# 08 - Section II Diagnostic Criteria and Codes

# 01 - Neurodevelopmental Disorders

# Neurodevelopmental Disorders

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Neurodevelopmental Disorders
The neurodevelopmental disorders are a group of conditions with onset in the
developmental period. The disorders typically manifest early in development, often before the
child enters school, and are characterized by developmental deficits or differences in brain
processes that produce impairments of personal, social, academic, or occupational functioning.
The range of developmental deficits or differences varies from very specific limitations of
learning or control of executive functions to global impairments of social skills or intellectual
ability. Once thought to be categorically defined, more recent dimensional approaches to
measurement of the symptoms demonstrate a range of severity, often without a very clear
boundary with typical development. Diagnosis of a disorder thus requires the presence of both
symptoms and impaired function.
The neurodevelopmental disorders frequently co-occur with one another; for example,
individuals with autism spectrum disorder often have intellectual developmental disorder
(intellectual disability), and many children with attention-deficit/hyperactivity disorder (ADHD)
also have a specific learning disorder. The neurodevelopmental disorders also frequently cooccur with other mental and behavioral disorders with onset in childhood (e.g., communication
disorders and autism spectrum disorder may be associated with anxiety disorders; ADHD with
oppositional 
defiant disorder; 
tics 
with 
obsessive-compulsive disorder). 
For some
neurodevelopmental disorders, the clinical presentation includes behaviors that are more frequent
or intense when compared with those of normal children of the same developmental age and
gender, as well as deficits and delays in achieving expected milestones. For example, autism
spectrum disorder is diagnosed only when the characteristic deficits of social communication are
accompanied by excessively repetitive behaviors, restricted interests, and insistence on
sameness.
Intellectual developmental disorder is characterized by deficits in general mental abilities,
such as reasoning, problem solving, planning, abstract thinking, judgment, academic learning,
and learning from experience. The deficits result in impairments of adaptive functioning, such
that the individual fails to meet standards of personal independence and social responsibility in
one or more aspects of daily life, including communication, social participation, academic or
occupational functioning, and personal independence at home or in community settings. Global
developmental delay, as its name implies, is diagnosed when an individual fails to meet expected
developmental milestones in several areas of intellectual functioning. The diagnosis is used for
individuals younger than 5 years who are unable to undergo systematic assessments of
intellectual functioning, and thus the clinical severity level cannot be reliably assessed.
Intellectual developmental disorder may result from an acquired insult during the developmental
period from, for example, a severe head injury, in which case a neurocognitive disorder also may
be diagnosed.
The communication disorders include language disorder, speech sound disorder, social

(pragmatic) communication disorder, and childhood-onset fluency disorder (stuttering). The first
three disorders are characterized by deficits in the development and use of language, speech, and
social communication, respectively. Social communication disorder is characterized by deficits
in both verbal and nonverbal communication skills that result in
social impairment and are not better explained by low abilities in structural language,
intellectual developmental disorder, or autism spectrum disorder. Childhood-onset fluency
disorder is characterized by disturbances of the normal fluency and motor production of speech,
including repetitive sounds or syllables, prolongation of consonants or vowel sounds, broken
words, blocking, or words produced with an excess of physical tension. Like other
neurodevelopmental disorders, communication disorders begin early in life and may produce
lifelong functional impairments.
Autism spectrum disorder is characterized by persistent deficits in social communication and
social interaction across multiple contexts, including deficits in social reciprocity, nonverbal
communicative behaviors used for social interaction, and skills in developing, maintaining, and
understanding relationships. In addition to the social communication deficits, the diagnosis of
autism spectrum disorder requires the presence of restricted, repetitive patterns of behavior,
interests, or activities. Because symptoms change with development and may be masked by
compensatory mechanisms, the diagnostic criteria may be met based on historical information,
although the current presentation must cause significant impairment.
Within the diagnosis of autism spectrum disorder, individual clinical characteristics are noted
through the use of specifiers (with or without accompanying intellectual impairment; with or
without accompanying structural language impairment; associated with a known genetic or other
medical condition or environmental factor; associated with a neurodevelopmental, mental, or
behavioral problem), as well as specifiers that describe the severity of autistic symptoms. These
specifiers provide clinicians with an opportunity to individualize the diagnosis and communicate
a richer clinical description of the affected individuals. For example, many individuals
previously diagnosed with Asperger’s disorder would now receive a diagnosis of autism
spectrum disorder without language or intellectual impairment.
ADHD is a neurodevelopmental disorder defined by impairing levels of inattention,
disorganization, and/or hyperactivity-impulsivity. Inattention and disorganization entail inability
to stay on task, seeming not to listen, and losing materials necessary for tasks, at levels that are
inconsistent with age or developmental level. Hyperactivity-impulsivity entails overactivity,
fidgeting, inability to stay seated, intruding into other people’s activities, and inability to wait—
symptoms that are excessive for age or developmental level. In childhood, ADHD frequently
overlaps with disorders that are often considered to be “externalizing disorders,” such as
oppositional defiant disorder and conduct disorder. ADHD often persists into adulthood, with
resultant impairments of social, academic, and occupational functioning.
Specific learning disorder, as the name implies, is diagnosed when there are specific deficits
in an individual’s ability to perceive or process information for learning academic skills
efficiently and accurately. This neurodevelopmental disorder first manifests during the years of
formal schooling and is characterized by persistent and impairing difficulties with learning
foundational academic skills in reading, writing, and/or math. The individual’s performance of

the affected academic skills is well below average for age, or acceptable performance levels are
achieved only with extraordinary effort. Specific learning disorder may occur in individuals
identified as intellectually gifted and manifest only when the learning demands or assessment
procedures (e.g., timed tests) pose barriers that cannot be overcome by their innate intelligence
and compensatory strategies. For all individuals, specific learning disorder can produce lifelong
impairments in activities dependent on the skills, including occupational performance.
The neurodevelopmental motor disorders include developmental coordination disorder,
stereotypic movement disorder, and tic disorders. Developmental coordination disorder is
characterized by deficits in the acquisition and execution of coordinated motor skills and is
manifested by clumsiness and slowness or inaccuracy of performance of
motor skills that cause interference with activities of daily living. Stereotypic movement
disorder is diagnosed when an individual has repetitive, seemingly driven, and apparently
purposeless motor behaviors, such as hand flapping, body rocking, head banging, self-biting, or
hitting. The movements interfere with social, academic, or other activities. If the behaviors cause
self-injury, this should be specified as part of the diagnostic description. Tic disorders are
characterized by the presence of motor or vocal tics, which are sudden, rapid, recurrent,
nonrhythmic, stereotyped motor movements or vocalizations. The duration, presumed etiology,
and clinical presentation define the specific tic disorder that is diagnosed: Tourette’s disorder,
persistent (chronic) motor or vocal tic disorder, provisional tic disorder, other specified tic
disorder, and unspecified tic disorder. Tourette’s disorder is diagnosed when the individual has
multiple motor and vocal tics that have been present for at least 1 year and that have a waxingwaning symptom course.
The use of specifiers for the neurodevelopmental disorder diagnoses enriches the clinical
description of the individual’s clinical course and current symptomatology. These include the
following: Severity specifiers are available for intellectual developmental disorder, autism
spectrum disorder, ADHD, specific learning disorder, and stereotypic movement disorder.
Specifiers indicative of current symptomatology are available for ADHD, specific learning
disorder, and persistent motor or vocal tic disorder. Autism spectrum disorder and stereotypic
movement disorder also include the specifier “associated with a known genetic or other medical
condition or environmental factor.” This specifier gives clinicians an opportunity to document
factors that may have played a role in the etiology of the disorder, as well as those that might
affect the clinical course.
Intellectual Developmental Disorders
Intellectual Developmental Disorder (Intellectual
Disability)

Diagnostic Criteria
Intellectual developmental disorder (intellectual disability) is a disorder with onset
during the developmental period that includes both intellectual and adaptive
functioning deficits in conceptual, social, and practical domains. The following three
criteria must be met:
A. Deficits in intellectual functions, such as reasoning, problem solving, planning,
abstract thinking, judgment, academic learning, and learning from experience,
confirmed by both clinical assessment and individualized, standardized
intelligence testing.
B. Deficits in adaptive functioning that result in failure to meet developmental and
sociocultural standards for personal independence and social responsibility.
Without ongoing support, the adaptive deficits limit functioning in one or more
activities of daily life, such as communication, social participation, and
independent living, across multiple environments, such as home, school, work,
and community.
C. Onset of intellectual and adaptive deficits during the developmental period.
Note: The term intellectual developmental disorder is used to clarify its relationship
with the WHO ICD-11 classification system, which uses the term Disorders of
Intellectual Development. The equivalent term intellectual disability is placed in
parentheses for continued use. The medical and research literature use both terms,
while intellectual disability is the term in common use by educational and other
professions, advocacy groups, and the lay public. In the United States, Public Law
111-256 (Rosa’s Law) changed all references to “mental retardation” in federal laws
to “intellectual disability.”
Specify current severity (see Table 1):
F70 Mild
F71 Moderate
F72 Severe
F73 Profound
TABLE 1 Severity levels for intellectual developmental disorder (intellectual
disability)
Severity
level
Conceptual domain
Social domain
Practical domain
Mild
For preschool children, there may be
Compared with typically developing
The individual may function age-

no obvious conceptual differences.
For school-age children and adults,
there are difficulties in learning
academic skills involving reading,
writing, arithmetic, time, or
money, with support needed in one
or more areas to meet age-related
expectations. In adults, abstract
thinking, executive function (i.e.,
planning, strategizing, priority
setting, and cognitive flexibility),
and short-term memory, as well as
functional use of academic skills
(e.g., reading, money
management), are impaired. There
is a somewhat concrete approach
to problems and solutions
compared with age-mates.
All through development, the
individual’s conceptual skills lag
markedly behind those of peers.
For preschoolers, language and
preacademic skills develop slowly.
For school-age children, progress
in reading, writing, mathematics,
and understanding of time and
money occurs slowly across the
school years and is markedly
limited compared with that of
peers. For adults, academic skill
development is typically at an
elementary level, and support is
required for all use of academic
skills in work and personal life.
Ongoing assistance on a daily
basis is needed to complete
conceptual tasks of day-to-day life,
and others may take over these
responsibilities fully for the
individual.
Moderate
Severe
Attainment of conceptual skills is
limited. The individual generally
has little understanding of written
language or of concepts involving
numbers, quantity, time, and
age-mates, the individual is
immature in social interactions.
For example, there may be
difficulty in accurately perceiving
peers’ social cues.
Communication, conversation, and
language are more concrete or
immature than expected for age.
There may be difficulties
regulating emotion and behavior in
age-appropriate fashion; these
difficulties are noticed by peers in
social situations. There is limited
understanding of risk in social
situations; social judgment is
immature for age, and the person
is at risk of being manipulated by
others (gullibility).
appropriately in personal care.
Individuals need some support
with complex daily living tasks in
comparison to peers. In adulthood,
supports typically involve grocery
shopping, transportation, home
and child-care organizing,
nutritious food preparation, and
banking and money management.
Recreational skills resemble those
of age-mates, although judgment
related to well-being and
organization around recreation
requires support. In adulthood,
competitive employment is often
seen in jobs that do not emphasize
conceptual skills. Individuals
generally need support to make
health care decisions and legal
decisions, and to learn to perform
a skilled vocation competently.
Support is typically needed to raise
a family.
The individual shows marked
The individual can care for personal
differences from peers in social
and communicative behavior
across development. Spoken
language is typically a primary
tool for social communication but
is much less complex than that of
peers. Capacity for relationships is
evident in ties to family and
friends, and the individual may
have successful friendships across
life and sometimes romantic
relations in adulthood. However,
individuals may not perceive or
interpret social cues accurately.
Social judgment and decisionmaking abilities are limited, and
caretakers must assist the person
with life decisions. Friendships
with typically developing peers are
often affected by communication
or social limitations. Significant
social and communicative support
is needed in work settings for
success.
needs involving eating, dressing,
elimination, and hygiene as an
adult, although an extended period
of teaching and time is needed for
the individual to become
independent in these areas, and
reminders may be needed.
Similarly, participation in all
household tasks can be achieved
by adulthood, although an
extended period of teaching is
needed, and ongoing supports will
typically occur for adult-level
performance. Independent
employment in jobs that require
limited conceptual and
communication skills can be
achieved, but considerable support
from coworkers, supervisors, and
others is needed to manage social
expectations, job complexities, and
ancillary responsibilities such as
scheduling, transportation, health
benefits, and money management.
A variety of recreational skills can
be developed. These typically
require additional supports and
learning opportunities over an
extended period of time.
Maladaptive behavior is present in
a significant minority and causes
social problems.
Spoken language is quite limited in
The individual requires support for
terms of vocabulary and grammar.
Speech may be single words or
phrases and may be supplemented
through augmentative means.
all activities of daily living,
including meals, dressing, bathing,
and elimination. The individual
requires supervision at all times.

money. Caretakers provide
extensive supports for problem
solving throughout life.
Speech and communication are
focused on the here and now
within everyday events. Language
is used for social communication
more than for explication.
Individuals understand simple
speech and gestural
communication. Relationships
with family members and familiar
others are a source of pleasure and
help.
The individual cannot make
responsible decisions regarding
well-being of self or others. In
adulthood, participation in tasks at
home, recreation, and work
requires ongoing support and
assistance. Skill acquisition in all
domains involves long-term
teaching and ongoing support.
Maladaptive behavior, including
self-injury, is present in a
significant minority.
Profound
Conceptual skills generally involve
the physical world rather than
symbolic processes. The individual
may use objects in goal-directed
fashion for self-care, work, and
recreation. Certain visuospatial
skills, such as matching and
sorting based on physical
characteristics, may be acquired.
However, co-occurring motor and
sensory impairments may prevent
functional use of objects.
The individual has very limited
understanding of symbolic
communication in speech or
gesture. He or she may understand
some simple instructions or
gestures. The individual expresses
his or her own desires and
emotions largely through
nonverbal, nonsymbolic
communication. The individual
enjoys relationships with wellknown family members,
caretakers, and familiar others, and
initiates and responds to social
interactions through gestural and
emotional cues. Co-occurring
sensory and physical impairments
may prevent many social
activities.
The individual is dependent on others
for all aspects of daily physical
care, health, and safety, although
he or she may be able to
participate in some of these
activities as well. Individuals
without severe physical
impairments may assist with some
daily work tasks at home, like
carrying dishes to the table. Simple
actions with objects may be the
basis of participation in some
vocational activities with high
levels of ongoing support.
Recreational activities may
involve, for example, enjoyment in
listening to music, watching
movies, going out for walks, or
participating in water activities, all
with the support of others. Cooccurring physical and sensory
impairments are frequent barriers
to participation (beyond watching)
in home, recreational, and
vocational activities. Maladaptive
behavior is present in a significant
minority.
Specifiers
The various levels of severity are defined on the basis of adaptive functioning, and not IQ scores,
because it is adaptive functioning that determines the level of supports required. Moreover, IQ
measures are less valid in the lower end of the IQ range.
Diagnostic Features
The essential features of intellectual developmental disorder (intellectual disability) are deficits
in general mental abilities (Criterion A) and impairment in everyday adaptive functioning, in
comparison to an individual’s age-, gender-, and socioculturally matched peers (Criterion B).
Onset is during the developmental period (Criterion C). The diagnosis of intellectual
developmental disorder is based on both clinical assessment and standardized testing of
intellectual functions, standardized neuropsychological tests, and standardized tests of adaptive
functioning.
Criterion A refers to intellectual functions that involve reasoning, problem solving, planning,
abstract thinking, judgment, learning from instruction and experience, and practical
understanding. Critical components include verbal comprehension, working memory, perceptual

reasoning, quantitative reasoning, abstract thought, and cognitive efficacy. Intellectual
functioning is typically measured with individually administered and psychometrically valid,
comprehensive, and culturally appropriate tests of intelligence. Individuals with intellectual
developmental disorder have scores of approximately two standard deviations or more below the
population mean, including a margin for measurement error (generally ± 5 points). On tests with
a standard deviation of 15 and a mean of 100, this involves a score of 65–75 (70 ± 5). Clinical
training and judgment are required to interpret test results and assess intellectual performance.
Factors that may affect test scores include practice effects (i.e., learning from repeated
testing) and the “Flynn effect” (i.e., overly high scores due to out-of-date test norms). Invalid
scores may result from the use of brief intelligence screening tests or group tests; highly
discrepant individual subtest scores may make an overall IQ score invalid. Instruments must be
normed for the individual’s sociocultural background and native language. Co-occurring
disorders that affect communication, language, and/or motor or sensory function may affect test
scores. Individual cognitive profiles based on neuropsychological testing as well as cross-battery
intellectual assessment (using multiple IQ or other cognitive tests to create a profile) are more
useful for understanding intellectual abilities than a single IQ score.
Such testing may identify areas of relative strengths and weaknesses, an assessment
important for academic and vocational planning. IQ test scores are approximations of conceptual
functioning but may be insufficient to assess reasoning in real-life situations and mastery of
practical tasks. For example, a person with deficits in intellectual functioning whose IQ score is
somewhat above 65–75 may nevertheless have such substantial adaptive behavior problems in
social judgment or other areas of adaptive functioning that the person’s actual functioning is
clinically comparable to that of individuals with a lower IQ score. Thus, clinical judgment is
important in interpreting the results of IQ tests, and using them as the sole criteria for the
diagnosis of an intellectual developmental disorder is insufficient.
Deficits in adaptive functioning (Criterion B) refer to how well a person meets community
standards of personal independence and social responsibility, in comparison to others of similar
age and sociocultural background. Adaptive functioning involves adaptive reasoning in three
domains: conceptual, social, and practical. The conceptual (academic) domain involves
competence in memory, language, reading, writing, math reasoning, acquisition of practical
knowledge, problem solving, and judgment in novel situations, among others. The social domain
involves awareness of others’ thoughts, feelings, and experiences; empathy; interpersonal
communication skills; friendship abilities; and social judgment, among others. The practical
domain involves learning and self-management across life settings, including personal care, job
responsibilities, money management, recreation, self-management of behavior, and school and
work task organization, among others. Intellectual capacity, education, motivation, socialization,
personality features, vocational opportunity, cultural experience, and coexisting other medical
conditions or mental disorders influence adaptive functioning.
Adaptive functioning is assessed using both clinical evaluation and individualized, culturally
appropriate, psychometrically sound measures. Standardized measures are used with
knowledgeable informants (e.g., parent or other family member; teacher; counselor; care
provider) and the individual to the extent possible. Additional sources of information include

educational, developmental, medical, and mental health evaluations. Scores from standardized
measures and interview sources must be interpreted using clinical judgment. When standardized
testing is difficult or impossible, because of a variety of factors (e.g., sensory impairment, severe
problem behavior), the individual may be diagnosed with unspecified intellectual developmental
disorder. Adaptive functioning may be difficult to assess in a controlled setting (e.g., prisons,
detention centers); if possible, corroborative information reflecting functioning outside those
settings should be obtained.
Criterion B is met when at least one domain of adaptive functioning—conceptual, social, or
practical—is sufficiently impaired that ongoing support is needed in order for the person to
perform adequately across multiple environments, such as home, school, work, and community.
Criterion C, onset during the developmental period, refers to recognition that intellectual and
adaptive deficits are present during childhood or adolescence.
A comprehensive evaluation includes an assessment of intellectual capacity and adaptive
functioning; identification of genetic and nongenetic etiologies; evaluation for associated
medical conditions (e.g., cerebral palsy, seizure disorder); and evaluation for co-occurring
mental, emotional, and behavioral disorders. Components of the evaluation may include basic
pre- and perinatal medical history, three-generational family pedigree, physical examination,
genetic evaluation (e.g., karyotype or chromosomal microarray analysis and testing for specific
genetic syndromes), and metabolic screening and neuroimaging assessment.
Associated Features
Intellectual developmental disorder is a heterogeneous condition with multiple causes. There
may be associated difficulties with social judgment; assessment of risk; self-management of
behavior, emotions, or interpersonal relationships; or motivation in school or
work environments. Because of a lack of awareness of risk and danger, accidental injury rates
may be increased. Lack of communication skills may predispose to disruptive and aggressive
behaviors. Gullibility is often a feature, involving naiveté in social situations and a tendency for
being easily led by others. Gullibility and lack of awareness of risk may result in exploitation by
others and possible victimization, fraud, unintentional criminal involvement, false confessions,
and risk for physical and sexual abuse. These associated features can be important in criminal
cases, including Atkins-type hearings involving the death penalty.
Beyond deficits in adaptive functioning, individuals also can become distressed about their
intellectual limitations. While such distress may not always be seen as having an impact on
functioning, distress can represent an important feature of the clinical scenario.
Prevalence
Intellectual developmental disorder has an overall general population prevalence of
approximately 10 per 1,000; however, the global prevalence varies by country and level of
development, being approximately 16 per 1,000 in middle-income countries and 9 per 1,000 in
high-income countries. The prevalence also varies by age, being higher in youth than in adults.
In the United States, prevalence per 1,000 population does not vary significantly by ethnoracial
groups.

Development and Course
Onset of intellectual developmental disorder is in the developmental period. The age and
characteristic features at onset depend on the etiology and severity of brain dysfunction. Delayed
motor, language, and social milestones may be identifiable within the first 2 years of life among
those with more severe intellectual developmental disorder, while mild levels may not be
identifiable until school age when difficulty with academic learning becomes apparent. All
criteria (including Criterion C) must be fulfilled by history or current presentation. Some
children younger than 5 years whose presentation will eventually meet criteria for intellectual
developmental disorder have deficits that meet criteria for global developmental delay.
When intellectual developmental disorder is associated with a genetic syndrome, there may
be a characteristic physical appearance (e.g., as in Down syndrome). Some syndromes have a
behavioral phenotype, which refers to specific behaviors that are characteristic of particular
genetic disorder (e.g., Lesch-Nyhan syndrome). In acquired forms, the onset may be abrupt
following an illness such as meningitis or encephalitis or head trauma occurring during the
developmental period. When intellectual developmental disorder results from a loss of
previously acquired cognitive skills, as in severe traumatic brain injury, the diagnoses of
intellectual developmental disorder and of a neurocognitive disorder may both be assigned.
Although intellectual developmental disorder is generally nonprogressive, in certain genetic
disorders (e.g., Rett syndrome) there are periods of worsening, followed by stabilization, and in
others (e.g., Sanfilippo syndrome, Down syndrome) progressive worsening of intellectual
function in varying degrees. In some cases, the progressive worsening of intellectual functioning
may represent the overlay of neurocognitive disorder that develops in adulthood (i.e., persons
with Down syndrome being at high risk for developing neurocognitive disorder due to
Alzheimer’s disease in adulthood). In this situation, both diagnoses, intellectual developmental
disorder and neurocognitive disorder, are given.
The disorder is generally lifelong, although severity levels may change over time. The course
may be influenced by underlying medical or genetic conditions and co-occurring conditions
(e.g., hearing or visual impairments, epilepsy). Early and ongoing interventions may improve
adaptive functioning throughout childhood and adulthood. In some cases, these result in
significant improvement of intellectual functioning, such that the
diagnosis of intellectual developmental disorder is no longer appropriate. Thus, it is common
practice when assessing infants and young children to delay diagnosis of intellectual
developmental disorder until after an appropriate course of intervention is provided. For older
children and adults, the extent of support provided may allow for full participation in all
activities of daily living and improved adaptive function. Diagnostic assessments must determine
whether improved adaptive skills are the result of a stable, generalized new skill acquisition (in
which case the diagnosis of intellectual developmental disorder may no longer be appropriate) or
whether the improvement is contingent on the presence of supports and ongoing interventions (in
which case the diagnosis of intellectual developmental disorder may still be appropriate).
Risk and Prognostic Factors

Genetic and physiological. Prenatal etiologies include genetic syndromes (e.g., sequence variations
or copy number variants involving one or more genes; chromosomal disorders), inborn errors of
metabolism, brain malformations, maternal disease (including placental disease), and
environmental influences (e.g., alcohol, other drugs, toxins, teratogens). Perinatal causes include
a variety of labor and delivery–related events leading to neonatal encephalopathy. Postnatal
causes include hypoxic ischemic injury, traumatic brain injury, infections, demyelinating
disorders, seizure disorders (e.g., infantile spasms), severe and chronic social deprivation, and
toxic metabolic syndromes and intoxications (e.g., lead, mercury).
Culture-Related Diagnostic Issues
Intellectual developmental disorder occurs across ethnoracial groups. Prevalence differences
across social and cultural contexts may be due to variation in environmental risks (e.g., perinatal
injury, chronic social deprivation) for the disorder that are associated with socioeconomic status
and access to quality health care. For example, in Western Australia, the population prevalence
of intellectual developmental disorder among Aboriginal children is 39 per 1,000 people, as
opposed to 16 per 1,000 for the more affluent non-Aboriginal youth population. Cultural
sensitivity and knowledge of sociostructural conditions are needed during assessment, and the
individual’s socioeconomic, ethnic, cultural, and linguistic background; available experiences;
and adaptive functioning within his or her community and cultural setting must be considered.
Cultural explanations for intellectual developmental disorder vary and may include cultural
beliefs about supernatural influences and punishment for presumed or actual wrongdoing by the
mother or parents, which can be associated with shame and underreporting of the disorder.
Sex- and Gender-Related Diagnostic Issues
Overall, males are more likely than females to be diagnosed with both mild (average male:female
ratio 1.6:1) and severe (average male:female ratio 1.2:1) forms of intellectual developmental
disorder. However, sex ratios vary widely in reported studies. Sex-linked genetic factors, sex
differences in other genetic factors such as specific copy number variants, and male vulnerability
to brain insult may account for some of the sex differences.
Association With Suicidal Thoughts or Behavior
Individuals with intellectual developmental disorder can be at risk for suicide associated with
comorbid mental disorder, higher intellectual and adaptive function, and immediate past
stressors. Comorbid mental disorder may manifest atypically in intellectual developmental
disorder; thus, recognizing comorbidity and screening for suicidal thoughts is important in the
assessment process, with particular attention to change in behavior of the individual.
Differential Diagnosis
The diagnosis of intellectual developmental disorder should be made whenever Criteria A, B,
and C are met. A diagnosis of intellectual developmental disorder should not be assumed
because of a particular genetic or medical condition. A genetic syndrome linked to intellectual
developmental disorder should be noted as a concurrent diagnosis with the intellectual

Major and mild neurocognitive disorders.
Communication disorders and specific learning disorder.
Autism spectrum disorder.
developmental disorder.
Intellectual developmental disorder is categorized as a
neurodevelopmental disorder and is distinct from the neurocognitive disorders, which are
characterized by a loss of cognitive functioning. Major neurocognitive disorder may co-occur
with intellectual developmental disorder (e.g., an individual with Down syndrome who develops
Alzheimer’s disease, or an individual with intellectual developmental disorder who loses further
cognitive capacity following a head injury). In such cases, the diagnoses of intellectual
developmental disorder and neurocognitive disorder may both be given. Moreover, when there is
stabilization of cognitive functioning following traumatic or nontraumatic brain injury with onset
in the developmental period (childhood and adolescence), and there is no continuing cognitive
decline, both neurocognitive disorder and intellectual developmental disorder diagnoses can be
used if diagnostic criteria are met for intellectual developmental disorder.
These neurodevelopmental disorders are
specific to the communication and learning domains and do not show deficits in intellectual and
adaptive behavior. They may co-occur with intellectual developmental disorder. Both diagnoses
are made if full criteria are met for intellectual developmental disorder and a communication
disorder or specific learning disorder.
Intellectual developmental disorder is common among individuals with
autism spectrum disorder. Assessment of intellectual ability may be complicated by socialcommunication and behavior deficits inherent to autism spectrum disorder, which may interfere
with understanding and complying with test procedures. Appropriate assessment of intellectual
functioning in autism spectrum disorder is essential, with reassessment across the developmental
period, because IQ scores in autism spectrum disorder may be unstable, particularly in early
childhood.
Comorbidity
Co-occurring neurodevelopmental and other mental and medical conditions are frequent in
intellectual developmental disorder, with rates of some conditions (e.g., mental disorders,
cerebral palsy, and epilepsy) three to four times higher than in the general population. The
prognosis and outcome of co-occurring diagnoses may be influenced by the presence of
intellectual developmental disorder. Assessment procedures may require modifications because
of associated disorders, including communication disorders, autism spectrum disorder, and
motor, sensory, or other disorders. Knowledgeable informants are essential for identifying
symptoms such as irritability, mood dysregulation, aggression, eating problems, and sleep
problems, and for assessing adaptive functioning in various community settings.
The most common co-occurring neurodevelopmental and other mental disorders are
attention-deficit/hyperactivity disorder; depressive and bipolar disorders; anxiety disorders;
autism spectrum disorder; stereotypic movement disorder (with or without self-injurious
behavior); impulse-control disorders; and major neurocognitive disorder. Major depressive
disorder may occur throughout the range of severity of intellectual developmental disorder. Selfinjurious behavior requires prompt diagnostic attention and may warrant a separate diagnosis of
stereotypic movement disorder. Individuals with intellectual developmental disorder, particularly
those with more severe intellectual developmental disorder, may also exhibit aggression and
disruptive behaviors, including harm of others or property destruction.

46
Individuals with intellectual developmental disorder disproportionately have more health
problems, including obesity, than the general population. Frequently they cannot verbalize
physical symptoms they are experiencing. This may lead to health problems being undiagnosed
and untreated.
Relationship to Other Classifications
ICD-11 uses the term disorders of intellectual development to indicate that these are disorders
that involve impaired brain functioning early in life. These disorders are described in ICD-11 as
a metasyndrome occurring in the developmental period analogous to dementia or major
neurocognitive disorder in later life. There are four subtypes of disorders of intellectual
development in ICD-11: mild, moderate, severe, and profound.
The American Association on Intellectual and Developmental Disabilities (AAIDD) uses the
term intellectual disability. The AAIDD’s classification is multidimensional rather than
categorical and is based on the disability construct. Rather than listing severity specifiers as is
done in DSM-5, the AAIDD emphasizes a profile of supports based on severity.
Global Developmental Delay
F88
This diagnosis is reserved for individuals under the age of 5 years when the clinical
severity level cannot be reliably assessed during early childhood. This category is
diagnosed when an individual fails to meet expected developmental milestones in
several areas of intellectual functioning, and applies to individuals who are unable to
undergo systematic assessments of intellectual functioning, including children who
are too young to participate in standardized testing. This category requires
reassessment after a period of time.
Unspecified Intellectual Developmental Disorder
(Intellectual Disability)
F79
This category is reserved for individuals over the age of 5 years when assessment of
the degree of intellectual developmental disorder (intellectual disability) by means of
locally available procedures is rendered difficult or impossible because of associated
sensory or physical impairments, as in blindness or prelingual deafness; locomotor
disability; or presence of severe problem behaviors or co-occurring mental disorder.
This category should only be used in exceptional circumstances and requires
reassessment after a period of time.

F80.2
Communication Disorders
Disorders of communication include deficits in language, speech, and communication. Speech is
the expressive production of sounds and includes an individual’s articulation, fluency, voice, and
resonance quality. Language includes the form, function, and use of a conventional system of
symbols (i.e., spoken words, sign language, written words, pictures) in a
rule-governed manner for communication. Communication includes any verbal or nonverbal
behavior (whether intentional or unintentional) that has the potential to influence the behavior,
ideas, or attitudes of another individual. Assessments of speech, language, and communication
abilities must take into account the individual's cultural and language context, particularly for
individuals growing up in bilingual environments. The standardized measures of language
development and of nonverbal intellectual capacity must be relevant for the cultural and
linguistic group (i.e., tests developed and standardized for one group may not provide
appropriate norms for a different group). The diagnostic category of communication disorders
includes the following: language disorder, speech sound disorder, childhood-onset fluency
disorder (stuttering), social (pragmatic) communication disorder, and unspecified communication
disorders Sex differences in the development of early communication may give rise to higher
prevalence rates of communication disorders in boys compared with girls. Given the associated
features of communication disorders and the relationship of communication to other
developmental domains, communication disorders have high rates of comorbidity with other
neurodevelopmental disorders (e.g., autism spectrum disorder, attention-deficit/hyperactivity
disorder (ADHD), specific learning disorder, intellectual developmental disorder [intellectual
disability]), mental disorders (e.g., anxiety disorders), and some medical conditions (e.g., seizure
disorders, specific chromosome abnormalities).
Language Disorder
Diagnostic Criteria
A. Persistent difficulties in the acquisition and use of language across modalities
(i.e., spoken, written, sign language, or other) due to deficits in comprehension
or production that include the following:
1. Reduced vocabulary (word knowledge and use).
2. Limited sentence structure (ability to put words and word endings together to
form sentences based on the rules of grammar and morphology).
3. Impairments in discourse (ability to use vocabulary and connect sentences to
explain or describe a topic or series of events or have a conversation).

B. Language abilities are substantially and quantifiably below those expected for
age, resulting in functional limitations in effective communication, social
participation, academic achievement, or occupational performance, individually
or in any combination.
C. Onset of symptoms is in the early developmental period.
D. The difficulties are not attributable to hearing or other sensory impairment, motor
dysfunction, or another medical or neurological condition and are not better
explained by intellectual developmental disorder (intellectual disability) or global
developmental delay.
Diagnostic Features
The essential features of language disorder are difficulties in the acquisition and use of language
due to deficits in the comprehension or production of vocabulary, grammar, sentence structure,
and discourse. The language deficits are evident in spoken communication, written
communication, or sign language. Language learning and use is dependent on both receptive and
expressive skills. Expressive ability refers to the production of vocal, gestural, or verbal signals,
while receptive ability refers to the process of receiving and comprehending language messages.
Language skills need to be assessed in both expressive and receptive modalities as these may
differ in severity.
Language disorder usually affects vocabulary and grammar, and these effects then limit the
capacity for discourse. The child’s first words and phrases are likely to be delayed
in onset; vocabulary size is smaller and less varied than expected; and sentences are shorter
and less complex with grammatical errors, especially in past tense. Deficits in comprehension of
language are frequently underestimated, as children may be good at using context to infer
meaning. There may be word-finding problems, impoverished verbal definitions, or poor
understanding of synonyms, multiple meanings, or word play appropriate for age and culture.
Problems with remembering new words and sentences are manifested by difficulties following
instructions of increasing length, difficulties rehearsing strings of verbal information (e.g.,
remembering a phone number or a shopping list), and difficulties remembering novel sound
sequences, a skill that may be important for learning new words. Difficulties with discourse are
shown by a reduced ability to provide adequate information about the key events and to narrate a
coherent story.
The language difficulty is manifest by abilities substantially and quantifiably below that
expected for age and significantly interfering with academic achievement, occupational
performance, effective communication, or socialization (Criterion B). A diagnosis of language
disorder is made based on the synthesis of the individual’s history, direct clinical observation in
different contexts (i.e., home, school, or work), and scores from standardized tests of language
ability that can be used to guide estimates of severity.
Associated Features

Environmental.
Genetic and physiological.
Normal variations in language.
Individuals, even children, can be adept at accommodating to their limited language. They may
appear to be shy or reticent to talk. Affected individuals may prefer to communicate only with
family members or other familiar individuals. Although these social indicators are not diagnostic
of a language disorder, if they are notable and persistent, they warrant referral for a full language
assessment.
Development and Course
Language acquisition is marked by changes from onset in toddlerhood to the adult level of
competency that appears during adolescence. Changes appear across the dimensions of language
(sounds, words, grammar, narratives/expository texts, and conversational skills) in age-graded
increments and synchronies. Language disorder emerges during the early developmental period;
however, there is considerable variation in early vocabulary acquisition and early word
combinations. Individual differences in early childhood are not, as single indicators, highly
predictive of later outcomes, although a late onset of language at age 24 months in a populationbased sample was the best predictor of outcomes at age 7 years. By age 4 years, individual
differences in language ability are more stable, with better measurement accuracy, and are highly
predictive of later outcomes. Language disorder diagnosed in children age 4 years and older is
likely to be stable over time and typically persists into adulthood, although the particular profile
of language strengths and deficits is likely to change over the course of development.
Language disorders can have social consequences across the lifespan. Children with language
disorders are at risk for peer victimization. For females with childhood language disorders, there
could be almost three times the risk compared with unaffected children for sexual assault in
adulthood.
Risk and Prognostic Factors
Children with receptive language impairments have a poorer prognosis than those with
predominantly expressive impairments. Receptive language impairments are more resistant to
treatment, and difficulties with reading comprehension are frequently seen.
Bilingualism does not cause or worsen a language disorder, but children who are
bilingual may demonstrate delays or differences in language development. A
language disorder in bilingual children will affect both languages; therefore, assessment across
both languages is important to consider.
Language disorders are highly heritable, and family members are more
likely to have a history of language impairment. Population-based twin studies consistently
report substantial heritability for language disorder, and molecular studies suggest multiple genes
interacting on causal pathways.
Differential Diagnosis
Language disorder needs to be distinguished from normal
developmental variations, and this distinction may be difficult to make before age 4 years.
Regional, social, or cultural/ethnic variations of language (e.g., dialects) must be considered

Hearing or other sensory impairment.
Intellectual developmental disorder (intellectual disability).
Autism spectrum disorder.
Neurological disorders.
Language regression.
F80.0
when an individual is being assessed for language impairment.
Hearing impairment needs to be excluded as the primary
cause of language difficulties. Language deficits may be associated with a hearing impairment,
other sensory deficit, or a speech-motor deficit. When language deficits are in excess of those
usually associated with these problems, a diagnosis of language disorder may be made.
Language 
impairment 
is 
often 
the
presenting feature of intellectual developmental disorder. However, the definitive diagnosis of
intellectual developmental disorder may not be made until the child is able to complete
standardized assessments. Language disorder can occur with varying degrees of intellectual
ability, and a discrepancy between verbal and nonverbal ability is not necessary for a diagnosis
of language disorder.
Autism spectrum disorder frequently manifests with delayed language
development. However, autism spectrum disorder is often accompanied by behaviors not present
in language disorder, such as lack of social interest or unusual social interactions (e.g., pulling
individuals by the hand without any attempt to look at them), odd play patterns (e.g., carrying
toys around but never playing with them), unusual communication patterns (e.g., knowing the
alphabet but not responding to own name), and rigid adherence to routines and repetitive
behaviors (e.g., flapping, spinning, echolalia).
Language disorder can be acquired in association with neurological
disorders, including epilepsy (e.g., acquired aphasia or Landau-Kleffner syndrome).
Loss of speech and language in a child at any age warrants thorough
assessment to determine if there is a specific neurological condition, such as Landau-Kleffner
syndrome. Language loss may be a symptom of seizures, and a diagnostic assessment is
necessary to exclude the presence of epilepsy (e.g., routine and sleep electroencephalogram).
Declines in critical social and communication behaviors during the first 2 years of life are
evident in most children presenting with autism spectrum disorder and should signal the need for
autism spectrum disorder assessment.
Comorbidity
Language disorder may be associated with other neurodevelopmental disorders in terms of
specific learning disorder (literacy and numeracy), intellectual developmental disorder, attentiondeficit/hyperactivity disorder, autism spectrum disorder, and developmental coordination
disorder. It is also associated with social (pragmatic) communication disorder. In clinical
samples, language disorder may co-occur with speech sound disorder, although data from a large
population-based sample of 6-year-old children in the United States suggest comorbidity might
be rare (1.3%). A positive family history of speech or language disorders is often present.
Speech Sound Disorder
Diagnostic Criteria

A. Persistent difficulty with speech sound production that interferes with speech
intelligibility or prevents verbal communication of messages.
B. The disturbance causes limitations in effective communication that interfere with
social participation, academic achievement, or occupational performance,
individually or in any combination.
C. Onset of symptoms is in the early developmental period.
D. The difficulties are not attributable to congenital or acquired conditions, such as
cerebral palsy, cleft palate, deafness or hearing loss, traumatic brain injury, or
other medical or neurological conditions.
Diagnostic Features
Speech sound production describes the clear articulation of the phonemes (i.e., individual
sounds) that in combination make up spoken words. Speech sound production requires both the
phonological knowledge of speech sounds and the ability to coordinate the movements of the
articulators (i.e., the jaw, tongue, and lips,) with breathing and vocalizing for speech. Children
with speech production difficulties may experience difficulty with phonological knowledge of
speech sounds or the ability to coordinate movements for speech in varying degrees. A speech
sound disorder is diagnosed when speech sound production is not what would be expected based
on the child’s age and developmental stage and when the deficits are not the result of a physical,
structural, neurological, or hearing impairment. Among typically developing children at age 3
years, overall speech should be intelligible, whereas at age 2 years, only 50% may be
understandable. Boys are more likely (range of 1.5–1.8 to 1.0) to have a speech sound disorder
than girls.
Associated Features
Language disorder may be found to co-occur with speech sound disorder, although cooccurrences are rare by age 6 years. A positive family history of speech or language disorders is
often present.
If the ability to rapidly coordinate the articulators is a particular aspect of difficulty, there
may be a history of delay or incoordination in acquiring skills that also utilize the articulators and
related facial musculature; among others, these skills include chewing, maintaining mouth
closure, and blowing the nose. Other areas of motor coordination may be impaired as in
developmental coordination disorder. The terms childhood apraxia of speech and verbal
dyspraxia are used for speech production problems with motor components.
Development and Course
Learning to produce speech sounds clearly and accurately and learning to produce connected
speech fluently are developmental skills. Articulation of speech sounds follows a developmental
pattern, which is reflected in the age norms of standardized tests. It is not unusual for typically
developing children to use developmental processes for shortening words and syllables as they
are learning to talk, but their progression in mastering speech sound production should result in
mostly intelligible speech by age 3 years. Children with speech sound disorder continue to use

Normal variations in speech.
Hearing or other sensory impairment.
Structural deficits.
Dysarthria.
Selective mutism.
immature phonological simplification processes past the age when most children can produce
words clearly.
Most speech sounds should be produced clearly and most words should be pronounced
accurately according to age and community norms by age 5 years. The most
frequently misarticulated sounds in English also tend to be learned later, leading them to be
called the “late eight” (l, r, s, z, th, ch, dzh, and zh). Misarticulation of any of these sounds by
itself could be considered within normal limits up to age 8 years; however, when multiple sounds
are involved, it is important to target some of those sounds as part of a plan to improve
intelligibility, rather than waiting until the age at which almost all children can produce them
accurately. Lisping (i.e., misarticulating sibilants) is particularly common and may involve
frontal or lateral patterns of airstream direction. It may be associated with a tongue-thrust
swallowing pattern.
Most children with speech sound disorder respond well to treatment, and speech difficulties
improve over time, and thus the disorder may not be lifelong. However, when a language
disorder is also present, the speech disorder has a poorer prognosis and may be associated with
specific learning disorder.
Differential Diagnosis
Regional, social, or cultural/ethnic variations of speech should be
considered before making the diagnosis. Bilingual children may demonstrate an overall lower
intelligibility rating, make more overall consonant and vowel errors, and produce more
uncommon error patterns than monolingual English-speaking children when assessed only in
English.
Those who are deaf or hard of hearing may have speech
sound production errors. When speech deficits are in excess of those usually associated with
these problems, a diagnosis of speech sound disorder may be made.
Speech impairment may be due to structural deficits (e.g., cleft palate).
Speech impairment may be attributable to a motor disorder, such as cerebral palsy.
Neurological signs, as well as distinctive features of voice, differentiate dysarthria from speech
sound disorder, although in young children (under 3 years) differentiation may be difficult,
particularly when there is no or minimal general body motor involvement (as in, e.g., WorsterDrought syndrome).
Limited use of speech may be a sign of selective mutism, an anxiety disorder
that is characterized by a lack of speech in one or more contexts or settings. Selective mutism
may develop in children with a speech disorder because of embarrassment about their
impairments, but many children with selective mutism exhibit normal speech in “safe” settings,
such as at home or with close friends.
Comorbidity
Speech may be differentially impaired in certain genetic conditions (e.g., Down syndrome, 22q
deletion, FoxP2 gene mutation). If present, these should also be coded.

F80.81
Childhood-Onset Fluency Disorder (Stuttering)
Diagnostic Criteria
A. Disturbances in the normal fluency and time patterning of speech that are
inappropriate for the individual’s age and language skills, persist over time, and
are characterized by frequent and marked occurrences of one (or more) of the
following:
1. Sound and syllable repetitions.
2. Sound prolongations of consonants as well as vowels.
3. Broken words (e.g., pauses within a word).
4. Audible or silent blocking (filled or unfilled pauses in speech).
5. Circumlocutions (word substitutions to avoid problematic words).
6. Words produced with an excess of physical tension.
7. Monosyllabic whole-word repetitions (e.g., “I-I-I-I see him”).
B. The disturbance causes anxiety about speaking or limitations in effective
communication, social participation, or academic or occupational performance,
individually or in any combination.
C. The onset of symptoms is in the early developmental period. (Note: Later-onset
cases are diagnosed as F98.5 adult-onset fluency disorder.)
D. The disturbance is not attributable to a speech-motor or sensory deficit,
dysfluency associated with neurological insult (e.g., stroke, tumor, trauma), or
another medical condition and is not better explained by another mental
disorder.
Diagnostic Features
The essential feature of childhood-onset fluency disorder (stuttering) is a disturbance in the
normal fluency and time patterning of speech that is inappropriate for the individual’s age. This
disturbance is characterized by frequent repetitions or prolongations of sounds or syllables and
by other types of speech dysfluencies, including broken words (e.g., pauses within a word),
audible or silent blocking (i.e., filled or unfilled pauses in speech), circumlocutions (i.e., word
substitutions to avoid problematic words), words produced with an excess of physical tension,
and monosyllabic whole-word repetitions (e.g., “I-I-I-I see him”). The disturbance in fluency
may interfere with academic or occupational achievement and with social communication. The
extent of the disturbance varies from situation to situation and often is more severe when there is
special pressure to communicate (e.g., giving a report at school, interviewing for a job).
Dysfluency is often absent during oral reading, singing, or talking to inanimate objects or to pets.

Genetic and physiological.
Associated Features
Fearful anticipation of the problem may develop. The speaker may attempt to avoid dysfluencies
by linguistic mechanisms (e.g., altering the rate of speech, avoiding certain words or sounds) or
by avoiding certain speech situations, such as telephoning or public speaking. In addition to
being features of the condition, stress and anxiety have been shown to exacerbate dysfluency.
Childhood-onset fluency disorder may also be accompanied by motor movements (e.g., eye
blinks, tics, tremors of the lips or face, jerking of the head, breathing movements, fist clenching).
Children with fluency disorder show a range of language abilities, and the relationship between
fluency disorder and language abilities is unclear.
Studies have shown both structural and functional neurological differences in children who
stutter. Males are more likely to stutter than females, with estimates varying depending on the
age and possible cause of stuttering. Causes of stuttering are multifactorial, including certain
genetic and neurophysiological factors.
Development and Course
Childhood-onset fluency disorder, or developmental stuttering, occurs by age 6 for 80%–90% of
affected individuals, with age at onset ranging from 2 to 7 years. The onset can be insidious or
more sudden. Typically, dysfluencies start gradually, with repetition of initial consonants, first
words of a phrase, or long words. The child may not be aware of dysfluencies. As the disorder
progresses, the dysfluencies become more frequent and interfering, occurring on the most
meaningful words or phrases in the utterance. As the child becomes aware of the speech
difficulty, he or she may develop mechanisms for avoiding the
dysfluencies and emotional responses, including avoidance of public speaking and use of short
and simple utterances. Longitudinal research shows that 65%–85% of children recover from the
dysfluency, with severity of fluency disorder at age 8 years predicting recovery or persistence
into adolescence and beyond.
Risk and Prognostic Factors
The risk of stuttering among first-degree biological relatives of
individuals with childhood-onset fluency disorder is more than three times the risk in the general
population. To date, mutations of four genes that underlie some cases of stuttering have been
identified.
Functional Consequences of Childhood-Onset Fluency Disorder
(Stuttering)
In addition to being features of the condition, stress and anxiety can exacerbate dysfluency.
Impairment of social functioning may result from this anxiety. Negative communication attitudes
may be a functional consequence of stuttering starting in the preschool years and increasing with
age.
Differential Diagnosis

Sensory deficits.
Normal speech dysfluencies.
Specific learning disorder, with impairment in reading.
Bilingualism.
Medication side effects.
Adult-onset dysfluencies.
Tourette’s disorder.
F80.82
Dysfluencies of speech may be associated with a hearing impairment or other
sensory deficit or a speech-motor deficit. When the speech dysfluencies are in excess of those
usually associated with these problems, a diagnosis of childhood-onset fluency disorder may be
made.
The disorder must be distinguished from normal dysfluencies that
occur frequently in young children, which include whole-word or phrase repetitions (e.g., “I
want, I want ice cream”), incomplete phrases, interjections, unfilled pauses, and parenthetical
remarks. If these difficulties increase in frequency or complexity as the child grows older, a
diagnosis of childhood-onset fluency disorder may be appropriate.
Children who have dysfluencies when they
read aloud may be diagnosed mistakenly as having a reading disorder. Oral reading fluency
typically is measured by timed assessments. Slower reading rates may not accurately reflect the
actual reading ability of children who stutter.
It is necessary to distinguish between dysfluencies resulting from attempts to learn
a new language and dysfluencies that indicate a fluency disorder, which typically appear in both
languages.
Stuttering may occur as a side effect of medication and may be detected
by a temporal relationship with exposure to the medication.
If onset of dysfluencies is during or after adolescence, it is an “adultonset dysfluency” rather than a neurodevelopmental disorder. Adult-onset dysfluencies are
associated with specific neurological insults and a variety of medical conditions and mental
disorders and may be specified with them, but they are not a DSM-5 diagnosis.
Vocal tics and repetitive vocalizations of Tourette’s disorder should be
distinguishable from the repetitive sounds of childhood-onset fluency disorder by their nature
and timing.
Comorbidity
Childhood-onset fluency disorder can co-occur with other disorders, such as attentiondeficit/hyperactivity disorder, autism spectrum disorder, intellectual developmental
disorder (intellectual disability), language disorder or specific learning disorder, seizure
disorders, social anxiety disorder, speech sound disorder, and other developmental disorders.
Social (Pragmatic) Communication Disorder
Diagnostic Criteria
A. Persistent difficulties in the social use of verbal and nonverbal communication as
manifested by all of the following:

1. Deficits in using communication for social purposes, such as greeting and
sharing information, in a manner that is appropriate for the social context.
2. Impairment of the ability to change communication to match context or the
needs of the listener, such as speaking differently in a classroom than on a
playground, talking differently to a child than to an adult, and avoiding use of
overly formal language.
3. Difficulties following rules for conversation and storytelling, such as taking
turns in conversation, rephrasing when misunderstood, and knowing how to
use verbal and nonverbal signals to regulate interaction.
4. Difficulties understanding what is not explicitly stated (e.g., making
inferences) and nonliteral or ambiguous meanings of language (e.g., idioms,
humor, metaphors, multiple meanings that depend on the context for
interpretation).
B. The deficits result in functional limitations in effective communication, social
participation, social relationships, academic achievement, or occupational
performance, individually or in combination.
C. The onset of the symptoms is in the early developmental period (but deficits may
not become fully manifest until social communication demands exceed limited
capacities).
D. The symptoms are not attributable to another medical or neurological condition
or to low abilities in the domains of word structure and grammar, and are not
better explained by autism spectrum disorder, intellectual developmental
disorder (intellectual disability), global developmental delay, or another mental
disorder.
Diagnostic Features
Social (pragmatic) communication disorder is characterized by a primary difficulty with
pragmatics (i.e., the social use of language and communication), as manifested by deficits in
understanding and following social rules of both verbal and nonverbal communication in
naturalistic contexts, changing language according to the needs of the listener or situation, and
following rules for conversations and storytelling. The deficits in social communication result in
functional limitations in effective communication, social participation, development of social
relationships, academic achievement, or occupational performance. The deficits are not better
explained by low abilities in the domains of structural language or cognitive ability or by autism
spectrum disorder.
Associated Features
The most common associated feature of social (pragmatic) communication disorder is language
impairment, which is characterized by a history of delay in reaching language milestones, and
historical, if not current, structural language problems (see “Language Disorder” earlier in this
chapter). Individuals with social communication deficits may

Genetic and physiological.
Autism spectrum disorder.
Attention-deficit/hyperactivity disorder.
avoid social interactions. Attention-deficit/hyperactivity disorder (ADHD), emotional and
behavioral problems, and specific learning disorders are also more common among affected
individuals.
Development and Course
Because social (pragmatic) communication depends on adequate developmental progress in
speech and language, diagnosis of social (pragmatic) communication disorder is rare among
children younger than 4 years. By age 4 or 5 years, most children should possess adequate
speech and language abilities to permit identification of specific deficits in social
communication. Milder forms of the disorder may not become apparent until early adolescence,
when language and social interactions become more complex.
The outcome of social (pragmatic) communication disorder is variable, with some children
improving substantially over time and others continuing to have difficulties persisting into
adulthood. Even among those who have significant improvements, the early deficits in
pragmatics may cause lasting impairments in social relationships and behavior and also low
performance of other related skills, such as written expression, reading comprehension, and oral
reading.
Risk and Prognostic Factors
A family history of autism spectrum disorder, communication
disorders, or specific learning disorder appears to increase the risk for social (pragmatic)
communication disorder; this includes siblings of children with these disorders who may present
with early symptoms of social (pragmatic) communication disorder.
Differential Diagnosis
Autism spectrum disorder is the primary diagnostic consideration for
individuals presenting with social communication deficits. The two disorders can be
differentiated by the presence in autism spectrum disorder of restricted/repetitive patterns of
behavior, interests, or activities and their absence in social (pragmatic) communication disorder.
Individuals with autism spectrum disorder may only display the restricted/repetitive patterns of
behavior, interests, and activities during the early developmental period, so a comprehensive
history should be obtained. Current absence of symptoms would not preclude a diagnosis of
autism spectrum disorder, if the restricted interests and repetitive behaviors were present in the
past. A diagnosis of social (pragmatic) communication disorder should be considered only if the
current symptoms or developmental history fails to reveal evidence of symptoms that meet the
diagnostic criteria for restricted/repetitive patterns of behavior, interests, or activities of autism
spectrum disorder (i.e., Criterion B) causing current impairment. The social communication
symptoms may be milder in social (pragmatic) communication disorder than in autism spectrum
disorder, although qualitatively similar.
Primary deficits of ADHD may cause impairments in social
communication and functional limitations of effective communication, social participation, or
academic achievement.

Social anxiety disorder.
Intellectual developmental disorder (intellectual disability) and global developmental delay.
F84.0
The symptoms of social (pragmatic) communication disorder overlap with
those of social anxiety disorder. The differentiating feature is the timing of the onset of
symptoms. In social (pragmatic) communication disorder, the individual has never had effective
social communication; in social anxiety disorder, the social communication skills developed
appropriately but are not utilized because of anxiety, fear, or distress about social interactions.
Social
communication skills may be deficient among individuals with global developmental delay or
intellectual developmental disorder, but a separate diagnosis is not given unless the social
communication deficits are clearly in excess of the intellectual limitations.
Unspecified Communication Disorder
F80.9
This category applies to presentations in which symptoms characteristic of
communication disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for communication disorder or for any of the disorders in the
neurodevelopmental disorders diagnostic class. The unspecified communication
disorder category is used in situations in which the clinician chooses not to specify
the reason that the criteria are not met for communication disorder or for a specific
neurodevelopmental disorder, and includes presentations in which there is
insufficient information to make a more specific diagnosis.
Autism Spectrum Disorder
Autism Spectrum Disorder
Diagnostic Criteria
A. Persistent deficits in social communication and social interaction across multiple
contexts, as manifested by all of the following, currently or by history (examples
are illustrative, not exhaustive; see text):
1. Deficits in social-emotional reciprocity, ranging, for example, from abnormal
social approach and failure of normal back-and-forth conversation; to reduced
sharing of interests, emotions, or affect; to failure to initiate or respond to

social interactions.
2. Deficits in nonverbal communicative behaviors used for social interaction,
ranging, for example, from poorly integrated verbal and nonverbal
communication; to abnormalities in eye contact and body language or deficits
in understanding and use of gestures; to a total lack of facial expressions and
nonverbal communication.
3. Deficits in developing, maintaining, and understanding relationships, ranging,
for example, from difficulties adjusting behavior to suit various social contexts;
to difficulties in sharing imaginative play or in making friends; to absence of
interest in peers.
B. Restricted, repetitive patterns of behavior, interests, or activities, as manifested
by at least two of the following, currently or by history (examples are illustrative,
not exhaustive; see text):
1. Stereotyped or repetitive motor movements, use of objects, or speech (e.g.,
simple motor stereotypies, lining up toys or flipping objects, echolalia,
idiosyncratic phrases).
2. Insistence on sameness, inflexible adherence to routines, or ritualized
patterns of verbal or nonverbal behavior (e.g., extreme distress at small
changes, difficulties with transitions, rigid thinking patterns, greeting rituals,
need to take same route or eat same food every day).
3. Highly restricted, fixated interests that are abnormal in intensity or focus (e.g.,
strong attachment to or preoccupation with unusual objects, excessively
circumscribed or perseverative interests).
4. Hyper- or hyporeactivity to sensory input or unusual interest in sensory
aspects of the environment (e.g., apparent indifference to pain/temperature,
adverse response to specific sounds or textures, excessive smelling or
touching of objects, visual fascination with lights or movement).
C. Symptoms must be present in the early developmental period (but may not
become fully manifest until social demands exceed limited capacities, or may be
masked by learned strategies in later life).
D. Symptoms cause clinically significant impairment in social, occupational, or other
important areas of current functioning.
E. These disturbances are not better explained by intellectual developmental
disorder (intellectual disability) or global developmental delay. Intellectual
developmental disorder and autism spectrum disorder frequently co-occur; to
make comorbid diagnoses of autism spectrum disorder and intellectual
developmental disorder, social communication should be below that expected for
general developmental level.
Note: Individuals with a well-established DSM-IV diagnosis of autistic disorder,
Asperger’s disorder, or pervasive developmental disorder not otherwise specified

should be given the diagnosis of autism spectrum disorder. Individuals who have
marked deficits in social communication, but whose symptoms do not otherwise
meet criteria for autism spectrum disorder, should be evaluated for social
(pragmatic) communication disorder.
Specify current severity based on social communication impairments and restricted,
repetitive patterns of behavior (see Table 2):
Requiring very substantial support
Requiring substantial support
Requiring support
Specify if:
With or without accompanying intellectual impairment
With or without accompanying language impairment
Specify if:
Associated with a known genetic or other medical condition or
environmental factor (Coding note: Use additional code to identify the
associated genetic or other medical condition.)
Associated with a neurodevelopmental, mental, or behavioral problem
Specify if:
With catatonia (refer to the criteria for catatonia associated with another mental
disorder, p. 135, for definition) (Coding note: Use additional code F06.1
catatonia associated with autism spectrum disorder to indicate the presence of
the comorbid catatonia.)
TABLE 2 Severity levels for autism spectrum disorder (examples of level of
support needs)
Severity level
Social communication
Restricted, repetitive behaviors
Level 3
“Requiring very substantial
support”
Severe deficits in verbal and nonverbal social
communication skills cause severe impairments
in functioning, very limited initiation of social
interactions, and minimal response to social
overtures from others. For example, a person
with few words of intelligible speech who rarely
initiates interaction and, when he or she does,
makes unusual approaches to meet needs only
and responds to only very direct social
approaches.
Inflexibility of behavior, extreme difficulty
coping with change, or other
restricted/repetitive behaviors markedly
interfere with functioning in all spheres.
Great distress/difficulty changing focus or
action.
Level 2
“Requiring substantial
support”
Marked deficits in verbal and nonverbal social
communication skills; social impairments
apparent even with supports in place; limited
initiation of social interactions; and reduced or
abnormal responses to social overtures from
others. For example, a person who speaks
simple sentences, whose interaction is limited to
narrow special interests, and who has markedly
Inflexibility of behavior, difficulty coping
with change, or other restricted/repetitive
behaviors appear frequently enough to be
obvious to the casual observer and
interfere with functioning in a variety of
contexts. Distress and/or difficulty
changing focus or action.

odd nonverbal communication.
Level 1
“Requiring support”
Without supports in place, deficits in social
communication cause noticeable impairments.
Difficulty initiating social interactions, and clear
examples of atypical or unsuccessful responses
to social overtures of others. May appear to
have decreased interest in social interactions.
For example, a person who is able to speak in
full sentences and engages in communication
but whose to-and-fro conversation with others
fails, and whose attempts to make friends are
odd and typically unsuccessful.
Inflexibility of behavior causes significant
interference with functioning in one or
more contexts. Difficulty switching
between activities. Problems of
organization and planning hamper
independence.
Recording Procedures
It may be helpful to note level of support needed for each of the two core psychopathological
domains in Table 2 (e.g., “requiring very substantial support for deficits in social communication
and requiring substantial support for restricted, repetitive behaviors”). Specification of “with
accompanying intellectual impairment” or “without accompanying
intellectual impairment” should be recorded next. Language impairment specification should be
recorded thereafter. If there is accompanying language impairment, the current level of verbal
functioning should be recorded (e.g., “with accompanying language impairment—no intelligible
speech” or “with accompanying language impairment—phrase speech”).
For autism spectrum disorder for which the specifiers “associated with a known genetic or
other medical condition or environmental factor” or “associated with a neurodevelopmental,
mental, or behavioral problem” are appropriate, record autism spectrum disorder associated with
(name of condition, disorder, or factor) (e.g., autism spectrum disorder associated with tuberous
sclerosis complex). These specifiers apply to presentations in which the listed condition or
problem is potentially relevant to the clinical care of the individual and do not necessarily
indicate that the condition or problem is causally related to the autism spectrum disorder. If the
associated neurodevelopmental, mental, or behavioral problem meets criteria for a
neurodevelopmental or other mental disorder, both autism spectrum disorder and the other
disorder should be diagnosed.
If catatonia is present, record separately “catatonia associated with autism spectrum
disorder.” For more information, see criteria for catatonia associated with another mental
disorder in the chapter “Schizophrenia Spectrum and Other Psychotic Disorders.”
Specifiers
The severity specifiers (see Table 2) may be used to describe succinctly the current
symptomatology (which might fall below level 1), with the recognition that severity may vary by
context and fluctuate over time. Severity of social communication difficulties and restricted,
repetitive behaviors should be separately rated. The descriptive severity categories should not be
used to determine eligibility for and provision of services. Indeed, individuals with relatively
better skills overall may experience different or even greater psychosocial challenges. Thus,
service needs can only be developed at an individual level and through discussion of personal
priorities and targets.

Regarding the specifier “with or without accompanying intellectual impairment,”
understanding the (often uneven) intellectual profile of a child or adult with autism spectrum
disorder is necessary for interpreting diagnostic features. Separate estimates of verbal and
nonverbal skill are necessary (e.g., using untimed nonverbal tests to assess potential strengths in
individuals with limited language).
To use the specifier “with or without accompanying language impairment,” the current level
of verbal functioning should be assessed and described. Examples of the specific descriptions for
“with accompanying language impairment” might include no intelligible speech (nonverbal),
single words only, or phrase speech. Language level in individuals “without accompanying
language impairment” might be further described as speaks in full sentences or has fluent speech.
Since receptive language may lag behind expressive language development in autism spectrum
disorder, receptive and expressive language skills should be considered separately.
The specifier “associated with a known genetic or other medical condition or environmental
factor” can be applied when an individual has a known genetic condition (e.g., Rett syndrome,
fragile X syndrome, Down syndrome), a known medical condition (e.g., epilepsy), or a history of
environmental exposure in utero to a known teratogen or infection (e.g., fetal valproate
syndrome, fetal alcohol syndrome, fetal rubella). This specifier should not be viewed as
synonymous with causation of autism spectrum disorder. A condition may be listed as being
associated with autism spectrum disorder when it is thought to be potentially clinically relevant
or inform care and not because the clinician is asserting a cause. Examples include autism
spectrum disorder associated with a unique genomic copy number variant that could be clinically
relevant even if the specific abnormality may not have directly caused nor have previously been
linked to autism spectrum disorder, or Crohn’s disease, which could exacerbate behavioral
symptoms.
The specifier “associated with a neurodevelopmental, mental, or behavioral problem” can be
applied to indicate problems (e.g., irritability, sleep problems, self-injurious behavior, or
developmental regression) that contribute to the functional formulation or are a focus of
treatment. Additional neurodevelopmental, mental, or behavioral disorders should also be noted
as separate diagnoses (e.g., attention-deficit/hyperactivity disorder; developmental coordination
disorder; disruptive behavior, impulse-control, and conduct disorders; anxiety, depressive, or
bipolar disorders; tics or Tourette’s disorder; feeding, elimination, or sleep disorders).
Catatonia can occur as a comorbid condition with autism spectrum disorder. In addition to
classic symptoms of posturing, negativism (opposition or no response to instructions or external
stimuli), mutism, and stupor, an increase or worsening of stereotypy and self-injurious behavior
may form part of the symptom complex of catatonia in the setting of autism spectrum disorder.
Diagnostic Features
The essential features of autism spectrum disorder are persistent impairment in reciprocal social
communication and social interaction (Criterion A), and restricted, repetitive patterns of
behavior, interests, or activities (Criterion B). These symptoms are present from early childhood
and limit or impair everyday functioning (Criteria C and D). The stage at which functional
impairment becomes obvious will vary according to characteristics of the individual and his or

her environment. Core diagnostic features are evident in the developmental period, but
intervention, compensation, and current supports may mask difficulties in at least some contexts.
Manifestations of the disorder also vary greatly depending on the severity of the autistic
condition, developmental level, chronological age, and possibly gender; hence, the term
spectrum. Individuals without cognitive or language impairment may have more subtle
manifestation of deficits (e.g., Criterion A, Criterion B) than individuals with accompanying
intellectual or language impairments and may be making great efforts to mask these deficits.
Criterion A deficits in social communication will be more subtle if an individual has better
overall communication skills (e.g., is verbally fluent, does not have intellectual impairments).
Similarly, Criterion B deficits (i.e., restricted patterns of behavior and interests) may be less
obvious if the interests are closer to age-typical norms (e.g., Ancient Egypt or trains as compared
to wiggling a string). Autism spectrum disorder encompasses disorders previously referred to as
early infantile autism, childhood autism, Kanner’s autism, high-functioning autism, atypical
autism, pervasive developmental disorder not otherwise specified, childhood disintegrative
disorder, and Asperger’s disorder.
The impairments in social communication and social interaction specified in Criterion A are
pervasive and sustained. Diagnoses are most valid and reliable when based on multiple sources
of information, including clinician’s observations, caregiver history, and, when possible, selfreport. Verbal and nonverbal deficits in social communication have varying manifestations,
depending on the individual’s age, intellectual level, and language ability, as well as other factors
such as treatment history and current support. Many individuals have language deficits, ranging
from complete lack of speech through language delays, poor comprehension of speech, echoed
speech, or stilted and overly literal language. Even when formal language skills (e.g.,
vocabulary, grammar) are intact, the use of language for reciprocal social communication is
impaired in autism spectrum disorder.
Deficits in social-emotional reciprocity (i.e., the ability to engage with others and share
thoughts and feelings) may be shown, for example, in young children with little or no initiation
of social interaction and no sharing of emotions, along with reduced or absent imitation of
others’ behavior. What language exists is often one-sided, lacking in social reciprocity, and used
to request or label rather than to comment, share feelings, or converse. In older children and
adults without intellectual impairments or language delays, deficits in
social-emotional reciprocity may be most apparent in difficulties processing and responding
to complex social cues (e.g., when and how to join a conversation, what not to say). Individuals
who have developed compensation strategies for some social challenges still struggle in novel or
unsupported situations and suffer from the effort and anxiety of consciously calculating what is
socially intuitive for most individuals. This behavior may contribute to lower ascertainment of
autism spectrum disorder in these individuals, perhaps especially in adult women. Thus, longer
assessments, observation in naturalistic settings, and inquiring about any tolls of social
interaction may be needed. If asked about the costs of social interaction, for example, these
individuals might respond that social interactions are exhausting for them, that they are unable to
concentrate because of the mental effort in monitoring social conventions, that their self-esteem
is adversely affected by being unable to be themselves, and so forth.

Deficits in nonverbal communicative behaviors used for social interaction are manifested by
absent, reduced, or atypical use of eye contact (relative to cultural norms), gestures, facial
expressions, body orientation, or speech intonation. An early feature of autism spectrum disorder
is impaired joint attention as manifested by a lack of pointing, showing, or bringing objects to
share interest with others, or failure to follow someone’s pointing or eye gaze. Individuals may
learn a few functional gestures, but their repertoire is smaller than that of others, and they often
fail to use expressive gestures spontaneously in communication. Among young people and adults
with fluent language, the difficulty in coordinating nonverbal communication with speech may
give the impression of odd, wooden, or exaggerated “body language” during interactions.
Impairment may be relatively subtle within individual modes (e.g., someone may have relatively
good eye contact when speaking) but noticeable in poor integration of eye contact, gesture, body
posture, prosody, and facial expression for social communication, or in difficulty maintaining
these for sustained periods or when under stress.
Deficits in developing, maintaining, and understanding relationships should be judged
against norms for age, gender, and culture. There may be absent, reduced, or atypical social
interest, manifested by rejection of others, passivity, or inappropriate approaches that seem
aggressive or disruptive. These difficulties are particularly evident in young children, in whom
there is often a lack of shared social play and imagination (e.g., age-appropriate flexible pretend
play) and, later, insistence on playing by very fixed rules. Older individuals may struggle to
understand what behavior is considered appropriate in one situation but not another (e.g., casual
behavior during a job interview), or the different ways that language may be used to
communicate (e.g., irony, white lies). There may be an apparent preference for solitary activities
or for interacting with much younger or older people. Frequently, there is a desire to establish
friendships without a complete or realistic idea of what friendship entails (e.g., one-sided
friendships or friendships based solely on shared special interests). Relationships with siblings,
coworkers, and caregivers are also important to consider (in terms of reciprocity).
Autism spectrum disorder is also defined by restricted, repetitive patterns of behavior,
interests, or activities (as specified in Criterion B), which show a range of manifestations
according to age and ability, intervention, and current supports. Stereotyped or repetitive
behaviors include simple motor stereotypies (e.g., hand flapping, finger flicking), repetitive use
of objects (e.g., spinning coins, lining up toys), and repetitive speech (e.g., echolalia, the delayed
or immediate parroting of heard words; use of “you” when referring to self; stereotyped use of
words, phrases, or prosodic patterns). Excessive adherence to routines and restricted patterns of
behavior may be manifest in resistance to change (e.g., distress at apparently small changes, such
as taking an alternative route to school or work; insistence on adherence to rules; rigidity of
thinking) or ritualized patterns of verbal or nonverbal behavior (e.g., repetitive questioning,
pacing a perimeter). Highly restricted, fixated interests in autism spectrum disorder tend to be
abnormal in intensity or focus (e.g., a toddler strongly attached to a pan or piece of string; a child
preoccupied with vacuum
cleaners; an adult spending hours writing out timetables). Some fascinations and routines
may relate to apparent hyper- or hyporeactivity to sensory input, manifested through extreme
responses to specific sounds or textures, excessive smelling or touching of objects, fascination

with lights or spinning objects, and sometimes apparent indifference to pain, heat, or cold.
Extreme reaction to or rituals involving taste, smell, texture, or appearance of food or excessive
food restrictions are common and may be a presenting feature of autism spectrum disorder.
Many individuals with autism spectrum disorder without intellectual or language
impairments learn to suppress repetitive behavior in public. In these individuals, repetitive
behaviors like rocking or finger flicking may serve an anxiolytic or self-soothing function.
Special interests may be a source of pleasure and motivation and provide avenues for
education and employment later in life. Diagnostic criteria may be met when restricted, repetitive
patterns of behavior, interests, or activities were clearly present during childhood or at some time
in the past, even if symptoms are no longer present.
Criterion D requires that the features must cause clinically significant impairment in social,
occupational, or other important areas of current functioning. Criterion E specifies that the social
communication deficits, although sometimes accompanied by intellectual developmental
disorder (intellectual disability), are not in line with the individual’s developmental level;
impairments exceed difficulties expected on the basis of developmental level.
Standardized behavioral diagnostic instruments with good psychometric properties, including
caregiver interviews, questionnaires and clinician observation measures, are available and can
improve reliability of diagnosis over time and across clinicians. However, the symptoms of
autism spectrum disorder occur as dimensions without universally accepted cutoff scores for
what would constitute a disorder. Thus, the diagnosis remains a clinical one, taking all available
information into account, and is not solely dictated by the score on a particular questionnaire or
observation measure.
Associated Features
Many individuals with autism spectrum disorder also have intellectual and/or language
impairment (e.g., slow to talk, language comprehension behind production). Even those with
average or high intelligence usually have an uneven profile of abilities. The gap between
intellectual and adaptive functional skills is often large. It is common for individuals with autism
to have theory-of-mind deficits (i.e., to have difficulty seeing the world from another person’s
perspective), but these are not necessarily present in all cases. Executive function deficits are
also common but not specific, as are difficulties with central coherence (i.e., being able to
understand context or to “see the big picture,” and thus tending to overfocus on detail).
Motor deficits are often present, including odd gait, clumsiness, and other abnormal motor
signs (e.g., walking on tiptoes). Self-injury (e.g., head banging, biting the wrist) may occur, and
disruptive/challenging behaviors are more common in children and adolescents with autism
spectrum disorder than other disorders, including intellectual developmental disorder. Some
individuals develop catatonic-like motor behavior (slowing and “freezing” mid-action), but these
are typically not of the magnitude of a catatonic episode. However, it is possible for individuals
with autism spectrum disorder to experience a marked deterioration in motor symptoms and
display a full catatonic episode with symptoms such as mutism, posturing, grimacing, and waxy
flexibility. The risk period for comorbid catatonia appears to be greatest in the adolescent years.
Prevalence
Frequencies for autism spectrum disorder across the United States have been reported to be

between 1% and 2% of the population, with similar estimates in child and adult
samples. However, prevalence appears to be lower among U.S. African American (1.1%) and
Latinx children (0.8%) compared with White children (1.3%), even after the effect of
socioeconomic resources is taken into account. The reported prevalence of autism spectrum
disorder may be affected by misdiagnosis, delayed diagnosis, or underdiagnosis of individuals
from some ethnoracial backgrounds. Prevalence across non-U.S. countries has approached 1% of
the population (0.62% median global prevalence), without substantial variation based on
geographic region or ethnicity and across child and adult samples. Globally, the male:female
ratio in well-ascertained epidemiological samples appears to be 3:1, with concerns about
underrecognition of autism spectrum disorder in women and girls.
Development and Course
The age and pattern of onset also should be noted for autism spectrum disorder. The behavioral
features of autism spectrum disorder first become evident in early childhood, with some cases
presenting a lack of interest in social interaction in the first year of life. Symptoms are typically
recognized during the second year of life (age 12–24 months) but may be seen earlier than 12
months if developmental delays are severe, or noted later than 24 months if symptoms are more
subtle. The pattern of onset description might include information about early developmental
delays or any losses of social or language skills. In cases where skills have been lost, parents or
caregivers may give a history of a gradual or relatively rapid deterioration in social behaviors or
language skills. Typically, this would occur between ages 12 and 24 months.
Prospective studies demonstrate that in most cases the onset of autism spectrum disorder is
associated with declines in critical social and communication behaviors in the first 2 years of life.
Such declines in functioning are rare in other neurodevelopmental disorders and may be an
especially useful indicator of the presence of autism spectrum disorder. In rare cases, there is
developmental regression occurring after at least 2 years of normal development (previously
described as childhood disintegrative disorder), which is much more unusual and warrants more
extensive medical investigation (i.e., continuous spike and waves during slow-wave sleep
syndrome and Landau-Kleffner syndrome). Often included in these encephalopathic conditions
are losses of skills beyond social communication (e.g., loss of self-care, toileting, motor skills)
(see also Rett syndrome in the section “Differential Diagnosis” for this disorder).
First symptoms of autism spectrum disorder frequently involve delayed language
development, often accompanied by lack of social interest or unusual social interactions (e.g.,
pulling individuals by the hand without any attempt to look at them), odd play patterns (e.g.,
carrying toys around but never playing with them), and unusual communication patterns (e.g.,
knowing the alphabet but not responding to own name). Deafness may be suspected but is
typically ruled out. During the second year, odd and repetitive behaviors and the absence of
typical play become more apparent. Since many typically developing young children have strong
preferences and enjoy repetition (e.g., eating the same foods, watching the same video multiple
times), distinguishing restricted and repetitive behaviors that are diagnostic of autism spectrum
disorder can be difficult in preschoolers. The clinical distinction is based on the type, frequency,
and intensity of the behavior (e.g., a child who daily lines up objects for hours and is very

distressed if any item is moved).
Autism spectrum disorder is not a degenerative disorder, and it is typical for learning and
compensation to continue throughout life. Symptoms are often most marked in early childhood
and early school years, with developmental gains typical in later childhood in at least some areas
(e.g., increased interest in social interaction). A small proportion of individuals deteriorate
behaviorally during adolescence, whereas most others improve. While it was once the case that
only a minority of individuals with autism spectrum disorder lived and worked independently in
adulthood, as diagnosis of autism spectrum
disorder is made more frequently in those who have superior language and intellectual
abilities, more individuals are able to find a niche that matches their special interests and skills
and thus are productively employed. Access to vocational rehabilitation services significantly
improves competitive employment outcomes for transition-age youth with autism spectrum
disorder.
In general, individuals with lower levels of impairment may be better able to function
independently. However, even these individuals may remain socially naive and vulnerable, have
difficulties organizing practical demands without aid, and are prone to anxiety and depression.
Many adults report using compensation strategies and coping mechanisms to mask their
difficulties in public but suffer from the stress and effort of maintaining a socially acceptable
facade. Relatively little is known about old age in autism spectrum disorder, but higher rates of
co-occurring medical conditions have been documented in the literature.
Some individuals come for first diagnosis in adulthood, perhaps prompted by the diagnosis of
autism in a child in the family or a breakdown of relations at work or home. Obtaining detailed
developmental history in such cases may be difficult, and it is important to consider self-reported
difficulties. Where clinical observation suggests criteria are currently met, autism spectrum
disorder may be diagnosed, particularly if supported by a history of poor social and
communication skills in childhood. A compelling report (by parents or another relative) that the
individual had ordinary and sustained reciprocal friendships and good nonverbal communication
skills throughout childhood would significantly lessen the likelihood of a diagnosis of autism
spectrum disorder; however, ambiguous or absent developmental information in itself is not
sufficient to rule out a diagnosis of autism spectrum disorder.
Manifestations of the social and communication impairments and restricted/repetitive
behaviors that define autism spectrum disorder are clear in the developmental period. In later
life, intervention or compensation, as well as current supports, may mask these difficulties in at
least some contexts. Overall, symptoms remain sufficient to cause current impairment in social,
occupational, or other important areas of functioning.
Risk and Prognostic Factors
The best established prognostic factors for individual outcome within autism spectrum disorder
are presence or absence of associated intellectual developmental disorder and language
impairment (e.g., functional language by age 5 years is a good prognostic sign) and additional
mental health problems. Epilepsy, as a comorbid diagnosis, is associated with greater intellectual
disability and lower verbal ability.

Environmental.
Genetic and physiological.
A variety of risk factors for neurodevelopmental disorders, such as advanced
parental age, extreme prematurity, or in utero exposures to certain drugs or teratogens like
valproic acid, may broadly contribute to risk of autism spectrum disorder.
Heritability estimates for autism spectrum disorder have ranged from
37% to higher than 90%, based on twin concordance rates, and a more recent five-country cohort
estimated heritability at 80%. Currently, as many as 15% of cases of autism spectrum disorder
appear to be associated with a known genetic mutation, with different de novo copy number
variants or de novo mutations in specific genes associated with the disorder in different families.
However, even when a known genetic mutation is associated with autism spectrum disorder, it
does not appear to be fully penetrant (i.e., not all individuals with that same genetic abnormality
will develop autism spectrum disorder). Risk for the majority of cases appears to be polygenic,
with perhaps hundreds of genetic loci making relatively small contributions. Whether these
findings apply to all racial/ethnic populations equally is unclear, given the limited inclusion of
communities of color in genetic research.
Culture-Related Diagnostic Issues
Cultural differences exist in norms for social interaction, nonverbal communication, and
relationships, but individuals with autism spectrum disorder are markedly impaired against the
norms for their cultural context. Culture influences the perception of autistic behaviors, the
perceived salience of some behaviors over others, and the expectations for child behavior and
parenting practices. Considerable discrepancies are found in age at diagnosis of autism spectrum
disorder in children from diverse ethnoracial backgrounds; most studies find delayed diagnosis
among socially oppressed ethnic and racialized children. In addition to being diagnosed later,
African American children are more often misdiagnosed with adjustment or conduct disorder
than are White children.
Sex- and Gender-Related Diagnostic Issues
Autism spectrum disorder is diagnosed three to four times more often in males than in females,
and on average, age at diagnosis is later in females. In clinic samples, females tend to be more
likely to show accompanying intellectual developmental disorder as well as epilepsy, suggesting
that girls without intellectual impairments or language delays may go unrecognized, perhaps
because of subtler manifestation of social and communication difficulties. In comparison with
males with autism spectrum disorder, females may have better reciprocal conversation, and be
more likely to share interests, to integrate verbal and nonverbal behavior, and to modify their
behavior by situation, despite having similar social understanding difficulties as males.
Attempting to hide or mask autistic behavior (e.g., by copying the dress, voice, and manner of
socially successful women) may also make diagnosis harder in some females. Repetitive
behaviors may be somewhat less evident in females than in males, on average, and special
interests may have a more social (e.g., a singer, an actor) or “normative” focus (e.g., horses),
while remaining unusual in their intensity. Relative to the general population, rates of gender
variance have been reported to be increased in autism spectrum disorder, with higher variance in
females compared with males.

Attention-deficit/hyperactivity disorder.
Intellectual developmental disorder (intellectual disability) without autism spectrum disorder.
Association With Suicidal Thoughts or Behavior
Individuals with autism spectrum disorder are at greater risk for suicide death compared with
those without autism spectrum disorder. Children with autism spectrum disorder who had
impaired social communication had a higher risk of self-harm with suicidal intent, suicidal
thoughts, and suicide plans by age 16 years as compared with those without impaired social
communication. Adolescents and young adults with autism spectrum disorder have an increased
risk of suicide attempts compared with age- and sex-matched control subjects, even after
adjustments for demographic factors and psychiatric comorbidities.
Functional Consequences of Autism Spectrum Disorder
In young children with autism spectrum disorder, lack of social and communication abilities may
hamper learning, especially learning through social interaction or in settings with peers. In the
home, insistence on routines and aversion to change, as well as sensory sensitivities, may
interfere with eating and sleeping and make routine care (e.g., haircuts, dental work) extremely
difficult. Adaptive skills are typically below measured IQ. Extreme difficulties in planning,
organization, and coping with change negatively impact academic achievement, even for
students with above-average intelligence. During adulthood, these individuals may have
difficulties establishing independence because of continued rigidity and difficulty with novelty.
Many individuals with autism spectrum disorder, even without intellectual developmental
disorder, have poor adult psychosocial functioning as indexed by measures such
as independent living and gainful employment. Functional consequences in old age are
unknown, but social isolation and communication problems (e.g., reduced help-seeking) are
likely to have consequences for health in older adulthood.
Co-occurring intellectual developmental disorder, epilepsy, mental disorders, and chronic
medical conditions may be associated with a higher risk of premature mortality for individuals
with autism spectrum disorder. Deaths from injury and poisoning are higher than for the general
population, as are deaths from suicide. Drowning is the leading cause of accidental death in
children with autism spectrum disorder.
Differential Diagnosis
Abnormalities of attention (overly focused or easily
distracted) are common in individuals with autism spectrum disorder, as is hyperactivity.
Moreover, some individuals with ADHD may exhibit social communication deficits such as
interrupting others, speaking too loudly, and not respecting personal space. Although potentially
difficult to discriminate ADHD from autism spectrum disorder, the developmental course and
absence of restricted, repetitive behaviors and unusual interests in ADHD help in differentiating
the two conditions. A concurrent diagnosis of ADHD should be considered when attentional
difficulties or hyperactivity exceeds that typically seen in individuals of comparable mental age,
and ADHD is one of the most common comorbidities in autism spectrum disorder.
Intellectual
developmental disorder without autism spectrum disorder may be difficult to differentiate from

Language disorders and social (pragmatic) communication disorder.
Selective mutism.
Stereotypic movement disorder.
Rett syndrome.
Symptoms associated with anxiety disorders.
autism spectrum disorder in very young children. Individuals with intellectual developmental
disorder who have not developed language or symbolic skills also present a challenge for
differential diagnosis, since repetitive behavior often occurs in such individuals as well. A
diagnosis of autism spectrum disorder in an individual with intellectual developmental disorder
is appropriate when social communication and interaction are significantly impaired relative to
the developmental level of the individual’s nonverbal skills (e.g., fine motor skills, nonverbal
problem solving). In contrast, intellectual developmental disorder is the appropriate diagnosis
when there is no apparent discrepancy between the level of social communicative skills and other
intellectual skills.
In some forms of language
disorder, there may be problems of communication and some secondary social difficulties.
However, specific language disorder is not usually associated with abnormal nonverbal
communication, nor with the presence of restricted, repetitive patterns of behavior, interests, or
activities.
When an individual shows impairment in social communication and social interactions but
does not show restricted and repetitive behavior or interests, criteria for social (pragmatic)
communication disorder, instead of autism spectrum disorder, may be met. The diagnosis of
autism spectrum disorder supersedes that of social (pragmatic) communication disorder
whenever the criteria for autism spectrum disorder are met, and care should be taken to enquire
carefully regarding past or current restricted/repetitive behavior.
In selective mutism, early development is not typically disturbed. The affected
child usually exhibits appropriate communication skills in certain contexts and settings. Even in
settings where the child is mute, social reciprocity is not impaired, nor are restricted or repetitive
patterns of behavior present.
Motor stereotypies are among the diagnostic characteristics of
autism spectrum disorder, so an additional diagnosis of stereotypic movement disorder is not
given when such repetitive behaviors are better explained by the presence
of autism spectrum disorder. However, when stereotypies cause self-injury and become a focus
of treatment, both diagnoses may be appropriate.
Disruption of social interaction may be observed during the regressive phase of
Rett syndrome (typically between ages 1 and 4 years); thus, a substantial proportion of affected
young girls may have a presentation that meets diagnostic criteria for autism spectrum disorder.
However, after this period, most individuals with Rett syndrome improve their social
communication skills, and autistic features are no longer a major area of concern. Consequently,
autism spectrum disorder should be considered only when all diagnostic criteria are met.
The overlap of anxiety symptoms with the core
symptoms of autism spectrum disorder can make the classification of anxiety symptoms in
autism spectrum disorder challenging. For example, social withdrawal and repetitive behaviors
are core features of autism spectrum disorder but may also be expressions of anxiety. The most
common anxiety disorders in autism spectrum disorder are specific phobia (in up to 30% of
cases), and social anxiety and agoraphobia (in as many as 17% of cases).

Obsessive-compulsive disorder.
Schizophrenia.
Personality disorders.
Repetitive behavior is a defining feature of both obsessivecompulsive disorder and autism spectrum disorder. In both conditions, repetitive behaviors are
considered to be inappropriate or odd. In obsessive-compulsive disorder, intrusive thoughts are
often related to contamination, organization, or sexual or religious themes. Compulsions are
performed in response to these intrusive thoughts in attempts to relieve anxiety. In autism
spectrum disorder, repetitive behaviors classically include more stereotyped motor behaviors,
such as hand flapping and finger shaking or more complex behaviors, such as insistence on
routines or lining up objects. Contrary to obsessive-compulsive disorder, repetitive behaviors in
autism spectrum disorder may be perceived as pleasurable and reinforcing.
Schizophrenia with childhood onset usually develops after a period of normal, or
near normal, development. A prodromal state has been described in which social impairment and
atypical interests and beliefs occur, which could be confused with the social deficits and
restricted fixated interests seen in autism spectrum disorder. Hallucinations and delusions, which
are defining features of schizophrenia, are not features of autism spectrum disorder. However,
clinicians must take into account the potential for individuals with autism spectrum disorder to
be concrete in their interpretation of questions regarding the key features of schizophrenia (e.g.,
“Do you hear voices when no one is there?” ”Yes [on the radio]”). Autism spectrum disorder and
schizophrenia can co-occur, and both should be diagnosed when criteria are met.
In adults without intellectual developmental disorder or significant
language impairment, some behaviors associated with autism spectrum disorder may be
perceived by others as symptoms of narcissistic, schizotypal, or schizoid personality disorder.
Schizotypal personality disorder in particular may intersect with autism spectrum disorder in
unusual preoccupations and perceptual experiences, odd thinking and speech, constricted affect
and social anxiety, lack of close friends, and odd or eccentric behavior. The early developmental
course of autism spectrum disorder (lack of imaginative play, restricted/repetitive behavior,
sensory sensitivities) is most helpful in differentiating it from personality disorders.
Comorbidity
Autism spectrum disorder is frequently associated with intellectual developmental disorder and
language disorder (i.e., an inability to comprehend and construct sentences with proper
grammar). Specific learning difficulties (literacy and numeracy) are common, as is
developmental coordination disorder.
Psychiatric comorbidities also co-occur in autism spectrum disorder. About 70% of
individuals with autism spectrum disorder may have one comorbid mental disorder, and 40%
may have two or more comorbid mental disorders. Anxiety disorders, depression, and ADHD are
particularly common. Avoidant/restrictive food intake disorder is a fairly frequent presenting
feature of autism spectrum disorder, and extreme and narrow food preferences may persist.
Among individuals who are nonverbal or have language deficits, observable signs such as
changes in sleep or eating and increases in challenging behavior should trigger an evaluation for
anxiety or depression, as well as for potential pain or discomfort from undiagnosed medical or
dental problems. Medical conditions commonly associated with autism spectrum disorder

include epilepsy and constipation.
Attention-Deficit/Hyperactivity Disorder
Attention-Deficit/Hyperactivity Disorder
Diagnostic Criteria
A. A persistent pattern of inattention and/or hyperactivity-impulsivity that interferes
with functioning or development, as characterized by (1) and/or (2):
1. Inattention: Six (or more) of the following symptoms have persisted for at
least 6 months to a degree that is inconsistent with developmental level and
that negatively impacts directly on social and academic/occupational
activities:
Note: The symptoms are not solely a manifestation of oppositional behavior,
defiance, hostility, or failure to understand tasks or instructions. For older
adolescents and adults (age 17 and older), at least five symptoms are
required.
a. Often fails to give close attention to details or makes careless mistakes in
schoolwork, at work, or during other activities (e.g., overlooks or misses
details, work is inaccurate).
b. Often has difficulty sustaining attention in tasks or play activities (e.g., has
difficulty remaining focused during lectures, conversations, or lengthy
reading).
c. Often does not seem to listen when spoken to directly (e.g., mind seems
elsewhere, even in the absence of any obvious distraction).
d. Often does not follow through on instructions and fails to finish
schoolwork, chores, or duties in the workplace (e.g., starts tasks but
quickly loses focus and is easily sidetracked).
e. Often has difficulty organizing tasks and activities (e.g., difficulty managing
sequential tasks; difficulty keeping materials and belongings in order;
messy, disorganized work; has poor time management; fails to meet
deadlines).
f. Often avoids, dislikes, or is reluctant to engage in tasks that require
sustained mental effort (e.g., schoolwork or homework; for older
adolescents and adults, preparing reports, completing forms, reviewing
lengthy papers).
g. Often loses things necessary for tasks or activities (e.g., school materials,
pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile

telephones).
h. Is often easily distracted by extraneous stimuli (for older adolescents and
adults, may include unrelated thoughts).
i. Is often forgetful in daily activities (e.g., doing chores, running errands; for
older adolescents and adults, returning calls, paying bills, keeping
appointments).
2. Hyperactivity and impulsivity: Six (or more) of the following symptoms
have persisted for at least 6 months to a degree that is inconsistent with
developmental level and that negatively impacts directly on social and
academic/occupational activities:
Note: The symptoms are not solely a manifestation of oppositional behavior,
defiance, hostility, or a failure to understand tasks or instructions. For older
adolescents and adults (age 17 and older), at least five symptoms are
required.
a. Often fidgets with or taps hands or feet or squirms in seat.
b. Often leaves seat in situations when remaining seated is expected (e.g.,
leaves his or her place in the classroom, in the office or other workplace,
or in other situations that require remaining in place).
c. Often runs about or climbs in situations where it is inappropriate. (Note: In
adolescents or adults, may be limited to feeling restless.)
d. Often unable to play or engage in leisure activities quietly.
e. Is often “on the go,” acting as if “driven by a motor” (e.g., is unable to be or
uncomfortable being still for extended time, as in restaurants, meetings;
may be experienced by others as being restless or difficult to keep up
with).
f. Often talks excessively.
g. Often blurts out an answer before a question has been completed (e.g.,
completes people’s sentences; cannot wait for turn in conversation).
h. Often has difficulty waiting his or her turn (e.g., while waiting in line).
i. Often interrupts or intrudes on others (e.g., butts into conversations,
games, or activities; may start using other people’s things without asking
or receiving permission; for adolescents and adults, may intrude into or
take over what others are doing).
B. Several inattentive or hyperactive-impulsive symptoms were present prior to age
12 years.
C. Several inattentive or hyperactive-impulsive symptoms are present in two or
more settings (e.g., at home, school, or work; with friends or relatives; in other
activities).
D. There is clear evidence that the symptoms interfere with, or reduce the quality of,

social, academic, or occupational functioning.
E. The symptoms do not occur exclusively during the course of schizophrenia or
another psychotic disorder and are not better explained by another mental
disorder (e.g., mood disorder, anxiety disorder, dissociative disorder, personality
disorder, substance intoxication or withdrawal).
Specify whether:
F90.2 Combined presentation: If both Criterion A1 (inattention) and Criterion
A2 (hyperactivity-impulsivity) are met for the past 6 months.
F90.0 Predominantly inattentive presentation: If Criterion A1 (inattention) is
met but Criterion A2 (hyperactivity-impulsivity) is not met for the past 6 months.
F90.1 Predominantly hyperactive/impulsive presentation: If Criterion A2
(hyperactivity-impulsivity) is met and Criterion A1 (inattention) is not met for the
past 6 months.
Specify if:
In partial remission: When full criteria were previously met, fewer than the full
criteria have been met for the past 6 months, and the symptoms still result in
impairment in social, academic, or occupational functioning.
Specify current severity:
Mild: Few, if any, symptoms in excess of those required to make the diagnosis
are present, and symptoms result in no more than minor impairments in social or
occupational functioning.
Moderate: Symptoms or functional impairment between “mild” and “severe” are
present.
Severe: Many symptoms in excess of those required to make the diagnosis, or
several symptoms that are particularly severe, are present, or the symptoms
result in marked impairment in social or occupational functioning.
Diagnostic Features
The essential feature of attention-deficit/hyperactivity disorder (ADHD) is a persistent pattern of
inattention and/or hyperactivity-impulsivity that interferes with functioning or development.
Inattention manifests behaviorally in ADHD as wandering off task, failing to follow through on
instructions or finishing work or chores, having difficulty sustaining focus, and being
disorganized and is not attributable to defiance or lack of comprehension. Hyperactivity refers to
excessive motor activity (such as a child running about) when it is not appropriate, or excessive
fidgeting, tapping, or talkativeness. In adults, hyperactivity may manifest as extreme restlessness
or wearing others out with their activity. Impulsivity refers to hasty actions that occur in the
moment without forethought, which may have potential for harm to the individual (e.g., darting
into the street without looking). Impulsivity may reflect a desire for immediate rewards or an
inability to delay gratification. Impulsive behaviors may manifest as social intrusiveness (e.g.,

interrupting others excessively) and/or as making important decisions without consideration of
long-term consequences (e.g., taking a job without adequate information).
ADHD begins in childhood. The requirement that several symptoms be present before age 12
years conveys the importance of a substantial clinical presentation during childhood. At the same
time, an earlier age at onset is not specified because of difficulties in establishing precise
childhood onset retrospectively. Adult recall of childhood symptoms tends to be unreliable, and
it is beneficial to obtain ancillary information. ADHD cannot be diagnosed in the absence of any
symptoms prior to age 12. When symptoms of what appears to be ADHD first occur after age 13,
they are more likely to be explained by another mental disorder or to represent the cognitive
effects of substance use.
Manifestations of the disorder must be present in more than one setting (e.g., home and
school, or home and work). Confirmation of substantial symptoms across settings typically
cannot be done accurately without consulting informants who have seen the individual in those
settings. Typically, symptoms vary depending on context within a given setting. Signs of the
disorder may be minimal or absent when the individual is receiving frequent rewards for
appropriate behavior, is under close supervision, is in a novel setting, is engaged in especially
interesting activities, has consistent external stimulation (e.g., via electronic screens), or is
interacting in one-on-one situations (e.g., the clinician's office).
Associated Features
Delays in language, motor, or social development are not specific to ADHD but often co-occur.
Emotional dysregulation or emotional impulsivity commonly occurs in children and adults with
ADHD. Individuals with ADHD self-report and are described by others as being quick to anger,
easily frustrated, and overreactive emotionally.
Even in the absence of a specific learning disorder, academic or work performance is often
impaired. Individuals with ADHD may exhibit neurocognitive deficits in a variety of areas,
including working memory, set shifting, reaction time variability, response inhibition, vigilance,
and planning/organization, although these tests are not sufficiently sensitive or specific to serve
as diagnostic indices.
Although ADHD is not associated with specific physical features, rates of minor physical
anomalies (e.g., hypertelorism, highly arched palate, low-set ears) may be elevated. Subtle motor
delays and other neurological soft signs may occur. (Note that marked co-occurring clumsiness
and motor delays should be coded separately [e.g., developmental coordination disorder].)
Children with neurodevelopmental disorders with a known cause (e.g., fragile X syndrome,
22q11 
deletion 
syndrome) 
may 
often 
also 
have 
symptoms 
of 
inattention 
and
impulsivity/hyperactivity; they should receive an ADHD diagnosis if their symptoms meet the
full criteria for the disorder.
Prevalence
Population surveys suggest that ADHD occurs worldwide in about 7.2% of children; however,
cross-national prevalence ranges widely, from 0.1% to 10.2% of children and adolescents.
Prevalence is higher in special populations such as foster children or correctional settings. In a

Temperamental.
Environmental.
Genetic and physiological.
Course modifiers.
cross-national meta-analysis, ADHD occurred in 2.5% of adults.
Development and Course
Many parents first observe excessive motor activity when the child is a toddler, but symptoms
are difficult to distinguish from highly variable normative behaviors before age 4 years. ADHD
is most often identified during elementary school years when inattention becomes more
prominent and impairing. The disorder is relatively stable through early adolescence, but some
individuals have a worsened course with development of antisocial behaviors. In most
individuals with ADHD, symptoms of motoric hyperactivity become less obvious in adolescence
and adulthood, but difficulties with restlessness, inattention, poor planning, and impulsivity
persist. A substantial proportion of children with ADHD remain relatively impaired into
adulthood.
In preschool, the main manifestation is hyperactivity. Inattention becomes more prominent
during elementary school. During adolescence, signs of hyperactivity (e.g., running and
climbing) are less common and may be confined to fidgetiness or an inner feeling of jitteriness,
restlessness, or impatience. In adulthood, along with inattention and restlessness, impulsivity
may remain problematic even when hyperactivity has diminished.
Risk and Prognostic Factors
ADHD is associated with reduced behavioral inhibition, effortful control, or
constraint; negative emotionality; and/or elevated novelty seeking. These traits may predispose
some children to ADHD but are not specific to the disorder.
Very low birth weight and degree of prematurity convey a greater risk for
ADHD; the more extreme the low weight, the greater the risk. Prenatal exposure to smoking is
associated with ADHD even after controlling for parental psychiatric history and socioeconomic
status. A minority of cases may be related to reactions to aspects of diet. Neurotoxin exposure
(e.g., lead), infections (e.g., encephalitis), and alcohol exposure in utero have been correlated
with subsequent ADHD, but it is not known whether these associations are causal.
The heritability of ADHD is approximately 74%. Large-scale genomewide association studies (GWAS) have identified a number of loci enriched in evolutionarily
constrained genomic regions and loss-of-function genes as well as around brain-expressed
regulatory regions. There is no single gene for ADHD.
Visual and hearing impairments, metabolic abnormalities, and nutritional deficiencies should
be considered as possible influences on ADHD symptoms. ADHD is elevated in individuals with
idiopathic epilepsy.
Family interaction patterns in early childhood are unlikely to cause ADHD but
may influence its course or contribute to secondary development of conduct problems.
Culture-Related Diagnostic Issues
Differences in ADHD prevalence across regions appear attributable mainly to different
diagnostic procedures and methodological practices, including using different diagnostic

interviews and differences in whether functional impairment was required and, if so, how it was
defined. Prevalence is also affected by cultural variation in attitudes toward behavioral norms
and expectations of children and youth in different social contexts, as well as cultural differences
in interpretations of children’s behaviors by parents and teachers, including differences by
gender. Clinical identification rates in the United States for African American and Latinx
populations tend to be lower than for non-Latinx White populations. Underdetection may result
from mislabeling of ADHD symptoms as oppositional or disruptive in socially oppressed ethnic
or racialized groups because of explicit or implicit clinician bias, leading to overdiagnosis of
disruptive disorders. Higher prevalence in non-Latinx White youth may also be influenced by
greater parental demand for diagnosis of behaviors seen as ADHD-related. Informant symptom
ratings may be influenced by the cultural background of the child and the informant, suggesting
that culturally competent diagnostic practices are relevant in assessing ADHD.
Sex- and Gender-Related Diagnostic Issues
ADHD is more frequent in males than in females in the general population, with a ratio of
approximately 2:1 in children and 1.6:1 in adults. Females are more likely than males to present
primarily with inattentive features. Sex differences in ADHD symptom severity may be due to
differing genetic and cognitive liabilities between sexes.
Diagnostic Markers
No biological marker is diagnostic for ADHD. Although ADHD has been associated with
elevated power of slow waves (4–7 Hz “theta”) as well as decreased power of fast waves (14–30
Hz “beta”), a later review found no differences in theta or beta power in either children or adults
with ADHD relative to control subjects.
Although some neuroimaging studies have shown differences in children with ADHD
compared with control subjects, meta-analysis of all neuroimaging studies do not show
differences between individuals with ADHD and control subjects. This likely is due to
differences in diagnostic criteria, sample size, task used, and technical aspects of the
neuroimaging technique. Until these issues are resolved, no form of neuroimaging can be used
for diagnosis of ADHD.
Association With Suicidal Thoughts or Behavior
ADHD is a risk factor for suicidal ideation and behavior in children. Similarly, in adulthood,
ADHD is associated with an increased risk of suicide attempt, when comorbid with mood,
conduct, or substance use disorders, even after controlling for comorbidity. Suicidal thoughts are
also more common in ADHD populations than in non-ADHD control subjects. ADHD predicted
persistence of suicidal thoughts in U.S. Army soldiers.
Functional Consequences of Attention-Deficit/Hyperactivity Disorder
ADHD is associated with reduced school performance and academic attainment. Academic
deficits, school-related problems, and peer neglect tend to be most associated with elevated
symptoms of inattention, whereas peer rejection and, to a lesser extent, accidental injury are most

Oppositional defiant disorder.
Intermittent explosive disorder.
Other neurodevelopmental disorders.
salient with marked symptoms of hyperactivity or impulsivity. Inadequate or variable selfapplication to tasks that require sustained effort is often interpreted by others as laziness,
irresponsibility, or failure to cooperate.
Young adults with ADHD have poor job stability. Adults with ADHD show poorer
occupational performance, attainment, attendance, and higher probability of unemployment, as
well as elevated interpersonal conflict. On average, individuals with ADHD obtain less
schooling, have poorer vocational achievement, and have reduced intellectual scores than their
peers, although there is great variability. In its severe form, the disorder is markedly impairing,
affecting social, familial, and scholastic/occupational adjustment.
Family relationships may be characterized by discord and negative interactions. Individuals
with ADHD have lower self-esteem relative to peers without ADHD. Peer relationships are often
disrupted by peer rejection, neglect, or teasing of the individual with ADHD.
Children with ADHD are significantly more likely than their peers without ADHD to
develop conduct disorder in adolescence and antisocial personality disorder in adulthood,
consequently increasing the likelihood for substance use disorders and incarceration. The risk of
subsequent substance use disorders is elevated, especially when conduct disorder or antisocial
personality disorder develops.
Individuals with ADHD are more likely than peers to be injured. Children and adults with
ADHD are at higher risk for suffering trauma and developing subsequent posttraumatic stress
syndrome. Traffic accidents and violations are more frequent in drivers with ADHD. Individuals
with ADHD have a higher overall mortality rate, largely because of accidents and injuries. There
may also be an elevated likelihood of obesity and hypertension among individuals with ADHD.
Differential Diagnosis
Individuals with oppositional defiant disorder may resist work or
school tasks that require self-application because they resist conforming to others' demands.
Their behavior is characterized by negativity, hostility, and defiance. These symptoms must be
differentiated from aversion to school or mentally demanding tasks because of difficulty in
sustaining mental effort, forgetting instructions, and impulsivity in individuals with ADHD.
Complicating the differential diagnosis is the fact that some individuals with ADHD may
develop secondary oppositional attitudes toward such tasks and devalue their importance.
ADHD and intermittent explosive disorder share high levels of
impulsive behavior. However, individuals with intermittent explosive disorder show serious
aggression toward others, which is not characteristic of ADHD, and they do not experience
problems with sustaining attention as seen in ADHD. In addition, intermittent explosive disorder
is rare in childhood. Intermittent explosive disorder may be diagnosed in the presence of ADHD.
The increased motoric activity that may occur in ADHD must
be distinguished from the repetitive motor behavior that characterizes stereotypic movement
disorder and some cases of autism spectrum disorder. In stereotypic movement disorder, the
motoric behavior is generally fixed and repetitive (e.g., body rocking, self-biting), whereas the
fidgetiness and restlessness in ADHD are typically generalized and not characterized by
repetitive stereotypic movements. In Tourette’s disorder, frequent multiple tics can be mistaken
for the generalized fidgetiness of ADHD. Prolonged observation may be needed to differentiate
fidgetiness from bouts of multiple tics.

Specific learning disorder.
Intellectual developmental disorder (intellectual disability).
Autism spectrum disorder.
Reactive attachment disorder.
Anxiety disorders.
Posttraumatic stress disorder.
Depressive disorders.
Bipolar disorder.
Children with specific learning disorder alone may appear inattentive
because of frustration, lack of interest, or limited ability in neurocognitive
processes, including working memory and processing speed, whereas their inattention is much
reduced when performing a skill that does not require the impaired cognitive process.
Symptoms of ADHD are common in
children with intellectual developmental disorder placed in academic settings that are
inappropriate to their intellectual ability. In such cases, the symptoms are not evident during
nonacademic tasks. A diagnosis of ADHD in intellectual developmental disorder requires that
inattention or hyperactivity be excessive for mental age.
Individuals with ADHD and those with autism spectrum disorder
exhibit inattention, social dysfunction, and difficult-to-manage behavior. The social dysfunction
and peer rejection seen in individuals with ADHD must be distinguished from the social
disengagement, isolation, and indifference to facial and tonal communication cues seen in
individuals with autism spectrum disorder. Children with autism spectrum disorder may display
tantrums because of an inability to tolerate a change from their expected course of events. In
contrast, children with ADHD may misbehave or have a tantrum during a major transition
because of impulsivity or poor self-control.
Children with reactive attachment disorder may show social
disinhibition, but not the full ADHD symptom cluster, and display other features such as a lack
of enduring relationships that are not characteristic of ADHD.
ADHD shares symptoms of inattention with anxiety disorders. Individuals
with ADHD are inattentive because of their preferential engagement with novel and stimulating
activities or preoccupation with enjoyable activities. This is distinguished from the inattention
attributable to worry and rumination seen in anxiety disorders. Restlessness might be seen in
anxiety disorders. However, in ADHD, the symptom is not associated with worry and
rumination.
Concentration difficulties associated with posttraumatic stress
disorder (PTSD) may be misdiagnosed in children as ADHD. Children younger than 6 years
often manifest PTSD in nonspecific symptoms such as restlessness, irritability, inattention, and
poor concentration, which can mimic ADHD. Parents may also minimize their children’s
trauma-related symptoms, and teachers and other caregivers are often unaware of the child’s
exposure to traumatic events. A comprehensive assessment of past exposure to traumatic events
can rule out PTSD.
Individuals with depressive disorders may present with inability to
concentrate. However, poor concentration in mood disorders becomes prominent only during a
depressive episode.
Individuals with bipolar disorder may have increased activity, poor
concentration, and increased impulsivity, but these features are episodic, unlike ADHD, in which
the symptoms are persistent. Moreover, in bipolar disorder, increased impulsivity or inattention
is accompanied by elevated mood, grandiosity, and other specific bipolar features. Children with

Disruptive mood dysregulation disorder.
Substance use disorders.
Personality disorders.
Psychotic disorders.
Medication-induced symptoms of ADHD.
Neurocognitive disorders.
ADHD may show significant changes in mood within the same day; such lability is distinct from
a manic or hypomanic episode, which must last 4 or more days to be a clinical indicator of
bipolar disorder, even in children. Bipolar disorder is rare in preadolescents, even when severe
irritability and anger are prominent, whereas ADHD is common among children and adolescents
who display excessive anger and irritability.
Disruptive mood dysregulation disorder is characterized by
pervasive irritability, and intolerance of frustration, but impulsiveness and disorganized attention
are not essential features. However, most children and adolescents with the disorder also have
symptoms that meet criteria for ADHD, which is diagnosed separately.
Differentiating ADHD from substance use disorders may be problematic
if the first presentation of ADHD symptoms follows the onset of abuse or
frequent use. Clear evidence of ADHD before substance misuse from informants or previous
records may be essential for differential diagnosis.
In adolescents and adults, it may be difficult to distinguish ADHD from
borderline, narcissistic, and other personality disorders. Some personality disorders tend to share
the features of disorganization, social intrusiveness, emotional dysregulation, and cognitive
dysregulation. However, ADHD is not characterized by fear of abandonment, self-injury,
extreme ambivalence, or other features of personality disorder. It may take extended clinical
observation, informant interview, or detailed history to distinguish impulsive, socially intrusive,
or inappropriate behavior from narcissistic, aggressive, or domineering behavior to make this
differential diagnosis.
ADHD is not diagnosed if the symptoms of inattention and hyperactivity
occur exclusively during the course of a psychotic disorder.
Symptoms of inattention, hyperactivity, or impulsivity
attributable to the use of medication (e.g., bronchodilators, isoniazid, neuroleptics [resulting in
akathisia], thyroid replacement medication) are diagnosed as other specified or unspecified other
(or unknown) substance–related disorders.
While impairment in complex attention may be one of the affected
cognitive domains in a neurocognitive disorder, it must represent a decline from a previous level
of performance in order to justify a diagnosis of major or mild neurocognitive disorder.
Moreover, major or mild neurocognitive disorder typically has its onset in adulthood. In contrast,
the inattention in ADHD must have been present prior to age 12 and does not represent a decline
from previous functioning.
Comorbidity
Although ADHD is more common in males, females with ADHD have higher rates of a number
of comorbid disorders, particularly oppositional defiant disorder, autism spectrum disorder, and
personality and substance use disorders. Oppositional defiant disorder co-occurs with ADHD in
approximately half of children with the combined presentation and about a quarter with the
predominantly inattentive presentation. Conduct disorder co-occurs in about a quarter of children

or adolescents with the combined presentation, depending on age and setting. Most children and
adolescents with disruptive mood dysregulation disorder have symptoms that also meet criteria
for ADHD; a lesser percentage of children with ADHD have symptoms that meet criteria for
disruptive mood dysregulation disorder. Anxiety disorders, major depressive disorder, obsessivecompulsive disorder, and intermittent explosive disorder occur in a minority of individuals with
ADHD but more often than in the general population. Although substance use disorders are
relatively more frequent among adults with ADHD in the general population, the disorders are
present in only a minority of adults with ADHD. In adults, antisocial and other personality
disorders may co-occur with ADHD.
ADHD may co-occur in variable symptom profiles with other neurodevelopmental disorders,
including specific learning disorder, autism spectrum disorder, intellectual developmental
disorder, language disorders, developmental coordination disorder, and tic disorders.
Comorbid sleep disorders in ADHD are associated with daytime impairments in cognition
(e.g., inattention). Many individuals with ADHD report daytime sleepiness that may meet criteria
for hypersomnolence disorder. One quarter to one-half of individuals with ADHD report sleep
difficulties; studies have shown an association of ADHD with insomnia, circadian rhythm sleepwake disorder, sleep-disordered breathing, and restless legs syndrome.
Individuals with ADHD have been found to have elevated rates of a number of medical
conditions, particularly allergy and autoimmune disorders, as well as epilepsy.
Other Specified Attention-Deficit/Hyperactivity Disorder
F90.8
This category applies to presentations in which symptoms characteristic of attentiondeficit/hyperactivity disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for attention-deficit/hyperactivity disorder or any of the disorders
in the neurodevelopmental disorders diagnostic class. The other specified attentiondeficit/hyperactivity disorder category is used in situations in which the clinician
chooses to communicate the specific reason that the presentation does not meet the
criteria for attention-deficit/hyperactivity disorder or any specific neurodevelopmental
disorder. This is done by recording “other specified attention-deficit/hyperactivity
disorder” followed by the specific reason (e.g., “with insufficient inattention
symptoms”).
Unspecified Attention-Deficit/Hyperactivity Disorder
F90.9

This category applies to presentations in which symptoms characteristic of attentiondeficit/hyperactivity disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for attention-deficit/hyperactivity disorder or any of the disorders
in the neurodevelopmental disorders diagnostic class. The unspecified attentiondeficit/hyperactivity disorder category is used in situations in which the clinician
chooses not to specify the reason that the criteria are not met for attentiondeficit/hyperactivity disorder or for a specific neurodevelopmental disorder, and
includes presentations in which there is insufficient information to make a more
specific diagnosis.
Specific Learning Disorder
Specific Learning Disorder
Diagnostic Criteria
A. Difficulties learning and using academic skills, as indicated by the presence of at
least one of the following symptoms that have persisted for at least 6 months,
despite the provision of interventions that target those difficulties:
1. Inaccurate or slow and effortful word reading (e.g., reads single words aloud
incorrectly or slowly and hesitantly, frequently guesses words, has difficulty
sounding out words).
2. Difficulty understanding the meaning of what is read (e.g., may read text
accurately but not understand the sequence, relationships, inferences, or
deeper meanings of what is read).
3. Difficulties with spelling (e.g., may add, omit, or substitute vowels or
consonants).
4. Difficulties with written expression (e.g., makes multiple grammatical or
punctuation errors within sentences; employs poor paragraph organization;
written expression of ideas lacks clarity).
5. Difficulties mastering number sense, number facts, or calculation (e.g., has
poor understanding of numbers, their magnitude, and relationships; counts on
fingers to add single-digit numbers instead of recalling the math fact as peers
do; gets lost in the midst of arithmetic computation and may switch
procedures).

6. Difficulties with mathematical reasoning (e.g., has severe difficulty applying
mathematical concepts, facts, or procedures to solve quantitative problems).
B. The affected academic skills are substantially and quantifiably below those
expected for the individual’s chronological age, and cause significant
interference with academic or occupational performance, or with activities of
daily living, as confirmed by individually administered standardized achievement
measures and comprehensive clinical assessment. For individuals age 17 years
and older, a documented history of impairing learning difficulties may be
substituted for the standardized assessment.
C. The learning difficulties begin during school-age years but may not become fully
manifest until the demands for those affected academic skills exceed the
individual’s limited capacities (e.g., as in timed tests, reading or writing lengthy
complex reports for a tight deadline, excessively heavy academic loads).
D. The learning difficulties are not better accounted for by intellectual disabilities,
uncorrected visual or auditory acuity, other mental or neurological disorders,
psychosocial adversity, lack of proficiency in the language of academic
instruction, or inadequate educational instruction.
Note: The four diagnostic criteria are to be met based on a clinical synthesis of the
individual’s history (developmental, medical, family, educational), school reports, and
psychoeducational assessment.
Coding note: Specify all academic domains and subskills that are impaired. When
more than one domain is impaired, each one should be coded individually according
to the following specifiers.
Specify if:
F81.0 With impairment in reading:
Word reading accuracy
Reading rate or fluency
Reading comprehension
Note: Dyslexia is an alternative term used to refer to a pattern of learning
difficulties characterized by problems with accurate or fluent word recognition,
poor decoding, and poor spelling abilities. If dyslexia is used to specify this
particular pattern of difficulties, it is important also to specify any additional
difficulties that are present, such as difficulties with reading comprehension or
math reasoning.
F81.81 With impairment in written expression:
Spelling accuracy
Grammar and punctuation accuracy
Clarity or organization of written expression

F81.2 With impairment in mathematics:
Number sense
Memorization of arithmetic facts
Accurate or fluent calculation
Accurate math reasoning
Note: Dyscalculia is an alternative term used to refer to a pattern of difficulties
characterized by problems processing numerical information, learning
arithmetic facts, and performing accurate or fluent calculations. If dyscalculia is
used to specify this particular pattern of mathematic difficulties, it is important
also to specify any additional difficulties that are present, such as difficulties
with math reasoning or word reasoning accuracy.
Specify current severity:
Mild: Some difficulties learning skills in one or two academic domains, but of
mild enough severity that the individual may be able to compensate or function
well when provided with appropriate accommodations or support services,
especially during the school years.
Moderate: Marked difficulties learning skills in one or more academic domains,
so that the individual is unlikely to become proficient without some intervals of
intensive 
and 
specialized 
teaching 
during 
the 
school 
years. 
Some
accommodations or supportive services at least part of the day at school, in the
workplace, or at home may be needed to complete activities accurately and
efficiently.
Severe: Severe difficulties learning skills, affecting several academic domains,
so that the individual is unlikely to learn those skills without ongoing intensive
individualized and specialized teaching for most of the school years. Even with
an array of appropriate accommodations or services at home, at school, or in the
workplace, the individual may not be able to complete all activities efficiently.
Recording Procedures
Each impaired academic domain and subskill of specific learning disorder should be recorded.
Because of ICD coding requirements, impairments in reading, impairments in written expression,
and impairments in mathematics, with their corresponding impairments in subskills, must be
coded and recorded separately. For example, impairments in reading and mathematics and
impairments in the subskills of reading rate or fluency, reading comprehension, accurate or
fluent calculation, and accurate math reasoning would be coded and recorded as F81.0 specific
learning disorder with impairment in reading, with impairment in reading rate or fluency, and
impairment in reading comprehension; F81.2 specific learning disorder with impairment in
mathematics, with impairment in accurate or fluent calculation and impairment in accurate math
reasoning.
Diagnostic Features

Specific learning disorder is a neurodevelopmental disorder with a biological origin that is the
basis for abnormalities at a cognitive level that are associated with the behavioral signs of the
disorder. The biological origin includes an interaction of genetic, epigenetic, and environmental
factors, which affect the brain’s ability to perceive or process verbal or nonverbal information
efficiently and accurately.
One essential feature of specific learning disorder is persistent difficulties learning keystone
academic skills (Criterion A), with onset during the years of formal schooling (i.e., the
developmental period). Key academic skills include reading of single words accurately and
fluently, reading comprehension, written expression and spelling, arithmetic calculation, and
mathematical reasoning (solving mathematical problems). In contrast to talking or walking,
which are acquired developmental milestones that emerge with brain maturation, academic skills
(e.g., reading, spelling, writing, mathematics) have to be taught and learned explicitly. Specific
learning disorder disrupts the normal pattern of learning academic skills; it is not simply a
consequence of lack of opportunity of learning or inadequate instruction. Difficulties mastering
these key academic skills may also impede learning in other academic subjects (e.g., history,
science, social studies), but those problems are attributable to difficulties learning the underlying
academic skills.
Difficulties learning to map letters with the sounds of one’s language—to read printed words
(often called dyslexia [specific learning disorder with impairment in reading])—is one of the
most common manifestations of specific learning disorder. The learning difficulties manifest as a
range of observable, descriptive behaviors or symptoms (as listed in Criteria A1–A6). These
clinical symptoms may be observed, probed by means of the clinical interview, or ascertained
from school reports, rating scales, or descriptions in previous educational or psychological
assessments. The learning difficulties are persistent, not transitory. In children and adolescents,
persistence is defined as restricted progress in learning (i.e., no evidence that the individual is
catching up with classmates) for at least 6 months despite the provision of extra help at home or
school. For example, difficulties learning to read single words that do not fully or rapidly remit
with the provision of instruction in phonological skills or word identification strategies may
indicate a specific learning disorder. Evidence of persistent learning difficulties may be derived
from cumulative school reports, portfolios of the child’s evaluated work, curriculum-based
measures, or clinical interview. In adults, persistent difficulty refers to ongoing difficulties in
literacy or numeracy skills that manifest during childhood or adolescence, as indicated by
cumulative evidence from school reports, evaluated portfolios of work, or previous assessments.
A second key feature is that the individual’s performance of the affected academic skills is
well below expected for age (Criterion B). One robust clinical indicator of difficulties learning
academic skills is low academic achievement for age or average achievement that is sustainable
only by extraordinarily high levels of effort or support. In children, the low academic skills cause
significant interference in school performance (as indicated by school reports and teacher’s
grades or ratings). Another clinical indicator, particularly in adults, is avoidance of activities that
require the academic skills. Also in adulthood, low academic skills interfere with occupational
performance or everyday activities requiring those skills (as indicated by self-report or report by
others). However, this criterion also requires psychometric evidence from an individually

administered, psychometrically sound and culturally appropriate test of academic achievement
that is norm-referenced or criterion-referenced. Academic skills are distributed along a
continuum, so there is no natural cutpoint that can be used to differentiate individuals with and
without specific learning disorder. Thus, any threshold used to specify what constitutes
significantly low academic achievement (e.g., academic skills well below age expectation) is to a
large extent arbitrary. Low achievement scores on one or more standardized tests or subtests
within an academic domain (i.e., at least 1.5 standard deviations [SD] below the population mean
for age, which translates to a standard score of 78 or less, which is below the 7th percentile) are
needed for the greatest diagnostic certainty. However, precise scores will vary according to the
particular standardized tests that are used. On the basis of clinical judgment, a more lenient
threshold may be used (e.g., 1.0 SD below the population mean for age), when learning
difficulties are supported by converging evidence from clinical assessment, academic history,
school reports, or test scores. Moreover, since standardized tests are not available in all
languages, the diagnosis may then be based in part on clinical judgment of scores on available
test measures.
A third core feature is that the learning difficulties are readily apparent in the early school
years in most individuals (Criterion C). However, in others, the learning difficulties may not
manifest fully until later school years, by which time learning demands have increased and
exceed the individual’s limited capacities.
Another key diagnostic feature is that the learning difficulties are considered “specific” for
four reasons. First, they are not better explained by intellectual developmental disorders
(intellectual developmental disorder [intellectual disability]; global developmental delay);
hearing or vision disorders; or neurological or motor disorders (Criterion D). Specific learning
disorder affects learning in individuals who otherwise demonstrate normal levels of intellectual
functioning (generally estimated by an IQ score of greater than about 70 [± 5 points allowing for
measurement error]). The phrase “unexpected academic
underachievement” is often cited as the defining characteristic of specific learning disorder in
that the specific learning disabilities are not part of a more general learning difficulty as
manifested in intellectual developmental disorder or global developmental delay.
Second, the learning difficulty cannot be attributed to more general external factors, such as
economic or environmental disadvantage, chronic absenteeism, or lack of education as typically
provided in the individual’s community context. Third, the learning difficulty cannot be
attributed to neurological (e.g., pediatric stroke) or motor disorders or to vision or hearing
disorders, which are often associated with problems learning academic skills but are
distinguishable by presence of neurological signs. Finally, the learning difficulty may be
restricted to one academic skill or domain (e.g., reading single words, retrieving or calculating
number facts).
Specific learning disorder may also occur in individuals identified as intellectually “gifted.”
These individuals may be able to sustain apparently adequate academic functioning by using
compensatory strategies, extraordinarily high effort, or support, until the learning demands or
assessment procedures (e.g., timed tests) pose barriers to their demonstrating their learning or
accomplishing required tasks. In these cases, the individual’s achievement scores will be low

relative to ability level or achievement in other domains, rather than to the population mean for
achievement.
Comprehensive assessment is required. Specific learning disorder can only be diagnosed
after formal education starts but can be diagnosed at any point afterward in children, adolescents,
or adults, providing there is evidence of onset during the years of formal schooling (i.e., the
developmental period). No single data source is sufficient for a diagnosis of specific learning
disorder. Rather, specific learning disorder is a clinical diagnosis based on a synthesis of the
individual’s medical, developmental, educational, and family history; the history of the learning
difficulty, including its previous and current manifestation; the impact of the difficulty on
academic, occupational, or social functioning; previous or current school reports; portfolios of
work requiring academic skills; curriculum-based assessments; and previous or current scores
from individual standardized tests of academic achievement. If an intellectual, sensory,
neurological, or motor disorder is suspected, then the clinical assessment for specific learning
disorder should also include methods appropriate for these disorders. Thus, comprehensive
assessment will involve professionals with expertise in specific learning disorder and
psychological/cognitive assessment. Since specific learning disorder typically persists into
adulthood, reassessment is rarely necessary, unless indicated by marked changes in the learning
difficulties (amelioration or worsening) or requested for specific purposes.
Associated Features
The symptoms of specific learning disorder (difficulty with aspects of reading, writing, or
mathematics) frequently co-occur. An uneven profile of abilities is common, such as a
combination of above-average abilities in drawing, design, and other visuospatial abilities, and
slow, effortful, and inaccurate reading and poor reading comprehension and written expression.
Specific learning disorder is frequently but not invariably preceded, in preschool years, by delays
in attention, language, or motor skills that may persist and co-occur with specific learning
disorder.
Individuals with specific learning disorder typically (but not invariably) exhibit poor
performance on psychological tests of cognitive processing. However, it remains unclear
whether these cognitive abnormalities are the cause, correlate, or consequence of the learning
difficulties. Cognitive deficits associated with difficulties learning to read words are well
documented, and there is a burgeoning understanding of the cognitive deficits associated with
difficulty acquiring mathematics skills, but cognitive deficits associated with other
manifestations of specific learning disorder (e.g., reading comprehension, written expression) are
underspecified.
Although individual cognitive deficits particularly contribute to each specific learning
disorder symptom, some cognitive deficits are shared across different specific learning disorder
subtypes (e.g., processing speed) and may contribute to co-occurring symptoms of specific
learning disorder. The co-occurring nature of the symptoms of specific learning disorder and the
shared cognitive deficits across the specific learning disorder subtypes suggest shared underlying
biological mechanisms.
Thus, individuals with similar behavioral symptoms or test scores are found to have a variety

of cognitive deficits, and many of these processing deficits are also found in other
neurodevelopmental disorders (e.g., attention-deficit/hyperactivity disorder [ADHD], autistic
spectrum disorder, communication disorders, developmental coordination disorder).
As a group, individuals with the disorder show circumscribed alterations in cognitive
processing and brain structure and function. Genetic differences are also evident at the group
level. However, cognitive testing, neuroimaging, or genetic testing are not useful for diagnosis at
this time, and assessment of cognitive processing deficits is not required for diagnostic
assessment.
Prevalence
The prevalence of specific learning disorder across the academic domains of reading, writing,
and mathematics is 5%–15% among school-age children in Brazil, Northern Ireland, and the
United States. Prevalence in adults is unknown.
Development and Course
Onset, recognition, and diagnosis of specific learning disorder usually occur during the
elementary school years when children are required to learn to read, spell, write, and learn
mathematics. However, precursors such as language delays or deficits, difficulties in rhyming or
counting, or difficulties with fine motor skills required for writing commonly occur in early
childhood before the start of formal schooling.
Manifestations may be behavioral (e.g., a reluctance to engage in learning; oppositional
behavior). Specific learning disorder is lifelong, but the course and clinical expression are
variable, in part depending on the interactions among the task demands of the environment, the
range and severity of the individual’s learning difficulties, the individual’s learning abilities,
comorbidity, and the available support systems and intervention. Nonetheless, problems with
reading fluency and comprehension, spelling, written expression, and numeracy skills in
everyday life typically persist into adulthood.
Changes in manifestation of symptoms occur with age, so that an individual may have a
persistent or shifting array of learning difficulties across the lifespan. Adults with specific
learning disorder appear to experience limitations and restrictions in activity and participation in
domains of communication, interpersonal interactions and community, and social and civic life.
Examples of symptoms that may be observed among preschool-age children include a lack of
interest in playing games with language sounds (e.g., repetition, rhyming), and they may have
trouble learning nursery rhymes. Preschool children with specific learning disorder may
frequently use baby talk, mispronounce words, and have trouble remembering names of letters,
numbers, or days of the week. They may fail to recognize letters in their own names and have
trouble learning to count. Kindergarten-age children with specific learning disorder may be
unable to recognize and write letters, may be unable to write their own names, or may have
persistent use of invented spelling beyond developmentally typical time frames.
They may have trouble breaking down spoken words into syllables (e.g., “cowboy” into
“cow” and “boy”) and trouble recognizing words that rhyme (e.g., cat, bat, hat). Kindergartenage children also may have trouble connecting letters with their sounds (e.g., letter b makes the
sound /b/) and may be unable to recognize phonemes (e.g., do not know which in a set of words
[e.g., dog, man, car] starts with the same sound as “cat”).

Specific learning disorder in elementary school–age children typically manifests as marked
difficulty learning letter-sound correspondence (particularly in English-speaking children),
fluent word decoding, spelling, or math facts; reading aloud is slow, inaccurate, and effortful,
and some children struggle to understand the magnitude that a spoken or written number
represents. Children in primary grades (grades 1–3) may continue to have problems recognizing
and manipulating phonemes, be unable to read common one-syllable words (such as mat or top),
and be unable recognize common irregularly spelled words (e.g., said, two). They may commit
reading errors that indicate problems in connecting sounds and letters (e.g., “big” for “got”) and
have difficulty sequencing numbers and letters. Children in grades 1–3 also may have difficulty
remembering number facts or arithmetic procedures for adding, subtracting, and so forth, and
may complain that reading or arithmetic is hard and avoid doing it. Children with specific
learning disorder in the middle grades (grades 4–6) may mispronounce or skip parts of long,
multisyllable words (e.g., say “conible” for “convertible,” “aminal” for “animal”) and confuse
words that sound alike (e.g., “tornado” for “volcano”). They may have trouble remembering
dates, names, and telephone numbers and may have trouble completing homework or tests on
time. Children in the middle grades also may have poor comprehension with or without slow,
effortful, and inaccurate reading, and they may have trouble reading small function words (e.g.,
that, the, an, in). They may have very poor spelling and poor written work. They may get the first
part of a word correctly, then guess wildly (e.g., read “clover” as “clock”), and may express fear
of reading aloud or refuse to read aloud.
By contrast, adolescents may have mastered word decoding, but reading remains slow and
effortful, and they are likely to show marked problems in reading comprehension and written
expression (including poor spelling) and poor mastery of math facts or mathematical problem
solving. During adolescence and into adulthood, individuals with specific learning disorder may
continue to make numerous spelling mistakes and read single words and connected text slowly
and with much effort, with trouble pronouncing multisyllable words. They may frequently need
to reread material to understand or get the main point and have trouble making inferences from
written text. Adolescents and adults may avoid activities that demand reading or arithmetic
(reading for pleasure, reading instructions). Adults with specific learning disorder have ongoing
spelling problems, slow and effortful reading, or problems making important inferences from
numerical information in work-related written documents. They may avoid both leisure and
work-related activities that demand reading or writing or use alternative approaches to access
print (e.g., text-to-speech/speech-to-text software, audiobooks, audiovisual media).
An alternative clinical expression is that of circumscribed learning difficulties that persist
across the lifespan, such as an inability to master the basic sense of number (e.g., to know which
of a pair of numbers or dots represents the larger magnitude), or lack of proficiency in word
identification or spelling. Avoidance of or reluctance to engage in activities requiring academic
skills is common in children, adolescents, and adults. Individuals with poor reading and math
skills are more likely to report socioemotional distress (e.g., sadness, loneliness) as they advance
across elementary grade levels.
Episodes of severe anxiety or anxiety disorders, including somatic complaints or panic
attacks, are common across the lifespan and accompany both the circumscribed and the broader

Environmental.
Genetic and physiological.
Course modifiers.
expression of learning difficulties.
Risk and Prognostic Factors
Environmental 
factors, 
including 
socioeconomic 
conditions 
(e.g., 
low
socioeconomic status) and exposure to neurotoxicants, increase the risk for specific learning
disorder or difficulties in reading and mathematics. Risks for specific learning disorder or
difficulties in reading and mathematics include prenatal or early-life exposure to any of the
following: air pollution, nicotine, polybrominated diphenyl ethers or polychlorinated biphenyls
(flame retardants), lead, or manganese.
Specific learning disorder appears to aggregate in families, particularly
when affecting reading, mathematics, and spelling. The relative risk of specific
learning disorder in reading or mathematics is substantially higher (e.g., 4–8 times and 5–10
times higher, respectively) in first-degree relatives of individuals with these learning difficulties
compared with those without them. Notably, rates vary depending on method of ascertainment
(objective testing or self-report) of parent diagnostic status. Family history of reading difficulties
(dyslexia) and parental literacy skills predict literacy problems or specific learning disorder in
offspring, indicating the combined role of genetic and environmental factors.
There is high heritability for both reading ability and reading disability in alphabetic and
nonalphabetic languages, including high heritability for most manifestations of learning abilities
and disabilities (e.g., heritability estimate values greater than 0.6). Covariation between various
manifestations of learning difficulties is high, suggesting that genes related to one presentation
are highly correlated with genes related to another manifestation.
Preterm delivery or very low birthweight is a risk for specific learning disorder. In
individuals with neurofibromatosis type 1, risk of specific learning disorder is high, with up to
75% of individuals demonstrating a learning disorder.
Marked problems with inattentive, internalizing, and externalizing behaviors in
preschool years are predictive of later difficulties in reading and mathematics (but not necessarily
specific learning disorder) and nonresponse to effective academic interventions. Language
impairment in preschool years is strongly associated with later impairment in reading (e.g., word
reading, reading comprehension). For example, delay or disorders in speech or language, or
impaired cognitive processing (e.g., phonological awareness, working memory, rapid serial
naming), may predict later specific learning disorder in reading and in written expression.
Additionally, a diagnosis of ADHD in childhood is associated with underachievement in reading
and math in adulthood. Comorbidity with ADHD is predictive of worse mental health outcome
than that associated with specific learning disorder without ADHD. Systematic, intensive,
individualized instruction, using evidence-based interventions, may improve or ameliorate the
learning difficulties in some individuals or promote the use of compensatory strategies in others,
thereby mitigating the otherwise poor outcomes.
Culture-Related Diagnostic Issues
Specific learning disorder occurs across linguistic and ethnoracial backgrounds and across

cultural and socioeconomic contexts but may vary in its manifestation according to the nature of
the spoken and written symbol systems and cultural and educational practices. For example, the
cognitive processing requirements of reading and of working with numbers vary greatly across
orthographies. In the English language, the observable hallmark clinical symptom of difficulties
learning to read is inaccurate and slow reading of single words; in other alphabetic languages
that have more direct mapping between sounds and letters (e.g., Spanish, German) and in
nonalphabetic languages (e.g., Chinese, Japanese), the hallmark feature is slow but accurate
reading. In English-language learners, assessment should include consideration of whether the
source of reading difficulties is a limited proficiency with English or a specific learning disorder.
Risk factors for specific learning disorder in English-language learners include a family history
of specific learning disorder or language delay in the native language, as well as learning
difficulties and deficits in phonological memory in English and failure to catch up with peers. If
there is suspicion of cultural or language differences (e.g., that an English-language learner is
influenced by limited English proficiency), the assessment needs to take into account the
individual’s language proficiency in his or her first or native language as well as in the second
language (in this example, English). Importantly, children who speak a language at home that
differs phonologically from the language of academic instruction are not more likely to have
phonological deficits than their peers who speak the same language at home and at school.
Comorbid reading difficulties may vary with different languages; for example, reading
difficulties are less frequent among Chinese-reading children with developmental coordination
disorder in Taiwan compared
with children in English-speaking countries, possibly because of the characteristics of the two
written languages (logographic vs. alphabetic). Considerations in assessment may include the
linguistic and cultural context in which the individual is living, as well as his or her educational
and learning history in the original linguistic and cultural context. Risk factors for learning
problems among refugee and migrant children include teacher stereotyping and low expectations,
bullying, ethnic and racialized discrimination, parental misunderstandings about educational
styles and expectations, trauma, and postmigration stressors.
Sex- and Gender-Related Diagnostic Issues
Specific learning disorder is more common in males than in females (ratios range from about 2:1
to 3:1) and cannot be attributed to factors such as ascertainment bias, definitional or
measurement variation, language, ethnoracial background, or socioeconomic status. Sex
differences in dyslexia (specific learning disorder with impairment in reading) may be partially
mediated by processing speed.
Association With Suicidal Thoughts or Behavior
In U.S. adolescents age 15 years in public school, poor reading ability was associated with
suicidal thoughts and behavior compared with adolescents with typical reading scores, even
when controlling for sociodemographic and psychiatric variables. In a population-based study of
adults in Canada, prevalence of lifetime suicide attempts among those with specific learning
disorder was higher than that among those without a specific learning disorder, even after

Normal variations in academic attainment.
Intellectual developmental disorder (intellectual disability).
Learning difficulties due to neurological or sensory disorders.
Neurocognitive disorders.
Attention-deficit/hyperactivity disorder.
adjustment for childhood adversities, history of mental illness and substance use, and
sociodemographic factors. Among those with specific learning disorder, a history of witnessing
chronic parental domestic violence and ever having had a major depressive disorder were
associated with increased risk for suicidal behavior.
Functional Consequences of Specific Learning Disorder
Specific learning disorder can have negative functional consequences across the lifespan,
including lower academic attainment, higher rates of high school dropout, lower rates of
postsecondary education, high levels of psychological distress and poorer overall mental health,
higher rates of unemployment and underemployment, and lower incomes. School dropout and
co-occurring depressive symptoms increase the risk for poor mental health outcomes, including
suicidal thoughts or behavior, whereas high levels of social or emotional support predict better
mental health outcomes.
Differential Diagnosis
Specific learning disorder is distinguished from normal
variations in academic attainment attributable to external factors (e.g., lack of educational
opportunity, consistently poor instruction, learning in a second language), because the learning
difficulties persist in the presence of adequate educational opportunity and exposure to the same
instruction as the peer group, and competency in the language of instruction, even when it is
different from one’s primary spoken language.
Specific learning disorder differs from
general learning difficulties associated with intellectual developmental disorder, because the
learning difficulties occur in the presence of normal levels of intellectual functioning (i.e., IQ
score of at least 70 ± 5). If intellectual developmental disorder is present, specific learning
disorder can be diagnosed only when the learning difficulties are in excess of those usually
associated with the intellectual developmental disorder.
Specific 
learning 
disorder 
is
distinguished from learning difficulties due to neurological or sensory disorders
(e.g., pediatric stroke, traumatic brain injury, hearing impairment, vision impairment), because in
these cases there are abnormal findings on neurological examination.
Specific learning disorder is distinguished from learning problems
associated with neurodegenerative cognitive disorders. In specific learning disorder, the clinical
expression of specific learning difficulties occurs during the developmental period, which
sometimes only becomes evident when learning demands have increased and exceed the
individual’s limited capacities (as may occur in adulthood), and the difficulties do not manifest
as a marked decline from a former state.
Specific learning disorder is distinguished from the poor
academic performance associated with ADHD, because in the latter condition the problems may
not necessarily reflect specific difficulties in learning academic skills but rather may reflect
difficulties in performing those skills. However, the co-occurrence of specific learning disorder

Psychotic disorders.
F82
and ADHD is more frequent than expected by chance. If criteria for both disorders are met, both
diagnoses can be given.
Specific learning disorder is distinguished from the cognitive-processing
difficulties associated with schizophrenia or other psychotic disorders, because with these
disorders there is a decline (often rapid) in these functional domains. However, deficits in
reading ability are more severe in specific learning disorder than what would be predicted by the
general cognitive impairments associated with schizophrenia. If criteria for both disorders are
met, both diagnoses can be given.
Comorbidity
The different types of specific learning disorder commonly co-occur with one another (e.g.,
specific learning disorder with impairment in mathematics and with impairment in reading) and
with other neurodevelopmental disorders (e.g., ADHD, communication disorders, developmental
coordination disorder, autism spectrum disorder) or other mental disorders (e.g., anxiety and
depressive disorders) or behavioral problems. Notably, estimates of the comorbidity of math and
reading difficulties vary depending on the tests used to define the math difficulty, likely because
the same symptom (e.g., arithmetic problems) can be associated with different cognitive deficits
(e.g., a deficit in language skills or a deficit in number processing). These comorbidities do not
necessarily exclude the diagnosis of specific learning disorder but may make testing and
differential diagnosis more difficult, because each of the co-occurring disorders independently
interferes with the execution of activities of daily living, including learning. Thus, clinical
judgment is required to attribute such impairment to learning difficulties. If there is an indication
that another diagnosis could account for the difficulties learning keystone academic skills
described in Criterion A, specific learning disorder should not be diagnosed.
Motor Disorders
Developmental Coordination Disorder
Diagnostic Criteria
A. The acquisition and execution of coordinated motor skills is substantially below
that expected given the individual’s chronological age and opportunity for skill
learning and use. Difficulties are manifested as clumsiness (e.g., dropping or
bumping into
objects) as well as slowness and inaccuracy of performance of motor skills (e.g.,
catching an object, using scissors or cutlery, handwriting, riding a bike, or
participating in sports).

B. The motor skills deficit in Criterion A significantly and persistently interferes with
activities of daily living appropriate to chronological age (e.g., self-care and selfmaintenance) and impacts academic/school productivity, prevocational and
vocational activities, leisure, and play.
C. Onset of symptoms is in the early developmental period.
D. The motor skills deficits are not better explained by intellectual developmental
disorder (intellectual disability) or visual impairment and are not attributable to a
neurological condition affecting movement (e.g., cerebral palsy, muscular
dystrophy, degenerative disorder).
Diagnostic Features
The diagnosis of developmental coordination disorder is made by a clinical synthesis of the
history (developmental and medical), physical examination, school or workplace report, and
individual assessment using psychometrically sound and culturally appropriate standardized
tests. The manifestation of impaired skills requiring motor coordination (Criterion A) varies with
age. Young children may be delayed in achieving motor milestones (i.e., sitting, crawling,
walking), although many achieve typical motor milestones. They also may be delayed in
developing skills such as negotiating stairs, pedaling, buttoning shirts, completing puzzles, and
using zippers. Even when the skill is achieved, movement execution may appear awkward, slow,
or less precise than that of peers. Older children and adults may display slow speed or inaccuracy
with motor aspects of activities such as assembling puzzles, building models, playing ball games
(especially in teams), handwriting, typing, driving, or carrying out self-care skills.
Developmental coordination disorder is diagnosed only if the impairment in motor skills
significantly interferes with the performance of, or participation in, daily activities in family,
social, school, or community life (Criterion B). Examples of such activities include getting
dressed, eating meals with age-appropriate utensils and without mess, engaging in physical
games with others, using specific tools in class such as rulers and scissors, and participating in
team exercise activities at school. Not only is ability to perform these actions impaired, but also
marked slowness in execution is common. Handwriting competence is frequently affected,
consequently affecting legibility and/or speed of written output and affecting academic
achievement (the impact is distinguished from specific learning difficulty by the emphasis on the
motoric component of written output skills). In adults, everyday skills in education and work,
especially those in which speed and accuracy are required, are affected by coordination
problems.
Criterion C states that the onset of symptoms of developmental coordination disorder must be
in the early developmental period. However, developmental coordination disorder is typically
not diagnosed before age 5 years because there is considerable variation in the age at acquisition
of many motor skills or a lack of stability of measurement in early childhood (e.g., some children
catch up) or because other causes of motor delay may not have fully manifested.
Criterion D specifies that the diagnosis of developmental coordination disorder is made if the
coordination difficulties are not better explained by visual impairment or attributable to a
neurological condition. Thus, visual function examination and neurological examination must be
included in the diagnostic evaluation. If intellectual developmental disorder (intellectual

Environmental.
Genetic and physiological.
disability) is present, the motor difficulties are in excess of those expected for the mental age;
however, no IQ cutoff or discrepancy criterion is specified.
Developmental coordination disorder does not have discrete subtypes; however, individuals
may be impaired predominantly in gross motor skills or in fine motor skills, including
handwriting skills.
Other terms used to describe developmental coordination disorder include childhood
dyspraxia, specific developmental disorder of motor function, and clumsy child syndrome.
Associated Features
Some children with developmental coordination disorder show additional (usually suppressed)
motor activity, such as choreiform movements of unsupported limbs or mirror movements. These
“overflow” movements are referred to as neurodevelopmental immaturities or neurological soft
signs rather than neurological abnormalities. In both current literature and clinical practice, their
role in diagnosis is still unclear, requiring further evaluation.
Prevalence
The prevalence of developmental coordination disorder in children ages 5–11 years ranges from
5% to 8% cross-nationally (in the United Kingdom, 1.8% of children age 7 years are diagnosed
with severe developmental coordination disorder and 3% with probable developmental
coordination disorder); and 7%–8% in Canada, Sweden, and Taiwan. Males are more often
affected than females, with a male:female ratio between 2:1 and 7:1.
Development and Course
The course of developmental coordination disorder is variable but stable at least to 1-year and 2year follow-up. Although there may be improvement in the longer term, problems with
coordinated movements continue through adolescence in an estimated 50%–70% of children.
Onset is in early childhood. Delayed motor milestones may be the first signs, or the disorder is
first recognized when the child attempts tasks such as holding a knife and fork, buttoning
clothes, or playing ball games. In middle childhood, there are difficulties with motor aspects of
assembling puzzles, building models, playing ball, and handwriting, as well as with organizing
belongings, when motor sequencing and coordination are required. In early adulthood, there is
continuing difficulty in learning new tasks involving complex/automatic motor skills, including
driving and using tools. Inability to take notes and handwrite quickly may affect performance in
the workplace. Co-occurrence with other disorders (see the section “Comorbidity” for this
disorder) has an additional impact on presentation, course, and outcome.
Risk and Prognostic Factors
Developmental coordination disorder is associated with prematurity and low birth
weight and with prenatal exposure to alcohol.
Impairments in underlying neurodevelopmental processes have been
found in visual-motor skills, including both visual-motor perception and spatial mentalizing.
Cerebellar dysfunction, which affects the ability to make rapid motoric adjustments as the

Course modifiers.
Motor impairments due to another medical condition.
Intellectual developmental disorder (intellectual disability).
complexity of the required movements increases, may also be involved. However, the precise
neural basis of developmental coordination disorder remains unclear. Because of the cooccurrence of developmental coordination disorder with other neurodevelopmental disorders,
including attention-deficit/hyperactivity disorder (ADHD), specific learning disabilities, and
autism spectrum disorder, shared genetic effect has been proposed. However, consistent cooccurrence in twins appears only in severe cases.
Individuals with ADHD and with developmental coordination disorder
demonstrate more impairment than individuals with ADHD without developmental coordination
disorder.
Culture-Related Diagnostic Issues
Developmental coordination disorder occurs across cultural, ethnoracial, and socioeconomic
contexts. At the same time, cultural variations in motor development (both accelerated and
delayed relative to U.S. norms) have been reported. These appear to be associated with
caregiving practices related to expectations of independent mobility during development,
inadequate opportunities for mobility among children in severe poverty, and differences in
measurement methodology. By definition, “activities of daily living” implies cultural differences
necessitating consideration of the context in which the individual child is living as well as
whether the child has had appropriate opportunities to learn and practice such activities. Higher
prevalence of developmental coordination disorder in studies of children from some low- and
middle-income countries may reflect the impact of socioeconomic disadvantage on motor
development.
Functional Consequences of Developmental Coordination Disorder
Developmental coordination disorder leads to impaired functional performance in activities of
daily living (Criterion B), and the impairment is increased with co-occurring conditions.
Consequences of developmental coordination disorder include reduced participation in team play
and sports; poor self-esteem and sense of self-worth; emotional or behavioral problems; impaired
academic achievement; poor physical fitness; reduced physical activity and obesity; and poor
health-related quality of life.
Differential Diagnosis
Problems in coordination may be associated
with visual function impairment and specific neurological disorders (e.g., cerebral palsy,
progressive lesions of the cerebellum, neuromuscular disorders). In such cases, there are
additional findings on neurological examination.
If intellectual developmental disorder is
present, motor competences may be impaired in accordance with the intellectual disability.
However, if the motor difficulties are in excess of what could be accounted for by the intellectual
developmental disorder, and criteria for developmental coordination disorder are met,
developmental coordination disorder can be diagnosed as well.

Attention-deficit/hyperactivity disorder.
Autism spectrum disorder.
Joint hypermobility syndrome.
F98.4
Individuals with ADHD may fall, bump into objects, or
knock things over. Careful observation across different contexts is required to ascertain if lack of
motor competence is attributable to distractibility and impulsiveness rather than to
developmental coordination disorder. If criteria for both ADHD and developmental coordination
disorder are met, both diagnoses can be given.
Individuals with autism spectrum disorder may be uninterested in
participating in tasks requiring complex coordination skills, such as ball sports, which will affect
test performance and function but not reflect core motor competence. Co-occurrence of
developmental coordination disorder and autism spectrum disorder is common. If criteria for
both disorders are met, both diagnoses can be given.
Individuals with syndromes causing hyperextensible joints (found
on physical examination; often with a complaint of pain) may present with symptoms similar to
those of developmental coordination disorder.
Comorbidity
Disorders that commonly co-occur with developmental coordination disorder include
communication disorders; specific learning disorder (especially reading and writing); problems
of inattention, including ADHD (the most frequent coexisting condition, with about 50% cooccurrence); autism spectrum disorder; disruptive and emotional behavior problems; and joint
hypermobility syndrome. Different clusters of co-occurrence may be present (e.g., a cluster with
severe reading disorders, fine motor problems, and handwriting problems; another cluster with
impaired movement control and motor planning). Presence of other disorders does not exclude
developmental coordination disorder but may make testing more difficult and may independently
interfere with the execution of activities of daily living, thus requiring examiner judgment in
ascribing impairment to motor skills.
Stereotypic Movement Disorder
Diagnostic Criteria
A. Repetitive, seemingly driven, and apparently purposeless motor behavior (e.g.,
hand shaking or waving, body rocking, head banging, self-biting, hitting own
body).
B. The repetitive motor behavior interferes with social, academic, or other activities
and may result in self-injury.
C. Onset is in the early developmental period.
D. The repetitive motor behavior is not attributable to the physiological effects of a
substance or neurological condition and is not better explained by another
neurodevelopmental or mental disorder (e.g., trichotillomania [hair-pulling
disorder], obsessive-compulsive disorder).

Specify if:
With self-injurious behavior (or behavior that would result in an injury if
preventive measures were not used)
Without self-injurious behavior
Specify if:
Associated 
with 
a 
known 
genetic 
or 
other 
medical 
condition,
neurodevelopmental disorder, or environmental factor (e.g., Lesch-Nyhan
syndrome, intellectual developmental disorder [intellectual disability], intrauterine
alcohol exposure)
Coding note: Use additional code to identify the associated genetic or other
medical condition, neurodevelopmental disorder, or environmental factor.
Specify current severity:
Mild: Symptoms are easily suppressed by sensory stimulus or distraction.
Moderate: Symptoms require explicit protective measures and behavioral
modification.
Severe: Continuous monitoring and protective measures are required to prevent
serious injury.
Recording Procedures
For stereotypic movement disorder that is associated with a known genetic or other medical
condition, neurodevelopmental disorder, or environmental factor, record stereotypic movement
disorder associated with (name of condition, disorder, or factor) (e.g., stereotypic movement
disorder associated with Lesch-Nyhan syndrome).
Specifiers
The severity of non-self-injurious stereotypic movements ranges from mild presentations that are
easily suppressed by a sensory stimulus or distraction to continuous movements that markedly
interfere with all activities of daily living. Self-injurious behaviors range in severity along
various dimensions, including the frequency, impact on adaptive functioning, and severity of
bodily injury (from mild bruising or erythema from hitting hand against body, to lacerations or
amputation of digits, to retinal detachment from head banging).
Diagnostic Features
The essential feature of stereotypic movement disorder is repetitive, seemingly driven, and
apparently purposeless motor behavior (Criterion A). These behaviors are often rhythmical
movements of the head, hands, or body without obvious adaptive function. The movements may
or may not respond to efforts to stop them. Among typically developing children, the repetitive
movements can usually be stopped when attention is directed to them
or when the child is distracted from performing them. Among children with neurodevelopmental

disorders, the behaviors are typically less responsive to such efforts. In other cases, the
individual demonstrates self-restraining behaviors (e.g., sitting on hands, wrapping arms in
clothing, finding a protective device).
The repertoire of behaviors is variable; each individual presents with his or her own
individually patterned, “signature” behavior. Examples of non-self-injurious stereotypic
movements include, but are not limited to, body rocking, bilateral flapping or rotating hand
movements, flicking or fluttering fingers in front of the face, arm waving or flapping, and head
nodding; mouth stretching is commonly seen in association with upper limb movements.
Stereotyped self-injurious behaviors include, but are not limited to, repetitive head banging, face
slapping, eye poking, and biting of hands, lips, or other body parts. Eye poking is particularly
concerning; it occurs more frequently among children with visual impairment. Multiple
movements may be combined (e.g., cocking the head, rocking the torso, waving a small string
repetitively in front of the face).
Stereotypic movements may occur many times during a day, lasting a few seconds to several
minutes or longer. Frequency can vary from many occurrences in a single day to several weeks
elapsing between episodes. The behaviors vary in context, occurring when the individual is
engrossed in other activities, when excited, stressed, fatigued, or bored. Criterion A requires that
the movements be “apparently” purposeless. However, some functions may be served by the
movements. For example, stereotypic movements might reduce anxiety in response to external
stressors.
Criterion B requires that the stereotypic movements interfere with social, academic, or other
activities and, in some children, may result in self-injury (or would if protective measures were
not used). The presence or absence of self-injurious behavior should be indicated using the
specifiers “with self-injurious behavior” or “without self-injurious behavior.” Onset of
stereotypic movements is in the early developmental period (Criterion C). Criterion D requires
that the repetitive, stereotyped behavior in stereotypic movement disorder is not attributable to
the physiological effects of a substance or neurological condition and is not better explained by
another neurodevelopmental or mental disorder. The presence of stereotypic movements may
indicate an undetected neurodevelopmental problem, especially in children ages 1–3 years.
Prevalence
Simple stereotypic movements (e.g., rocking) are common in young typically developing
children (e.g., 5%–19% in the United Kingdom and United States). Complex stereotypic
movements are much less common (occurring in approximately 3%–4%). Between 4% and 16%
of individuals with intellectual developmental disorder (intellectual disability) in samples from
high-income countries engage in stereotypy and self-injury. The risk is greater in individuals
with severe intellectual developmental disorder. Among individuals with intellectual
developmental disorder living in residential facilities, 10%–15% may have stereotypic
movement disorder with self-injury. Repetitive and restricted behaviors and interests may be risk
markers for the onset of self-injury, aggression, and destruction in children with severe
intellectual developmental disorder.
Development and Course
Stereotypic movements typically begin within the first 3 years of life. Simple stereotypic

Environmental.
Genetic and physiological.
Normal development.
movements are common in infancy and may be involved in acquisition of motor mastery. In
children who develop complex motor stereotypies, approximately 80% exhibit symptoms before
age 24 months, 12% between 24 and 35 months, and 8% at 36 months or older. In most typically
developing children, the severity and frequency of stereotyped movements diminish over time.
Onset of complex motor stereotypies may be in infancy or later in the developmental period.
Among individuals with intellectual developmental
disorder, the stereotyped, self-injurious behaviors may persist for years, even though the
typography or pattern of self-injury may change.
Risk and Prognostic Factors
Social isolation is a risk factor for self-stimulation that may progress to
stereotypic movements with repetitive self-injury. Environmental stress may also trigger
stereotypic behavior. Fear may alter physiological state, resulting in increased frequency of
stereotypic behaviors.
Stereotypic movement disorder is believed to be somewhat heritable
based on the high frequency of cases that have a positive family history of motor stereotypies.
Significant reduction in the putamen volume in children with stereotypies suggests that distinct
cortical-striatal pathways associated with habitual behaviors (i.e., premotor to posterior putamen
circuits) may be the underlying anatomical site in complex motor stereotypies. Lower cognitive
functioning is linked to greater risk for stereotypic behaviors and poorer response to
interventions. Stereotypic movements are more frequent among individuals with moderate-tosevere/profound intellectual developmental disorder, who by virtue of a particular syndrome
(e.g., Rett syndrome) or environmental factor (e.g., an environment with relatively insufficient
stimulation) seem to be at higher risk for stereotypies. Repetitive self-injurious behavior may be
a behavioral phenotype in neurogenetic syndromes. For example, in Lesch-Nyhan syndrome,
there are both stereotypic dystonic movements and self-mutilation of fingers, lip biting, and other
forms of self-injury unless the individual is restrained, and in Rett syndrome and Cornelia de
Lange syndrome, self-injury may result from the hand-to-mouth stereotypies. Stereotypic
behaviors may also result from a painful medical condition (e.g., middle ear infection, dental
problems, gastroesophageal reflux).
Culture-Related Diagnostic Issues
Stereotypic repetitive behaviors, with or without self-injury, variedly manifest in many cultures.
Cultural attitudes toward unusual behaviors may result in delayed diagnosis. Overall cultural
tolerance and attitudes toward stereotypic movement vary and must be considered.
Differential Diagnosis
Simple stereotypic movements are common in infancy and early childhood.
Rocking may occur in the transition from sleep to awake, a behavior that usually resolves with
age. Complex stereotypies are less common in typically developing children and can usually be
suppressed by distraction or sensory stimulation. The individual’s daily routine is rarely affected,

Autism spectrum disorder.
Tic disorders.
Obsessive-compulsive and related disorders.
Other neurological and medical conditions.
and the movements generally do not cause the child distress. The diagnosis would not be
appropriate in these circumstances.
Stereotypic movements may be a presenting symptom of autism
spectrum disorder and should be considered when repetitive movements and behaviors are being
evaluated. Deficits of social communication and reciprocity manifesting in autism spectrum
disorder are generally absent in stereotypic movement disorder, and thus social interaction, social
communication, and rigid repetitive behaviors and interests are distinguishing features. When
autism spectrum disorder is present, stereotypic movement disorder is diagnosed only when there
is self-injury or when the stereotypic behaviors are sufficiently severe to become a focus of
treatment.
Typically, stereotypies have an earlier age at onset (before 3 years) than do tics,
which have a mean age at onset of 4–6 years. They also are consistent and fixed in their pattern
or topography compared with tics, which are variable in their presentation,
typically changing in character over time. Stereotypies may involve arms, hands, or the entire
body, while tics commonly involve eyes, face, head, and shoulders. Stereotypies are more fixed,
rhythmic, and prolonged in duration than tics, which, generally, are brief, rapid, random, and
fluctuating. Stereotypies are ego-syntonic (children enjoy them) as opposed to tics, which are
usually ego-dystonic. Tics wax and wane in location and time and are uniquely associated with
premonitory urge (a physical feeling that precedes many tic movements). Tics and stereotypic
movements are both reduced by distraction.
Stereotypic movement disorder is distinguished from
obsessive-compulsive disorder (OCD) by the absence of obsessions, as well as by the nature of
the repetitive behaviors. In OCD the individual feels driven to perform repetitive behaviors in
response to an obsession or according to rules that must be applied rigidly, whereas in
stereotypic movement disorder the behaviors are seemingly driven but apparently purposeless.
Trichotillomania (hair-pulling disorder) and excoriation (skin-picking) disorder are characterized
by body-focused repetitive behaviors (i.e., hair pulling and skin picking) that may be seemingly
driven but that are not apparently purposeless, and that may not be patterned or rhythmical.
Furthermore, onset in trichotillomania and excoriation disorder is not typically in the early
developmental period, but rather around puberty or later.
The diagnosis of stereotypic movements requires the
exclusion of habits, mannerisms, paroxysmal dyskinesias, and benign hereditary chorea. A
neurological history and examination are required to assess features suggestive of other
disorders, such as myoclonus, dystonia, tics, and chorea. Involuntary movements associated with
a neurological condition may be distinguished by their signs and symptoms. For example,
repetitive, stereotypic movements in tardive dyskinesia can be distinguished by a history of
chronic neuroleptic use and characteristic oral or facial dyskinesia or irregular trunk or limb
movements. These types of movements do not result in self-injury. Stereotypies are a common
manifestation of a variety of neurogenetic disorders, such as Lesch-Nyhan syndrome, Rett
syndrome, fragile X syndrome, Cornelia de Lange syndrome, and Smith-Magenis syndrome. For
stereotypic movement disorder that is associated with a known genetic or other medical

Substance-induced repetitive behaviors.
Functional (conversion) stereotypies.
F95.2
F95.1
condition, neurodevelopmental disorder, or environmental factor, record stereotypic movement
disorder associated with (name of condition, disorder, or factor) (e.g., stereotypic movement
disorder associated with Lesch-Nyhan syndrome).
A diagnosis of stereotypic movement disorder is not
appropriate for repetitive skin picking or scratching associated with amphetamine intoxication or
abuse. In such cases, the diagnosis substance/medication-induced obsessive-compulsive and
related disorder would apply.
Stereotyped 
movements 
must 
be 
distinguished 
from
functional (conversion) movements. Sudden onset, distractibility, changing pattern with
unexplained improvement or aggravation, and the coexistence of other symptoms of functional
neurological symptom disorder (conversion disorder) are some of the typical features that help
identify functional stereotypies.
Comorbidity
Common comorbidities in children with chronic motor stereotypies include attention-deficit
hyperactivity disorder, motor coordination problems, tics/Tourette’s disorder, and anxiety.
Tic Disorders
Diagnostic Criteria
Note: A tic is a sudden, rapid, recurrent, nonrhythmic motor movement or
vocalization.
Tourette’s Disorder
A. Both multiple motor and one or more vocal tics have been present at
some time during the illness, although not necessarily concurrently.
B. The tics may wax and wane in frequency but have persisted for more than 1 year
since first tic onset.
C. Onset is before age 18 years.
D. The disturbance is not attributable to the physiological effects of a substance
(e.g., cocaine) or another medical condition (e.g., Huntington’s disease, postviral
encephalitis).
Persistent (Chronic) Motor or Vocal Tic Disorder
A. Single or multiple motor or vocal tics have been present during the
illness, but not both motor and vocal.
B. The tics may wax and wane in frequency but have persisted for more than 1 year
since first tic onset.

F95.0
C. Onset is before age 18 years.
D. The disturbance is not attributable to the physiological effects of a substance
(e.g., cocaine) or another medical condition (e.g., Huntington’s disease, postviral
encephalitis).
E. Criteria have never been met for Tourette’s disorder.
Specify if:
With motor tics only
With vocal tics only
Provisional Tic Disorder
A. Single or multiple motor and/or vocal tics.
B. The tics have been present for less than 1 year since first tic onset.
C. Onset is before age 18 years.
D. The disturbance is not attributable to the physiological effects of a substance
(e.g., cocaine) or another medical condition (e.g., Huntington’s disease, postviral
encephalitis).
E. Criteria have never been met for Tourette’s disorder or persistent (chronic) motor
or vocal tic disorder.
Specifiers
The “motor tics only” or “vocal tics only” specifier is only required for persistent (chronic)
motor or vocal tic disorder.
Diagnostic Features
Tic disorders comprise five diagnostic categories: Tourette’s disorder, persistent (chronic) motor
or vocal tic disorder, provisional tic disorder, and the other specified and unspecified tic
disorders. Diagnosis for any of the specific tic disorders is based on the presence of motor and/or
vocal tics (Criterion A), duration of tics (Criterion B), age at onset (Criterion C), and absence of
any known cause such as another medical condition or substance use (Criterion D). The tic
disorder diagnoses are hierarchical in order (i.e., Tourette’s disorder, followed by persistent
[chronic] motor or vocal tic disorder, followed by provisional tic
disorder, followed by the other specified and unspecified tic disorders). Once a tic disorder at
one level of the hierarchy is diagnosed, a lower hierarchy diagnosis cannot be made (Criterion
E).
Tics are typically sudden, rapid, recurrent, nonrhythmic motor movements or vocalizations.
Some motor tics can be slower twisting or tightening movements that occur over varying lengths
of time. An individual may exhibit various tics over time, but, at any point in time, the tic
repertoire may recur in a characteristic fashion. Although tics can include almost any muscle
group or vocalization, certain tics, such as eye blinking or throat clearing, are common across

patient populations. There is often a localized uncomfortable sensation (premonitory sensation)
prior to a tic, and most individuals report an “urge” to tic. Consequently, tics are generally
experienced as involuntary, but some tics can be voluntarily suppressed for varying lengths of
time.
Explicit discussion of tics can serve as a trigger. Likewise, observing a gesture or sound in
another person may result in an individual with a tic disorder making a similar gesture or sound,
which may be incorrectly perceived by others as purposeful. This can be particularly problematic
when the individual is interacting with authority figures who do not have an adequate
understanding of tic disorders (e.g., teachers, supervisors, police).
Tics are classically categorized as either simple or complex. Simple motor tics are
characterized by the limited involvement of specific muscle groups, often are of short duration,
and can include eye blinks, facial grimaces, shoulder shrugs, or extension of the extremities.
Simple vocal tics include throat clearing, sniffs, chirps, barks, or grunting often caused by
contraction of the diaphragm or muscles of the oropharynx. Complex motor tics are of longer
duration and often include a combination of simple tics such as simultaneous head turning and
shoulder shrugging. Complex tics can appear purposeful, such as head gestures or torso
movements. They can also include imitations of someone else’s movements (echopraxia) or
sexual or taboo gestures (copropraxia). Similarly, complex vocal tics have linguistic meaning
(words or partial words) and can include repeating one’s own sounds or words (palilalia),
repeating the last-heard word or phrase (echolalia), or uttering socially unacceptable words,
including obscenities, or ethnic, racial, or religious slurs (coprolalia). Importantly, coprolalia is
an abrupt, sharp bark or grunt utterance and lacks the prosody of similar inappropriate speech
observed in human interactions.
The presence of motor and/or vocal tics varies across the five tic disorders (Criterion A). For
Tourette’s disorder, both motor and vocal tics must be present (though not necessarily
concurrently), whereas for persistent (chronic) motor or vocal tic disorder, only motor or only
vocal tics are present. For provisional tic disorder, motor and/or vocal tics may be present. For
other specified or unspecified tic disorders, the tics or tic-like symptoms are best characterized as
tics but are atypical in presentation or age at onset, or have a known etiology.
The 1-year minimum duration criterion (Criterion B) assures that individuals diagnosed with
either Tourette’s disorder or persistent (chronic) motor or vocal tic disorder have had persistent
symptoms. Tics wax and wane in severity, and some individuals may have tic-free intervals of
weeks to months; however, an individual who has had tics of greater than 1 year’s duration since
first tic onset would be considered to have persistent symptoms regardless of intermittent tic-free
periods. For an individual with motor and/or vocal tics for less than 1 year since first tic onset, a
provisional tic disorder diagnosis can be considered. The onset of tics must occur prior to age 18
years (Criterion C). Tic disorders typically begin in the prepubertal period, with an average age
at onset between 4 and 6 years, and with the incidence of first-onset tic disorders decreasing in
the later teen years. First onset of tics in adulthood is exceedingly rare and is often associated
with exposures to illicit substances (e.g., excessive cocaine use), is the result of a central nervous
system insult, or is related to a functional neurological disorder. Although first onset of tics is
uncommon in teenagers and adults, it is not uncommon for adolescents and adults to present for
an initial diagnostic assessment and, when carefully evaluated, provide a history of milder tics
dating

95
back to childhood, even if earlier phases of development included tic-free periods of months
or years. First-onset abnormal movements suggestive of tics that occur outside of the usual age
range should result in evaluation for other movement disorders, including functional tic-like
complex movements or vocalizations.
Tics cannot be attributable to the physiological effects of a substance or another medical
condition (Criterion D). When there is strong evidence from the history, physical examination,
and/or laboratory results to suggest a plausible, proximal, and probable cause for a tic disorder, a
diagnosis of other specified tic disorder should be used.
Having previously met diagnostic criteria for Tourette’s disorder negates a possible diagnosis
of persistent (chronic) motor or vocal tic disorder (Criterion E). Similarly, a previous diagnosis
of persistent (chronic) motor or vocal tic disorder negates a diagnosis of provisional tic disorder
or other specified or unspecified tic disorder (Criterion E).
Prevalence
Tics are common in childhood but transient in most cases. A national survey in the United States
estimated 3 per 1,000 for the prevalence of clinically identified cases. The frequency of
identified cases was lower among African Americans and Latinx individuals, which may be
related to differences in access to care. The estimated prevalence of Tourette’s disorder in
Canada ranges from 3 to 9 per 1,000 in school-age children. Globally, males are more commonly
affected than females, with the ratio varying from 2:1 to 4:1. Epidemiological studies have
shown tics to be present in children from all continents, but exact prevalence rates are influenced
by methodological differences in research.
Development and Course
First onset of tics is typically between ages 4 and 6 years. Eye blinking is highly characteristic as
an initial symptom. Peak severity occurs between ages 10 and 12 years, with a decline in severity
during adolescence. Many adults with tic disorders experience diminished symptoms. However,
a percentage of individuals will have persistently severe or worsening symptoms in adulthood.
Tics manifest similarly in all age groups and across the lifespan. Tics wax and wane in
severity (frequency and intensity) and over time change with regard to the affected muscle
groups and nature of vocalizations. Many individuals, including young children, report that their
tics are associated with a localized bodily sensation preceding the tic and a premonitory urge to
move. It can be difficult to find words to describe these premonitory sensations and urges. Tics
associated with a premonitory urge may be experienced as not completely “involuntary” in that
the urge and the tic can be resisted. An individual may also feel the need to perform a tic
repeatedly or in a specific way until the individual feels that the tic has been done “just right.”
Often there is a feeling of relief and tension reduction following the expression of the tic or a
series of tics.
The vulnerability toward developing co-occurring conditions changes as individuals pass
through the age of risk for various co-occurring conditions. For example, prepubertal children
with tic disorders are more likely to exhibit co-occurring attention-deficit/hyperactivity disorder
(ADHD), obsessive-compulsive disorder (OCD), and separation anxiety disorder. Teenagers and
adults are more vulnerable to developing mood and anxiety disorders as well as substance use

Environmental.
Genetic and physiological.
Course modifiers.
disorders.
Risk and Prognostic Factors
Early in brain development, a number of environmental risk factors have been
identified, including advanced paternal age as well as pre- and perinatal adverse events (e.g.,
impaired fetal growth, maternal intrapartum fever, maternal smoking, severe maternal
psychosocial stress, preterm birth, breech presentation, and cesarean delivery).
Genetic factors influence tic expression and severity. The heritability of
tic disorders is estimated to be 70%–85%, and there are no differences in familial risk or
heritability between males and females. Important risk alleles for Tourette’s disorder and rare
genetic variants in families with tic disorders have been identified. Common genetic variants
have also been identified. They are shared across tic disorders in a graded fashion that correlates
with disease severity. Indeed, tic disorders likely exist along a continuous developmental
spectrum, based on both their phenomenology and their genetic background.
Chronic tic disorders have shared genetic variance with OCD, ADHD, and other
neurodevelopmental disorders, including autism spectrum disorder. In addition, individuals with
tic disorders are at increased risk to develop an autoimmune disorder (e.g., Hashimoto’s
thyroiditis). It is increasingly evident that the immune system and neuroinflammation play
important roles in the pathobiology of tics in at least a subset of affected individuals (e.g., those
with Sydenham's chorea). However, more work is needed to understand the biobehavioral
underpinnings and the potential causative role of infections for other neuropsychiatric conditions,
including pediatric acute-onset neuropsychiatric syndrome and pediatric autoimmune
neuropsychiatric disorder associated with streptococcal infections.
Tics are increased by anxiety, excitement, and exhaustion and are better during
calm, focused activities. For example, many individuals typically have fewer tics when engaged
in tasks that require focused attention and motor control. Stressful/exciting events (e.g., taking a
test, participating in exciting activities) often make tics worse.
Culture-Related Diagnostic Issues
Tic disorders do not appear to vary in clinical characteristics, course, or etiology by ethnic,
racialized, and cultural background, but these backgrounds may affect how tic disorders are
perceived and managed in the family and community, influencing patterns of help seeking and
choices of treatment, such as age at presentation at specialty services. For example, preferred
social distance from individuals with tic disorders (e.g., when working or studying together) was
greater in a Korean sample than in U.S. studies.
Sex- and Gender-Related Diagnostic Issues
Males are more commonly affected than females, but there are no sex differences in the kinds of
tics, age at onset, or course. Women with persistent tic disorders may be more likely to
experience anxiety and depression.
Association With Suicidal Thoughts or Behavior

Abnormal movements that may accompany other medical conditions, including other
movement disorders.
Paroxysmal dyskinesias.
A matched case-cohort study in Sweden from 1969 to 2013 demonstrated that individuals with
Tourette’s disorder or persistent (chronic) motor or vocal tic disorder have a substantially
increased risk of suicide attempts (odds ratio 3.86) and suicide death (odds ratio 4.39), even after
adjustment for psychiatric comorbidities, compared with matched general population control
subjects. Persistence of tics after young adulthood and a prior suicide attempt were the strongest
predictors of suicide death. Case-control data suggest that about 1 in 10 youth with persistent
(chronic) motor or vocal tic disorder has suicidal thoughts and/or behaviors, particularly in the
context of anger/frustration and associated with anxiety/depression, social problems or
withdrawal, aggression and internalizing problems, tic severity, and related impairment.
Functional Consequences of Tic Disorders
Many individuals with mild to moderate tic severity experience no distress or impairment in
functioning and may even be unaware of their tics. Individuals with more severe
symptoms generally have more impairment in daily living, but even individuals with moderate or
even severe tic disorders may function well. The presence of a co-occurring condition, such as
ADHD or OCD, can have greater impact on functioning than the tics themselves. Less
commonly, tics disrupt functioning in daily activities and result in social isolation, interpersonal
conflict, peer victimization, inability to work or to go to school, and lower quality of life. Often
individuals with tics have difficulty focusing their attention on work-related tasks while they are
actively trying to suppress their tics. The individual also may experience substantial
psychological distress and even suicidal thoughts. Rare complications of Tourette’s disorder
include physical injury, such as eye injury (from hitting oneself in the face), and orthopedic and
neurological injury (e.g., disc disease related to forceful head and neck movements).
Differential Diagnosis
Motor stereotypies are defined as involuntary rhythmic, repetitive, predictable movements that
appear purposeful but serve no obvious adaptive function. They are often self-soothing or
pleasurable and stop with distraction. Examples include repetitive hand waving/rotating, arm
flapping, and finger wiggling. Motor stereotypies can usually be differentiated from tics based on
the former’s earlier age at onset (often younger than 3 years), prolonged duration (seconds to
minutes), being repetitive and rhythmic in form and location, lacking a premonitory sensation or
urge, and cessation with distraction (e.g., hearing name called or being touched). Chorea
represents rapid, random, continual, abrupt, irregular, unpredictable, nonstereotyped actions that
are usually bilateral and affect all parts of the body (i.e., face, trunk, and limbs). The timing,
direction, and distribution of movements vary from moment to moment, and movements usually
worsen during attempted voluntary action. Dystonia is the simultaneous sustained contraction of
both agonist and antagonist muscles, resulting in a distorted posture or movement of parts of the
body. Dystonic postures are often triggered by attempts at voluntary movements and are not seen
during sleep.
Paroxysmal dyskinesias are characterized by episodic involuntary

Myoclonus.
Obsessive-compulsive and related disorders.
Functional tic disorder.
dystonic or choreoathetoid movements that are precipitated by voluntary movement or exertion
and less commonly arise from normal background activity.
Myoclonus is characterized by a sudden unidirectional movement that is often
nonrhythmic. It may be worsened by movement and occur during sleep. Myoclonus is
differentiated from tics by its rapidity, lack of suppressibility, and absence of a premonitory
sensation or urge.
Differentiating compulsions in OCD from complex
tics may be difficult, especially because they frequently co-occur in the same individual. The
compulsions of OCD are aimed at preventing or reducing anxiety or distress and are usually
performed in response to an obsession (e.g., fear of contamination). In contrast, many individuals
with a tic disorder feel the need to perform the action in a particular fashion, equally on both
sides of the body a certain number of times or until a “just right” feeling is achieved. Bodyfocused repetitive behavior disorders (i.e., persistent hair-pulling, skin-picking, nail-biting) are
more goal-directed and complex than tics.
Functional disorders should also be considered when an individual
presents with “tic attacks” that can go on for extended periods of time lasting from 15 minutes to
several hours.
Comorbidity
Many medical and psychiatric conditions have been described as co-occurring with tic disorders,
and ADHD, disruptive behavior, and OCD and related disorders are particularly
common. Children with ADHD may demonstrate disruptive behavior, social immaturity, and
learning difficulties that may interfere with academic progress and interpersonal relationships
and lead to greater impairment than that caused by a tic disorder. The obsessive-compulsive
symptoms observed in tic disorders tend to have an earlier age at onset and often are
characterized by a need for symmetry and exactness and/or forbidden or taboo thoughts (e.g.,
aggressive, sexual, or religious obsessions and related compulsions). Individuals with tic
disorders can also have other movement disorders (e.g., Sydenham’s chorea, stereotypic
movement disorder) and other neurodevelopmental and psychiatric conditions, such as autism
spectrum disorder and specific learning disorder. As noted earlier, teenagers and adults with a tic
disorder are at increased risk for developing a mood, anxiety, or substance use disorder.
Other Specified Tic Disorder
F95.8
This category applies to presentations in which symptoms characteristic of a tic
disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for a tic disorder or any of the disorders in the neurodevelopmental

disorders diagnostic class. The other specified tic disorder category is used in
situations in which the clinician chooses to communicate the specific reason that the
presentation does not meet the criteria for a tic disorder or any specific
neurodevelopmental disorder. This is done by recording “other specified tic disorder”
followed by the specific reason (e.g., “with onset after age 18 years”).
Unspecified Tic Disorder
F95.9
This category applies to presentations in which symptoms characteristic of a tic
disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for a tic disorder or for any of the disorders in the neurodevelopmental
disorders diagnostic class. The unspecified tic disorder category is used in situations
in which the clinician chooses not to specify the reason that the criteria are not met
for a tic disorder or for a specific neurodevelopmental disorder and includes
presentations in which there is insufficient information to make a more specific
diagnosis.
Other Neurodevelopmental Disorders
Other Specified Neurodevelopmental Disorder
F88
This category applies to presentations in which symptoms characteristic of a
neurodevelopmental disorder that cause impairment in social, occupational, or other
important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the neurodevelopmental disorders diagnostic class. The other
specified neurodevelopmental disorder category is used in situations in which the
clinician chooses to communicate the specific reason that the presentation does not
meet the criteria for any specific neurodevelopmental disorder. This is done by
recording “other specified neurodevelopmental disorder” followed by the specific
reason (e.g., “neurodevelopmental disorder associated with prenatal alcohol
exposure”).
An example of a presentation that can be specified using the “other specified”
designation is the following:

Neurodevelopmental disorder associated with prenatal alcohol exposure:
Neurodevelopmental disorder associated with prenatal alcohol exposure is
characterized by a range of developmental disabilities following exposure to
alcohol in utero.
Unspecified Neurodevelopmental Disorder
F89
This category applies to presentations in which symptoms characteristic of a
neurodevelopmental disorder that cause impairment in social, occupational, or other
important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the neurodevelopmental disorders diagnostic class. The unspecified
neurodevelopmental disorder category is used in situations in which the clinician
chooses not to specify the reason that the criteria are not met for a specific
neurodevelopmental disorder and includes presentations in which there is
insufficient information to make a more specific diagnosis (e.g., in emergency room
settings).

# 02 - Schizophrenia Spectrum and Other Psychotic Di

# Schizophrenia Spectrum and Other Psychotic Disorders

101

Schizophrenia Spectrum and Other Psychotic
Disorders
Schizophrenia spectrum and other psychotic disorders include schizophrenia, other
psychotic disorders, and schizotypal (personality) disorder. They are defined by abnormalities in
one or more of the following five domains: delusions, hallucinations, disorganized thinking
(speech), grossly disorganized or abnormal motor behavior (including catatonia), and negative
symptoms.
Key Features That Define the Psychotic Disorders
Delusions
Delusions are fixed beliefs that are not amenable to change in light of conflicting evidence. Their
content may include a variety of themes (e.g., persecutory, referential, somatic, religious,
grandiose). Persecutory delusions (i.e., belief that one is going to be harmed, harassed, and so
forth by an individual, organization, or other group) are most common. Referential delusions
(i.e., belief that certain gestures, comments, environmental cues, and so forth are directed at
oneself) are also common. Grandiose delusions (i.e., when an individual believes that he or she
has exceptional abilities, wealth, or fame) and erotomanic delusions (i.e., when an individual
believes falsely that another person is in love with him or her) are also seen. Nihilistic delusions
involve the conviction that a major catastrophe will occur, and somatic delusions focus on
preoccupations regarding health and organ function.
Delusions are deemed bizarre if they are clearly implausible and not understandable to sameculture peers and do not derive from ordinary life experiences. An example of a bizarre delusion
is the belief that an outside force has removed his or her internal organs and replaced them with
someone else’s organs without leaving any wounds or scars. An example of a nonbizarre
delusion is the belief that one is under surveillance by the police, despite a lack of convincing
evidence. Delusions that express a loss of control over mind or body are generally considered to
be bizarre; these include the belief that one’s thoughts have been “removed” by some outside
force (thought withdrawal), that alien thoughts have been put into one’s mind (thought
insertion), or that one’s body or actions are being acted on or manipulated by some outside force
(delusions of control).
The distinction between a delusion and a strongly held idea is sometimes difficult to
determine and depends in part on the degree of conviction with which the belief is held despite
clear or reasonable contradictory evidence regarding its veracity. Assessing delusions in
individuals from a variety of cultural backgrounds can be difficult. Some religious and
supernatural beliefs (e.g., evil eye, causing illness through curses, influence of spirits) may be
viewed as bizarre and possibly delusional in some cultural contexts but be generally accepted in

others. However, elevated religiosity can be a feature of many presentations of psychosis.
Individuals who have experienced torture, political violence, or discrimination can report
fears that may be misjudged as persecutory delusions; these may represent instead intense fears
of recurrence or posttraumatic symptoms. A careful evaluation of whether the
person’s fears are justified given the nature of the trauma can help to differentiate appropriate
fears from persecutory delusions.
Hallucinations
Hallucinations are perception-like experiences that occur without an external stimulus. They are
vivid and clear, with the full force and impact of normal perceptions, and not under voluntary
control. They may occur in any sensory modality, but auditory hallucinations are the most
common in schizophrenia and related disorders. Auditory hallucinations are usually experienced
as voices, whether familiar or unfamiliar, that are perceived as distinct from the individual’s own
thoughts. The hallucinations must occur in the context of a clear sensorium; those that occur
while falling asleep (hypnagogic) or waking up (hypnopompic) are considered to be within the
range of normal experience. Hallucinations may be a normal part of religious experience in
certain cultural contexts.
Disorganized Thinking (Speech)
Disorganized thinking (formal thought disorder) is typically inferred from the individual’s
speech. The individual may switch from one topic to another (derailment or loose associations).
Answers to questions may be obliquely related or completely unrelated (tangentiality). Rarely,
speech may be so severely disorganized that it is nearly incomprehensible and resembles
receptive aphasia in its linguistic disorganization (incoherence or “word salad”). Because mildly
disorganized speech is common and nonspecific, the symptom must be severe enough to
substantially impair effective communication. The severity of the impairment may be difficult to
evaluate if the person making the diagnosis comes from a different linguistic background than
that of the person being examined. For example, some religious groups engage in glossolalia
(“speaking in tongues”); others describe experiences of possession trance (trance states in which
personal identity is replaced by an external possessing identity). These phenomena are
characterized by disorganized speech. These instances do not represent signs of psychosis unless
they are accompanied by other clearly psychotic symptoms. Less severe disorganized thinking or
speech may occur during the prodromal and residual periods of schizophrenia.
Grossly Disorganized or Abnormal Motor Behavior (Including
Catatonia)
Grossly disorganized or abnormal motor behavior may manifest itself in a variety of ways,
ranging from childlike “silliness” to unpredictable agitation. Problems may be noted in any form
of goal-directed behavior, leading to difficulties in performing activities of daily living.
Catatonic behavior is a marked decrease in reactivity to the environment. This ranges from
resistance to instructions (negativism); to maintaining a rigid, inappropriate or bizarre posture; to
a complete lack of verbal and motor responses (mutism and stupor). It can also include

purposeless and excessive motor activity without obvious cause (catatonic excitement). Other
features are repeated stereotyped movements, staring, grimacing, and the echoing of speech.
Although catatonia has historically been associated with schizophrenia, catatonic symptoms are
nonspecific and may occur in other mental disorders (e.g., bipolar or depressive disorders with
catatonia) and in medical conditions (catatonic disorder due to another medical condition).
Negative Symptoms
Negative symptoms account for a substantial portion of the morbidity associated with
schizophrenia but are less prominent in other psychotic disorders. Two negative symptoms are
particularly prominent in schizophrenia: diminished emotional expression and avolition.
Diminished emotional expression includes reductions in the expression of emotions in the
face, eye contact, intonation of speech (prosody), and movements of the hand, head, and face that
normally give an emotional emphasis to speech. Avolition is a decrease in motivated selfinitiated purposeful activities. The individual may sit for long periods of time and show little
interest in participating in work or social activities. Other negative symptoms include alogia,
anhedonia, and asociality. Alogia is manifested by diminished speech output. Anhedonia is the
decreased ability to experience pleasure. Individuals with schizophrenia can still enjoy a
pleasurable activity in the moment and can recall it, but show a reduction in the frequency of
engaging in pleasurable activity. Asociality refers to the apparent lack of interest in social
interactions and may be associated with avolition, but it can also be a manifestation of limited
opportunities for social interactions.
Disorders in This Chapter
This chapter is organized along a gradient of psychopathology. Clinicians should first consider
conditions that do not reach full criteria for a psychotic disorder or are limited to one domain of
psychopathology. Then they should consider time-limited conditions. Finally, the diagnosis of a
schizophrenia spectrum disorder requires the exclusion of another condition that may give rise to
psychosis.
Schizotypal personality disorder is noted within this chapter as it is considered within the
schizophrenia spectrum, although its full description is found in the chapter “Personality
Disorders.” The diagnosis schizotypal personality disorder captures a pervasive pattern of social
and interpersonal deficits, including reduced capacity for close relationships; cognitive or
perceptual distortions; and eccentricities of behavior, usually beginning by early adulthood but in
some cases first becoming apparent in childhood and adolescence. Abnormalities of beliefs,
thinking, and perception are below the threshold for the diagnosis of a psychotic disorder.
Two conditions are defined by abnormalities limited to one domain of psychosis: delusions
or catatonia. Delusional disorder is characterized by at least 1 month of delusions but no other
psychotic symptoms. Catatonia is described later in the chapter and further in this discussion.
Brief psychotic disorder lasts more than 1 day and remits by 1 month. Schizophreniform
disorder is characterized by a symptomatic presentation equivalent to that of schizophrenia
except for its duration (less than 6 months) and the absence of a requirement for a decline in

functioning.
Schizophrenia lasts for at least 6 months and includes at least 1 month of active-phase
symptoms. In schizoaffective disorder, a mood episode and the active-phase symptoms of
schizophrenia occur together and were preceded or are followed by at least 2 weeks of delusions
or hallucinations without prominent mood symptoms.
Psychotic disorders may be induced by substances, medications, toxins, and other medical
conditions. In substance/medication-induced psychotic disorder, the psychotic symptoms are
judged to be a direct physiological consequence of a drug of abuse, a medication, or toxin
exposure and cease after removal of the agent. In psychotic disorder due to another medical
condition, the psychotic symptoms are judged to be a direct physiological consequence of
another medical condition.
Catatonia can occur in several disorders, including neurodevelopmental, psychotic, bipolar,
depressive, and other mental disorders. This chapter also includes the diagnoses catatonia
associated with another mental disorder (catatonia specifier), catatonic disorder due to another
medical condition, and unspecified catatonia, and the diagnostic criteria for all three conditions
are described together.
Other specified and unspecified schizophrenia spectrum and other psychotic disorders are
included for classifying psychotic presentations that do not meet the criteria for any of the
specific psychotic disorders, or psychotic symptomatology about which there is inadequate or
contradictory information.
Clinician-Rated Assessment of Symptoms and Related Clinical
Phenomena in Psychosis
Psychotic disorders are heterogeneous, and the severity of symptoms can predict important
aspects of the illness, such as the degree of cognitive or neurobiological deficits. To move the
field forward, a detailed framework for the assessment of severity is included in Section III,
“Assessment Measures,” which may help with treatment planning, prognostic decision-making,
and research on pathophysiological mechanisms. Section III, “Assessment Measures,” also
contains dimensional assessments of the primary symptoms of psychosis, including
hallucinations, delusions, disorganized speech (except for substance/medication-induced
psychotic disorder and psychotic disorder due to another medical condition), abnormal
psychomotor behavior, and negative symptoms, as well as dimensional assessments of
depression and mania. The severity of mood symptoms in psychosis has prognostic value and
guides treatment. Thus, dimensional assessments of depression and mania for all psychotic
disorders alert clinicians to mood pathology and the need to treat where appropriate. The Section
III scale also includes a dimensional assessment of cognitive impairment. Many individuals with
psychotic disorders have impairments in a range of cognitive domains that predict functional
status. Clinical neuropsychological assessment can help guide diagnosis and treatment, but brief
assessments without formal neuropsychological assessment can provide useful information that
can be sufficient for diagnostic purposes. Formal neuropsychological testing, when conducted,
should be administered and scored by personnel trained in the use of testing instruments. If a

F22
formal neuropsychological assessment is not conducted, the clinician should use the best
available information to make a judgment. Further research on these assessments is necessary to
determine their clinical utility; thus, the assessments available in Section III should serve as a
prototype to stimulate such research.
Cultural Considerations in the Assessment of Psychotic Symptoms
Diagnostic accuracy and the quality of treatment planning may be enhanced by interview
approaches, scales, and tools that have been adapted or validated for the person’s culture and by
using a cultural formulation interview (see Section III, “Culture and Psychiatric Diagnosis”).
Assessing psychosis through interpreters or in a second or third language must avoid the
misunderstanding of unfamiliar metaphors as delusions.
Schizotypal (Personality) Disorder
Criteria and text for schizotypal personality disorder can be found in the chapter “Personality
Disorders.” Because this disorder is considered part of the schizophrenia spectrum of disorders,
and is labeled in this section of ICD-10 as schizotypal disorder, it is listed in this chapter and
discussed in detail in the DSM-5 chapter “Personality Disorders.”
Delusional Disorder
Diagnostic Criteria
A. The presence of one (or more) delusions with a duration of 1 month or longer.
B. Criterion A for schizophrenia has never been met.
Note: Hallucinations, if present, are not prominent and are related to the
delusional theme (e.g., the sensation of being infested with insects associated
with delusions of infestation).
C. Apart from the impact of the delusion(s) or its ramifications, functioning is not
markedly impaired, and behavior is not obviously bizarre or odd.
D. If manic or major depressive episodes have occurred, these have been brief
relative to the duration of the delusional periods.
E. The disturbance is not attributable to the physiological effects of a substance or
another medical condition and is not better explained by another mental
disorder, such as body dysmorphic disorder or obsessive-compulsive disorder.
Specify whether:
Erotomanic type: This subtype applies when the central theme of the delusion
is that another person is in love with the individual.

Grandiose type: This subtype applies when the central theme of the delusion is
the conviction of having some great (but unrecognized) talent or insight or having
made some important discovery.
Jealous type: This subtype applies when the central theme of the individual’s
delusion is that his or her spouse or lover is unfaithful.
Persecutory type: This subtype applies when the central theme of the delusion
involves the individual’s belief that he or she is being conspired against, cheated,
spied on, followed, poisoned or drugged, maliciously maligned, harassed, or
obstructed in the pursuit of long-term goals.
Somatic type: This subtype applies when the central theme of the delusion
involves bodily functions or sensations.
Mixed type: This subtype applies when no one delusional theme predominates.
Unspecified type: This subtype applies when the dominant delusional belief
cannot be clearly determined or is not described in the specific types (e.g.,
referential delusions without a prominent persecutory or grandiose component).
Specify if:
With bizarre content: Delusions are deemed bizarre if they are clearly
implausible, not understandable, and not derived from ordinary life experiences
(e.g., an individual’s belief that a stranger has removed his or her internal organs
and replaced them with someone else’s organs without leaving any wounds or
scars).
Specify if:
The following course specifiers are only to be used after a 1-year duration of the
disorder:
First episode, currently in acute episode: First manifestation of the disorder
meeting the defining diagnostic symptom and time criteria. An acute episode is a
time period in which the symptom criteria are fulfilled.
First episode, currently in partial remission: Partial remission is a time period
during which an improvement after a previous episode is maintained and in
which the defining criteria of the disorder are only partially fulfilled.
First episode, currently in full remission: Full remission is a period of time
after a previous episode during which no disorder-specific symptoms are
present.
Multiple episodes, currently in acute episode
Multiple episodes, currently in partial remission
Multiple episodes, currently in full remission
Continuous: Symptoms fulfilling the diagnostic symptom criteria of the disorder
are remaining for the majority of the illness course, with subthreshold symptom
periods being very brief relative to the overall course.
Unspecified

Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of
psychosis, including delusions, hallucinations, disorganized speech, abnormal
psychomotor
behavior, and negative symptoms. Each of these symptoms may be rated for its
current severity (most severe in the last 7 days) on a 5-point scale ranging from
0 (not present) to 4 (present and severe). (See Clinician-Rated Dimensions of
Psychosis Symptom Severity in the chapter “Assessment Measures.”)
Note: Diagnosis of delusional disorder can be made without using this severity
specifier.
Subtypes
In erotomanic type, the central theme of the delusion is that another person is in love with the
individual. The person about whom this conviction is held is usually of higher status (e.g., a
famous individual or a superior at work) but can be a complete stranger. Efforts to contact the
object of the delusion are common. In grandiose type, the central theme of the delusion is the
conviction of having some great talent or insight or of having made some important discovery.
Less commonly, the individual may have the delusion of having a special relationship with a
prominent individual or of being a prominent person (in which case the actual individual may be
regarded as an impostor). Grandiose delusions may have a religious content. In jealous type, the
central theme of the delusion is that of an unfaithful partner. This belief is arrived at without due
cause and is based on incorrect inferences supported by small bits of “evidence” (e.g., disarrayed
clothing). The individual with the delusion usually confronts the spouse or lover and attempts to
intervene in the imagined infidelity. In persecutory type, the central theme of the delusion
involves the individual’s belief of being conspired against, cheated, spied on, followed,
poisoned, maliciously maligned, harassed, or obstructed in the pursuit of long-term goals. Small
slights may be exaggerated and become the focus of a delusional system. The affected individual
may engage in repeated attempts to obtain satisfaction by legal or legislative action. Individuals
with persecutory delusions are often resentful and angry and may resort to violence against those
they believe are hurting them. In somatic type, the central theme of the delusion involves bodily
functions or sensations. Somatic delusions can occur in several forms. Most common is the belief
that the individual emits a foul odor; that there is an infestation of insects on or in the skin; that
there is an internal parasite; or that parts of the body are not functioning.
Diagnostic Features
The essential feature of delusional disorder is the presence of one or more delusions that persist
for at least 1 month (Criterion A). A diagnosis of delusional disorder is not given if the
individual has ever had a symptom presentation that met Criterion A for schizophrenia (Criterion
B). Apart from the direct impact of the delusions, impairments in psychosocial functioning may
be more circumscribed than those seen in other psychotic disorders such as schizophrenia, and
behavior is not obviously bizarre or odd (Criterion C). If mood episodes occur concurrently with

Genetic and physiological.
the delusions, the total duration of these mood episodes is brief relative to the total duration of
the delusional periods (Criterion D). The delusions are not attributable to the physiological
effects of a substance (e.g., cocaine) or another medical condition (e.g., Alzheimer’s disease) and
are not better explained by another mental disorder, such as body dysmorphic disorder or
obsessive-compulsive disorder (Criterion E).
In addition to the delusions identified in the diagnostic criteria, the assessment of cognition,
depression, and mania symptom domains is vital for making critically important distinctions
between the various schizophrenia spectrum and other psychotic disorders. Whereas delusions
are a sine qua non of delusional disorder, hallucinations and negative symptoms are uncommon
and disorganization is rare. By definition, the presence of catatonia in conjunction with delusions
rules out delusional disorder, because Criterion A for schizophrenia would be met. A subset of
cases has prominent depressive symptoms, but cognitive impairment and mania are rarely
demonstrated.
Associated Features
Social, marital, or work problems can result from the delusional beliefs of delusional disorder.
Individuals with delusional disorder may be able to factually describe that others view their
beliefs as irrational but are unable to accept this themselves (i.e., there may be “factual insight”
but no true insight). Many individuals develop irritable or dysphoric mood, which can sometimes
be understood as a reaction to their delusional beliefs. Anger and violent behavior can occur with
persecutory, jealous, and erotomanic types. The individual may engage in litigious or
antagonistic behavior (e.g., sending hundreds of letters of protest to the government). Legal
difficulties can occur, particularly in jealous and erotomanic types.
Prevalence
The lifetime prevalence of delusional disorder has been estimated at around 0.2% in a Finnish
sample, and the most frequent subtype is persecutory. Delusional disorder, jealous type, is
probably more common in men than in women, but there are no major sex or gender differences
in the overall frequency of delusional disorder or in the content of the delusions.
Development and Course
On average, global functioning is generally better than that observed in schizophrenia. Although
the diagnosis is generally stable, a proportion of individuals go on to develop schizophrenia.
Whereas about a third of individuals with delusional disorder of 1–3 months’ duration
subsequently receive a diagnosis of schizophrenia, the diagnosis of delusional disorder is much
less likely to change if the duration of the disorder is greater than 6–12 months. Although
delusional disorder can occur in younger age groups, it may be more prevalent in older
individuals.
Risk and Prognostic Factors
Delusional disorder has a significant familial relationship with both
schizophrenia and schizotypal personality disorder.

Obsessive-compulsive and related disorders.
Delirium, major neurocognitive disorder, and psychotic disorder due to another medical
condition.
Substance/medication-induced psychotic disorder.
Schizophrenia and schizophreniform disorder.
Culture-Related Diagnostic Issues
An individual’s cultural and religious background must be taken into account in evaluating the
possible presence of delusional disorder; in fact, some traditional beliefs unfamiliar to Western
cultures may be wrongly labeled as delusional, so their context must be carefully assessed. The
nature and content of delusions also vary among different cultural groups.
Functional Consequences of Delusional Disorder
The functional impairment is usually more circumscribed than that seen with other psychotic
disorders, although in some cases, the impairment may be substantial and include poor
occupational functioning and social isolation. When poor psychosocial functioning is present,
delusional beliefs themselves often play a significant role. A common characteristic of
individuals with delusional disorder is the apparent normality of their behavior and appearance
when their delusional ideas are not being discussed or acted on. Men with delusional disorder
generally have more severe symptoms and worse functional outcomes compared with women.
Differential Diagnosis
If an individual with obsessive-compulsive disorder is
completely convinced that his or her obsessive-compulsive disorder beliefs are true, then the
diagnosis of obsessive-compulsive disorder, with absent insight/delusional
beliefs specifier, should be given rather than a diagnosis of delusional disorder. Similarly, if an
individual with body dysmorphic disorder is completely convinced that his or her body
dysmorphic disorder beliefs are true, then the diagnosis of body dysmorphic disorder, with
absent insight/delusional beliefs specifier, should be given rather than a diagnosis of delusional
disorder.
Individuals with these disorders may present with symptoms that suggest delusional disorder.
For example, simple persecutory delusions in the context of major neurocognitive disorder
would be diagnosed as major neurocognitive disorder, with behavioral disturbance.
A 
substance/medication-induced 
psychotic
disorder cross-sectionally may be identical in symptomatology to delusional disorder but can be
distinguished by the chronological relationship of substance use to the onset and remission of the
delusional beliefs.
Delusional disorder can be distinguished from
schizophrenia and schizophreniform disorder by the absence of the other characteristic
symptoms of the active phase of schizophrenia. Furthermore, the quality of delusions can help
distinguish between schizophrenia and delusional disorder. In schizophrenia, delusions show
greater disorganization (the degree to which delusions are internally consistent, logical, and
systematized), whereas in delusional disorder, they show greater conviction (the degree to which
the individual is convinced of the reality of the delusion), greater extension (the degree to which
the delusion involves various areas of the individual’s life), and greater pressure (the degree to

Depressive and bipolar disorders and schizoaffective disorder.
F23
which the individual is preoccupied and concerned with the expressed delusion).
These disorders may be distinguished
from delusional disorder by the temporal relationship between the mood disturbance and the
delusions and by the severity of the mood symptoms. If delusions occur exclusively during mood
episodes, the diagnosis is major depressive or bipolar disorder, with psychotic features. Mood
symptoms that meet full criteria for a mood episode can be superimposed on delusional disorder.
Delusional disorder can be diagnosed only if the total duration of all mood episodes remains
brief relative to the total duration of the delusional disturbance. If not, then a diagnosis of other
specified or unspecified schizophrenia spectrum and other psychotic disorder accompanied by
other specified depressive disorder, unspecified depressive disorder, other specified bipolar and
related disorder, or unspecified bipolar and related disorder is appropriate.
Brief Psychotic Disorder
Diagnostic Criteria
A. Presence of one (or more) of the following symptoms. At least one of these must
be (1), (2), or (3):
1. Delusions.
2. Hallucinations.
3. Disorganized speech (e.g., frequent derailment or incoherence).
4. Grossly disorganized or catatonic behavior.
Note: Do not include a symptom if it is a culturally sanctioned response.
B. Duration of an episode of the disturbance is at least 1 day but less than 1 month,
with eventual full return to premorbid level of functioning.
C. The disturbance is not better explained by major depressive or bipolar disorder
with psychotic features or another psychotic disorder such as schizophrenia or
catatonia, and is not attributable to the physiological effects of a substance (e.g.,
a drug of abuse, a medication) or another medical condition.
Specify if:
With marked stressor(s) (brief reactive psychosis): If symptoms occur in
response to events that, singly or together, would be markedly stressful to
almost anyone in similar circumstances in the individual’s culture.
Without marked stressor(s): If symptoms do not occur in response to events
that, singly or together, would be markedly stressful to almost anyone in similar
circumstances in the individual’s culture.
With peripartum onset: If onset is during pregnancy or within 4 weeks

postpartum.
Specify if:
With catatonia (refer to the criteria for catatonia associated with another mental
disorder, p. 135, for definition).
Coding note: Use additional code F06.1 catatonia associated with brief
psychotic disorder to indicate the presence of the comorbid catatonia.
Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of
psychosis, including delusions, hallucinations, disorganized speech, abnormal
psychomotor behavior, and negative symptoms. Each of these symptoms may
be rated for its current severity (most severe in the last 7 days) on a 5-point
scale ranging from 0 (not present) to 4 (present and severe). (See ClinicianRated Dimensions of Psychosis Symptom Severity in the chapter “Assessment
Measures.”)
Note: Diagnosis of brief psychotic disorder can be made without using this
severity specifier.
Diagnostic Features
The essential feature of brief psychotic disorder is a disturbance that involves at least one of the
following positive psychotic symptoms: delusions, hallucinations, disorganized speech (e.g.,
frequent derailment or incoherence), or grossly abnormal psychomotor behavior, including
catatonia (Criterion A). An episode of the disturbance lasts at least 1 day but less than 1 month,
and the individual eventually has a full return to the premorbid level of functioning (Criterion B).
The disturbance is not better explained by a depressive or bipolar disorder with psychotic
features, by schizoaffective disorder, or by schizophrenia and is not attributable to the
physiological effects of a substance (e.g., a hallucinogen) or another medical condition (e.g.,
subdural hematoma) (Criterion C).
In addition to the four symptom domain areas identified in the diagnostic criteria, the
assessment of cognition, depression, and mania symptom domains is vital for making critically
important distinctions between the various schizophrenia spectrum and other psychotic disorders.
Associated Features
Individuals with brief psychotic disorder typically experience emotional turmoil or
overwhelming confusion. They may have rapid shifts from one intense affect to another.
Although the disturbance is brief, the level of impairment may be severe, and supervision may be
required to ensure that nutritional and hygienic needs are met and that the individual is protected
from the consequences of poor judgment, cognitive impairment, or acting on the basis of
delusions. There appears to be an increased risk of suicidal behavior, particularly during the
acute episode.
Prevalence

Other medical conditions.
Substance-related disorders.
Depressive and bipolar disorders.
Brief psychotic disorder may account for 2%–7% of cases of first-onset psychosis in several
countries.
Development and Course
Brief psychotic disorder may appear in adolescence or early adulthood, and onset can occur
across the life span, with the average age at onset being the mid 30s. By definition, a diagnosis of
brief psychotic disorder requires a full remission of all symptoms and an eventual full return to
the premorbid level of functioning within 1 month of the onset of the disturbance. In some
individuals, the duration of psychotic symptoms may be quite brief (e.g., a few days).
Although brief psychotic disorder by definition reaches a full remission within 1 month,
subsequently more than 50% of the individuals experience a relapse. Despite the possibility of
relapse, for most individuals, outcome is favorable in terms of social functioning and
symptomatology.
In less than half of cases diagnosed with DSM-IV brief psychotic disorder or ICD-10 acute
and transient psychotic disorder, the diagnosis changes—more often to schizophrenia spectrum
disorders and less often to affective disorders or to other psychotic disorders.
Culture-Related Diagnostic Issues
It is important to distinguish symptoms of brief psychotic disorder from culturally sanctioned
response patterns. For example, in some religious ceremonies, an individual may report hearing
voices, but these do not generally persist and are not perceived as abnormal by most members of
the individual’s community. In a wide range of cultural contexts, it would be common or
expected for bereaved relatives to hear, see, or interact with the spirit of a recently deceased
loved one without notable pathological sequelae. In addition, cultural and religious background
must be taken into account when considering whether beliefs are delusional.
Differential Diagnosis
A variety of medical conditions can manifest with psychotic symptoms
of short duration. Psychotic disorder due to another medical condition or a delirium is diagnosed
when there is evidence from the history, physical examination, or laboratory tests that the
delusions or hallucinations are the direct physiological consequence of a specific medical
condition (e.g., Cushing’s syndrome, brain tumor) (see “Psychotic Disorder Due to Another
Medical Condition” later in this chapter).
Substance/medication-induced psychotic disorder, substance-induced
delirium, and substance intoxication are distinguished from brief psychotic disorder by the fact
that a substance (e.g., a drug of abuse, a medication, exposure to a toxin) is judged to be
etiologically related to the psychotic symptoms (see “Substance/Medication-Induced Psychotic
Disorder” later in this chapter). Laboratory tests, such as a urine drug screen or a blood alcohol
level, may be helpful in making this determination, as may a careful history of substance use
with attention to temporal relationships between substance intake and onset of the symptoms and
to the nature of the substance being used.
The diagnosis of brief psychotic disorder cannot be made if the
psychotic symptoms are better explained by a mood episode (i.e., the psychotic symptoms occur
exclusively during a full major depressive, manic, or mixed episode).

Other psychotic disorders.
Malingering and factitious disorders.
Personality disorders.
F20.81
If the psychotic symptoms persist for 1 month or longer, the diagnosis
is either schizophreniform disorder, delusional disorder, depressive disorder with psychotic
features, bipolar disorder with psychotic features, or other specified or
unspecified schizophrenia spectrum and other psychotic disorder, depending on the other
symptoms in the presentation. The differential diagnosis between brief psychotic disorder and
schizophreniform disorder is difficult when the psychotic symptoms have remitted before 1
month in response to successful treatment with medication. Careful attention should be given to
the possibility that a recurrent disorder (e.g., bipolar disorder, recurrent acute exacerbations of
schizophrenia) may be responsible for any recurring psychotic episodes.
An episode of factitious disorder with predominantly
psychological signs and symptoms may have the appearance of brief psychotic disorder, but in
such cases there is evidence that the symptoms are intentionally produced. When malingering
involves apparently psychotic symptoms, there is usually evidence that the illness is being
feigned for an understandable goal.
In certain individuals with personality disorders, psychosocial stressors
may precipitate brief periods of psychotic symptoms. These symptoms are usually transient and
do not warrant a separate diagnosis. If psychotic symptoms persist for at least 1 day, an
additional diagnosis of brief psychotic disorder may be appropriate.
Schizophreniform Disorder
Diagnostic Criteria
A. Two (or more) of the following, each present for a significant portion of time
during a 1-month period (or less if successfully treated). At least one of these
must be (1), (2), or (3):
1. Delusions.
2. Hallucinations.
3. Disorganized speech (e.g., frequent derailment or incoherence).
4. Grossly disorganized or catatonic behavior.
5. Negative symptoms (i.e., diminished emotional expression or avolition).
B. An episode of the disorder lasts at least 1 month but less than 6 months. When
the diagnosis must be made without waiting for recovery, it should be qualified
as “provisional.”
C. Schizoaffective disorder and depressive or bipolar disorder with psychotic
features have been ruled out because either 1) no major depressive or manic
episodes have occurred concurrently with the active-phase symptoms, or 2) if
mood episodes have occurred during active-phase symptoms, they have been

present for a minority of the total duration of the active and residual periods of
the illness.
D. The disturbance is not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication) or another medical condition.
Specify if:
With good prognostic features: This specifier requires the presence of at least
two of the following features: onset of prominent psychotic symptoms within 4
weeks of the first noticeable change in usual behavior or functioning; confusion
or perplexity; good premorbid social and occupational functioning; and absence
of blunted or flat affect.
Without good prognostic features: This specifier is applied if two or more of
the above features have not been present.
Specify if:
With catatonia (refer to the criteria for catatonia associated with another mental
disorder, p. 135, for definition).
Coding note: Use additional code F06.1 catatonia associated with
schizophreniform disorder to indicate the presence of the comorbid catatonia.
Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of
psychosis, including delusions, hallucinations, disorganized speech, abnormal
psychomotor behavior, and negative symptoms. Each of these symptoms may
be rated for its current severity (most severe in the last 7 days) on a 5-point
scale ranging from 0 (not present) to 4 (present and severe). (See ClinicianRated Dimensions of Psychosis Symptom Severity in the chapter “Assessment
Measures.”)
Note: Diagnosis of schizophreniform disorder can be made without using this
severity specifier.
Note: For additional information on Associated Features, Development and Course
(age-related factors), Culture-Related Diagnostic Issues, Sex- and Gender-Related
Diagnostic Issues, Differential Diagnosis, and Comorbidity, see the corresponding
sections in Schizophrenia.
Diagnostic Features
The characteristic symptoms of schizophreniform disorder are identical to those of schizophrenia
(Criterion A). Schizophreniform disorder is distinguished by its difference in duration: the total
duration of the illness, including prodromal, active, and residual phases, is at least 1 month but
less than 6 months (Criterion B). The duration requirement for schizophreniform disorder is
intermediate between that for brief psychotic disorder, which lasts more than 1 day and remits by
1 month, and schizophrenia, which lasts for at least 6 months. The diagnosis of schizophreniform

Genetic and physiological.
disorder is made under two conditions: 1) when an episode of illness lasts between 1 and 6
months and the individual has already recovered, and 2) when an individual is symptomatic for
less than the 6 months’ duration required for the diagnosis of schizophrenia but has not yet
recovered. In this case, the diagnosis should be noted as “schizophreniform disorder
(provisional)” because it is uncertain if the individual will recover from the disturbance within
the 6-month period. If the disturbance persists beyond 6 months, the diagnosis should be changed
to schizophrenia.
Another distinguishing feature of schizophreniform disorder is the lack of a criterion
requiring impaired social and occupational functioning. While such impairments may potentially
be present, they are not necessary for a diagnosis of schizophreniform disorder.
In addition to the five symptom domain areas identified in the diagnostic criteria, the
assessment of cognition, depression, and mania symptom domains is vital for making critically
important distinctions between the various schizophrenia spectrum and other psychotic disorders.
Associated Features
As with schizophrenia, currently there are no laboratory or psychometric tests for
schizophreniform disorder. There are multiple brain regions where neuroimaging,
neuropathological, and neurophysiological research has indicated abnormalities, but none are
diagnostic.
Prevalence
Incidence of schizophreniform disorder across sociocultural settings is likely similar to that
observed in schizophrenia. In the United States and other high-income countries, the incidence is
low, possibly fivefold less than that of schizophrenia. In lower-income countries, the incidence
may be higher, especially for the specifier “with good prognostic features”; in some of these
settings schizophreniform disorder may be as common as schizophrenia.
Development and Course
The development of schizophreniform disorder is similar to that of schizophrenia. About onethird of individuals with an initial diagnosis of schizophreniform disorder (provisional) recover
within the 6-month period and schizophreniform disorder is their final diagnosis. The majority of
the remaining two-thirds of individuals will eventually receive a diagnosis of schizophrenia or
schizoaffective disorder.
Risk and Prognostic Factors
Relatives of individuals with schizophreniform disorder have an
increased risk for schizophrenia.
Functional Consequences of Schizophreniform Disorder
For the majority of individuals with schizophreniform disorder who eventually receive a
diagnosis of schizophrenia or schizoaffective disorder, the functional consequences are similar to
the consequences of those disorders. Most individuals experience dysfunction in several areas of

Other mental disorders and medical conditions.
Brief psychotic disorder.
F20.9
daily functioning, such as school or work, interpersonal relationships, and self-care. Individuals
who recover from schizophreniform disorder have better functional outcomes.
Differential Diagnosis
A wide variety of mental disorders and medical
conditions can manifest with psychotic symptoms that must be considered in the differential
diagnosis of schizophreniform disorder. These include psychotic disorder due to another medical
condition or its treatment; delirium or major neurocognitive disorder; substance/medicationinduced psychotic disorder or delirium; major depressive or bipolar disorder with psychotic
features; schizoaffective disorder; other specified or unspecified bipolar and related disorder;
major depressive or bipolar disorder with catatonic features; schizophrenia; delusional disorder;
other specified or unspecified schizophrenia spectrum and other psychotic disorder; schizotypal,
schizoid, or paranoid personality disorders; autism spectrum disorder; disorders presenting in
childhood with disorganized speech; attention-deficit/hyperactivity disorder; obsessivecompulsive disorder; posttraumatic stress disorder; and traumatic brain injury.
Since the diagnostic criteria for schizophreniform disorder and schizophrenia differ primarily
in duration of illness, the discussion of the differential diagnosis of schizophrenia also applies to
schizophreniform disorder.
Schizophreniform disorder differs in duration from brief psychotic
disorder, which has a duration of less than 1 month.
Schizophrenia
Diagnostic Criteria
A. Two (or more) of the following, each present for a significant portion of time
during a 1-month period (or less if successfully treated). At least one of these
must be (1), (2), or (3):
1. Delusions.
2. Hallucinations.
3. Disorganized speech (e.g., frequent derailment or incoherence).
4. Grossly disorganized or catatonic behavior.
5. Negative symptoms (i.e., diminished emotional expression or avolition).
B. For a significant portion of the time since the onset of the disturbance, level of
functioning in one or more major areas, such as work, interpersonal relations, or
self-care, is markedly below the level achieved prior to the onset (or when the
onset is in childhood or adolescence, there is failure to achieve expected level of
interpersonal, academic, or occupational functioning).

C. Continuous signs of the disturbance persist for at least 6 months. This 6-month
period must include at least 1 month of symptoms (or less if successfully treated)
that meet Criterion A (i.e., active-phase symptoms) and may include periods of
prodromal or residual symptoms. During these prodromal or residual periods, the
signs of the disturbance may be manifested by only negative symptoms or by
two or more symptoms listed in Criterion A present in an attenuated form (e.g.,
odd beliefs, unusual perceptual experiences).
D. Schizoaffective disorder and depressive or bipolar disorder with psychotic
features have been ruled out because either 1) no major depressive or manic
episodes have occurred concurrently with the active-phase symptoms, or 2) if
mood episodes have occurred during active-phase symptoms, they have been
present for a minority of the total duration of the active and residual periods of
the illness.
E. The disturbance is not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication) or another medical condition.
F. If there is a history of autism spectrum disorder or a communication disorder of
childhood onset, the additional diagnosis of schizophrenia is made only if
prominent delusions or hallucinations, in addition to the other required symptoms
of schizophrenia, are also present for at least 1 month (or less if successfully
treated).
Specify if:
The following course specifiers are only to be used after a 1-year duration of the
disorder and if they are not in contradiction to the diagnostic course criteria.
First episode, currently in acute episode: First manifestation of the disorder
meeting the defining diagnostic symptom and time criteria. An acute episode is a
time period in which the symptom criteria are fulfilled.
First episode, currently in partial remission: Partial remission is a period of
time during which an improvement after a previous episode is maintained and in
which the defining criteria of the disorder are only partially fulfilled.
First episode, currently in full remission: Full remission is a period of time
after a previous episode during which no disorder-specific symptoms are
present.
Multiple episodes, currently in acute episode: Multiple episodes may be
determined after a minimum of two episodes (i.e., after a first episode, a
remission and a minimum of one relapse).
Multiple episodes, currently in partial remission
Multiple episodes, currently in full remission
Continuous: Symptoms fulfilling the diagnostic symptom criteria of the disorder
are remaining for the majority of the illness course, with subthreshold symptom
periods being very brief relative to the overall course.
Unspecified

Specify if:
With catatonia (refer to the criteria for catatonia associated with another mental
disorder, p. 135, for definition).
Coding note: Use additional code F06.1 catatonia associated with
schizophrenia to indicate the presence of the comorbid catatonia.
Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of
psychosis, including delusions, hallucinations, disorganized speech, abnormal
psychomotor behavior, and negative symptoms. Each of these symptoms may
be rated for its current severity (most severe in the last 7 days) on a 5-point
scale ranging from 0 (not present) to 4 (present and severe). (See ClinicianRated Dimensions of Psychosis Symptom Severity in the chapter “Assessment
Measures.”)
Note: Diagnosis of schizophrenia can be made without using this severity
specifier.
Diagnostic Features
The characteristic symptoms of schizophrenia involve a range of cognitive, behavioral, and
emotional dysfunctions, but no single symptom is pathognomonic of the disorder. The diagnosis
involves the recognition of a constellation of signs and symptoms associated with impaired
occupational or social functioning. Individuals with the disorder will vary substantially on most
features, as schizophrenia is a heterogeneous clinical syndrome.
At least two Criterion A symptoms must be present for a significant portion of time during a
1-month period or longer. At least one of these symptoms must be the clear presence of
delusions (Criterion A1), hallucinations (Criterion A2), or disorganized speech (Criterion A3).
Grossly disorganized or catatonic behavior (Criterion A4) and negative symptoms (Criterion A5)
may also be present. In those situations in which the active-phase symptoms remit within a
month in response to treatment, Criterion A is still met if the clinician estimates that they would
have persisted in the absence of treatment.
Schizophrenia involves impairment in one or more major areas of functioning (Criterion B).
If the disturbance begins in childhood or adolescence, the expected level of function is not
attained. Comparing the individual with unaffected siblings may be helpful. The dysfunction
persists for a substantial period during the course of the disorder and does not appear to be a
direct result of any single feature. Avolition (i.e., reduced drive to pursue goal-directed behavior;
Criterion A5) is linked to the social dysfunction described under Criterion B. There is also strong
evidence for a relationship between cognitive impairment (see the section “Associated Features”
for this disorder) and functional impairment in individuals with schizophrenia.
Some signs of the disturbance must persist for a continuous period of at least 6 months
(Criterion C). Prodromal symptoms often precede the active phase, and residual symptoms may
follow it, characterized by mild or subthreshold forms of hallucinations or delusions. Individuals

may express a variety of unusual or odd beliefs that are not of delusional proportions (e.g., ideas
of reference or magical thinking); they may have unusual perceptual experiences (e.g., sensing
the presence of an unseen person); their speech may be generally understandable but vague; and
their behavior may be unusual but not grossly disorganized (e.g., mumbling in public). Negative
symptoms are common in the prodromal and residual phases and can be severe. Individuals who
had been socially active may become withdrawn from previous routines. Such behaviors are
often the first sign of a disorder.
Mood symptoms and full mood episodes are common in schizophrenia and may be
concurrent with active-phase symptomatology. However, as distinct from a psychotic mood
disorder, a schizophrenia diagnosis requires the presence of delusions or hallucinations in the
absence of mood episodes. In addition, mood episodes, taken in total, should be present for only
a minority of the total duration of the active and residual periods of the illness.
In addition to the five symptom domain areas identified in the diagnostic criteria, the
assessment of cognition, depression, and mania symptom domains is vital for making critically
important distinctions between the various schizophrenia spectrum and other psychotic disorders.
Associated Features
Individuals with schizophrenia may display inappropriate affect (e.g., laughing in the absence of
an appropriate stimulus); a dysphoric mood that can take the form of depression, anxiety, or
anger; a disturbed sleep pattern (e.g., daytime sleeping and nighttime activity); and a lack of
interest in eating or food refusal. Depersonalization, derealization, and somatic concerns may
occur and sometimes reach delusional proportions. Anxiety and phobias are common. Cognitive
deficits in schizophrenia are common and are strongly linked to vocational and functional
impairments. These deficits can include decrements in declarative memory, working memory,
language function, and other executive functions, as well as slower processing speed.
Abnormalities in sensory processing and inhibitory capacity, as well as reductions in attention,
are also found. Some individuals with schizophrenia show social cognition deficits, including
deficits in the ability to infer the intentions of other people (theory of mind), and may attend to
and then interpret irrelevant events or stimuli as meaningful, perhaps leading to the generation of
explanatory delusions. These impairments frequently persist during symptomatic remission.
Some individuals with psychosis may lack insight or awareness of their disorder (i.e.,
anosognosia). This lack of “insight” includes unawareness of symptoms of schizophrenia and
may be present throughout the entire course of the illness. Unawareness of illness is typically a
symptom of schizophrenia itself rather than a coping strategy. It is comparable to the lack of
awareness of neurological deficits following brain damage, termed anosognosia. This symptom
is the most common predictor of nonadherence to treatment, and it predicts higher relapse rates,
increased number of involuntary treatments, poorer psychosocial functioning, aggression, and a
poorer course of illness.
Hostility and aggression can be associated with schizophrenia, although spontaneous or
random assault is uncommon. Aggression is more frequent for younger males and for individuals
with a past history of violence, nonadherence to treatment, substance abuse, and impulsivity. It
should be noted that the vast majority of persons with schizophrenia are not aggressive and are

more frequently victimized than are individuals in the general population.
Currently, there are no radiological, laboratory, or psychometric tests for the disorder.
Differences are evident in multiple brain regions between groups of healthy individuals and
persons with schizophrenia, including evidence from neuroimaging, neuropathological, and
neurophysiological studies. Differences are also evident in cellular architecture, white matter
connectivity, and gray matter volume in a variety of regions such as the prefrontal and temporal
cortices. Reduced overall brain volume has been observed, as well as increased brain volume
reduction with age. Brain volume reductions with age are more pronounced in individuals with
schizophrenia than in healthy individuals. Finally, individuals with schizophrenia appear to differ
from individuals without the disorder in eye-tracking and electrophysiological indices.
Neurological soft signs common in individuals with schizophrenia include impairments in
motor coordination, sensory integration, and motor sequencing of complex movements; left-right
confusion; and disinhibition of associated movements. In addition, minor physical anomalies of
the face and limbs may occur.
Prevalence
The estimated lifetime prevalence of schizophrenia is approximately 0.3%–0.7%, with variation
over a fivefold range in meta-analyses of nationally representative surveys. Studies have shown
increased prevalence and incidence of schizophrenia for some groups based on migration and
refugee status, urbanicity, and the economic status and latitude of the country. It is important to
note that the reported prevalence and incidence of schizophrenia may be affected by the fact that
some groups are more likely to be misdiagnosed or overdiagnosed.
The sex ratio differs across samples and populations: for example, presentations with
prominent negative symptoms and longer duration of disorder (associated with poorer outcome)
show higher incidence rates for men, whereas definitions allowing for the inclusion of more
mood symptoms and brief presentations (associated with better outcome) show equivalent risks
for both sexes. A large worldwide study, which was based on a range of definitions of
schizophrenia, found no difference in prevalence between the sexes.
Development and Course
The requisite psychotic features of the schizophrenia diagnosis typically emerge between the late
teens and the mid-30s; onset prior to adolescence is rare. The peak onset age occurs in the earlyto mid-20s for men and in the late-20s for women. The onset may be abrupt or insidious, but the
majority of individuals manifest a slow and gradual development of a variety of clinically
significant signs and symptoms, particularly social withdrawal, emo-tional changes, and
cognitive changes producing a deterioration in role functioning. Half of these individuals display
depressive symptoms. Prognosis is influenced both by dura-tion and by severity of illness and
gender. Men, especially those with long duration of psychosis before treatment and lower
premorbid adjustment, have more prominent negative symptoms, cognitive impairment, and
generally worse functional outcomes than women. Sociocognitive deficits may manifest during
development and precede the emergence of psychosis, taking the form of stable impairments
during adulthood, refractory to antipsychotic medications.

Environmental.
Course and outcome in schizophrenia are heterogeneous, and prognosis is uncertain at the
onset of psychosis. Although most individuals with schizophrenia remain vulnerable to
exacerbation of psychotic symptoms and a chronic course defined by symptoms and functional
impairment is common, many individuals experience periods of remission and even recovery.
According to a meta-analysis of 79 longitudinal studies of first-episode psychosis with more than
1 year of follow-up, the pooled remission rate (qualitatively defined as mild or absent symptoms
for at least 6 months) for first-episode schizophrenia was 56% and the pooled recovery rate
(qualitatively defined as symptomatic and functional improvement for greater than 2 years) was
30%. A different meta-analysis of 50 studies of individuals with broadly defined schizophrenia
(i.e., schizophrenia, schizophreniform, schizoaffective, or delusional disorder) found that the
median proportion of individuals who met recovery criteria (at most mild symptoms and
improvements in social and/or occupational functioning persisting for at least 2 years) was
13.5%. There is a tendency for reduced psychotic experiences during late life. In addition to
psychosis, cognitive impairment and negative symptom pathology are core features of
schizophrenia, and the course for these characteristic features is different from that of positive
psychotic symptoms. Cognition tends to decline during development prior to full psychosis and
is relatively stable over the longer term. Negative symptoms, if present during development, also
tend to be relatively stable traits over time. Negative symptoms that begin after psychosis onset
are more variable and may reflect secondary causes. A degree of chronicity is required for a
diagnosis of schizophrenia, and long-term course reflects a need for mental health care and living
support in many individuals. While schizophrenia is generally not a progressive
neurodegenerative disorder, life challenges, changing lifestyle, and persistent symptoms may
lead to progressive dysfunction in more severe chronic cases.
The essential features of schizophrenia are the same in childhood, but it is more difficult to
make the diagnosis. In children, delusions and hallucinations may be less elaborate than in
adults, and visual hallucinations are more common and should be distinguished from normal
fantasy play. Disorganized speech occurs in many disorders with childhood onset (e.g., autism
spectrum disorder), as does disorganized behavior (e.g., attention-deficit/hyperactivity disorder).
These symptoms should not be attributed to schizophrenia
without due consideration of the more common disorders of childhood. Childhood-onset
cases tend to resemble poor-outcome adult cases, with gradual onset and prominent negative
symptoms. Children who later receive the diagnosis of schizophrenia are more likely to have
experienced nonspecific emotional-behavioral disturbances and psychopathology, intellectual
and language alterations, and subtle motor delays.
Late-onset cases (i.e., onset after age 40 years) are overrepresented by women, who may
have married. Often, the course is characterized by a predominance of psychotic symptoms with
preservation of affect and social functioning. Such late-onset cases can still meet the diagnostic
criteria for schizophrenia, but it is not yet clear whether this is the same condition as
schizophrenia diagnosed prior to midlife (e.g., prior to age 55 years).
Risk and Prognostic Factors
Season of birth has been linked to the incidence of schizophrenia, including late

Genetic and physiological.
winter/early spring in some locations and summer for the deficit form of the disease. The
incidence of schizophrenia and related disorders may be higher for children growing up in an
urban environment, for refugees, for some migrant groups, and for socially oppressed groups
facing discrimination. There is evidence that social deprivation, social adversity, and
socioeconomic factors may be associated with increased rates of this disorder. Among
individuals with schizophrenia and other psychotic disorders, the severity of positive and
negative symptoms appears to be correlated with the severity of adverse childhood experiences,
such as trauma and neglect. Higher rates of schizophrenia for some ethnic and racialized groups
have been documented when they live in areas with lower proportions of people from the same
ethnicity or racialized group. The reasons for this are not completely clear but appear related to
several factors, including the following: 1) higher levels of discrimination or fear of
discrimination; 2) less social support and more stigmatization of those with schizophrenia; 3)
higher social isolation; and 4) decreased availability of and access to normalizing explanations of
perceptual experiences and abnormal beliefs reported by individuals at high risk for developing
schizophrenia.
There is a strong contribution for genetic factors in determining risk for
schizophrenia, although most individuals who have been diagnosed with schizophrenia have no
family history of psychosis. Liability is conferred by a spectrum of risk alleles, common and
rare, with each allele contributing only a small fraction to the total population variance. The risk
alleles identified to date are also associated with other mental disorders, including bipolar
disorder, depression, and autism spectrum disorder.
Pregnancy and birth complications with hypoxia and greater paternal age are associated with
a higher risk of schizophrenia for the developing fetus. In addition, other prenatal and perinatal
adversities, including stress, infection, malnutrition, maternal diabetes, and other medical
conditions, have been linked with schizophrenia. However, the vast majority of offspring with
these risk factors do not develop schizophrenia.
Culture-Related Diagnostic Issues
The form and content of schizophrenia symptoms can vary cross-culturally, including the
following ways: the relative proportion of visual and auditory hallucinations (e.g., while auditory
hallucinations tend to be more common than visual hallucinations around the world, the relative
proportion of visual hallucinations may be particularly higher in some regions compared with
others); the specific content of the delusions (e.g., persecutory, grandiose, somatic) and
hallucinations (e.g., command, abusive, religious); and the level of fear associated with them.
Cultural and socioeconomic factors must be considered, particularly when the individual and the
clinician do not share the same cultural and socioeconomic background. Ideas that appear to be
delusional in one cultural context (e.g., evil eye, causing illness through curses, influences of
spirits) may be commonly held in others.
In some cultural contexts, visual or auditory hallucinations with a religious content (e.g., hearing
God’s voice) are a normal part of religious experience. In addition, the assessment of
disorganized speech may be made difficult by linguistic variation in narrative styles across
cultures. The assessment of affect requires sensitivity to differences in styles of emotional

expression, eye contact, and body language, which vary across cultures. If the assessment is
conducted in a language that is different from the individual’s primary language, care must be
taken to ensure that alogia is not related to linguistic barriers. In certain cultures, distress may
take the form of hallucinations or pseudo-hallucinations and overvalued ideas that may present
clinically similar to true psychosis but are normative to the individual’s subgroup. Misdiagnosis
of schizophrenia in individuals with mood disorders with psychotic features or with other
psychiatric disorders is more likely to occur in members of underserved ethnic and racialized
groups (in the United States, especially among African Americans). This may be attributable to
clinical bias, racism, or discrimination leading to limited quality of information and potential
misinterpretation of symptoms.
Sex- and Gender-Related Diagnostic Issues
A number of features distinguish the clinical expression of schizophrenia in women and men.
The age at onset is later in women, with a second midlife peak. Symptoms tend to be more
affect-laden among women, and there are more psychotic symptoms, as well as a greater
propensity for psychotic symptoms to worsen in later life. Other symptom differences include
less frequent negative symptoms and disorganization. Finally, social functioning tends to remain
better preserved in women. There are, however, frequent exceptions to these general caveats.
Psychotic symptoms have been observed to worsen during the premenstrual time period
when estrogen levels are dropping; consequently, increased psychiatric admission rates are seen
in women with schizophrenia just before and during menses. Lower estrogen levels resulting
from menopause may be another factor associated with the second peak of onset in women in
midlife. Similarly, psychotic symptoms appear to improve during pregnancy when estrogen
levels are high and worsen again postpartum when estrogen levels precipitously drop.
Association With Suicidal Thoughts or Behavior
Approximately 5%–6% of individuals with schizophrenia die by suicide, about 20% attempt
suicide on one or more occasions, and many more have significant suicidal ideation. Suicidal
behavior is sometimes in response to command hallucinations to harm oneself or others. Suicide
risk remains high over the whole lifespan for men and women, although it may be especially
high for younger men with comorbid substance use. Other risk factors include depressive
symptoms, hopelessness, being unemployed, the period after a psychotic episode or hospital
discharge, number of psychiatric admissions, closeness to onset of illness, and older age at
illness onset. A systematic review and meta-analysis of longitudinal studies found that the odds
of suicidal behavior during follow-up after first-episode psychosis were higher among
individuals with depressive symptoms during first-episode psychosis compared with those
without. A meta-analysis of a large number of studies of the relationship of schizophrenia with
suicidal behavior found that alcohol, tobacco, and drug abuse; depression; number of
hospitalizations; physical comorbidity; and family history of depression and suicidal behavior
increased the risk of suicide attempt. Risk factors for suicide included male sex, being younger,
having a higher IQ, history of attempts, hopelessness, and poor adherence to treatment.
Functional Consequences of Schizophrenia
Schizophrenia is associated with significant social and occupational dysfunction. Among

Major depressive or bipolar disorder with psychotic or catatonic features.
Schizoaffective disorder.
Schizophreniform disorder and brief psychotic disorder.
Delusional disorder.
Schizotypal personality disorder.
Obsessive-compulsive disorder and body dysmorphic disorder.
Posttraumatic stress disorder.
Autism spectrum disorder or communication disorders.
individuals with schizophrenia, deficits in reading ability are more severe than what would
be predicted by the general cognitive impairments associated with the disorder. Such deficits can
be conceptualized as a secondary or acquired dyslexia that underlies the academic impairment
observed in schizophrenia. Making educational progress and maintaining employment are
frequently impaired by avolition or other disorder manifestations, even when the cognitive skills
are sufficient for the tasks at hand. Most individuals are employed at a lower level than their
parents, and most, particularly men, do not marry or have limited social contacts outside of their
family.
Differential Diagnosis
The 
distinction 
between
schizophrenia and major depressive or bipolar disorder with psychotic features or with catatonia
depends on the temporal relationship between the mood disturbance and the psychosis, and on
the severity of the depressive or manic symptoms. If delusions or hallucinations occur
exclusively during a major depressive or manic episode, the diagnosis is depressive or bipolar
disorder with psychotic features.
A diagnosis of schizoaffective disorder requires that a major depressive
or manic episode occur concurrently with the active-phase symptoms and that the mood
symptoms be present for a majority of the total duration of the active periods.
These disorders are of shorter duration than
schizophrenia as specified in Criterion C, which requires 6 months of symptoms. In
schizophreniform disorder, the disturbance is present less than 6 months, and in brief psychotic
disorder, symptoms are present at least 1 day but less than 1 month.
Delusional disorder can be distinguished from schizophrenia by the absence
of the other symptoms characteristic of schizophrenia (e.g., delusions, prominent auditory or
visual hallucinations, disorganized speech, grossly disorganized or catatonic behavior, negative
symptoms).
Schizotypal personality disorder may be distinguished from
schizophrenia by subthreshold symptoms that are associated with persistent personality features.
Individuals 
with 
obsessivecompulsive disorder and body dysmorphic disorder may present with poor or absent insight, and
the preoccupations may reach delusional proportions. But these disorders are distinguished from
schizophrenia by their prominent obsessions, compulsions, preoccupations with appearance or
body odor, hoarding, or body-focused repetitive behaviors.
Posttraumatic stress disorder may include flashbacks that have a
hallucinatory quality, and hypervigilance may reach paranoid proportions. But a traumatic event
and characteristic symptom features relating to reliving or reacting to the event are required to
make the diagnosis of posttraumatic stress disorder.
These disorders may also have symptoms
resembling a psychotic episode but are distinguished by their respective deficits in social

Other mental disorders associated with a psychotic episode.
Substance/medication-induced psychotic disorder.
interaction with repetitive and restricted behaviors and other cognitive and communication
deficits. An individual with autism spectrum disorder or communication disorder must have
symptoms that meet full criteria for schizophrenia, with prominent hallucinations or delusions
for at least 1 month, in order to be diagnosed with schizophrenia as a comorbid condition.
The diagnosis of schizophrenia is made
only when the psychotic episode is persistent and not attributable to the physiological effects of a
substance or another medical condition. Individuals with a delirium or major or minor
neurocognitive disorder may present with psychotic symptoms,
but these would have a temporal relationship to the onset of cognitive changes consistent with
those disorders.
Individuals with substance/medication-induced
psychotic disorder may present with symptoms characteristic of Criterion A for schizophrenia,
but the substance/medication-induced psychotic disorder can usually be distinguished by the
chronological relationship of substance use to the onset and remission of the psychosis in the
absence of substance use.
Comorbidity
Rates of comorbidity with substance-related disorders are high in schizophrenia. Over half of
individuals with schizophrenia have tobacco use disorder and smoke cigarettes regularly.
Comorbidity with anxiety disorders is increasingly recognized in schizophrenia. Rates of
obsessive-compulsive disorder and panic disorder are elevated in individuals with schizophrenia
compared with the general population. Schizotypal or paranoid personality disorder may
sometimes precede the onset of schizophrenia.
Life expectancy is reduced in individuals with schizophrenia because of associated medical
conditions. Weight gain, diabetes, metabolic syndrome, and cardiovascular and pulmonary
disease are more common in schizophrenia than in the general population. Poor engagement in
health maintenance behaviors (e.g., cancer screening, exercise) increases the risk of chronic
disease, but other disorder factors, including medications, lifestyle, cigarette smoking, and diet,
may also play a role. A shared vulnerability for psychosis and medical conditions may explain
some of the medical comorbidity of schizophrenia.
Schizoaffective Disorder
Diagnostic Criteria
A. An uninterrupted period of illness during which there is a major mood episode
(major depressive or manic) concurrent with Criterion A of schizophrenia.
Note: The major depressive episode must include Criterion A1: Depressed
mood.

B. Delusions or hallucinations for 2 or more weeks in the absence of a major mood
episode (depressive or manic) during the lifetime duration of the illness.
C. Symptoms that meet criteria for a major mood episode are present for the
majority of the total duration of the active and residual portions of the illness.
D. The disturbance is not attributable to the effects of a substance (e.g., a drug of
abuse, a medication) or another medical condition.
Specify whether:
F25.0 Bipolar type: This subtype applies if a manic episode is part of the
presentation. Major depressive episodes may also occur.
F25.1 Depressive type: This subtype applies if only major depressive episodes
are part of the presentation.
Specify if:
With catatonia (refer to the criteria for catatonia associated with another mental
disorder, p. 135, for definition).
Coding note: Use additional code F06.1 catatonia associated with
schizoaffective disorder to indicate the presence of the comorbid catatonia.
Specify if:
The following course specifiers are only to be used after a 1-year duration of the
disorder and if they are not in contradiction to the diagnostic course criteria.
First episode, currently in acute episode: First manifestation of the disorder
meeting the defining diagnostic symptom and time criteria. An acute episode is a
time period in which the symptom criteria are fulfilled.
First episode, currently in partial remission: Partial remission is a time period
during which an improvement after a previous episode is maintained and in
which the defining criteria of the disorder are only partially fulfilled.
First episode, currently in full remission: Full remission is a period of time
after a previous episode during which no disorder-specific symptoms are
present.
Multiple episodes, currently in acute episode: Multiple episodes may be
determined after a minimum of two episodes (i.e., after a first episode, a
remission and a minimum of one relapse).
Multiple episodes, currently in partial remission
Multiple episodes, currently in full remission
Continuous: Symptoms fulfilling the diagnostic symptom criteria of the disorder
are remaining for the majority of the illness course, with subthreshold symptom
periods being very brief relative to the overall course.
Unspecified
Specify current severity:

Severity is rated by a quantitative assessment of the primary symptoms of
psychosis, including delusions, hallucinations, disorganized speech, abnormal
psychomotor behavior, and negative symptoms. Each of these symptoms may
be rated for its current severity (most severe in the last 7 days) on a 5-point
scale ranging from 0 (not present) to 4 (present and severe). (See ClinicianRated Dimensions of Psychosis Symptom Severity in the chapter “Assessment
Measures.”)
Note: Diagnosis of schizoaffective disorder can be made without using this
severity specifier.
Diagnostic Features
The diagnosis of schizoaffective disorder is based on the assessment of an uninterrupted period
of illness during which the individual continues to display active or residual symptoms of
psychotic illness. The diagnosis is usually, but not necessarily, made during the period of
psychotic illness. At some time during the period, Criterion A for schizophrenia has to be met.
Criteria B (social dysfunction), C (6-month duration), and F (exclusion of autism spectrum
disorder or other communication disorder of childhood onset) for schizophrenia do not have to
be met. In addition to meeting Criterion A for schizophrenia, there is a major mood episode
(major depressive or manic) (Criterion A for schizoaffective disorder). Because loss of interest or
pleasure is common in schizophrenia, to meet Criterion A for schizoaffective disorder, the major
depressive episode must include pervasive depressed mood (i.e., the presence of markedly
diminished interest or pleasure is not sufficient). Episodes of depression or mania are present for
the majority of the total duration of the illness (i.e., after Criterion A has been met) (Criterion C
for schizoaffective disorder). To separate schizoaffective disorder from a depressive or bipolar
disorder with psychotic features, delusions or hallucinations must be present for at least 2 weeks
in the absence of a major mood episode (depressive or manic) at some point during the lifetime
duration of the illness (Criterion B for schizoaffective disorder). The symptoms must not be
attributable to the effects of a substance or another medical condition (Criterion D for
schizoaffective disorder).
Criterion C for schizoaffective disorder specifies that mood symptoms meeting criteria for a
major mood episode must be present for the majority of the total duration of the active and
residual portion of the illness. Criterion C requires the assessment of mood symptoms for the
entire lifetime course of a psychotic illness. If the mood symptoms are present
for only a relatively brief period, the diagnosis is schizophrenia, not schizoaffective disorder.
When deciding whether an individual’s presentation meets Criterion C, the clinician should
review the total duration of psychotic illness (i.e., both active and residual symptoms) and
determine when significant mood symptoms (untreated or in need of treatment with
antidepressant and/or mood-stabilizing medication) accompanied the psychotic symptoms. This
determination requires sufficient historical information and clinical judgment. For example, an
individual with a 4-year history of active and residual symptoms of schizophrenia develops
depressive and manic episodes that, taken together, do not occupy more than 1 year during the 4-

year history of psychotic illness. This presentation would not meet Criterion C.
In addition to the five symptom domain areas identified in the diagnostic criteria, the
assessment of cognition, depression, and mania symptom domains is vital for making critically
important distinctions between the various schizophrenia spectrum and other psychotic disorders.
Associated Features
Occupational and social functioning is frequently impaired, but this is not a defining criterion (in
contrast to schizophrenia). Restricted social contact and difficulties with self-care are associated
with schizoaffective disorder, but negative symptoms may be less severe and less persistent than
those seen in schizophrenia. Anosognosia (i.e., poor insight) is also common in schizoaffective
disorder, but the deficits in insight may be less severe and pervasive than those in schizophrenia.
Individuals with schizoaffective disorder may be at increased risk for later developing episodes
of major depressive disorder or bipolar disorder if mood symptoms continue following the
remission of symptoms meeting Criterion A for schizophrenia. There may be associated alcohol
and other substance-related disorders.
There are no tests or biological measures that can provide definitive assistance in making the
diagnosis of schizoaffective disorder. Neuropsychological testing typically shows cognitive
deficits in areas such as executive function, verbal memory, and speed of processing, and these
may be less pronounced than in schizophrenia. Schizoaffective disorder is often characterized by
gray matter volume loss on brain imaging, in much the same way that schizophrenia is.
Prevalence
Schizoaffective disorder appears to be about one-third as common as schizophrenia. Lifetime
prevalence of schizoaffective disorder was estimated to be 0.3% in a Finnish sample and is
higher in women than in men when DSM-IV diagnostic criteria were used. This rate would be
expected to be lower because of the more stringent requirement of DSM-5 Criterion C (i.e.,
mood symptoms meeting criteria for a major mood episode must be present for the majority of
the total duration of the active and residual portion of the illness).
Development and Course
The typical age at onset of schizoaffective disorder is early adulthood, although onset can occur
anytime from adolescence to late in life. A significant number of individuals diagnosed with
another psychotic illness initially will receive the diagnosis schizoaffective disorder later when
the pattern of mood episodes has become more apparent, whereas others may be diagnosed with
mood disorders before independent psychotic symptoms are detected.
Conversely, some individuals will have a change in diagnosis from schizoaffective disorder
to a mood disorder or to schizophrenia over time. A change in diagnosis from schizoaffective
disorder to schizophrenia was more common than a change to mood disorder
under DSM-IV criteria, and that difference is expected to be more pronounced under DSM-5
as the current Criterion C for schizoaffective disorder has become more stringent, requiring
mood symptoms to be present for the majority of the illness as compared with the DSM-IV
definition, which only required mood symptoms to be present for a “substantial” portion. The

Genetic and physiological.
prognosis for schizoaffective disorder is somewhat better than the prognosis for schizophrenia
but worse than the prognosis for mood disorders.
Schizoaffective disorder may occur in a variety of temporal patterns. The following is a
typical pattern: An individual may have pronounced auditory hallucinations and persecutory
delusions for 2 months before the onset of a prominent major depressive episode. The psychotic
symptoms and the full major depressive episode are then present for 4 months. Then, the
individual recovers completely from the major depressive episode, but the psychotic symptoms
persist for another month before they too disappear. During this period of illness, the individual’s
symptoms concurrently met criteria for a major depressive episode and Criterion A for
schizophrenia, and during this same period of illness, auditory hallucinations and delusions were
present both before and after the depressive phase. The total period of illness lasted for about 7
months, with psychotic symptoms alone present during the initial 2 months, both depressive and
psychotic symptoms present during the next 4 months, and psychotic symptoms alone present
during the last month. In this instance, the depressive episode was present for a majority of the
total duration of the psychotic disturbance, and thus the presentation qualifies for a diagnosis of
schizoaffective disorder.
The temporal relationship between the mood symptoms and the psychotic symptoms across
the lifespan is variable. Depressive or manic symptoms can occur before the onset of psychosis,
during acute psychotic episodes, during residual periods, and after cessation of psychosis. For
example, an individual might present with prominent mood symptoms during the prodromal
stage of schizophrenia. This pattern is not necessarily indicative of schizoaffective disorder,
since it is the co-occurrence of psychotic and mood symptoms that is diagnostic. For an
individual with symptoms that clearly meet the criteria for schizoaffective disorder but who on
further follow-up only presents with residual psychotic symptoms (such as subthreshold
psychosis and/or prominent negative symptoms), the diagnosis may be changed to schizophrenia,
as the total proportion of psychotic illness compared with mood symptoms becomes more
prominent. Schizoaffective disorder, bipolar type, may be more common in young adults,
whereas schizoaffective disorder, depressive type, may be more common in older adults.
Risk and Prognostic Factors
Among individuals with schizophrenia, there may be an increased risk
for schizoaffective disorder in first-degree relatives. The risk for schizoaffective disorder may
also be increased among individuals who have a first-degree relative with bipolar disorder or
schizoaffective disorder itself. The molecular genetic composite signatures known as polygenic
risk scores for schizophrenia, bipolar disorder, and major depressive disorder may all be elevated
in schizoaffective disorder.
Culture-Related Diagnostic Issues
Cultural and socioeconomic factors must be considered, particularly when the individual and the
clinician do not share the same cultural and economic background. Ideas that appear to be
delusional in one cultural context (e.g., evil eye, causing illness through curses, influences of
spirits) may be commonly held in others. There is also some evidence in the literature that
African American and Hispanic populations whose symptoms meet criteria for schizoaffective
disorder are more likely to be diagnosed with schizophrenia. To mitigate the impact of clinician

Other mental disorders and medical conditions.
Psychotic disorder due to another medical condition.
Schizophrenia, bipolar, and depressive disorders.
bias, care must be taken to ensure a comprehensive evaluation that includes both psychotic and
mood symptoms.
Association With Suicidal Thoughts or Behavior
The lifetime risk of suicide for schizophrenia and schizoaffective disorder is 5%, and the
presence of depressive symptoms is correlated with a higher risk for suicide. There is evidence
that suicide rates are higher in North American populations than in European, Eastern European,
South American, and Indian populations of individuals with schizophrenia or schizoaffective
disorder.
Functional Consequences of Schizoaffective Disorder
Schizoaffective disorder is associated with global dysfunction, including in social and
occupational domains, but dysfunction is not a diagnostic criterion (as it is for schizophrenia),
and there is substantial variability between individuals diagnosed with schizoaffective disorder.
Differential Diagnosis
A wide variety of psychiatric and medical conditions
can manifest with psychotic and mood symptoms and must be considered in the differential
diagnosis of schizoaffective disorder. These include delirium; major neurocognitive disorder;
substance/medication-induced psychotic disorder or neurocognitive disorder; bipolar disorders,
with psychotic features; major depressive disorder, with psychotic features; depressive or bipolar
disorders, with catatonic features; schizotypal, schizoid, or paranoid personality disorder; brief
psychotic disorder; schizophreniform disorder; schizophrenia; delusional disorder; and other
specified and unspecified schizophrenia spectrum and other psychotic disorders.
Other medical conditions and substance use can
manifest with a combination of psychotic and mood symptoms, and thus psychotic disorder due
to another medical condition needs to be excluded.
Distinguishing 
schizoaffective 
disorder 
from
schizophrenia and from depressive and bipolar disorders with psychotic features is often
difficult. Criterion C is designed to separate schizoaffective disorder from schizophrenia, and
Criterion B is designed to distinguish schizoaffective disorder from a depressive or bipolar
disorder with psychotic features. More specifically, schizoaffective disorder can be distinguished
from a major depressive or bipolar disorder with psychotic features based on the presence of
prominent delusions and/or hallucinations for at least 2 weeks in the absence of a major mood
episode. In contrast, in depressive or bipolar disorder with psychotic features, the psychotic
features only occur during the mood episode(s). Because the relative proportion of mood to
psychotic symptoms may change over time, the appropriate diagnosis may change from and to
schizoaffective disorder. (For example, a diagnosis of schizoaffective disorder for a severe and
prominent major depressive episode lasting 4 months during the first 6 months of a chronic
psychotic illness would be changed to schizophrenia if active psychotic or prominent residual
symptoms persist over several years without a recurrence of another mood episode.) Achieving
greater clarity about the relative proportion of mood to psychotic symptoms over time and about

their concurrence may require collateral information from medical records and from informants.
Comorbidity
Many individuals diagnosed with schizoaffective disorder are also diagnosed with other mental
disorders, especially substance use disorders and anxiety disorders. Similarly, the incidence of
medical conditions, including metabolic syndrome, is increased above base rate for the general
population and leads to decreased life expectancy.
Substance/Medication-Induced Psychotic Disorder
Diagnostic Criteria
A. Presence of one or both of the following symptoms:
1. Delusions.
2. Hallucinations.
B. There is evidence from the history, physical examination, or laboratory findings
of both (1) and (2):
1. The symptoms in Criterion A developed during or soon after substance
intoxication or withdrawal or after exposure to or withdrawal from a
medication.
2. The involved substance/medication is capable of producing the symptoms in
Criterion A.
C. The disturbance is not better explained by a psychotic disorder that is not
substance/medication-induced. Such evidence of an independent psychotic
disorder could include the following:
The symptoms preceded the onset of the substance/medication use; the
symptoms persist for a substantial period of time (e.g., about 1 month) after
the cessation of acute withdrawal or severe intoxication; or there is other
evidence of an independent non-substance/medication-induced psychotic
disorder (e.g., a history of recurrent non-substance/medication-related
episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Note: This diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the symptoms in Criterion A
predominate in the clinical picture and when they are sufficiently severe to warrant
clinical attention.

Coding note: The ICD-10-CM codes for the [specific substance/medication]-induced
psychotic disorders are indicated in the table below. Note that the ICD-10-CM code
depends on whether or not there is a comorbid substance use disorder present for
the same class of substance. In any case, an additional separate diagnosis of a
substance use disorder is not given. If a mild substance use disorder is comorbid
with the substance-induced psychotic disorder, the 4th position character is “1,” and
the clinician should record “mild [substance] use disorder” before the substanceinduced psychotic disorder (e.g., “mild cocaine use disorder with cocaine-induced
psychotic disorder”). If a moderate or severe substance use disorder is comorbid
with the substance-induced psychotic disorder, the 4th position character is “2,” and
the clinician should record “moderate [substance] use disorder” or “severe
[substance] use disorder,” depending on the severity of the comorbid substance use
disorder. If there is no comorbid substance use disorder (e.g., after a one-time heavy
use of the substance), then the 4th position character is “9,” and the clinician should
record only the substance-induced psychotic disorder.
ICD-10-CM
With mild use
disorder
With moderate or
severe use disorder
Without use
disorder
Alcohol
F10.159
F10.259
F10.959
Cannabis
F12.159
F12.259
F12.959
Phencyclidine
F16.159
F16.259
F16.959
Other hallucinogen
F16.159
F16.259
F16.959
Inhalant
F18.159
F18.259
F18.959
Sedative, hypnotic, or anxiolytic
F13.159
F13.259
F13.959
Amphetamine-type substance (or other
stimulant)
F15.159
F15.259
F15.959
Cocaine
F14.159
F14.259
F14.959
Other (or unknown) substance
F19.159
F19.259
F19.959
Specify (see Table 1 in the chapter “Substance-Related and Addictive Disorders,”
which indicates whether “with onset during intoxication” and/or “with onset during
withdrawal” applies to a given substance class; or specify “with onset after
medication use”):
With onset during intoxication: If criteria are met for intoxication with the
substance and the symptoms develop during intoxication.
With onset during withdrawal: If criteria are met for withdrawal from the
substance and the symptoms develop during, or shortly after, withdrawal.
With onset after medication use: If symptoms developed at initiation of
medication, with a change in use of medication, or during withdrawal of
medication.

Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of
psychosis, including delusions, hallucinations, abnormal psychomotor behavior,
and negative symptoms. Each of these symptoms may be rated for its current
severity (most severe in the last 7 days) on a 5-point scale ranging from 0 (not
present) to 4 (present and severe). (See Clinician-Rated Dimensions of
Psychosis Symptom Severity in the chapter “Assessment Measures.”)
Note: Diagnosis of substance/medication-induced psychotic disorder can be
made without using this severity specifier.
Recording Procedures
The name of the substance/medication-induced psychotic disorder begins with the specific
substance (e.g., cocaine, dexamethasone) that is presumed to be causing the delusions or
hallucinations. The diagnostic code is selected from the table included in the criteria set, which is
based on the drug class and presence or absence of a comorbid substance use disorder. For
substances that do not fit into any of the classes (e.g., dexamethasone), the code for “other (or
unknown) substance” should be used; and in cases in which a substance is judged to be an
etiological factor but the specific class of substance is unknown, the same code should also be
used.
When recording the name of the disorder, the comorbid substance use disorder (if any) is
listed first, followed by the word “with,” followed by the name of the substance-induced
psychotic disorder, followed by the specification of onset (i.e., onset during intoxication, onset
during withdrawal). For example, in the case of delusions occurring during intoxication in a man
with a severe cocaine use disorder, the diagnosis is F14.259 severe cocaine use disorder with
cocaine-induced psychotic disorder, with onset during intoxication. A separate diagnosis of the
comorbid severe cocaine use disorder is not given. If the substance-induced psychotic disorder
occurs without a comorbid substance use disorder (e.g., after a one-time heavy use of the
substance), no accompanying substance use disorder is noted (e.g., F16.959 phencyclidineinduced psychotic disorder, with onset during intoxication). When more than one substance is
judged to play a significant role in the development of psychotic symptoms, each should be listed
separately (e.g., F12.259 severe cannabis use disorder with cannabis-induced psychotic disorder,
with onset during intoxication; F16.159 mild phencyclidine use disorder with phencyclidineinduced psychotic disorder, with onset during intoxication).
Diagnostic Features
The essential features of substance/medication-induced psychotic disorder are prominent
delusions and/or hallucinations (Criterion A) that are judged to be due to the physiological
effects of a substance/medication (i.e., a drug of abuse, a medication, or a toxin exposure)
(Criterion B). Hallucinations that the individual realizes are substance/medication-induced are
not included here and instead would be diagnosed as substance intoxication or substance
withdrawal with the accompanying specifier “with perceptual disturbances” (applies to alcohol

withdrawal; cannabis intoxication; sedative, hypnotic, or anxiolytic withdrawal; and stimulant
intoxication).
A substance/medication-induced psychotic disorder is distinguished from an independent
psychotic disorder by considering the onset, course, and other factors. For drugs of abuse, there
must be evidence from the history, physical examination, or laboratory findings of substance use,
intoxication, or withdrawal. Substance/medication-induced psychotic disorders arise during or
soon after exposure to or withdrawal from a medication or after substance intoxication or
withdrawal but can persist for weeks, whereas independent psychotic disorders may precede the
onset of substance/medication use or may occur during times of sustained abstinence. Once
initiated, the psychotic symptoms may continue as long as the substance/medication use
continues. Another consideration is the presence of features that are atypical of an independent
psychotic disorder (e.g., atypical age at onset or course). For example, the appearance of
delusions de novo in a male person older than 35 years without a known history of an
independent psychotic disorder should suggest the possibility of a substance/medication-induced
psychotic disorder. Even a prior history of an independent psychotic disorder does not rule out
the possibility of a substance/medication-induced psychotic disorder. In contrast, factors that
suggest that the psychotic symptoms are better accounted for by an independent psychotic
disorder include persistence of psychotic symptoms for a substantial period of time (i.e., a month
or more) after the end of substance intoxication or acute substance withdrawal or after cessation
of medication use; or a history of prior recurrent independent psychotic disorders. Other causes
of psychotic symptoms must be considered even in an individual with substance intoxication or
withdrawal, because substance use problems are not uncommon among individuals with nonsubstance/medication-induced psychotic disorders.
In addition to the two symptom domain areas identified in the diagnostic criteria (i.e.,
delusions and hallucinations), the assessment of cognition, depression, and mania symptom
domains is vital for making critically important distinctions between the various schizophrenia
spectrum and other psychotic disorders.
Associated Features
Psychotic disorders can occur in association with intoxication with the following classes of
substances: alcohol; cannabis; hallucinogens, including phencyclidine and related substances;
inhalants; sedatives, hypnotics, and anxiolytics; stimulants (including cocaine); and other (or
unknown) substances. Psychotic disorders can occur in association with withdrawal from the
following classes of substances: alcohol; sedatives, hypnotics, and anxiolytics; and other (or
unknown) substances.
Some of the medications reported to evoke psychotic symptoms include anesthetics and
analgesics, anticholinergic agents, anticonvulsants, antihistamines, antihypertensive and
cardiovascular 
medications, 
antimicrobial 
medications, 
antiparkinsonian 
medications,
chemotherapeutic agents (e.g., cyclosporine, procarbazine), corticosteroids, gastrointestinal
medications, muscle relaxants, nonsteroidal anti-inflammatory medications, other over-thecounter medications (e.g., phenylephrine, pseudoephedrine), antidepressant medication, and
disulfiram. Toxins reported to induce psychotic symptoms include anticholinesterase,

organophosphate insecticides, sarin and other nerve gases, carbon monoxide, carbon dioxide, and
volatile substances such as fuel or paint.
Prevalence
Prevalence of substance/medication-induced psychotic disorder in the general population is
unknown. Between 7% and 25% of individuals presenting with a first episode of psychosis in
different settings are reported to have substance/medication-induced psychotic disorder.
Development and Course
The initiation of the psychotic symptoms may vary considerably with the substance. For
example, smoking a high dose of cocaine may produce psychosis within minutes, whereas days
or weeks of high-dose alcohol or sedative use may be required to produce psychosis. Alcoholinduced psychotic disorder, with hallucinations, usually occurs only after prolonged, heavy
ingestion of alcohol in individuals who have moderate to severe alcohol use disorder, and the
hallucinations are generally auditory in nature.
Psychotic disorders induced by amphetamine-type substances and cocaine share similar
clinical features. Persecutory delusions may rapidly develop shortly after use of amphetamine or
a similarly acting sympathomimetic. The hallucination of bugs or vermin crawling in or under
the skin (formication) can lead to scratching and extensive skin excoriations. Cannabis-induced
psychotic disorder may develop shortly after high-dose cannabis use and usually involves
persecutory delusions, marked anxiety, emotional lability, and depersonalization. The disorder
usually remits within a day but in some cases may persist longer.
Substance/medication-induced psychotic disorder may at times persist when the offending
agent is removed, such that it may be difficult initially to distinguish it from an independent
psychotic disorder. Agents such as amphetamine-type substances, phencyclidine, and cocaine
have been reported to evoke temporary psychotic states that can sometimes persist for weeks or
longer despite removal of the agent and treatment with neuroleptic medication. In later life,
polypharmacy for medical conditions and exposure to medications for parkinsonism,
cardiovascular disease, and other medical disorders may be associated with a greater likelihood
of psychosis induced by prescription medications as opposed to substances of abuse.
According to data from a Danish registry study that followed cases of substance-induced
psychosis longitudinally over 20 years, roughly one-third (32%) of individuals with substanceinduced psychosis are later diagnosed with a schizophrenia spectrum disorder (26%) or a bipolar
disorder (8%), with the highest rate (44%) for cannabis-induced psychotic disorder.
Diagnostic Markers
With substances for which relevant blood levels are available (e.g., blood alcohol level, other
quantifiable blood levels such as digoxin), the presence of a level consistent with toxicity may
increase diagnostic certainty.
Functional Consequences of Substance/Medication-Induced Psychotic
Disorder

Substance intoxication or substance withdrawal.
Independent psychotic disorder.
Psychotic disorder due to another medical condition.
Other specified or unspecified schizophrenia spectrum and other psychotic disorder.
Substance/medication-induced psychotic disorder is typically severely disabling and
consequently is observed most frequently in emergency departments, as individuals are often
brought to the acute-care setting when it occurs. However, the disability is typically self-limited
and resolves upon removal of the offending agent.
Differential Diagnosis
Individuals intoxicated with stimulants, cannabis,
the opioid meperidine, or phencyclidine, or those withdrawing from alcohol or sedatives, may
experience altered perceptions that they recognize as drug effects. If reality testing for these
experiences remains intact (i.e., the individual recognizes that the perception is substance
induced and neither believes in nor acts on it), the diagnosis is not substance/medication-induced
psychotic disorder. Instead, substance intoxication or substance withdrawal, with perceptual
disturbances, is diagnosed (e.g., cocaine intoxication, with perceptual disturbances). “Flashback”
hallucinations that can occur long after the use of hallucinogens has stopped are diagnosed as
hallucinogen persisting perception disorder. If substance/medication-induced psychotic
symptoms occur exclusively during the course of a delirium, as in severe forms of alcohol
withdrawal, the psychotic symptoms are considered to be an associated feature of the delirium
and are not diagnosed separately. Delusions in the context of a major or mild neurocognitive
disorder would be diagnosed as major or mild neurocognitive disorder, with behavioral
disturbance.
A 
substance/medication-induced 
psychotic 
disorder 
is
distinguished from an independent psychotic disorder, such as schizophrenia, schizoaffective
disorder, delusional disorder, brief psychotic disorder, other specified schizophrenia spectrum
and other psychotic disorder, or unspecified schizophrenia spectrum and other psychotic
disorder, by the fact that a substance is judged to be etiologically related to the symptoms.
A 
substance/medication-induced 
psychotic
disorder due to a prescribed treatment for a mental disorder or medical condition must have its
onset while the individual is receiving the medication (or during withdrawal, if there is a
withdrawal syndrome associated with the medication). Because individuals with medical
conditions often take medications for those conditions, the clinician must consider the possibility
that the psychotic symptoms are caused by the physiological consequences of the medical
condition itself rather than the medication, in which case psychotic disorder due to another
medical condition is diagnosed. The history often provides the primary basis for such a
judgment. At times, a change in the treatment for the medical condition (e.g., medication
substitution or discontinuation) may be needed to determine empirically for that individual
whether the medication is the causative agent. If the clinician has ascertained that the disturbance
is attributable to both a medical condition and substance/medication use, both diagnoses (i.e.,
psychotic disorder due to another medical condition and substance/medication-induced psychotic
disorder) may be given.
The 
psychotic
symptoms included in the diagnosis of substance/medication-induced psy-chotic disorder are
limited to either delusions or hallucinations. Individuals with other

substance-induced psychotic symptoms (e.g., disorganized or catatonic behavior; disorganized
speech; incoherence or irrational content) should be classified in the category other specified or
unspecified schizophrenia spectrum and other psychotic disorder.
Psychotic Disorder Due to Another Medical Condition
Diagnostic Criteria
A. Prominent hallucinations or delusions.
B. There is evidence from the history, physical examination, or laboratory findings
that the disturbance is the direct pathophysiological consequence of another
medical condition.
C. The disturbance is not better explained by another mental disorder.
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Specify whether:
Code based on predominant symptom:
F06.2 With delusions: If delusions are the predominant symptom.
F06.0 With hallucinations: If hallucinations are the predominant symptom.
Coding note: Include the name of the other medical condition in the name of the
mental disorder (e.g., F06.2 psychotic disorder due to malignant lung neoplasm, with
delusions). The other medical condition should be coded and listed separately
immediately before the psychotic disorder due to the medical condition (e.g., C34.90
malignant lung neoplasm; F06.2 psychotic disorder due to malignant lung neoplasm,
with delusions).
Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of
psychosis, including delusions, hallucinations, abnormal psychomotor behavior,
and negative symptoms. Each of these symptoms may be rated for its current
severity (most severe in the last 7 days) on a 5-point scale ranging from 0 (not
present) to 4 (present and severe). (See Clinician-Rated Dimensions of
Psychosis Symptom Severity in the chapter “Assessment Measures.”)
Note: Diagnosis of psychotic disorder due to another medical condition can be
made without using this severity specifier.
Specifiers
In addition to the symptom domain areas identified in the diagnostic criteria, the assessment of
cognition, depression, and mania symptom domains is vital for making critically important
distinctions between the various schizophrenia spectrum and other psychotic disorders.

Diagnostic Features
The essential features of psychotic disorder due to another medical condition are prominent
delusions or hallucinations that are judged to be attributable to the physiological effects of
another medical condition and are not better explained by another mental disorder (e.g., the
symptoms are not a psychologically mediated response to a severe medical condition, in which
case a diagnosis of brief psychotic disorder, with marked stressor, would be appropriate).
Hallucinations can occur in any sensory modality (i.e., visual, olfactory, gustatory, tactile, or
auditory), but certain etiological factors are likely to evoke specific hallucinatory phenomena.
Olfactory hallucinations are suggestive of temporal lobe epilepsy, for example. Hallucinations
may vary from simple and unformed to highly complex and organized, depending on etiological
and environmental factors. Psychotic disorder due to another medical condition is generally not
diagnosed if the individual maintains reality testing for the hallucinations and appreciates that
they result from the medical condition. Delusions may have a variety of themes, including
somatic, grandiose, religious, and, most commonly, persecutory. On the whole, however,
associations between delusions and particular medical conditions appear to be less specific than
is the case for hallucinations.
Although there are no infallible guidelines to determine whether the psychotic disturbance is
etiologically attributable to another medical condition, three considerations can provide some
guidance: biological plausibility, temporality, and typicality. First, the presence of a medical
condition that has the potential to cause psychotic symptoms through a putative physiological
mechanism (e.g., severe, generalized infection; porphyria; lupus; temporal lobe epilepsy) must
be identified (biological plausibility). The second consideration is whether there is a temporal
association between the onset, exacerbation, or remission of the medical condition and that of the
psychotic disturbance (temporality). The third consideration in favor of a medical etiology of the
psychotic symptoms is the presence of features that would be atypical for an independent
psychotic disorder (e.g., atypical age at onset, presence of visual or olfactory hallucinations)
(typicality). Finally, causes of psychotic symptoms other than the physiological effects of a
medical condition need to be considered and ruled out (e.g., substance/medication-induced
psychotic disorder, psychotic symptoms occurring as side effects of the treatment of the medical
condition).
The temporal association of the onset or exacerbation of the medical condition offers the
greatest diagnostic certainty that the delusions or hallucinations are attributable to a medical
condition. Additional factors may include concomitant treatments for the underlying medical
condition that confer a risk for psychosis independently, such as steroid treatment for
autoimmune disorders.
The diagnosis of psychotic disorder due to another medical condition depends on the clinical
condition of each individual, and the diagnostic tests will vary according to that condition. A
wide variety of medical conditions may cause psychotic symptoms. These include neurological
conditions (e.g., neoplasms, cerebrovascular disease, Huntington’s disease, Parkinson’s disease,
multiple sclerosis, epilepsy, auditory or visual nerve injury or impairment, deafness, migraine,
central nervous system infections), endocrine conditions (e.g., hyper- and hypothyroidism,

hyper- and hypoparathyroidism, hyper- and hypoadrenocorticism), metabolic conditions (e.g.,
hypoxia, hypercarbia, hypoglycemia), vitamin B12 deficiency, fluid or electrolyte imbalances,
hepatic or renal diseases, and autoimmune disorders with central nervous system involvement
(e.g., systemic lupus erythematosus, N-methyl-D-aspartate [NMDA] receptor autoimmune
encephalitis). The associated physical examination findings, laboratory findings, and patterns of
prevalence or onset reflect the etiological medical condition.
Prevalence
Prevalence rates for psychotic disorder due to another medical condition are difficult to estimate
given the wide variety of underlying medical etiologies. Lifetime prevalence has been estimated
to range from 0.21% to 0.54% in studies in Sweden and Finland. When the prevalence findings
are stratified by age group, individuals older than 65 years have a significantly greater prevalence
of 0.74% compared with those in younger age groups in Finland. Rates of psychosis also vary
according to the underlying medical condition; conditions most commonly associated with
psychosis include untreated endocrine and metabolic disorders, autoimmune disorders (e.g.,
systemic lupus erythematosus, NMDA receptor autoimmune encephalitis), or temporal lobe
epilepsy. Psychosis attributable to epilepsy
has been further differentiated into ictal, postictal, and interictal psychosis. The most common of
these is postictal psychosis, observed in 2%–7.8% of individuals with epilepsy. Among older
individuals, there may be a higher prevalence of the disorder in women, although additional sexor gender-related features are not clear and vary considerably with the sex and gender
distributions of the underlying medical conditions. An estimated 60% of older individuals with
new-onset psychosis have a medical etiology for their psychotic symptoms.
Development and Course
Psychotic disorder due to another medical condition may be a single transient state or it may be
recurrent, cycling with exacerbations and remissions of the underlying medical condition.
Although treatment of the underlying medical condition often results in a resolution of the
psychosis, this is not always the case, and psychotic symptoms may persist long after the medical
event (e.g., psychotic disorder due to focal brain injury). In the context of chronic conditions
such as multiple sclerosis or chronic interictal psychosis of epilepsy, the psychosis may assume a
long-term course.
The expression of psychotic disorder due to another medical condition does not differ
substantially in phenomenology depending on age at occurrence. However, older age groups
have a higher prevalence of the disorder, which is most likely due to the increasing medical
burden associated with advanced age and the cumulative effects of deleterious exposures and
age-related processes (e.g., atherosclerosis). The nature of the underlying medical conditions is
likely to change across the lifespan, with younger age groups more affected by epilepsy, head
trauma, autoimmune, and neoplastic diseases of early to midlife, and older age groups more
affected by a neurodegenerative disease (e.g., Alzheimer’s), stroke disease, anoxic events, and
multiple system comorbidities. Underlying factors with increasing age, such as preexisting
cognitive impairment as well as vision and hearing impairments, may incur a greater risk for

Course modifiers.
Delirium and major or mild neurocognitive disorder.
Substance/medication-induced psychotic disorder.
Psychotic disorder.
psychosis, possibly by serving to lower the threshold for experiencing psychosis.
Risk and Prognostic Factors
Identification and treatment of the underlying medical condition has the
greatest impact on course, although preexisting central nervous system injury may confer a
worse course outcome (e.g., head trauma, cerebrovascular disease).
Association With Suicidal Thoughts or Behavior
Suicide risk in the context of psychotic disorder due to another medical condition is not clearly
delineated, although certain conditions such as epilepsy and multiple sclerosis are associated
with increased rates of suicide, which may be further increased in the presence of psychosis.
Functional Consequences of Psychotic Disorder Due to Another
Medical Condition
Functional disability is typically severe in the context of psychotic disorder due to another
medical condition but will vary considerably by the type of condition and likely improve with
successful resolution of the condition.
Differential Diagnosis
Hallucinations and delusions commonly occur in
the context of a delirium; a separate diagnosis of psychotic disorder due to
another medical condition is not given if the delusions and/or hallucinations occur exclusively
during the course of a delirium. On the other hand, a diagnosis of psychotic disorder due to
another medical condition may be given in addition to a diagnosis of major or mild
neurocognitive disorder if the delusions or hallucinations are judged to be a physiological
consequence of the pathological process causing the neurocognitive disorder (e.g., psychotic
disorder due to Lewy body disease, with delusions).
If there is evidence of recent or prolonged
substance use (including medications with psychoactive effects), withdrawal from a substance or
medication that can cause psychotic symptoms on withdrawal, or exposure to a toxin (e.g., LSD
[lysergic acid diethylamide] intoxication, alcohol withdrawal), a substance/medication-induced
psychotic disorder should be considered. Symptoms that occur during or shortly after (i.e., within
4 weeks) of substance intoxication or withdrawal or after medication use may be especially
indicative of a substance-induced psychotic disorder, depending on the character, duration, or
amount of the substance used. If the clinician has ascertained that the disturbance is due to both a
medical condition and substance use, both diagnoses (i.e., psychotic disorder due to another
medical condition and substance/medication-induced psychotic disorder) can be given.
Psychotic disorder due to another medical condition must be distinguished
from a psychotic disorder that is not due to another medical condition (e.g., schizophrenia,
delusional disorder, schizoaffective disorder) or a major depressive or bipolar disorder, with
psychotic features. In psychotic disorders and in depressive or bipolar disorders, with psychotic

features, no specific and direct causative physiological mechanisms associated with a medical
condition can be demonstrated. Late age at onset and the absence of a personal or family history
of schizophrenia or delusional disorder suggest the need for a thorough assessment to rule out the
diagnosis of psychotic disorder due to another medical condition. Auditory hallucinations that
involve voices speaking complex sentences are more characteristic of schizophrenia than of
psychotic disorder due to a medical condition. While certain symptoms suggest a medical or
toxic etiology (e.g., visual or olfactory hallucinations, dreamlike quality of delusions [individual
as uninvolved observer]), there are no pathognomonic signs or symptoms that unequivocally
point clinicians either way. Visual hallucinations are not uncommon in schizophrenia or bipolar
disorder, and olfactory hallucinations (e.g., unpleasant smells) are also consistent with a
diagnosis of schizophrenia. Thus, clinicians should not give undue weight to any one particular
hallucination alone when deciding between a psychiatric and a medical cause for
psychopathology.
Comorbidity
Psychotic disorder due to another medical condition in individuals older than 80 years is
associated with concurrent major neurocognitive disorder (dementia). Alzheimer’s disease is
commonly accompanied by psychosis, and psychosis is a defining feature in Lewy body disease.
Catatonia
Catatonia can occur in the context of several disorders, including neurodevelopmental, psychotic,
bipolar, and depressive disorders, and other medical conditions (e.g., cerebral folate deficiency,
rare autoimmune and paraneoplastic disorders). The manual does not treat catatonia as an
independent class but recognizes a) catatonia associated with another
mental disorder (i.e., a neurodevelopmental, psychotic disorder, a bipolar disorder, a depressive
disorder, or other mental disorder), b) catatonic disorder due to another medical condition, and c)
unspecified catatonia.
Catatonia is defined by the presence of 3 or more of 12 psychomotor features in the
diagnostic criteria for catatonia associated with another mental disorder and catatonic disorder
due to another medical condition. The essential feature of catatonia is a marked psychomotor
disturbance that may involve decreased motor activity, decreased engagement during interview
or physical examination, or excessive and peculiar motor activity. The clinical presentation of
catatonia can be puzzling, as the psychomotor disturbance may range from marked
unresponsiveness to marked agitation. Motoric immobility may be severe (stupor) or moderate
(catalepsy and waxy flexibility). Similarly, decreased engagement may be severe (mutism) or
moderate (negativism). Excessive and peculiar motor behaviors can be complex (e.g.,
stereotypy) or simple (agitation) and may include echolalia and echopraxia. In extreme cases, the
same individual may wax and wane between decreased and excessive motor activity. The
seemingly opposing clinical features, variable manifestations of the diagnosis, and overemphasis
in teaching on rare, severe signs such as waxy flexibility contribute to a lack of awareness and

decreased recognition of catatonia. During severe stages of catatonia, the individual may need
careful supervision to avoid self-harm or harming others. There are potential risks from
malnutrition, exhaustion, thromboembolism, pressure ulcers, muscle contractions, hyperpyrexia
and self-inflicted injury.
Catatonia Associated With Another Mental Disorder
(Catatonia Specifier)
F06.1
A. The clinical picture is dominated by three (or more) of the following symptoms:
1. Stupor (i.e., no psychomotor activity; not actively relating to environment).
2. Catalepsy (i.e., passive induction of a posture held against gravity).
3. Waxy flexibility (i.e., slight, even resistance to positioning by examiner).
4. Mutism (i.e., no, or very little, verbal response [exclude if known aphasia]).
5. Negativism (i.e., opposition or no response to instructions or external stimuli).
6. Posturing (i.e., spontaneous and active maintenance of a posture against
gravity).
7. Mannerism (i.e., odd, circumstantial caricature of normal actions).
8. Stereotypy 
(i.e., 
repetitive, 
abnormally 
frequent, 
non-goal-directed
movements).
9. Agitation, not influenced by external stimuli.
10. Grimacing.
11. Echolalia (i.e., mimicking another’s speech).
12. Echopraxia (i.e., mimicking another’s movements).
Coding note: Indicate the name of the associated mental disorder when recording
the name of the condition (i.e., F06.1 catatonia associated with major depressive
disorder). Code first the associated mental disorder (e.g., neurodevelopmental
disorder, brief psychotic disorder, schizophreniform disorder, schizophrenia,
schizoaffective disorder, bipolar disorder, major depressive disorder, or other mental
disorder) (e.g., F25.1 schizoaffective disorder, depressive type; F06.1 catatonia
associated with schizoaffective disorder).
Diagnostic Features
Catatonia associated with another mental disorder (catatonia specifier) may be used when criteria
are met for catatonia during the course of a neurodevelopmental, psychotic, bipolar, depressive,
or other mental disorder. The catatonia specifier is appropriate when the clinical picture is
characterized by marked psychomotor disturbance and involves at least three of the 12 diagnostic

F06.1
features listed in Criterion A. Catatonia is typically diagnosed in an inpatient setting and occurs
in up to 35% of individuals with schizophrenia, but the majority of catatonia cases involve
individuals with depressive or bipolar disorders. Meta-analysis of clinical samples indicated that
approximately 9% of patients had catatonia. Before the catatonia specifier is used in
neurodevelopmental, psychotic, bipolar, depressive, or other mental disorders, a wide variety of
other medical conditions need to be ruled out; these conditions include, but are not limited to,
medical conditions due to infectious, metabolic, or neurological conditions (see “Catatonic
Disorder Due to Another Medical Condition”). Catatonia can also be a side effect of a
medication (see the chapter “Medication-Induced Movement Disorders and Other Adverse
Effects of Medication”). Because of the seriousness of the complications, particular attention
should be paid to the possibility that the catatonia is attributable to G21.0 neuroleptic malignant
syndrome.
Culture-Related Diagnostic Issues
The association between catatonia and mood disorders has been found in a wide range of cultural
contexts.
Catatonic Disorder Due to Another Medical Condition
Diagnostic Criteria
A. The clinical picture is dominated by three (or more) of the following symptoms:
1. Stupor (i.e., no psychomotor activity; not actively relating to environment).
2. Catalepsy (i.e., passive induction of a posture held against gravity).
3. Waxy flexibility (i.e., slight, even resistance to positioning by examiner).
4. Mutism (i.e., no, or very little, verbal response [Note: not applicable if there is
an established aphasia]).
5. Negativism (i.e., opposition or no response to instructions or external stimuli).
6. Posturing (i.e., spontaneous and active maintenance of a posture against
gravity).
7. Mannerism (i.e., odd, circumstantial caricature of normal actions).
8. Stereotypy 
(i.e., 
repetitive, 
abnormally 
frequent, 
non-goal-directed
movements).
9. Agitation, not influenced by external stimuli.
10. Grimacing.
11. Echolalia (i.e., mimicking another’s speech).
12. Echopraxia (i.e., mimicking another’s movements).
B. There is evidence from the history, physical examination, or laboratory findings
that the disturbance is the direct pathophysiological consequence of another
medical condition.

C. The disturbance is not better explained by another mental disorder (e.g., a manic
episode).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Coding note: Include the name of the medical condition in the name of the mental
disorder (e.g., F06.1 catatonic disorder due to hepatic encephalopathy). The other
medical condition should be coded and listed separately immediately before the
catatonic 
disorder 
due 
to 
the 
medical 
condition 
(e.g., 
K72.90 
hepatic
encephalopathy; F06.1 catatonic disorder due to hepatic encephalopathy).
Diagnostic Features
The essential feature of catatonic disorder due to another medical condition is the presence of
catatonia that is judged to be attributed to the physiological effects of another medical condition.
Catatonia can be diagnosed by the presence of at least 3 of the 12 clinical features in Criterion A.
There must be evidence from the history, physical examination, or laboratory findings that the
catatonia is attributable to another medical condition (Criterion B). The diagnosis is not given if
the catatonia is better explained by another mental disorder (e.g., manic episode) (Criterion C) or
if it occurs exclusively during the course of a delirium (Criterion D).
Associated Features
A variety of medical conditions may cause catatonia, especially neurological conditions (e.g.,
neoplasms, head trauma, cerebrovascular disease, encephalitis) and metabolic conditions (e.g.,
hypercalcemia, hepatic encephalopathy, homocystinuria, diabetic ketoacidosis). The associated
physical examination findings, laboratory findings, and patterns of prevalence and onset reflect
those of the etiological medical condition.
Differential Diagnosis
A separate diagnosis of catatonic disorder due to another medical condition is not given if the
catatonia occurs exclusively during the course of a delirium or neuroleptic malignant syndrome.
However, even though a separate diagnosis of catatonia cannot be made, research suggests that
catatonia symptoms occur in a significant proportion of delirium cases. If the individual is
currently taking neuroleptic medication, consideration should be given to medication-induced
movement disorders (e.g., abnormal positioning may be due to neuroleptic-induced acute
dystonia) or neuroleptic malignant syndrome (e.g., catatonic-like features may be present, along
with associated vital sign and/or laboratory abnormalities). Catatonic symptoms may be present
in any of the following five psychotic disorders: brief psychotic disorder, schizophreniform
disorder, schizophrenia, schizoaffective disorder, and substance/medication-induced psychotic
disorder. It may also be present in some of the neurodevelopmental disorders, in all of the bipolar
and depressive disorders, and in other mental disorders.

Unspecified Catatonia
This category applies to presentations in which symptoms characteristic of catatonia
cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning but either the nature of the underlying mental disorder
or other medical condition is unclear, full criteria for catatonia are not met, or there is
insufficient information to make a more specific diagnosis (e.g., in emergency room
settings).
 
Coding note: Code first R29.818 other symptoms involving nervous and
musculoskeletal systems, followed by F06.1 unspecified catatonia.
Other Specified Schizophrenia Spectrum and Other
Psychotic Disorder
F28
This category applies to presentations in which symptoms characteristic of a
schizophrenia spectrum and other psychotic disorder that cause clinically significant
distress or impairment in social, occupational, or other important areas of functioning
predominate but do not meet the full criteria for any of the disorders in the
schizophrenia spectrum and other psychotic disorders diagnostic class. The other
specified schizophrenia spectrum and other psychotic disorder category is used in
situations in which the clinician chooses to communicate the specific reason that the
presentation does not meet the criteria for any specific schizophrenia spectrum and
other psychotic disorder. This is done by recording “other specified schizophrenia
spectrum and other psychotic disorder” followed by the specific reason (e.g.,
“persistent auditory hallucinations”).
Examples of presentations that can be specified using the “other specified”
designation include the following:
1. Persistent auditory hallucinations occurring in the absence of any other
features.
2. Delusions with significant overlapping mood episodes: This includes
persistent delusions with periods of overlapping mood episodes that are present
for a substantial portion of the delusional disturbance (such that the criterion
stipulating only brief mood disturbance in delusional disorder is not met).
3. Attenuated psychosis syndrome: This syndrome is characterized by
psychotic-like symptoms that are below a threshold for full psychosis (e.g., the
symptoms are less severe and more transient, and insight is relatively
maintained).

4. Delusional symptoms in the context of relationship with an individual with
prominent delusions: In the context of a relationship, the delusional material
from the individual with a psychotic disorder provides content for the same
delusions held by the other person who may not otherwise have symptoms that
meet criteria for a psychotic disorder.
Unspecified Schizophrenia Spectrum and Other
Psychotic Disorder
F29
This category applies to presentations in which symptoms characteristic of a
schizophrenia spectrum and other psychotic disorder that cause clinically significant
distress or impairment in social, occupational, or other important areas of functioning
predominate but do not meet the full criteria for any of the disorders in the
schizophrenia spectrum and other psychotic disorders diagnostic class. The
unspecified schizophrenia spectrum and other psychotic disorder category is used in
situations in which the clinician chooses not to specify the reason that the criteria are
not met for a specific schizophrenia spectrum and other psychotic disorder and
includes presentations in which there is insufficient information to make a more
specific diagnosis (e.g., in emergency room settings).

# 03 - Bipolar and Related Disorders

# Bipolar and Related Disorders

139

Bipolar and Related Disorders
Bipolar and related disorders are found between the chapters on schizophrenia
spectrum and other psychotic disorders and depressive disorders in DSM-5-TR in recognition of
their place as a bridge between those two diagnostic classes in terms of symptomatology, family
history, and genetics. The diagnoses included in this chapter are bipolar I disorder, bipolar II
disorder, cyclothymic disorder, substance/medication-induced bipolar and related disorder,
bipolar and related disorder due to another medical condition, other specified bipolar and related
disorder, and unspecified bipolar and related disorder.
The bipolar I disorder criteria represent the modern understanding of the classic manicdepressive disorder or affective psychosis described in the nineteenth century, differing from that
classic description only to the extent that neither psychosis nor the lifetime experience of a major
depressive episode is a requirement. However, the vast majority of individuals whose symptoms
meet the criteria for a fully syndromal manic episode also experience major depressive episodes
during the course of their lives.
Bipolar II disorder, requiring the lifetime experience of at least one major depressive episode
and at least one hypomanic episode (but no history of mania), is no longer thought to be a less
severe condition than bipolar I disorder, largely because of the burden of depression in bipolar II
disorder and because the instability of mood experienced by individuals with bipolar II disorder
is often accompanied by serious impairment in work and social functioning.
The diagnosis of cyclothymic disorder is given to adults who experience at least 2 years (for
children, a full year) of both hypomanic and depressive periods without ever fulfilling the criteria
for an episode of mania, hypomania, or major depression.
A large number of substances of abuse, some prescribed medications, and several medical
conditions can be associated with manic-like phenomena. This fact is recognized in the
diagnoses of substance/medication-induced bipolar and related disorder and bipolar and related
disorder due to another medical condition.
The recognition that there are individuals who experience bipolar-like phenomena with
symptoms that do not meet the criteria for bipolar I, bipolar II, or cyclothymic disorder is
reflected in the availability of the other specified bipolar and related disorder category. Specific
criteria for a disorder involving short-duration hypomania are provided in Section III in the hope
of encouraging further study of this presentation of bipolar disorder symptomatology and its
course.
Bipolar I Disorder
Diagnostic Criteria

For a diagnosis of bipolar I disorder, it is necessary to meet the following criteria for
a manic episode. The manic episode may have been preceded by and may be
followed by hypomanic or major depressive episodes.
Manic Episode
A. A distinct period of abnormally and persistently elevated, expansive, or irritable
mood and abnormally and persistently increased activity or energy, lasting at
least 1 week and present most of the day, nearly every day (or any duration if
hospitalization is necessary).
B. During the period of mood disturbance and increased energy or activity, three (or
more) of the following symptoms (four if the mood is only irritable) are present to
a significant degree and represent a noticeable change from usual behavior:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are racing.
5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant
external stimuli), as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or
sexually) or psychomotor agitation (i.e., purposeless non-goal-directed
activity).
7. Excessive involvement in activities that have a high potential for painful
consequences (e.g., engaging in unrestrained buying sprees, sexual
indiscretions, or foolish business investments).
C. The mood disturbance is sufficiently severe to cause marked impairment in
social or occupational functioning or to necessitate hospitalization to prevent
harm to self or others, or there are psychotic features.
D. The episode is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication, other treatment) or another medical condition.
Note: A full manic episode that emerges during antidepressant treatment (e.g.,
medication, electroconvulsive therapy) but persists at a fully syndromal level
beyond the physiological effect of that treatment is sufficient evidence for a
manic episode and, therefore, a bipolar I diagnosis.
Note: Criteria A–D constitute a manic episode. At least one lifetime manic episode is
required for the diagnosis of bipolar I disorder.
Hypomanic Episode
A. A distinct period of abnormally and persistently elevated, expansive, or irritable
mood and abnormally and persistently increased activity or energy, lasting at
least 4 consecutive days and present most of the day, nearly every day.

B. During the period of mood disturbance and increased energy and activity, three
(or more) of the following symptoms (four if the mood is only irritable) have
persisted, represent a noticeable change from usual behavior, and have been
present to a significant degree:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are racing.
5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant
external stimuli), as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or
sexually) or psychomotor agitation.
7. Excessive involvement in activities that have a high potential for painful
consequences (e.g., engaging in unrestrained buying sprees, sexual
indiscretions, or foolish business investments).
C. The episode is associated with an unequivocal change in functioning that is
uncharacteristic of the individual when not symptomatic.
D. The disturbance in mood and the change in functioning are observable by
others.
E. The episode is not severe enough to cause marked impairment in social or
occupational functioning or to necessitate hospitalization. If there are psychotic
features, the episode is, by definition, manic.
F. The episode is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication, other treatment) or another medical condition.
Note: A full hypomanic episode that emerges during antidepressant treatment
(e.g., medication, electroconvulsive therapy) but persists at a fully syndromal
level beyond the physiological effect of that treatment is sufficient evidence for a
hypomanic episode diagnosis. However, caution is indicated so that one or two
symptoms (particularly increased irritability, edginess, or agitation following
antidepressant use) are not taken as sufficient for diagnosis of a hypomanic
episode, nor necessarily indicative of a bipolar diathesis.
Note: Criteria A–F constitute a hypomanic episode. Hypomanic episodes are
common in bipolar I disorder but are not required for the diagnosis of bipolar I
disorder.
Major Depressive Episode
A. Five (or more) of the following symptoms have been present during the same 2week period and represent a change from previous functioning; at least one of
the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.

Note: Do not include symptoms that are clearly attributable to another medical
condition.
1. Depressed mood most of the day, nearly every day, as indicated by either
subjective report (e.g., feels sad, empty, or hopeless) or observation made by
others (e.g., appears tearful). (Note: In children and adolescents, can be
irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most of
the day, nearly every day (as indicated by either subjective account or
observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of
more than 5% of body weight in a month), or decrease or increase in appetite
nearly every day. (Note: In children, consider failure to make expected weight
gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others,
not merely subjective feelings of restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be
delusional) nearly every day (not merely self-reproach or guilt about being
sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day
(either by subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation
without a specific plan, or a suicide attempt or a specific plan for committing
suicide.
B. The symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
C. The episode is not attributable to the physiological effects of a substance or
another medical condition.
Note: Criteria A–C constitute a major depressive episode. Major depressive
episodes are common in bipolar I disorder but are not required for the diagnosis of
bipolar I disorder.
Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses from
a natural disaster, a serious medical illness or disability) may include the feelings of
intense sadness, rumination about the loss, insomnia, poor appetite, and weight loss
noted in Criterion A, which may resemble a depressive episode. Although such
symptoms may be understandable or considered appropriate to the loss, the
presence of a major depressive episode in addition to the normal response to a
significant loss should also be carefully considered. This decision inevitably requires

the exercise of clinical judgment based on the individual’s history and the cultural
norms for the expression of distress in the context of loss.1
Bipolar I Disorder
A. Criteria have been met for at least one manic episode (Criteria A–D under
“Manic Episode” above).
B. At least one manic episode is not better explained by schizoaffective disorder
and is not superimposed on schizophrenia, schizophreniform disorder,
delusional disorder, or other specified or unspecified schizophrenia spectrum
and other psychotic disorder.
Coding and Recording Procedures
The diagnostic code for bipolar I disorder is based on type of current or most recent
episode and its status with respect to current severity, presence of psychotic
features, and remission status. Current severity and psychotic features are only
indicated if full criteria are currently met for a manic or major depressive episode.
Remission specifiers are only indicated if the full criteria are not currently met for a
manic, hypomanic, or major depressive episode. Codes are as follows:
Bipolar I disorder
Current or
most
recent
episode
manic
Current or
most recent
episode
hypomanic*
Current or
most
recent
episode
depressed
Current or
most recent
episode
unspecified**
Mild (p. 175)
F31.11
NA
F31.31
NA
Moderate (p. 175)
F31.12
NA
F31.32
NA
Severe (p. 175)
F31.13
NA
F31.4
NA
With psychotic features*** (p. 173)
F31.2
NA
F31.5
NA
In partial remission (p. 175)
F31.73
F31.71
F31.75
NA
In full remission (p. 175)
F31.74
F31.72
F31.76
NA
Unspecified
F31.9
F31.9
F31.9
NA
*Severity and psychotic specifiers do not apply; code F31.0 for cases not in remission.
**Severity, psychotic, and remission specifiers do not apply. Code F31.9.
***If psychotic features are present, code the “with psychotic features” specifier irrespective of episode severity.
In recording the name of a diagnosis, terms should be listed in the following order:
bipolar I disorder, type of current episode (or most recent episode if bipolar I
disorder is in partial or full remission), severity/psychotic/remission specifiers,
followed by as many of the following specifiers without codes as apply to the
current episode (or the most recent episode if bipolar I disorder is in partial or full
remission). Note: The specifiers “with rapid cycling” and “with seasonal pattern”
describe the pattern of mood episodes.

Specify if:
With anxious distress (pp. 169–170)
With mixed features (pp. 170–171)
With rapid cycling (p. 171)
With melancholic features (pp. 171–172)
With atypical features (pp. 172–173)
With mood-congruent psychotic features (p. 173; applies to manic episode
and/or major depressive episode)
With mood-incongruent psychotic features (p. 173; applies to manic episode
and/or major depressive episode)
With catatonia (p. 173). Coding note: Use additional code F06.1.
With peripartum onset (pp. 173–174)
With seasonal pattern (pp. 174–175)
Diagnostic Features
Bipolar I disorder is characterized by a clinical course of recurring mood episodes (manic,
depressive, and hypomanic), but the occurrence of at least one manic episode is necessary for the
diagnosis of bipolar I disorder. The essential feature of a manic episode is a distinct period
during which there is an abnormally, persistently elevated, expansive, or irritable mood and
persistently increased activity or energy that is present for most of the day, nearly every day, for
a period of at least 1 week (or any duration if hospitalization is necessary), accompanied by at
least three additional symptoms from Criterion B. If the mood is irritable rather than elevated or
expansive, at least four Criterion B symptoms must be present.
Mood in a manic episode is often described as euphoric, excessively cheerful, high, or
“feeling on top of the world.” In some cases, the mood is of such a highly infectious quality that
it is easily recognized as excessive and may be characterized by unlimited and
haphazard enthusiasm for interpersonal, sexual, or occupational interactions. For example,
the individual may spontaneously start extensive conversations with strangers in public. Often
the predominant mood is irritable rather than elevated, particularly when the individual’s wishes
are denied or if the individual has been using substances. Rapid shifts in mood over brief periods
of time may occur and are referred to as lability (i.e., the alternation among euphoria, dysphoria,
and irritability). In children, happiness, silliness, and “goofiness” are normal in many social
contexts; however, if these symptoms are recurrent, inappropriate to the context, and beyond
what is expected for the developmental level of the child, they may meet the Criterion A mood
requirement of abnormally elevated mood. For the happiness or silliness of a child to meet
Criterion A, it must be distinctly increased from the child’s baseline and accompanied by
persistently increased activity or energy levels that to those who know the child well are clearly
unusual for that child. For a child’s symptoms to meet criteria for a manic episode, the symptoms

must also meet Criterion B for mania and must also represent a change from the child’s usual
baseline.
During the manic episode, the individual may engage in multiple overlapping new projects.
The projects are often initiated with little knowledge of the topic, and nothing seems out of the
individual’s reach. The increased activity or energy levels may manifest at unusual hours of the
day, such as during the individual’s normal sleep phase.
Inflated self-esteem is typically present, ranging from uncritical self-confidence to marked
grandiosity, and may reach delusional proportions (Criterion B1). Despite lack of any particular
experience or talent, the individual may embark on complex tasks such as writing a novel or
seeking publicity for some impractical invention. Grandiose delusions (e.g., of having a special
relationship to a famous person) are common. In children, overestimation of abilities and belief
that, for example, they are the best at a sport or the smartest in the class is normal; however,
when such beliefs are present despite clear evidence to the contrary or the child attempts feats
that are clearly dangerous and, most important, represent a change from the child’s normal
behavior, the grandiosity criterion should be considered satisfied.
One of the most common features is a decreased need for sleep (Criterion B2), which is
distinct from insomnia (during which the individual wants to sleep or feels the need to sleep but
is unable to). The individual may sleep little, if at all, or may awaken several hours earlier than
usual, feeling rested and full of energy. When the sleep disturbance is severe, the individual may
go for days without sleep, yet not feel tired. Often decreased need for sleep heralds the onset of a
manic episode.
Speech can be rapid, pressured, loud, and difficult to interrupt (Criterion B3). Individuals
may talk continuously and without regard for others’ wishes to communicate, often in an
intrusive manner or without concern for the relevance of what is said. Speech is sometimes
characterized by jokes, puns, amusing irrelevancies, and theatricality, with dramatic mannerisms,
singing, and excessive gesturing. Loudness and forcefulness of speech often become more
important than what is conveyed. If the individual’s mood is more irritable than expansive,
speech may be marked by complaints, hostile comments, or angry tirades, particularly if attempts
are made to interrupt the individual. Both Criterion A and Criterion B symptoms may be
accompanied by symptoms of the opposite (i.e., depressive) pole (see “with mixed features”
specifier, pp. 170–171).
Often the individual’s thoughts race at a rate faster than can be expressed through speech
(Criterion B4). Frequently there is flight of ideas evidenced by a nearly continuous flow of
accelerated speech, with abrupt shifts from one topic to another. When flight of ideas is severe,
speech may become disorganized, incoherent, and particularly distressing to the individual.
Sometimes thoughts are experienced as so crowded that it is very difficult to speak.
Distractibility (Criterion B5) is evidenced by an inability to censor immaterial external
stimuli (e.g., the interviewer’s attire, background noises or conversations, furnishings in the
room) and often prevents individuals experiencing mania from holding a rational conversation or
attending to instructions.
The increase in goal-directed activity (Criterion B6) often consists of excessive planning and
participation in multiple activities, including sexual, occupational, political, or religious

activities. Increased sexual drive, fantasies, and behavior are often present. Individuals in a
manic episode usually show increased sociability (e.g., renewing old acquaintances or calling or
contacting friends or even strangers), without regard to the intrusive, domineering, and
demanding nature of these interactions. They often also display psychomotor agitation or
restlessness (i.e., purposeless activity) by pacing or by holding multiple conversations
simultaneously. Some individuals write excessive letters, e-mails, text messages, and so forth, on
many different topics to friends, public figures, or the media.
The increased activity criterion can be difficult to ascertain in children; however, when the
child takes on many tasks simultaneously, starts devising elaborate and unrealistic plans for
projects, develops previously absent and developmentally inappropriate sexual preoccupations
(not accounted for by sexual abuse or exposure to sexually explicit material), then Criterion B
might be met based on clinical judgment. It is essential to determine whether the behavior
represents a change from the child’s baseline behavior; occurs most of the day, nearly every day
for the requisite time period; and occurs in temporal association with other symptoms of mania.
The expansive mood, excessive optimism, grandiosity, and poor judgment often lead to
reckless involvement in activities such as spending sprees, giving away possessions, reckless
driving, foolish business investments, and sexual indiscretions that are unusual for the individual,
even though these activities are likely to have catastrophic consequences (Criterion B7). The
individual may purchase many unneeded items without the money to pay for them and, in some
cases, give them away. Sexual indiscretions may include infidelity or indiscriminate sexual
encounters with strangers, often disregarding the risk of sexually transmitted diseases or
interpersonal consequences.
The manic episode must result in marked impairment in social or occupational functioning
(e.g., financial losses, loss of employment, school failure, divorce) or require hospitalization to
prevent harm to self or others (e.g., physical exhaustion or hyperthermia from manic excitement,
self-injurious behavior). By definition, the presence of psychotic features during a manic episode
also satisfies Criterion C.
Manic symptoms or syndromes that are attributable to the direct physiological effects of a
drug of abuse (e.g., in the context of cocaine or amphetamine intoxication), the side effects of
medications or treatments (e.g., steroids, L-dopa, antidepressants, stimulants), or another medical
condition do not count toward the diagnosis of bipolar I disorder. However, a fully syndromal
manic episode that arises during treatment (e.g., with medications, electroconvulsive therapy,
light therapy) and persists beyond the physiological effect of the inducing agent (e.g., after a
medication is fully out of the individual’s system or the effects of electroconvulsive therapy
would be expected to have dissipated completely) is sufficient evidence for a manic episode that
is considered due to bipolar I disorder (Criterion D). Caution is indicated so that one or two
symptoms (particularly increased irritability, edginess, or agitation following antidepressant use)
are not taken as sufficient for diagnosis of a manic or hypomanic episode, nor necessarily an
indication of a bipolar disorder diathesis. Although not essential to a diagnosis of bipolar I
disorder, hypomanic or depressive episodes often precede or follow a manic episode. Full
descriptions of the diagnostic features of a hypomanic episode may be found within the text for
bipolar II disorder, and the features of a major depressive episode are described within the text
for major depressive disorder.

Associated Features
During a manic episode, individuals often do not perceive that they are ill or in need of treatment
and vehemently resist efforts to be treated. Individuals may change their dress, makeup, or
personal appearance to a more sexually suggestive or flamboyant style. Some perceive a sharper
sense of smell, hearing, or vision. Gambling and antisocial behaviors
may accompany the manic episode. Mood may shift very rapidly to anger or depression; some
individuals may become hostile and physically threatening to others and, when delusional,
become physically assaultive or suicidal. Serious consequences of a manic episode (e.g.,
involuntary hospitalization, difficulties with the law, serious financial difficulties) often result
from poor judgment, loss of insight, and hyperactivity. Depressive symptoms occur in some 35%
of manic episodes (see “with mixed features” specifier, p. 170), and mixed features are
associated with poorer outcome and increased suicide attempts. Bipolar I disorder is also
associated with significant decrements in quality of life and well-being.
Trait-like features associated with the diagnosis include hyperthymic, depressive,
cyclothymic, anxious, and irritable temperaments, sleep and circadian rhythm disturbances,
reward sensitivity, and creativity. Having a first-degree relative with bipolar disorder increases
the risk of diagnosis approximately 10-fold.
Prevalence
The 12-month prevalence of DSM-5 bipolar I disorder in a nationally representative U.S. adult
sample was 1.5% and did not differ between men (1.6%) and women (1.5%). Compared with
non-Hispanic Whites, prevalence of bipolar I disorder appears to be higher among Native
Americans and lower among African Americans, Hispanics, and Asians/Pacific Islanders.
Twelve-month prevalence of DSM-IV bipolar I disorder across 11 countries ranged from 0.0% to
0.6% and was greater in high-income countries than in low- and middle-income countries, except
in Japan, where prevalence was low (0.01%). The lifetime prevalence ratio in men to women is
approximately 1.1:1.
Development and Course
The peak age at onset of bipolar I disorder across studies is between 20 and 30 years, but onset
occurs throughout the life cycle. In the United States, mean age at onset of DSM-5 bipolar I
disorder is 22 years and slightly younger for women (21.5 years) than for men (23.0 years). In a
comparison of six international sites, median age at onset of DSM-IV-TR bipolar I disorder was
24.3 years. Special considerations are necessary to apply the diagnosis in children. Because
children of the same chronological age may be at different developmental stages, it is difficult to
define with precision what is “normal” or “expected” at any given point. Therefore, each child
should be judged according to his or her own baseline in determining whether a particular
behavior is “normal” or evidence of a manic episode. Although age at first onset may occur in
the 60s or 70s, onset of manic symptoms (e.g., sexual or social disinhibition) in late mid-life or
late-life should prompt consideration of medical conditions (e.g., frontotemporal neurocognitive
disorder) and of substance ingestion or withdrawal.

Environmental.
Genetic and physiological.
More than 90% of individuals who have a single manic episode go on to have recurrent mood
episodes. Approximately 60% of manic episodes occur immediately before a major depressive
episode. Individuals with bipolar I disorder who have multiple (four or more) mood episodes
(major depressive, manic, or hypomanic) occurring in the prior 12 months receive the specifier
“with rapid cycling,” a common variant associated with poorer outcomes. About half of
individuals diagnosed with bipolar disorder exhibit a predominant polarity (relapse tending to be
either depressive or manic), with one international study of bipolar I disorder finding 31.3% with
predominant mania, 21.4% with predominant depression, and 47.3% without polarity
predominance.
The course of bipolar I disorder is highly heterogeneous. Some patterns have been noted
across episodes (e.g., a manic episode with psychotic features may be associated with psychotic
features in subsequent manic episodes). Polarity of first episode tends to be associated with
predominant polarity of future episodes and clinical features (e.g., depressive onset is associated
with greater density of depressive episodes and suicidal behavior). The
presence of mixed features in a manic episode is associated with a poorer prognosis, poorer
lithium response, and suicidal behavior.
Risk and Prognostic Factors
Childhood 
adversity 
(including 
early 
emotional 
trauma, 
parental
psychopathology, and family conflict) is a known risk factor for bipolar disorder and appears to
predispose to early onset of bipolar disorder. Childhood adversity is also associated with poorer
prognosis and a worse clinical picture that may include medical or psychiatric comorbidities,
suicide, and associated psychotic features. More proximally, recent life stress and other negative
life events increase depressive relapse risk in individuals diagnosed with bipolar disorder,
whereas manic relapse appears to be specifically linked to goal-attainment life events (e.g.,
getting married, completing a degree). Cannabis and other substance use is associated with
exacerbation of manic symptoms among individuals diagnosed with bipolar disorder, as well as
first onset of manic symptoms in the general population. There is some evidence that becoming
married is less common among individuals with bipolar disorder than in the general population
and that a diagnosis of bipolar disorder is associated with being previously as opposed to
currently married.
Genetic processes strongly affect predisposition to bipolar disorder,
with heritability estimates around 90% in some twin studies. Risk of bipolar disorder in the
general population is around 1%, while risk in a first-degree relative is 5%–10%. However,
monozygotic concordance rates are significantly less than 100% (40%–70%), indicating that
much risk is left unexplained by genes alone. The mechanism of heritability is not Mendelian,
and involves multiple genes (or more complex genetic mechanisms) of small effect, interacting
with each other, the environment, and random factors. Emerging genetic findings suggest that
mania- and depression-proneness are inherited separately, and bipolar disorder shares a genetic
origin with schizophrenia.

Culture-Related Diagnostic Issues
Bipolar I disorder symptoms tend to be consistent across cultural contexts, but some variation
exists in symptom expression and interpretation. For example, individuals from different cultural
backgrounds with bipolar I disorder, with psychotic features, may vary in the prevalence of flight
of ideas or types of delusions (e.g., grandiose, persecutory, sexual, religious, or somatic).
Cultural factors may affect disorder prevalence. For example, countries with reward-oriented
cultural values that place significance on individual pursuit of reward have a relatively higher
prevalence of bipolar disorder. In the United States, individuals with bipolar disorder had an
earlier age at onset than those in Europe and were more likely to have a family history of
psychiatric disorder.
Culture also influences clinician diagnostic practices regarding bipolar disorder. Compared
with non-Latinx Whites in the United States, African Americans with bipolar I disorder are at
higher risk of being misdiagnosed with schizophrenia. Possible reasons include underrecognition
of mood symptoms, cultural and linguistic misunderstanding between clinicians and the
individuals presenting for treatment (e.g., misinterpretation of cultural mistrust as paranoia),
more florid psychotic symptoms at presentation due to delay in receiving services, and diagnoses
based on shorter clinical assessments. These factors may result in discriminatory misdiagnosis of
schizophrenia, particularly in African Americans with mood disorders who present with
psychotic features.
Sex- and Gender-Related Diagnostic Issues
Women may be more likely to experience rapid cycling and mixed states, and to have patterns of
comorbidity that differ from those of men, including higher rates of lifetime eating
disorders. Women with bipolar I or II disorder are more likely to experience depressive
symptoms than are men. They also have a higher lifetime risk of alcohol use disorder than do
men and a much greater likelihood of alcohol use disorder than do women in the general
population.
Some women with bipolar disorder experience exacerbation of mood symptoms during the
premenstrual time period, and this has been associated with a worse course of illness. Many
women with bipolar disorder also report severe emotional disturbances during perimenopause
when estrogen levels are decreasing. There does not appear to be an increased risk of mood
episodes in pregnant women with bipolar disorder except in those who discontinue medications
for pregnancy. In contrast, there is strong and consistent evidence for an increased risk of mood
episodes (both depression and mania) in women with bipolar I disorder in the postpartum period.
The specifier “with peripartum onset” should be used for mood episodes that begin during
pregnancy or within 4 weeks of delivery. “Postpartum psychosis” typically resembles a manic or
mixed mood episode with psychotic symptoms and is strongly associated with bipolar I disorder.
Association With Suicidal Thoughts or Behavior
The lifetime risk of suicide in individuals with bipolar disorder is estimated to be 20- to 30-fold
greater than in the general population. An estimated 5%–6% of individuals with bipolar disorders

Major depressive disorder.
Other bipolar disorders.
Generalized anxiety disorder, panic disorder, posttraumatic stress disorder, or other anxiety
disorders.
Bipolar and related disorder due to another medical condition.
die by suicide. While suicide attempts are higher in women, lethal suicide is more common in
men with bipolar disorder. A past history of suicide attempt and percent days spent depressed in
the past year are associated with greater risk of suicide attempts or completions. Nearly half of
individuals whose symptoms meet criteria for bipolar disorder have an alcohol use disorder, and
those with both disorders are at greater risk for suicide attempt and suicide death.
Functional Consequences of Bipolar I Disorder
Approximately 30% of individuals with bipolar disorder show severe impairment in work role
functioning, although many individuals return to a fully functional level between episodes.
Functional recovery lags substantially behind recovery from symptoms, especially with respect
to occupational recovery, resulting in lower socioeconomic status despite equivalent levels of
education when compared with the general population. Cognitive impairments persist through
the lifespan, even during euthymic periods, and may contribute to vocational and interpersonal
difficulties. Higher level of self-perceived stigma is associated with lower level of functioning.
Differential Diagnosis
There is a risk of misdiagnosing bipolar I disorder as unipolar
depression because of the prominence of depression in the presentation of bipolar I disorder: 1)
the first episode of bipolar disorder is often depressive, 2) depressive symptoms are the most
frequent symptoms experienced across the long-term course of bipolar I disorder, and 3) the
problem for which individuals typically seek help is depression. When the individual presents in
an episode of major depression, it is therefore important to actively probe for a history of mania
or hypomania. Factors that might indicate that the diagnosis is bipolar I disorder rather than
major depressive disorder in an individual presenting with a current depressive episode include
family history of bipolar disorder, onset of illness in early 20s, numerous past episodes, presence
of psychotic symptoms, and a history of lack of response to antidepressant treatment or the
emergence of a manic episode during antidepressant treatment (e.g., medication,
electroconvulsive therapy).
Bipolar II disorder, cyclothymic disorder, and other specified bipolar and
related disorder are similar to bipolar I disorder by virtue of their including
periods of hypomanic symptoms in their presentations but are differentiated from bipolar I
disorder by the absence of any manic episodes.
A
careful history of symptoms is needed to differentiate generalized anxiety disorder from bipolar
disorder, as anxious ruminations may be mistaken for racing thoughts (and vice versa), and
efforts to minimize anxious feelings may be taken as impulsive behavior. Similarly, symptoms of
posttraumatic stress disorder need to be differentiated from bipolar disorder. It is helpful to
assess the episodic nature of the symptoms described (classical bipolar I is episodic), as well as
to consider symptom triggers, in making this differential diagnosis.
The diagnosis of bipolar and related

Substance/medication-induced bipolar and related disorder.
Schizoaffective disorder.
Attention-deficit/hyperactivity disorder.
Disruptive mood dysregulation disorder.
Personality disorders.
disorder due to another medical condition should be made instead of bipolar I disorder if the
manic episodes are judged, based on history, laboratory findings, or physical examination, to be
the direct physiological consequence of another medical condition (e.g., Cushing’s disease,
multiple sclerosis).
A substance/medication-induced bipolar
and related disorder is distinguished from bipolar I disorder by the fact that a substance (e.g.,
stimulants, phencyclidine) or medication (e.g., steroids) is judged to be etiologically related to
the manic episode. Because individuals with a manic episode have a tendency to overuse
substances during an episode, it is important to determine whether the substance use is a
consequence of a primary manic episode or whether the manic-like episode has been caused by
the substance use. In some cases, a definitive diagnosis may involve establishing that the manic
symptoms remain once the individual is no longer using the substance. Note that manic episodes
emerging in the context of treatment with an antidepressant medication but that persist at a fully
syndromal level beyond the physiological effect of the medication warrant a diagnosis of bipolar
I disorder rather than substance/medication-induced bipolar and related disorder.
Schizoaffective disorder is characterized by periods in which manic and
major depressive episodes are concurrent with the active phase symptoms of schizophrenia and
periods in which delusions or hallucinations occur for at least 2 weeks in the absence of a manic
or major depressive episode. The diagnosis is “bipolar I disorder, with psychotic features” if the
psychotic symptoms have occurred exclusively during manic and major depressive episodes.
Attention-deficit/hyperactivity disorder is characterized by
persistent symptoms of inattention, hyperactivity, and impulsivity, which may resemble the
symptoms of a manic episode (e.g., distractibility, increased activity, impulsive behavior) and
have their onset by age 12. In contrast, the symptoms of mania in bipolar I disorder occur in
distinct episodes and typically begin in late adolescence or early adulthood.
In individuals with severe irritability, particularly children
and adolescents, care must be taken to apply the diagnosis of bipolar I disorder only to those who
have had a clear episode of mania or hypomania—that is, a distinct time period, of the required
duration, during which the irritability was clearly different from the individual’s baseline and
was accompanied by the onset of the other characteristic symptoms of mania (e.g., grandiosity,
decreased need for sleep, pressured speech, involvement in activities with a high potential for
painful consequences). When a child’s irritability is persistent and particularly severe, the
diagnosis of disruptive mood dysregulation disorder would be more appropriate. Indeed, when
any child is being assessed for mania, it is essential that the symptoms represent a clear change
from the child’s typical behavior.
Personality disorders such as borderline personality disorder may have
substantial symptomatic overlap with bipolar I disorder, since mood lability and impulsivity are
common in both conditions. In order to make a diagnosis of bipolar I disorder, symptoms of
mood lability and impulsivity must represent a distinct episode of illness, or there must be a
noticeable increase in these symptoms over the individual’s baseline in order to justify an
additional diagnosis of bipolar I disorder.

F31.81
Comorbidity
Co-occurring mental disorders are the norm in bipolar I disorder, with the majority of individuals
having a history of three or more disorders. The most frequently comorbid disorders are anxiety
disorders, alcohol use disorder, other substance use disorder, and attention-deficit/hyperactivity
disorder. Sociocultural factors influence the pattern of comorbid conditions in bipolar disorder.
For example, countries with cultural prohibitions against alcohol or other substance use may
have a lower prevalence of substance use comorbidity. Bipolar I disorder is frequently associated
with borderline, schizotypal, and antisocial personality disorder. In particular, although the
underlying nature of the relationship between bipolar I disorder and borderline personality
disorder is unclear, the substantial comorbidity between the two may reflect similarities in
phenomenology (i.e., misdiagnosing the emotional extremes of borderline personality disorder as
bipolar I disorder), the influence of borderline personality features on vulnerability to bipolar I
disorder, and the impact of early childhood adversity on the development of both bipolar I and
borderline personality disorder.
Individuals with bipolar I disorder also have high rates of serious co-occurring and often
untreated medical conditions, which largely explain the shortened life expectancy of those with
bipolar disorder. Comorbidities appear in multiple organ systems, with cardiovascular and
autoimmune diseases, obstructive sleep apnea, metabolic syndrome, and migraine more common
among individuals with bipolar disorder than in the general population. Comorbid
overweight/obesity is a particular concern for individuals with bipolar disorder and is associated
with poor treatment outcomes.
Bipolar II Disorder
Diagnostic Criteria
For a diagnosis of bipolar II disorder, it is necessary to meet the following criteria for
a current or past hypomanic episode and the following criteria for a current or past
major depressive episode:
Hypomanic Episode
A. A distinct period of abnormally and persistently elevated, expansive, or irritable
mood and abnormally and persistently increased activity or energy, lasting at
least 4 consecutive days and present most of the day, nearly every day.
B. During the period of mood disturbance and increased energy and activity, three
(or more) of the following symptoms have persisted (four if the mood is only
irritable), represent a noticeable change from usual behavior, and have been
present to a significant degree:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are racing.

151
5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant
external stimuli), as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or
sexually) or psychomotor agitation.
7. Excessive involvement in activities that have a high potential for painful
consequences (e.g., engaging in unrestrained buying sprees, sexual
indiscretions, or foolish business investments).
C. The episode is associated with an unequivocal change in functioning that is
uncharacteristic of the individual when not symptomatic.
D. The disturbance in mood and the change in functioning are observable by
others.
E. The episode is not severe enough to cause marked impairment in social or
occupational functioning or to necessitate hospitalization. If there are psychotic
features, the episode is, by definition, manic.
F. The episode is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication, other treatment) or another medical condition.
Note: A full hypomanic episode that emerges during antidepressant treatment
(e.g., medication, electroconvulsive therapy) but persists at a fully syndromal
level beyond the physiological effect of that treatment is sufficient evidence for a
hypomanic episode diagnosis. However, caution is indicated so that one or two
symptoms (particularly increased irritability, edginess, or agitation following
antidepressant use) are not taken as sufficient for diagnosis of a hypomanic
episode, nor necessarily indicative of a bipolar diathesis.
Major Depressive Episode
A. Five (or more) of the following symptoms have been present during the same 2week period and represent a change from previous functioning; at least one of
the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.
Note: Do not include symptoms that are clearly attributable to a medical
condition.
1. Depressed mood most of the day, nearly every day, as indicated by either
subjective report (e.g., feels sad, empty, or hopeless) or observation made by
others (e.g., appears tearful). (Note: In children and adolescents, can be
irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most of
the day, nearly every day (as indicated by either subjective account or
observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of
more than 5% of body weight in a month), or decrease or increase in appetite
nearly every day. (Note: In children, consider failure to make expected weight

gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others,
not merely subjective feelings of restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be
delusional) nearly every day (not merely self-reproach or guilt about being
sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day
(either by subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation
without a specific plan, or a suicide attempt or a specific plan for committing
suicide.
B. The symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
C. The episode is not attributable to the physiological effects of a substance or
another medical condition.
Note: Criteria A–C constitute a major depressive episode.
Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses from
a natural disaster, a serious medical illness or disability) may include the feelings of
intense sadness, rumination about the loss, insomnia, poor appetite, and weight loss
noted in Criterion A, which may resemble a depressive episode. Although such
symptoms may be understandable or considered appropriate to the loss, the
presence of a major depressive episode in addition to the normal response to a
significant loss should be carefully considered. This decision inevitably requires the
exercise of clinical judgment based on the individual’s history and the cultural norms
for the expression of distress in the context of loss.1
Bipolar II Disorder
A. Criteria have been met for at least one hypomanic episode (Criteria A–F under
“Hypomanic Episode” above) and at least one major depressive episode (Criteria
A–C under “Major Depressive Episode” above).
B. There has never been a manic episode.
C. At least one hypomanic episode and at least one major depressive episode are
not better explained by schizoaffective disorder and are not superimposed on
schizophrenia, schizophreniform disorder, delusional disorder, or other specified
or unspecified schizophrenia spectrum and other psychotic disorder.
D. The symptoms of depression or the unpredictability caused by frequent
alternation between periods of depression and hypomania causes clinically
significant distress or impairment in social, occupational, or other important

areas of functioning.
Coding and Recording Procedures
Bipolar II disorder has one diagnostic code: F31.81. Its status with respect to current
severity, presence of psychotic features, course, and other specifiers cannot be
coded but should be indicated in writing (e.g., F31.81 bipolar II disorder, current
episode depressed, moderate severity, with mixed features; F31.81 bipolar II
disorder, most recent episode depressed, in partial remission).
Specify current or most recent episode:
Hypomanic
Depressed
If current episode is hypomanic (or most recent episode if bipolar II disorder is in
partial or full remission):
In recording the diagnosis, terms should be listed in the following order: bipolar II
disorder, current or most recent episode hypomanic, in partial remission/in full
remission (p. 175) (if full criteria for a hypomanic episode are not currently met),
plus any of the following hypomanic episode specifiers that are applicable. Note:
The specifiers “with rapid cycling” and “with seasonal pattern” describe the
pattern of mood episodes.
Specify if:
With anxious distress (p. 169–170)
With mixed features (pp. 170–171)
With rapid cycling (p. 171)
With peripartum onset (pp. 173–174)
With seasonal pattern (pp. 174–175)
If current episode is depressed (or most recent episode if bipolar II disorder is in
partial or full remission):
In recording the diagnosis, terms should be listed in the following order: bipolar II
disorder, current or most recent episode depressed, mild/moderate/severe (if full
criteria for a major depressive episode are currently met), in partial remission/in
full remission (if full criteria for a major depressive episode are not currently met)
(p. 175), plus any of the following major depressive episode specifiers that are
applicable. Note: The specifiers “with rapid cycling” and “with seasonal pattern”
describe the pattern of mood episodes.
Specify if:
With anxious distress (pp. 169–170)
With mixed features (pp. 170–171)
With rapid cycling (p. 171)
With melancholic features (pp. 171–172)

With atypical features (pp. 172–173)
With mood-congruent psychotic features (p. 173)
With mood-incongruent psychotic features (p. 173)
With catatonia (p. 173). Coding note: Use additional code F06.1.
With peripartum onset (pp. 172–174)
With seasonal pattern (pp. 174–175)
Specify course if full criteria for a mood episode are not currently met:
In partial remission (p. 175)
In full remission (p. 175)
Specify severity if full criteria for a major depressive episode are currently met:
Mild (p. 175)
Moderate (p. 175)
Severe (p. 175)
Diagnostic Features
Bipolar II disorder is characterized by a clinical course of recurring mood episodes consisting of
one or more major depressive episodes (Criteria A–C under “Major Depressive Episode”) and at
least one hypomanic episode (Criteria A–F under “Hypomanic Episode”). A diagnosis of a major
depressive episode requires that there be a period of depressed mood, or as an alternative,
marked diminished interest or pleasure, for most of the day nearly every day, lasting for a
minimum of 2 weeks. The depressed mood or loss of interest must be accompanied by additional
symptoms occurring nearly every day (e.g., sleep disturbance, psychomotor agitation or
retardation) for a total of at least five symptoms. The diagnosis of a hypomanic episode requires
that there be a distinct period of
abnormally and persistently elevated, expansive, or irritable mood and abnormally and
persistently increased activity or energy for most of the day, nearly every day, for at least 4
consecutive days accompanied by three (or four if mood is only irritable) additional symptoms
(e.g., inflated self-esteem, decreased need for sleep, distractibility) that persist and represent a
noticeable change from usual behavior and functioning. By definition, psychotic symptoms do
not occur in hypomanic episodes, and they appear to be less frequent in the major depressive
episodes in bipolar II disorder than in those of bipolar I disorder. The presence of a manic
episode during the course of illness precludes the diagnosis of bipolar II disorder (Criterion B
under “Bipolar II Disorder”). Moreover, for depressive and hypomanic episodes to count toward
the diagnosis of bipolar II disorder, at least one of the depressive episodes and at least one of the
hypomanic episodes must not be attributable to the physiological effects of a substance (i.e.,
medication, drug of abuse, or toxin exposure) or another medical condition. Note that hypomanic
episodes that emerge during antidepressant treatment and persist for at least 4 days at a fully
syndromal level beyond the physiological effects of the treatment are not considered to be

substance-induced and do count toward the diagnosis of bipolar II disorder. In addition, at least
one hypomanic episode and at least one major depressive episode are not explained by a
diagnosis of schizoaffective disorder and are not superimposed on schizophrenia,
schizophreniform disorder, delusional disorder, or other specified or unspecified schizophrenia
spectrum or other psychotic disorder (Criterion C under “Bipolar II Disorder”). The depressive
episodes or the pattern of unpredictable mood changes must cause clinically significant distress
or impairment in social, occupational, or other important areas of functioning (Criterion D under
“Bipolar II Disorder”). The recurrent major depressive episodes are often more frequent and
lengthier than those occurring in bipolar I disorder.
Individuals with bipolar II disorder typically present to a clinician during a major depressive
episode. They are unlikely to complain initially of hypomania, because either they do not
recognize the symptoms of hypomania or they consider hypomania desirable. Hypomanic
episodes by definition do not cause significant impairment. Instead, the impairment results from
the major depressive episodes or from a persistent pattern of unpredictable mood changes and
fluctuating, unreliable interpersonal or occupational functioning. Individuals with bipolar II
disorder may not view the hypomanic episodes as pathological or disadvantageous, although
others may be troubled by the individual’s erratic behavior. Clinical information from other
informants, such as close friends or relatives, is often useful in establishing the diagnosis of
bipolar II disorder.
A hypomanic episode should not be confused with the several days of euthymia and restored
energy or activity that may follow remission of a major depressive episode. Despite the
substantial differences in duration and severity between a manic and hypomanic episode, bipolar
II disorder is not a “milder form” of bipolar I disorder. Compared to individuals with bipolar I
disorder, individuals with bipolar II disorder have greater chronicity of illness and spend, on
average, more time in the depressive phase of their illness, which can be severe and/or disabling.
Although the diagnostic requirements for major depressive episodes are identical whether
they occur in the context of bipolar II disorder or major depressive disorder, certain clinical
features of the episodes may hint at possible differential diagnosis. For instance, the coexistence
of both insomnia and hypersomnia is not uncommon in major depressive episodes in both bipolar
II disorder and major depressive disorder; however, both insomnia and hypersomnia are
overrepresented among women with bipolar II disorder. Similarly, atypical depressive symptoms
(hypersomnia, hyperphagia) are common in both disorders, but more so in those with bipolar II
disorder.
Depressive symptoms co-occurring with a hypomanic episode or hypomanic symptoms cooccurring with a depressive episode are common in individuals with bipolar II disorder and are
overrepresented in females, particularly hypomania with mixed features.
Individuals experiencing hypomania with mixed features may not label their symptoms as
hypomania, but instead experience them as depression with increased energy or irritability.
Associated Features
A common feature of bipolar II disorder is impulsivity, which can contribute to suicide attempts

and substance use disorders.
There may be heightened levels of creativity during hypomanic episodes in some individuals
with a bipolar II disorder. However, that relationship may be nonlinear; that is, greater lifetime
creative accomplishments have been associated with milder forms of bipolar disorder, and higher
creativity has been found in unaffected family members. The individual’s attachment to the
prospect of heightened creativity during hypomanic episodes may contribute to ambivalence
about seeking treatment or undermine adherence to treatment.
Prevalence
The 12-month prevalence of bipolar II disorder in the United States is 0.8%. The 12-month
prevalence internationally is 0.3%. The prevalence rate of pediatric bipolar II disorder is difficult
to establish. DSM-IV bipolar I, bipolar II, and bipolar disorder not otherwise specified yield a
combined prevalence rate of 1.8% in U.S. and non-U.S. community samples, with higher rates
(2.7% inclusive) in youth age 12 years or older.
Development and Course
Although bipolar II disorder can begin in late adolescence and throughout adulthood, average
age at onset is the mid-20s, which is slightly later than for bipolar I disorder but earlier than for
major depressive disorder. Age at onset does not reliably distinguish between bipolar I and II
disorder. The illness most often begins with a depressive episode and is not recognized as bipolar
II disorder until a hypomanic episode occurs; this happens in about 12% of individuals with the
initial diagnosis of major depressive disorder. Anxiety, substance use, or eating disorders may
also precede the diagnosis, complicating its detection. Many individuals experience several
episodes of major depression prior to the first recognized hypomanic episode, with typically a
more than 10-year lag between illness onset and the diagnosis of a bipolar disorder.
Bipolar II disorder is a highly recurrent disorder, with over 50% of individuals experiencing
a new episode within a year after their first episode. Individuals with bipolar II disorder also
have more seasonal variation in mood compared to those with bipolar I disorder.
The number of lifetime episodes (both hypomanic and major depressive episodes) tends to be
higher for bipolar II disorder than for major depressive disorder or bipolar I disorder. However,
individuals with bipolar I disorder are actually more likely to experience hypomanic symptoms
than are individuals with bipolar II disorder. The interval between mood episodes in the course
of bipolar II disorder tends to decrease as the individual ages. While the hypomanic episode is
the feature that defines bipolar II disorder, depressive episodes are more enduring and disabling
over time. Despite the predominance of depression, once a hypomanic episode has occurred, the
diagnosis becomes bipolar II disorder and never reverts to major depressive disorder.
Approximately 5%–15% of individuals with bipolar II disorder have multiple (four or more)
mood episodes (hypomanic or major depressive) within the previous 12 months. If this pattern is
present, it is noted by the specifier “with rapid cycling.” Rapid cycling is more common in
women and may reflect an overall worsening of the bipolar disorder.
Switching from a depressive episode to a manic or hypomanic episode (with or without
mixed features) may occur, both spontaneously and during treatment for depression.

Genetic and physiological.
Course modifiers.
About 5%–15% of individuals with bipolar II disorder will ultimately develop a manic
episode, which changes the diagnosis to bipolar I disorder, regardless of subsequent course.
Making the diagnosis in children is often a challenge, especially in those with irritability and
hyperarousal that is nonepisodic (i.e., lacks the well-demarcated periods of altered mood).
Nonepisodic irritability in youth is associated with an elevated risk for anxiety disorders and
major depressive disorder, but not bipolar disorder, in adulthood. Persistently irritable youth
have lower familial rates of bipolar disorder than do youth who have bipolar disorder. For a
hypomanic episode to be diagnosed, the child’s symptoms must exceed what is expected in a
given environment and culture for the child’s developmental stage. Similar to adults, youth with
bipolar II disorder spend less time hypomanic compared to those with bipolar I disorder, and the
initial presenting episode is typically depression. Compared with adult onset of bipolar II
disorder, childhood or adolescent onset of the disorder may be associated with a more severe
lifetime course.
The 3-year incidence rate of first-onset bipolar II disorder in adults older than 60 years is
0.34%. However, distinguishing individuals older than 60 years with bipolar II disorder by late
versus early age at onset does not appear to have any clinical utility. The presence of cooccurring hypomanic symptoms during a depressive episode is more common during bipolar II
depressive episodes relative to depressive episodes occurring in the context of major depression
and may help distinguish older individuals with bipolar II disorder from those with major
depressive disorder. In any later life presentation of bipolar disorder, it is important to consider
medical factors, including possible medical and neurological causes of new symptoms.
Risk and Prognostic Factors
The risk of bipolar II disorder tends to be highest among relatives of
individuals with bipolar II disorder, as opposed to individuals with bipolar I disorder or major
depressive disorder. About a third of individuals with bipolar II disorder reported a family
history of bipolar disorder. There may be genetic factors influencing the age at onset for bipolar
disorders. Th ere is also evidence that bipolar II disorder may have a genetic architecture that is
at least partially distinct from bipolar I disorder and from schizophrenia.
A rapid-cycling pattern is associated with a poorer prognosis. Return to
previous level of social function for individuals with bipolar II disorder is more likely for
individuals of younger age and with less severe depression, suggesting adverse effects of
prolonged illness on recovery. More education, fewer years of illness, and being married are
independently associated with functional recovery in individuals with bipolar disorder, even after
diagnostic type (I vs. II), current depressive symptoms, and presence of psychiatric comorbidity
are taken into account.
Sex- and Gender-Related Diagnostic Issues
Whereas the gender ratio for bipolar I disorder is equal, findings on gender differences in bipolar
II disorder are mixed, differing by type of sample (i.e., registry, community, or clinical) and
country of origin. There is little to no evidence of bipolar gender differences in the general
population, whereas some, but not all, clinical samples suggest that bipolar II disorder is more
common in women than in men, which may reflect gender differences in treatment seeking or
other factors.

Major depressive disorder.
Patterns of illness and comorbidity, however, seem to differ by sex, with females being more
likely than males to report hypomania with mixed depressive features and a rapid-cycling course.
Childbirth may also be a specific trigger for a hypomanic episode, which can occur in 10%–20%
of females in nonclinical populations and most typically in the early postpartum period.
Distinguishing hypomania from the elated mood and reduced sleep
that normally accompany the birth of a child may be challenging. Postpartum hypomania
may foreshadow the onset of a depression that occurs in about half of females who experience
postpartum “highs.” The perimenopause transition can also be a time of mood instability in
bipolar II disorder. No major sex differences have been found in several clinical variables,
including rates of depressive episodes, age at and polarity of onset, symptoms, and severity of
the illness.
Association With Suicidal Thoughts or Behavior
Approximately one-third of individuals with bipolar II disorder report a lifetime history of
suicide attempt. The risk and incidence of attempted suicide in bipolar II and bipolar I disorder
appear to be similar. Overall there appears to be about equal rates of suicide attempts and suicide
deaths across individuals with bipolar II and bipolar I disorder, although overall the rates for both
attempts and deaths are significantly higher than in the general population. Time spent in a
depressive episode is associated more significantly with the diagnosis of bipolar I or bipolar II in
terms of suicide attempt risk. However, the lethality of attempts, as defined by a lower ratio of
attempts to suicide deaths, may be higher in individuals with bipolar II disorder compared to
individuals with bipolar I disorder. There may be an association between genetic markers and
increased risk for suicidal behavior in individuals with bipolar disorder, including a 6.5-fold
higher risk of suicide among first-degree relatives of bipolar II probands compared with firstdegree relatives of bipolar I probands.
Functional Consequences of Bipolar II Disorder
Although many individuals with bipolar II disorder return to a fully functional level between
mood episodes, at least 15% continue to have some interepisode dysfunction, and 20% transition
directly into another mood episode without interepisode recovery. Functional recovery lags
substantially behind recovery from symptoms of bipolar II disorder, especially in regard to
occupational recovery, resulting in lower socioeconomic status despite equivalent levels of
education with the general population. Individuals with bipolar II disorder perform more poorly
than healthy individuals on cognitive tests. Cognitive impairments associated with bipolar II
disorder may contribute to vocational difficulties. Prolonged unemployment in individuals with
bipolar disorder is associated with more episodes of depression, older age, increased rates of
current panic disorder, and lifetime history of alcohol use disorder.
Differential Diagnosis
Major depressive disorder is characterized by the absence of both
manic episodes and hypomanic episodes. Given that the presence of some manic or hypomanic

Cyclothymic disorder.
Schizophrenia.
Schizoaffective disorder.
Bipolar and related disorder due to another medical condition.
Substance/medication-induced bipolar and related disorder.
symptoms (e.g., fewer symptoms or shorter duration than required for hypomania) may still be
compatible with a diagnosis of major depressive disorder, it is important to ascertain whether the
symptoms meet criteria for a hypomanic episode to determine whether it is more appropriate to
make the diagnosis of bipolar II disorder. Depressive episodes dominate the overall course of
illness for most individuals with bipolar II disorder, contributing to the decade-long lag between
illness onset and the diagnosis of bipolar II disorder. Because the diagnostic criteria for major
depressive episode are identical in major depressive disorder and bipolar II disorder, the
diagnosis of bipolar II disorder can be made only by eliciting information about at least one prior
hypomanic episode in order to distinguish the bipolar II disorder from major depressive disorder.
In cyclothymic disorder, there are numerous periods of hypomanic
symptoms that do not meet symptom or duration criteria for a hypomanic episode and numerous
periods of depressive symptoms that do not meet symptom or duration criteria for a major
depressive episode. Bipolar II disorder is distinguished from cyclothymic disorder by the
presence of one or more hypomanic episodes and one or more major depressive episodes.
Schizophrenia is characterized by active-phase psychotic symptoms that may be
accompanied by major depressive episodes. The diagnosis of schizophrenia is made if no major
depressive episodes have occurred concurrently with the active-phase symptoms. If they have
occurred concurrently, the diagnosis of schizophrenia is made if the major depressive episodes
have been present for only a minority of the time. The diagnosis is bipolar II disorder, with
psychotic features, if the psychotic symptoms have occurred exclusively during major depressive
episodes.
Schizoaffective disorder is characterized by periods in which depressive
symptoms are concurrent with the active-phase symptoms of schizophrenia and periods in which
delusions or hallucinations occur for at least 2 weeks in the absence of a major depressive
episode. The diagnosis is bipolar II disorder, with psychotic features, if the psychotic symptoms
have occurred exclusively during major depressive episodes.
The diagnosis of bipolar and related
disorder due to another medical condition should be made instead of bipolar II disorder if the
hypomanic episodes are judged, based on history, laboratory findings, or physical examination,
to be the direct physiological consequence of another medical condition (e.g., Cushing’s disease,
multiple sclerosis).
A substance/medication-induced bipolar
and related disorder is distinguished from bipolar II disorder by the fact that a substance (e.g.,
stimulants, phencyclidine) or medication (e.g., steroids) is judged to be etiologically related to
the hypomanic and major depressive episodes. Because individuals with a hypomanic episode
have a tendency to overuse substances during an episode, it is important to determine whether
the substance use is a consequence of a primary hypomanic episode or whether the hypomaniclike episode has been caused by the substance use. In some cases, a definitive diagnosis may
involve establishing that the hypomanic symptoms or depressive symptoms remain once the
individual is no longer using the substance. Note that hypomanic episodes emerging in the
context of treatment with an antidepressant medication but persisting at a fully syndromal level

Attention-deficit/hyperactivity disorder.
Personality disorders.
Other bipolar disorders.
beyond the physiological effect of the medication warrant a diagnosis of bipolar II disorder
rather than substance/medication-induced bipolar and related disorder.
Attention-deficit/hyperactivity disorder (ADHD) may be
misdiagnosed as bipolar II disorder, especially in adolescents and children. Many symptoms of
ADHD, such as excessive talking, distractibility, and less need for sleep, overlap with the
symptoms of hypomania. The double counting of symptoms toward both ADHD and bipolar II
disorder can be avoided if the clinician clarifies whether the symptoms represent a distinct
episode and if the noticeable increase over baseline required for the diagnosis of bipolar II
disorder is present.
The same convention as applies for ADHD also applies when evaluating an
individual for a personality disorder such as borderline personality disorder because mood
lability and impulsivity are common in both personality disorders and bipolar II disorder.
Symptoms must represent a distinct episode, and the noticeable increase over baseline required
for the diagnosis of bipolar II disorder must be present. A diagnosis of a personality disorder
should not be made during an untreated mood episode unless the lifetime history supports the
presence of a personality disorder.
Diagnosis of bipolar II disorder should be differentiated from bipolar I
disorder by carefully considering whether there have been any past episodes of mania and from
other specified and unspecified bipolar and related disorders by confirming the presence of fully
syndromal hypomania and depression.
Comorbidity
Bipolar II disorder is more often than not associated with one or more co-occurring mental
disorders, with anxiety disorders being the most common. Approximately 60% of individuals
with bipolar II disorder have three or more co-occurring mental disorders; 75% have an anxiety
disorder, most commonly social anxiety (38%), specific phobia (36%), and generalized anxiety
(30%). Lifetime prevalence of comorbid anxiety disorder does not differ between bipolar I and
bipolar II disorders but is associated with a worse course of illness. Children and adolescents
with bipolar II disorder have a higher rate of co-occurring anxiety disorders compared to those
with bipolar I disorder, and the anxiety disorder most often predates the bipolar disorder.
Anxiety and substance use disorders occur in individuals with bipolar II disorder at a higher
rate than in the general population. It should be noted that co-occurring anxiety and substance
use disorder do not seem to follow a course of illness that is truly independent from that of
bipolar II disorder, but rather have strong associations with mood states. For example, anxiety
disorders tend to associate most with depressive symptoms, and substance use disorders are
moderately associated with hypomanic symptoms.
The prevalence of substance use disorders appears to be similar between bipolar I and bipolar
II disorders, most commonly alcohol use (42%) and cannabis use (20%) disorders. Sociocultural
factors influence the pattern of comorbid conditions in bipolar II disorder. For example,
countries with cultural prohibitions against alcohol or other substance use may have a lower
prevalence of substance use comorbidity.
Individuals with bipolar II disorder appear to have lower rates of comorbid posttraumatic

F34.0
stress disorder compared to individuals with bipolar I disorder.
Approximately 14% of individuals with bipolar II disorder have at least one lifetime eating
disorder, with binge-eating disorder being more common than bulimia nervosa and anorexia
nervosa.
Premenstrual syndrome and premenstrual dysphoric disorder are common in women with
bipolar disorder, especially in those with bipolar II disorder. Among women who have
premenstrual syndrome and/or premenstrual dysphoric disorder, bipolar mood symptoms and
lability may be more severe.
Individuals with bipolar II disorder also have comorbid medical conditions, which have the
potential to substantially complicate course and prognosis. These include cardiovascular disease,
migraine, and autoimmune disorders.
Cyclothymic Disorder
Diagnostic Criteria
A. For at least 2 years (at least 1 year in children and adolescents) there have been
numerous periods with hypomanic symptoms that do not meet criteria for a
hypomanic episode and numerous periods with depressive symptoms that do
not meet criteria for a major depressive episode.
B. During the above 2-year period (1 year in children and adolescents), Criterion A
symptoms have been present for at least half the time and the individual has not
been without the symptoms for more than 2 months at a time.
C. Criteria for a major depressive, manic, or hypomanic episode have never been
met.
D. The symptoms in Criterion A are not better explained by schizoaffective disorder,
schizophrenia, schizophreniform disorder, delusional disorder, or other specified
or unspecified schizophrenia spectrum and other psychotic disorder.
E. The symptoms are not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication) or another medical condition (e.g.,
hyperthyroidism).
F. The symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Specify if:
With anxious distress (see pp. 169–170)
Diagnostic Features
The essential feature of cyclothymic disorder is a chronic, fluctuating mood disturbance

involving numerous periods of hypomanic symptoms and periods of depressive symptoms
(Criterion A). The hypomanic symptoms are of insufficient number, severity, pervasiveness,
and/or duration to meet full criteria for a hypomanic episode, and the depressive symptoms are of
insufficient number, severity, pervasiveness, and/or duration to meet full criteria for a major
depressive episode. During the initial 2-year period (1 year for children or adolescents), the
symptoms must be persistent (present more days than not), and any symptom-free intervals last
no longer than 2 months (Criterion B). The diagnosis of cyclothymic disorder is made only if the
criteria for a major depressive, manic, or hypomanic episode have never been met (Criterion C).
If an individual with cyclothymic disorder subsequently (i.e., after the initial 2 years in adults
or 1 year in children or adolescents) experiences a major depressive, manic, or hypomanic
episode, the diagnosis changes to major depressive disorder, bipolar I disorder, or other specified
or unspecified bipolar and related disorder (subclassified as hypomanic episode without prior
major depressive episode), respectively, and the cyclothymic disorder diagnosis is dropped.
The cyclothymic disorder diagnosis is not made if the pattern of mood swings is better
explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional
disorder, or other specified and unspecified schizophrenia spectrum and other psychotic
disorders (Criterion D), in which case the mood symptoms are considered associated features of
the psychotic disorder. The mood disturbance must also not be attributable to the physiological
effects of a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g.,
hyperthyroidism) (Criterion E). Although some individuals may function particularly well during
some of the periods of hypomania, over the prolonged course of the disorder, there must be
clinically significant distress or impairment in social, occupational, or other important areas of
functioning as a result of the mood disturbance (Criterion F). The prolonged pattern of repeated,
often unpredictable mood changes may lead to impairment attributable to the negative effects of
the symptoms themselves combined with negative effects that the pattern of unpredictability and
inconsistency has on interpersonal functioning and role performance (i.e., familial, occupational
roles).
Prevalence
The lifetime prevalence of cyclothymic disorder in the United States and Europe is
approximately 0.4%–2.5%. Prevalence in mood disorders clinics may range from 3% to 5%. In
the general population, cyclothymic disorder is apparently equally common in males and
females. In clinical settings, females with cyclothymic disorder may be more likely to present for
treatment than males.
Development and Course
Cyclothymic disorder usually begins in adolescence or early adult life and is sometimes
considered to reflect a temperamental predisposition to other disorders in this chapter. The vast
majority of youth with cyclothymic disorder experience the onset of mood symptoms before age
10. Cyclothymic disorder usually has an insidious onset and a persistent course. There is a 15%–
50% risk that an individual with cyclothymic disorder will

Genetic and physiological.
Bipolar and related disorder due to another medical condition.
Substance/medication-induced bipolar and related disorder and substance/medication-induced
depressive disorder.
Bipolar I disorder, with rapid cycling, and bipolar II disorder, with rapid cycling.
Borderline personality disorder.
subsequently develop bipolar I disorder or bipolar II disorder; diagnostic conversion rates are
higher in youth than in adults. Onset of persistent, fluctuating hypomanic and depressive
symptoms late in adult life needs to be clearly differentiated from bipolar and related disorder
due to another medical condition and depressive disorder due to another medical condition (e.g.,
multiple sclerosis) before the cyclothymic disorder diagnosis is assigned.
Risk and Prognostic Factors
Major depressive disorder, bipolar I disorder, and bipolar II disorder
are more common among first-degree biological relatives of individuals with cyclothymic
disorder than in the general population. There may also be an increased familial risk of
substance-related disorders. Cyclothymic disorder may be more common in the first-degree
biological relatives of individuals with bipolar I disorder than in the general population.
Differential Diagnosis
The diagnosis of bipolar and related
disorder due to another medical condition is made when the mood disturbance is judged to be
attributable to the physiological effect of a specific, usually chronic medical condition (e.g.,
hyperthyroidism). This determination is based on the history, physical examination, and/or
laboratory findings. If it is judged that the hypomanic and depressive symptoms are not the
physiological consequence of the medical condition, then the primary mental disorder (i.e.,
cyclothymic disorder) and the medical condition are coded. For example, this would be the case
if the mood symptoms are considered to be the psychological (not the physiological)
consequence of having a chronic medical condition, or if there is no etiological relationship
between the hypomanic and depressive symptoms and the medical condition.
Substance/medication-induced bipolar and related disorder and substance/medication-induced
depressive disorder are distinguished from cyclothymic disorder by the judgment that a
substance/medication (especially stimulants) is etiologically related to the mood disturbance. The
frequent mood swings in these disorders that are suggestive of cyclothymic disorder usually
resolve following cessation of substance/medication use.
Both 
disorders 
may
resemble cyclothymic disorder by virtue of the frequent marked shifts in mood. By definition, in
cyclothymic disorder the criteria for a major depressive, manic, or hypomanic episode have
never been met, whereas the bipolar I disorder and bipolar II disorder specifier “with rapid
cycling” requires that full mood episodes be present.
Borderline personality disorder is associated with recurrent, brief
marked shifts in mood that may suggest cyclothymic disorder. Engagement in potentially selfdamaging behaviors can be seen in both conditions but would need to occur in the context of
other hypomanic symptoms to be related to cyclothymia. Mood instability in borderline
personality disorder occurs in the domains of anxiety, irritability, and sadness, whereas elation,
euphoria, and/or increased energy are not characteristic features of borderline personality
disorder. If the criteria are met for both disorders, both borderline personality disorder and
cyclothymic disorder may be diagnosed.

Comorbidity
Substance-related disorders and sleep disorders (i.e., difficulties in initiating and maintaining
sleep) may be present in individuals with cyclothymic disorder. Rates of comorbid
psychiatric disorders in children with cyclothymic disorder treated in outpatient psychiatric
settings are greater than those in children with disruptive behavior/attention-deficit/hyperactivity
disorder and similar to those in children with bipolar I or II disorder.
Substance/Medication-Induced Bipolar and Related
Disorder
Diagnostic Criteria
A. A prominent and persistent disturbance in mood that predominates in the clinical
picture and is characterized by abnormally elevated, expansive, or irritable mood
and abnormally increased activity or energy.
B. There is evidence from the history, physical examination, or laboratory findings
of both (1) and (2):
1. The symptoms in Criterion A developed during or soon after substance
intoxication or withdrawal or after exposure to or withdrawal from a
medication.
2. The involved substance/medication is capable of producing the symptoms in
Criterion A.
C. The disturbance is not better explained by a bipolar or related disorder that is not
substance/medication-induced. Such evidence of an independent bipolar or
related disorder could include the following:
The symptoms precede the onset of the substance/medication use; the
symptoms persist for a substantial period of time (e.g., about 1 month) after
the cessation of acute withdrawal or severe intoxication; or there is other
evidence 
suggesting 
the 
existence 
of 
an 
independent 
nonsubstance/medication-induced bipolar and related disorder (e.g., a history of
recurrent non-substance/medication-related episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Note: This diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the symptoms in Criterion A
predominate in the clinical picture and when they are sufficiently severe to warrant

clinical attention.
Coding note: The ICD-10-CM codes for the [specific substance/medication]-induced
bipolar and related disorders are indicated in the table below. Note that the ICD-10CM code depends on whether or not there is a comorbid substance use disorder
present for the same class of substance. In any case, an additional separate
diagnosis of a substance use disorder is not given. If a mild substance use disorder
is comorbid with the substance-induced bipolar and related disorder, the 4th position
character is “1,” and the clinician should record “mild [substance] use disorder”
before the substance-induced bipolar and related disorder (e.g., “mild cocaine use
disorder with cocaine-induced bipolar and related disorder”). If a moderate or severe
substance use disorder is comorbid with the substance-induced bipolar and related
disorder, the 4th position character is “2,” and the clinician should record “moderate
[substance] use disorder” or “severe [substance] use disorder,” depending on the
severity of the comorbid substance use disorder. If there is no comorbid substance
use disorder (e.g., after a one-time heavy use of the substance), then the 4th
position character is “9,” and the clinician should record only the substance-induced
bipolar and related disorder.
ICD-10-CM
With mild use
disorder
With moderate or
severe use disorder
Without use
disorder
Alcohol
F10.14
F10.24
F10.94
Phencyclidine
F16.14
F16.24
F16.94
Other hallucinogen
F16.14
F16.24
F16.94
Sedative, hypnotic, or anxiolytic
F13.14
F13.24
F13.94
Amphetamine-type substance (or other
stimulant)
F15.14
F15.24
F15.94
Cocaine
F14.14
F14.24
F14.94
Other (or unknown) substance
F19.14
F19.24
F19.94
Specify (see Table 1 in the chapter “Substance-Related and Addictive Disorders,”
which indicates whether “with onset during intoxication” and/or “with onset during
withdrawal” applies to a given substance class; or specify “with onset after
medication use”):
With onset during intoxication: If criteria are met for intoxication with the
substance and the symptoms develop during intoxication.
With onset during withdrawal: If criteria are met for withdrawal from the
substance and the symptoms develop during, or shortly after, withdrawal.
With onset after medication use: If symptoms developed at initiation of
medication, with a change in use of medication, or during withdrawal of
medication.

Recording Procedures
The name of the substance/medication-induced bipolar and related disorder begins with the
specific substance (e.g., cocaine, dexamethasone) that is presumed to be causing the bipolar
mood symptoms. The diagnostic code is selected from the table included in the criteria set,
which is based on the drug class and presence or absence of a comorbid substance use disorder.
For substances that do not fit into any of the classes (e.g., dexamethasone), the code for “other
(or unknown) substance” should be used; and in cases in which a substance is judged to be an
etiological factor but the specific class of substance is unknown, the same code should also be
used.
When recording the name of the disorder, the comorbid substance use disorder (if any) is
listed first, followed by the word “with,” followed by the name of the substance-induced bipolar
and related disorder, followed by the specification of onset (i.e., onset during intoxication, onset
during withdrawal). For example, in the case of irritable symptoms occurring during intoxication
in a man with a severe cocaine use disorder, the diagnosis is F14.24 severe cocaine use disorder
with cocaine-induced bipolar and related disorder, with onset during intoxication. A separate
diagnosis of the comorbid severe cocaine use disorder is not given. If the substance-induced
bipolar and related disorder occurs without a comorbid substance use disorder (e.g., after a onetime heavy use of the substance), no accompanying substance use disorder is noted (e.g., F15.94
amphetamine-induced bipolar and related disorder, with onset during intoxication). When more
than one substance is judged to play a significant role in the development of bipolar mood
symptoms, each should be listed separately (e.g., F15.24 severe methylphenidate use disorder
with methylphenidate-induced bipolar and related disorder, with onset during intoxication;
F19.94 dexamethasone-induced bipolar and related disorder, with onset during intoxication).
Diagnostic Features
The essential feature of substance/medication-induced bipolar and related disorder is a prominent
and persistent disturbance in mood that predominates in the clinical picture and is characterized
by abnormally elevated, expansive, or irritable mood and abnormally increased activity or energy
(Criterion A); these symptoms are judged to be attributable to the effects of a substance (e.g., a
drug of abuse, a medication, or a toxin exposure) (Criterion B).
To meet criteria for the diagnosis, the abnormally elevated, expansive, or irritable mood and
increased activity or energy must have developed during or soon after substance intoxication or
withdrawal or after exposure to or withdrawal from a medication, as evidenced by clinical
history, physical examination, or laboratory findings (Criterion B1), and the involved
substance/medication must be capable of producing the abnormally elevated, expansive, or
irritable mood and increased activity or energy (Criterion B2). In addition, the abnormally
elevated, expansive, or irritable mood and increased activity or energy are not better explained
by a non-substance/medication-induced bipolar and related disorder.
Evidence of an independent bipolar and related disorder includes the observation that the
abnormally elevated, expansive, or irritable mood and increased activity or energy preceded the
onset of substance/medication use, the symptoms persist beyond a substantial period of time after
the cessation of acute withdrawal or severe intoxication (i.e., usually longer than 1 month), or

there is other evidence that suggests the existence of an independent non-substance/medicationinduced bipolar and related disorder (Criterion C), such as a history of recurrent non-substanceinduced manic episodes. Diagnosis of substance/medication-induced bipolar and related disorder
should not be made when symptoms occur exclusively during the course of a delirium (Criterion
D). Finally, the diagnosis requires that the substance/medication-induced symptoms cause
clinically significant distress or impairment in social, occupational, or other important areas of
functioning (Criterion E). The substance-induced bipolar and related disorder diagnosis should
be made instead of a diagnosis of substance intoxication or substance withdrawal only when the
symptoms in Criterion A predominate in the clinical picture and are sufficiently severe to
warrant independent clinical attention.
A key exception to the diagnosis of substance/medication-induced bipolar and related
disorder is the case of hypomania or mania that occurs after antidepressant medication use or
other treatments and persists beyond the physiological effects of the medication. The persistence
of hypomania or mania is considered an indicator of true bipolar disorder, not
substance/medication-induced bipolar and related disorder. Similarly, individuals with apparent
electroconvulsive therapy–induced manic or hypomanic episodes that persist beyond the
physiological effects of the treatment are diagnosed with bipolar disorder, not
substance/medication-induced bipolar and related disorder. Furthermore, substance/medicationinduced bipolar and related symptoms may suggest an underlying bipolar diathesis in individuals
previously not diagnosed with bipolar disorders.
Side effects of some antidepressants and other psychotropic drugs (e.g., edginess, agitation)
may resemble the primary symptoms of a manic syndrome, but they are fundamentally distinct
from bipolar symptoms and are insufficient for the diagnosis. That is, the criterion symptoms of
mania/hypomania have specificity (simple agitation is not the same as excess involvement in
purposeful activities), and a sufficient number of symptoms must be present (not just one or two
symptoms) to make these diagnoses. In particular, the appearance of one or two nonspecific
symptoms—irritability, edginess, or agitation during antidepressant treatment—in the absence of
a full manic or hypomanic syndrome should not be taken to support a diagnosis of a bipolar
disorder.
Associated Features
Substances/medications that are typically considered to be associated with substance/medicationinduced bipolar and related disorder include the stimulant class of drugs, as
well as phencyclidine and steroids; however, a number of potential substances continue to
emerge as new compounds are synthesized (e.g., so-called bath salts).
Prevalence
Limited epidemiological data exist regarding the prevalence of substance/medication-induced
mania or bipolar disorder. Prevalence of substance-induced bipolar disorder will depend on
substance availability and level of substance use in a society; for example, countries with cultural
prohibitions against alcohol or other substance use may have a lower prevalence of substance-

Substance intoxication and substance withdrawal.
related disorders.
Development and Course
In phencyclidine-induced mania, the initial presentation may be one of a delirium with affective
features, which then becomes an atypically appearing manic or mixed manic state. This condition
follows the ingestion or inhalation quickly, usually within hours or, at the most, a few days. In
stimulant-induced manic or hypomanic states, the response is in minutes to 1 hour after one or
several ingestions or injections. The episode is very brief and typically resolves over 1–2 days.
With corticosteroids and some immunosuppressant medications, the mania (or mixed or
depressed state) usually follows several days of ingestion, and the higher doses appear to have a
much greater likelihood of producing bipolar symptoms.
Diagnostic Markers
Determination of the substance of use can be made through markers in the blood or urine to
corroborate diagnosis.
Differential Diagnosis
Substance/medication-induced bipolar and related disorder should be differentiated from other
bipolar disorders, substance intoxication, substance withdrawal, substance-induced delirium, and
medication side effects (as noted earlier). A full manic episode that emerges during
antidepressant treatment (e.g., medication, electroconvulsive therapy) but persists at a fully
syndromal level beyond the physiological effect of that treatment is sufficient evidence for a
bipolar I diagnosis. A full hypomanic episode that emerges during antidepressant treatment (e.g.,
medication, electroconvulsive therapy) but persists at a fully syndromal level beyond the
physiological effect of that treatment is sufficient evidence for a bipolar II diagnosis only if
preceded by a major depressive episode.
Euphoria, irritability, and increased energy may
occur in substance intoxication (e.g., stimulant intoxication) or substance withdrawal (e.g.,
cannabis withdrawal). The diagnosis of the substance-specific intoxication or substance-specific
withdrawal will usually suffice to categorize the symptom presentation. A diagnosis of
substance/medication-induced bipolar and related disorder either with onset during intoxication
or with onset during withdrawal should be made instead of a diagnosis of substance intoxication
or substance withdrawal when the euphoric or irritable mood or increased energy symptoms are
predominant in the clinical picture and are sufficiently severe to warrant clinical attention.
Comorbidity
Comorbidities are those associated with the use of illicit substances (in the case of illegal
stimulants or phencyclidine) or diversion of prescribed stimulants. Comorbidities related to
steroid or immunosuppressant medications are those medical indications for these preparations.
Delirium can occur before or along with manic symptoms in individuals ingesting phencyclidine
or those who are prescribed steroid medications or other immunosuppressant medications.

Bipolar and Related Disorder Due to Another Medical
Condition
Diagnostic Criteria
A. A prominent and persistent disturbance in mood that predominates in the clinical
picture and is characterized by abnormally elevated, expansive, or irritable mood
and abnormally increased activity or energy.
B. There is evidence from the history, physical examination, or laboratory findings
that the disturbance is the direct pathophysiological consequence of another
medical condition.
C. The disturbance is not better explained by another mental disorder.
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning, or necessitates
hospitalization to prevent harm to self or others, or there are psychotic features.
Coding note: The ICD-10-CM code depends on the specifier (see below).
Specify if:
F06.33 With manic features: Full criteria are not met for a manic or hypomanic
episode.
F06.33 With manic- or hypomanic-like episode: Full criteria are met except
Criterion D for a manic episode or except Criterion F for a hypomanic episode.
F06.34 With mixed features: Symptoms of depression are also present but do
not predominate in the clinical picture.
Coding note: Include the name of the other medical condition in the name of the
mental disorder (e.g., F06.33 bipolar disorder due to hyperthyroidism, with manic
features). The other medical condition should also be coded and listed separately
immediately before the bipolar and related disorder due to the medical condition
(e.g., E05.90 hyperthyroidism; F06.33 bipolar disorder due to hyperthyroidism, with
manic features).
Diagnostic Features
The essential features of bipolar and related disorder due to another medical condition are
presence of a prominent and persistent period of abnormally elevated, expansive, or irritable
mood and abnormally increased activity or energy predominating in the clinical picture
(Criterion A) that is attributable to another medical condition (Criterion B). In most cases the
manic or hypomanic picture may appear during the initial presentation of the medical condition
(i.e., within 1 month); however, there are exceptions, especially in chronic medical conditions
that might worsen or relapse and herald the appearance of the manic or hypomanic picture.
Bipolar and related disorder due to another medical condition would not be diagnosed when the

manic or hypomanic episodes definitely preceded the medical condition, because the proper
diagnosis would be bipolar disorder (except in the unusual circumstance in which all preceding
manic or hypomanic episodes—or, when only one such episode has occurred, the preceding
manic or hypomanic episode—were associated with ingestion of a substance/medication). The
diagnosis of bipolar and related disorder due to another medical condition should not be made
during the course of a delirium (Criterion D). The manic or hypomanic episode in bipolar and
related disorder due to another medical condition must cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning to qualify for this
diagnosis (Criterion E).
Associated Features
The listing of medical conditions that are said to be able to induce mania is never complete, and
the clinician’s best judgment is the essence of this diagnosis. Among the best known of the
medical conditions that can cause a bipolar manic or hypomanic condition are Cushing’s disease
and multiple sclerosis, as well as stroke and traumatic brain injuries. Antibodies to the N-methylD-aspartate (NMDA) receptor have been associated with manic or mixed mood and psychotic
symptoms. In such cases, the causative medical condition would be anti-NMDA receptor
encephalitis.
Development and Course
Bipolar and related disorder due to another medical condition usually has its onset acutely or
subacutely within the first weeks or month of the onset of the associated medical condition.
However, this is not always the case, as a worsening or later relapse of the associated medical
condition may precede the onset of the manic or hypomanic syndrome. The clinician must make
a clinical judgment in these situations about whether the medical condition is causative, based on
temporal sequence as well as plausibility of a causal relationship. Finally, the condition may
remit before or just after the medical condition remits, particularly when treatment of the
manic/hypomanic symptoms is effective.
Culture-Related Diagnostic Issues
Culture-related differences, to the extent that there is any evidence, pertain to those associated
with the medical condition (e.g., rates of multiple sclerosis and stroke vary around the world
based on dietary factors, genetic factors, and other environmental factors).
Sex- and Gender-Related Diagnostic Issues
Gender differences pertain to those associated with the medical condition (e.g., systemic lupus
erythematosus is more common in females; stroke is somewhat more common in middle-age
males compared with females).
Diagnostic Markers
Diagnostic markers pertain to those associated with the medical condition (e.g., steroid levels in

Delirium and major or mild neurocognitive disorder.
Symptoms of catatonia and acute anxiety.
Medication-induced depressive or manic symptoms.
blood or urine to help corroborate the diagnosis of Cushing’s disease, which can be associated
with manic or depressive syndromes; laboratory tests confirming the diagnosis of multiple
sclerosis).
Functional Consequences of Bipolar and Related Disorder Due to
Another Medical Condition
Functional consequences of the bipolar symptoms may exacerbate impairments associated with
the medical condition and may incur worse outcomes because of interference with medical
treatment.
Differential Diagnosis
A separate diagnosis of bipolar and related
disorder due to another medical condition is not given if the mood disturbance occurs exclusively
during the course of a delirium. However, a diagnosis of bipolar and related disorder due to
another medical condition may be given in addition to a diagnosis of major or mild
neurocognitive disorder if the mood disturbance is judged to be a physiological consequence of
the pathological process causing the neurocognitive disorder and if symptoms of irritability or
elevated mood are a prominent part of the clinical presentation.
It is important to differentiate symptoms of mania from
excited catatonic symptoms and from agitation related to acute anxiety states.
An important differential diagnostic observation
is that the other medical condition may be treated with medications (e.g., steroids or alphainterferon) that can induce depressive or manic symptoms. In these cases, clinical judgment
using all of the evidence in hand is the best way to try to separate the most likely and/or the most
important of two etiological factors (i.e., association with the medical condition vs. a
substance/medication-induced syndrome). The differential diagnosis of the associated medical
conditions is relevant but largely beyond the scope of the present manual.
Comorbidity
Conditions comorbid with bipolar and related disorder due to another medical condition are
those associated with the medical conditions of etiological relevance. Delirium can occur before
or along with manic symptoms in individuals with Cushing’s disease.
Other Specified Bipolar and Related Disorder
F31.89
This category applies to presentations in which symptoms characteristic of a bipolar
and related disorder that cause clinically significant distress or impairment in social,

occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the bipolar and related disorders diagnostic
class. The other specified bipolar and related disorder category is used in situations
in which the clinician chooses to communicate the specific reason that the
presentation does not meet the criteria for any specific bipolar and related disorder.
This is done by recording “other specified bipolar and related disorder” followed by
the specific reason (e.g., “short-duration cyclothymia”).
Examples of presentations that can be specified using the “other specified”
designation include the following:
1. Short-duration hypomanic episodes (2–3 days) and major depressive
episodes: A lifetime history of one or more major depressive episodes in
individuals whose presentation has never met full criteria for a manic or
hypomanic episode but who have experienced two or more episodes of shortduration hypomania that meet the full symptomatic criteria for a hypomanic
episode but that only last for 2–3 days. The episodes of hypomanic symptoms do
not overlap in time with the major depressive episodes, so the disturbance does
not meet criteria for major depressive episode, with mixed features.
2. Hypomanic episodes with insufficient symptoms and major depressive
episodes: A lifetime history of one or more major depressive episodes in
individuals whose presentation has never met full criteria for a manic or
hypomanic episode but who have experienced one or more episodes of
hypomania that do not meet full symptomatic criteria (i.e., at least 4 consecutive
days of elevated mood and one or two of the other symptoms of a hypomanic
episode, or irritable mood and two or three of the other symptoms of a
hypomanic episode). The episodes of hypomanic symptoms do not overlap in
time with the major depressive episodes, so the disturbance does not meet
criteria for major depressive episode, with mixed features.
3. Hypomanic episode without prior major depressive episode: One or more
hypomanic episodes in an individual whose presentation has never met full
criteria for a major depressive episode or a manic episode.
4. Short-duration cyclothymia (less than 24 months): Multiple episodes of
hypomanic symptoms that do not meet criteria for a hypomanic episode and
multiple episodes of depressive symptoms that do not meet criteria for a major
depressive episode that persist over a period of less than 24 months (less than
12 months for children or adolescents) in an individual whose presentation has
never met full criteria for a major depressive, manic, or hypomanic episode and
does not meet criteria for any psychotic disorder. During the course of the
disorder, the hypomanic or depressive symptoms are present for more days than
not, the individual has not been without symptoms for more than 2 months at a
time, and the symptoms cause clinically significant distress or impairment.
5. Manic episode superimposed on schizophrenia, schizophreniform disorder,
delusional disorder, or other specified and unspecified schizophrenia spectrum

and other psychotic disorder. Note: Manic episodes that are part of
schizoaffective disorder do not merit an additional diagnosis of other specified
bipolar and related disorder.
Unspecified Bipolar and Related Disorder
F31.9
This category applies to presentations in which symptoms characteristic of a bipolar
and related disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the bipolar and related disorders diagnostic
class. The unspecified bipolar and related disorder category is used in situations in
which the clinician chooses not to specify the reason that the criteria are not met for
a specific bipolar and related disorder, and includes presentations in which there is
insufficient information to make a more specific diagnosis (e.g., in emergency room
settings).
Unspecified Mood Disorder
F39
This category applies to presentations in which symptoms characteristic of a mood
dis-order that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not at the
time of the evaluation meet the full criteria for any of the disorders in either the
bipolar or the depressive disorders diagnostic classes and in which it is difficult to
choose between unspecified bipolar and related disorder and unspecified depressive
disorder (e.g., acute agitation).
Specifiers for Bipolar and Related Disorders
Specify if:
With anxious distress: The presence of at least two of the following symptoms
during the majority of days of the current manic, hypomanic, or major depressive
episode in bipolar I disorder (or the most recent episode if bipolar I disorder is in
partial or full remission); or of the current hypomanic or major depressive
episode in bipolar II disorder (or the most recent episode if bipolar II disorder is
in partial or full remission); or during the majority of symptomatic days in
cyclothymic disorder:

1. Feeling keyed up or tense.
2. Feeling unusually restless.
3. Difficulty concentrating because of worry.
4. Fear that something awful may happen.
5. Feeling that the individual might lose control of himself or herself.
Specify current severity:
Mild: Two symptoms.
Moderate: Three symptoms.
Moderate-severe: Four or five symptoms.
Severe: Four or five symptoms with motor agitation.
Note: Anxious distress has been noted as a prominent feature of both bipolar
and major depressive disorders in both primary care and specialty mental
health settings. High levels of anxiety have been associated with higher
suicide risk, longer duration of illness, and greater likelihood of treatment
nonresponse. As a result, it is clinically useful to specify accurately the
presence and severity levels of anxious distress for treatment planning and
monitoring of response to treatment.
With mixed features: The mixed features specifier can apply to the current
manic, hypomanic, or major depressive episode in bipolar I disorder (or the most
recent episode if bipolar I disorder is in partial or full remission) or to the current
hypomanic or major depressive episode in bipolar II disorder (or the most recent
episode if bipolar II disorder is in partial or full remission):
Manic or hypomanic episode, with mixed features:
A. Full criteria are met for a manic episode or hypomanic episode, and at least
three of the following symptoms are present during the majority of days of
the current or most recent episode of mania or hypomania:
1. Prominent dysphoria or depressed mood as indicated by either
subjective report (e.g., feels sad or empty) or observation made by
others (e.g., appears tearful).
2. Diminished interest or pleasure in all, or almost all, activities (as
indicated by either subjective account or observation made by others).
3. Psychomotor retardation nearly every day (observable by others; not
merely subjective feelings of being slowed down).
4. Fatigue or loss of energy.
5. Feelings of worthlessness or excessive or inappropriate guilt (not merely
self-reproach or guilt about being sick).
6. Recurrent thoughts of death (not just fear of dying), recurrent suicidal
ideation without a specific plan, or a suicide attempt or a specific plan for

committing suicide.
B. Mixed symptoms are observable by others and represent a change from the
person’s usual behavior.
C. For individuals whose symptoms meet full episode criteria for both mania
and depression simultaneously, the diagnosis should be manic episode,
with mixed features, due to the marked impairment and clinical severity of
full mania.
D. The mixed symptoms are not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication or other treatment).
Depressive episode, with mixed features:
A. Full criteria are met for a major depressive episode, and at least three of the
following manic/hypomanic symptoms are present during the majority of
days of the current or most recent episode of depression:
1. Elevated, expansive mood.
2. Inflated self-esteem or grandiosity.
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are racing.
5. Increase in energy or goal-directed activity (either socially, at work or
school, or sexually).
6. Increased or excessive involvement in activities that have a high
potential for painful consequences (e.g., engaging in unrestrained buying
sprees, sexual indiscretions, or foolish business investments).
7. Decreased need for sleep (feeling rested despite sleeping less than
usual; to be contrasted with insomnia).
B. Mixed symptoms are observable by others and represent a change from the
person’s usual behavior.
C. For individuals whose symptoms meet full episode criteria for both mania
and depression simultaneously, the diagnosis should be manic episode,
with mixed features.
D. The mixed symptoms are not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication or other treatment).
Note: Mixed features associated with a major depressive episode have been
found to be a significant risk factor for the development of bipolar I or bipolar II
disorder. As a result, it is clinically useful to note the presence of this specifier
for treatment planning and monitoring of response to treatment.
With rapid cycling: Presence of at least four mood episodes in the previous 12
months that meet the criteria for manic, hypomanic, or major depressive episode
in bipolar I disorder or that meet the criteria for hypomanic or major depressive

episode in bipolar II disorder.
Note: Episodes are demarcated by either partial or full remissions of at least 2
months or a switch to an episode of the opposite polarity (e.g., major
depressive episode to manic episode).
Note: The essential feature of a rapid-cycling bipolar disorder is the
occurrence of at least four mood episodes during the previous 12 months.
These episodes can occur in any combination and order. The episodes must
meet both the duration and the symptom number criteria for a major
depressive, manic, or hypomanic episode and must be demarcated by either a
period of full remission or a switch to an episode of the opposite polarity.
Manic and hypomanic episodes are counted as being on the same pole.
Except for the fact that they occur more frequently, the episodes that occur in
a rapid-cycling pattern are no different from those that occur in a non-rapidcycling pattern. Mood episodes that count toward defining a rapid-cycling
pattern exclude those episodes directly caused by a substance (e.g., cocaine,
corticosteroids) or another medical condition.
With melancholic features:
A. One of the following is present during the most severe period of the current
major depressive episode (or the most recent major depressive episode if
bipolar I or bipolar II disorder is currently in partial or full remission):
1. Loss of pleasure in all, or almost all, activities.
2. Lack of reactivity to usually pleasurable stimuli (does not feel much better,
even temporarily, when something good happens).
B. Three (or more) of the following:
1. A distinct quality of depressed mood characterized by profound
despondency, despair, and/or moroseness or by so-called empty mood.
2. Depression that is regularly worse in the morning.
3. Early-morning awakening (i.e., at least 2 hours before usual awakening).
4. Marked psychomotor agitation or retardation.
5. Significant anorexia or weight loss.
6. Excessive or inappropriate guilt.
Note: The specifier “with melancholic features” is applied if these features
are present at the most severe stage of the episode. There is a nearcomplete absence of the capacity for pleasure, not merely a diminution. A
guideline for evaluating the lack of reactivity of mood is that even highly
desired events are not associated with marked brightening of mood. Either
mood does not brighten at all, or it brightens only partially (e.g., up to 20%–
40% of normal for only minutes at a time). The “distinct quality” of mood

that is characteristic of the “with melancholic features” specifier is
experienced as qualitatively different from that during a nonmelancholic
depressive episode. A depressed mood that is described as merely more
severe, longer lasting, or present without a reason is not considered
distinct in quality. Psychomotor changes are nearly always present and are
observable by others.
 Melancholic features exhibit only a modest tendency to repeat across
episodes in the same individual. They are more frequent in inpatients, as
opposed to outpatients; are less likely to occur in milder than in more
severe major depressive episodes; and are more likely to occur in
individuals with psychotic features.
With atypical features: This specifier is applied when these features predominate
during the majority of days of the current major depressive episode (or the most
recent major depressive episode if bipolar I or bipolar II disorder is currently in
partial or full remission).
A. Mood reactivity (i.e., mood brightens in response to actual or potential positive
events).
B. Two (or more) of the following:
1. Significant weight gain or increase in appetite.
2. Hypersomnia.
3. Leaden paralysis (i.e., heavy, leaden feelings in arms or legs).
4. A long-standing pattern of interpersonal rejection sensitivity (not limited to
episodes of mood disturbance) that results in significant social or
occupational impairment.
C. Criteria are not met for “with melancholic features” or “with catatonia” during
the same episode.
Note: “Atypical depression” has historical significance (i.e., atypical in
contradistinction to the more classical agitated, “endogenous” presentations of
depression that were the norm when depression was rarely diagnosed in
outpatients and almost never in adolescents or younger adults) and today
does not connote an uncommon or unusual clinical presentation as the term
might imply.
 Mood reactivity is the capacity to be cheered up when presented with
positive events (e.g., a visit from children, compliments from others). Mood
may become euthymic (not sad) even for extended periods of time if the
external circumstances remain favorable. Increased appetite may be
manifested by an obvious increase in food intake or by weight gain.
Hypersomnia may include either an extended period of nighttime sleep or
daytime napping that totals at least 10 hours of sleep per day (or at least 2
hours more than when not depressed). Leaden paralysis is defined as feeling
heavy, leaden, or weighted down, usually in the arms or legs. This sensation is
generally present for at least an hour a day but often lasts for many

173
hours at a time. Unlike the other atypical features, pathological sensitivity to
perceived interpersonal rejection is a trait that has an early onset and persists
throughout most of adult life. Rejection sensitivity occurs both when the person
is and is not depressed, though it may be exacerbated during depressive
periods.
With psychotic features: Delusions or hallucinations are present at any time in
the current manic or major depressive episode in bipolar I disorder (or the most
recent manic or major depressive episode if bipolar I disorder is currently in
partial or full remission) or in the current major depressive episode in bipolar II
disorder (or the most recent major depressive episode if bipolar II disorder is
currently in partial or full remission). If psychotic features are present, specify if
mood-congruent or mood-incongruent:
When applied to current or most recent manic episode (in bipolar I disorder):
With mood-congruent psychotic features: The content of all delusions
and hallucinations is consistent with the typical manic themes of grandiosity,
invulnerability, etc., but may also include themes of suspiciousness or
paranoia, especially with respect to others’ doubts about the individual’s
capacities, accomplishments, and so forth.
With mood-incongruent psychotic features: The content of the delusions
and hallucinations does not involve typical manic themes as described
above, or the content is a mixture of mood-incongruent and mood-congruent
themes.
When applied to current or most recent major depressive episode (in bipolar I
disorder or bipolar II disorder):
With mood-congruent psychotic features: The content of all delusions
and hallucinations is consistent with the typical depressive themes of
personal inadequacy, guilt, disease, death, nihilism, or deserved
punishment.
With mood-incongruent psychotic features: The content of the delusions
and hallucinations does not involve typical depressive themes of personal
inadequacy, guilt, disease, death, nihilism, or deserved punishment, or the
content is a mixture of mood-incongruent and mood-congruent themes.
With catatonia: This specifier is applied to the current manic or major
depressive episode in bipolar I disorder (or the most recent manic or major
depressive episode if bipolar I disorder is currently in partial or full remission)
or to the current major depressive episode in bipolar II disorder (or the most
recent major depressive episode if bipolar II disorder is currently in partial or
full remission) if catatonic features are present during most of the episode.
See criteria for catatonia associated with a mental disorder in the chapter
“Schizophrenia Spectrum and Other Psychotic Disorders.”

With peripartum onset: This specifier is applied to the current manic,
hypomanic, or major depressive episode in bipolar I disorder (or the most
recent manic, hypomanic, or major depressive episode if bipolar I disorder is
currently in partial or full remission) or to the current hypomanic or major
depressive episode in bipolar II disorder (or the most recent hypomanic or
major depressive episode if bipolar II disorder is currently in partial or full
remission) if onset of mood symptoms occurs during pregnancy or in the 4
weeks following delivery.
Note: Mood episodes can have their onset either during pregnancy or
postpartum. About 50% of postpartum major depressive episodes begin
prior to delivery. Thus, these episodes are referred to collectively as
peripartum episodes.
 Between conception and birth, about 9% of women will experience a
major depressive episode. The best estimate for prevalence of a major
depressive episode between birth and 12 months postpartum is just below
7%.
 Peripartum-onset mood episodes can present either with or without
psychotic features. Infanticide (a rare occurrence) is most often associated
with postpartum
psychotic episodes that are characterized by command hallucinations to kill
the infant or delusions that the infant is possessed, but psychotic symptoms
can also occur in severe postpartum mood episodes without such specific
delusions or hallucinations.
 Postpartum mood (major depressive or manic) episodes with psychotic
features appear to occur in from 1 in 500 to 1 in 1,000 deliveries and may be
more common in primiparous women. The risk of postpartum episodes with
psychotic features is particularly increased for women with prior postpartum
psychotic mood episodes but is also elevated for those with a prior history of
a depressive or bipolar disorder (especially bipolar I disorder) and those with
a family history of bipolar disorders.
 Once a woman has had a postpartum episode with psychotic features, the
risk of recurrence with each subsequent delivery is between 30% and 50%.
Postpartum episodes must be differentiated from delirium occurring in the
postpartum period, which is distinguished by a fluctuating level of
awareness or attention.
 Peripartum-onset depressive disorders must be distinguished from the
much more common “maternity blues,” or what is known in lay terms as
“baby blues.” Maternity blues is not considered to be a mental disorder and
is characterized by sudden changes in mood (e.g., the sudden onset of
tearfulness in the absence of depression) that do not cause functional
impairment and that are likely caused by physiological changes occurring
after delivery. It is temporary and self-limited, typically improving quickly

(within a week) without the need for treatment. Other symptoms of maternity
blues include sleep disturbance and even confusion that can occur shortly
after delivery.
 Perinatal women may be at higher risk for depressive disorders due to
thyroid abnormalities as well as other medical conditions that can cause
depressive symptoms. If the depressive symptoms are judged to be due to
another medical condition related to the perinatal period, depressive
disorder due to another medical condition should be diagnosed instead of a
major depressive episode, with peripartum onset.
With seasonal pattern: This specifier applies to the lifetime pattern of mood
episodes. The essential feature is a regular seasonal pattern of at least one
type of episode (i.e., mania, hypomania, or depression). The other types of
episodes may not follow this pattern. For example, an individual may have
seasonal manias but have depressions that do not regularly occur at a specific
time of year.
A. There has been a regular temporal relationship between the onset of manic,
hypomanic, or major depressive episodes and a particular time of the year
(e.g., in the fall or winter) in bipolar I or bipolar II disorder.
Note: Do not include cases in which there is an obvious effect of seasonally
related psychosocial stressors (e.g., regularly being unemployed every
winter).
B. Full remissions (or a change from major depression to mania or hypomania
or vice versa) also occur at a characteristic time of the year (e.g.,
depression disappears in the spring).
C. In the last 2 years, the individual’s manic, hypomanic, or major depressive
episodes have demonstrated a temporal seasonal relationship, as defined
above, and no nonseasonal episodes of that polarity have occurred during
that 2-year period.
D. Seasonal manias, hypomanias, or depressions (as described above)
substantially outnumber any nonseasonal manias, hypomanias, or
depressions that may have occurred over the individual’s lifetime.
Note: The specifier “with seasonal pattern” can apply to the pattern of major
depressive episodes in bipolar I and bipolar II disorder, to the pattern of
manic episodes
and hypomanic episodes in bipolar I disorder, and to the pattern of
hypomanic episodes in bipolar II disorder. The essential feature is the onset
and remission of major depressive, manic, or hypomanic episodes at
characteristic times of the year. In most cases, the seasonal major
depressive episodes begin in fall or winter and remit in spring. Less
commonly, there may be recurrent summer depressive episodes. This

pattern of onset and remission of episodes must have occurred during at
least a 2-year period, without any nonseasonal episodes occurring during
this period. In addition, the seasonal depressive, manic, or hypomanic
episodes must substantially outnumber any nonseasonal depressive, manic,
or hypomanic episodes over the individual’s lifetime.
 This specifier does not apply to those situations in which the pattern is
better explained by seasonally linked psychosocial stressors (e.g., seasonal
unemployment or school schedule). It is unclear whether a seasonal pattern
of major depressive episodes is more likely in recurrent major depressive
disorder or in bipolar disorders. However, within the bipolar disorders group,
a seasonal pattern of major depressive episodes appears to be more likely
in bipolar II disorder than in bipolar I disorder. In some individuals, the onset
of manic or hypomanic episodes may also be linked to a particular season,
with peak seasonality of mania or hypomania from spring through summer.
 The prevalence of winter-type seasonal pattern appears to vary with
latitude, age, and sex. Prevalence increases with higher latitudes. Age is
also a strong predictor of seasonality, with younger persons at higher risk for
winter depressive episodes.
Specify if:
In partial remission: Symptoms of the immediately previous manic, hypomanic,
or major depressive episode are present but full criteria are not met, or there is a
period lasting less than 2 months without any significant symptoms of a manic,
hypomanic, or major depressive episode following the end of such an episode.
In full remission: During the past 2 months, no significant signs or symptoms of
the disturbance were present.
Specify current severity of manic episode:
Severity is based on the number of criterion symptoms, the severity of those
symptoms, and the degree of functional disability.
Mild: Minimum symptom criteria are met for a manic episode.
Moderate: Very significant increase in activity or impairment in judgment.
Severe: Almost continual supervision is required in order to prevent physical
harm to self or others.
Specify current severity of major depressive episode:
Severity is based on the number of criterion symptoms, the severity of those
symptoms, and the degree of functional disability.
Mild: Few, if any, symptoms in excess of those required to make the diagnosis
are present, the intensity of the symptoms is distressing but manageable, and
the symptoms result in minor impairment in social or occupational functioning.
Moderate: The number of symptoms, intensity of symptoms, and/or functional
impairment are between those specified for “mild” and “severe.”
Severe: The number of symptoms is substantially in excess of that required to
make the diagnosis, the intensity of the symptoms is seriously distressing and

unmanageable, and the symptoms markedly interfere with social and
occupational functioning.
1In distinguishing grief from a major depressive episode (MDE), it is useful to consider that in grief the predominant affect is
feelings of emptiness and loss, while in an MDE it is persistent depressed mood and the inability to anticipate happiness or
pleasure. The dysphoria in grief is likely to decrease in intensity over days to weeks and occurs in waves, the so-called pangs of
grief. These waves tend to be associated with thoughts or reminders of the deceased. The depressed mood of an MDE is more
persistent and not tied to specific thoughts or preoccupations. The pain of grief may be accompanied by positive emotions and
humor that are uncharacteristic of the pervasive unhappiness and misery characteristic of an MDE. The thought content
associated with grief generally features a preoccupation with thoughts and memories of the deceased, rather than the self-critical
or pessimistic ruminations seen in an MDE. In grief, self-esteem is generally preserved, whereas in an MDE, feelings of
worthlessness and self-loathing are common. If self-derogatory ideation is present in grief, it typically involves perceived failings
vis-à-vis the deceased (e.g., not visiting frequently enough, not telling the deceased how much he or she was loved). If a bereaved
individual thinks about death and dying, such thoughts are generally focused on the deceased and possibly about “joining” the
deceased, whereas in an MDE such thoughts are focused on ending one’s own life because of feeling worthless, undeserving of
life, or unable to cope with the pain of depression.
1In distinguishing grief from a major depressive episode (MDE), it is useful to consider that in grief the predominant affect is
feelings of emptiness and loss, while in an MDE it is persistent depressed mood and the inability to anticipate happiness or
pleasure. The dysphoria in grief is likely to decrease in intensity over days to weeks and occurs in waves, the so-called pangs of
grief. These waves tend to be associated with thoughts or reminders of the deceased. The depressed mood of an MDE is more
persistent and not tied to specific thoughts or preoccupations. The pain of grief may be accompanied by positive emotions and
humor that are uncharacteristic of the pervasive unhappiness and misery characteristic of an MDE. The thought content
associated with grief generally features a preoccupation with thoughts and memories of the deceased, rather than the self-critical
or pessimistic ruminations seen in an MDE. In grief, self-esteem is generally preserved, whereas in an MDE feelings of
worthlessness and self-loathing are common. If self-derogatory ideation is present in grief, it typically involves perceived failings
vis-à-vis the deceased (e.g., not visiting frequently enough, not telling the deceased how much he or she was loved). If a bereaved
individual thinks about death and dying, such thoughts are generally focused on the deceased and possibly about “joining” the
deceased, whereas in an MDE such thoughts are focused on ending one’s own life because of feeling worthless, undeserving of
life, or unable to cope with the pain of depression.

# 04 - Depressive Disorders

# Depressive Disorders

177

Depressive Disorders
Depressive disorders include disruptive mood dysregulation disorder, major
depressive disorder (including major depressive episode), persistent depressive disorder,
premenstrual dysphoric disorder, substance/medication-induced depressive disorder, depressive
disorder due to another medical condition, other specified depressive disorder, and unspecified
depressive disorder. The common feature of all of these disorders is the presence of sad, empty,
or irritable mood, accompanied by related changes that significantly affect the individual’s
capacity to function (e.g., somatic and cognitive changes in major depressive disorder and
persistent depressive disorder). What differs among them are issues of duration, timing, or
presumed etiology.
In order to address concerns in the United States and, increasingly, internationally about the
potential for the overdiagnosis and treatment of bipolar disorder in children, a new diagnosis,
disruptive mood dysregulation disorder, referring to the presentation of children with persistent
irritability and frequent episodes of extreme behavioral dyscontrol, is added to the depressive
disorders for children up to 12 years of age. Its placement in this chapter reflects the finding that
children with this symptom pattern typically develop unipolar depressive disorders or anxiety
disorders, rather than bipolar disorders, as they mature into adolescence and adulthood.
Major depressive disorder represents the classic condition in this group of disorders. It is
characterized by discrete episodes of at least 2 weeks’ duration (although most episodes last
considerably longer) involving clear-cut changes in affect, cognition, and neurovegetative
functions and interepisode remissions. A diagnosis based on a single episode is possible,
although the disorder is a recurrent one in the majority of cases. Careful consideration should be
given to the delineation of normal sadness and grief from a major depressive episode.
Bereavement may induce great suffering, but it does not typically induce an episode of major
depressive disorder. When they do occur together, the depressive symptoms and functional
impairment tend to be more severe and the prognosis is worse compared with bereavement that
is not accompanied by major depressive disorder. Bereavement-related major depressive
episodes tend to occur in persons with other vulnerabilities to depressive disorders.
A more chronic form of depression, persistent depressive disorder, can be diagnosed when
the mood disturbance continues for at least 2 years in adults or 1 year in children. This diagnosis,
new in DSM-5, includes the DSM-IV diagnostic categories of chronic major depression and
dysthymia.
After careful scientific review of the evidence, premenstrual dysphoric disorder has been
moved from an appendix of DSM-IV (“Criteria Sets and Axes Provided for Further Study”) to
Section II of DSM-5. Almost 20 years of additional research on this condition has confirmed a
specific and treatment-responsive form of depressive disorder that begins sometime following
ovulation and remits within a few days of menses and has a marked impact on functioning.
A large number of substances of abuse, some prescribed medications, and several medical

F34.81
conditions can be associated with depression-like phenomena. This fact is recognized in the
diagnoses of substance/medication-induced depressive disorder and depressive disorder due to
another medical condition.
Disruptive Mood Dysregulation Disorder
Diagnostic Criteria
A. Severe recurrent temper outbursts manifested verbally (e.g., verbal rages)
and/or behaviorally (e.g., physical aggression toward people or property) that are
grossly out of proportion in intensity or duration to the situation or provocation.
B. The temper outbursts are inconsistent with developmental level.
C. The temper outbursts occur, on average, three or more times per week.
D. The mood between temper outbursts is persistently irritable or angry most of the
day, nearly every day, and is observable by others (e.g., parents, teachers,
peers).
E. Criteria A–D have been present for 12 or more months. Throughout that time,
the individual has not had a period lasting 3 or more consecutive months without
all of the symptoms in Criteria A–D.
F. Criteria A and D are present in at least two of three settings (i.e., at home, at
school, with peers) and are severe in at least one of these.
G. The diagnosis should not be made for the first time before age 6 years or after
age 18 years.
H. By history or observation, the age at onset of Criteria A–E is before 10 years.
I. There has never been a distinct period lasting more than 1 day during which the
full symptom criteria, except duration, for a manic or hypomanic episode have
been met.
Note: Developmentally appropriate mood elevation, such as occurs in the
context of a highly positive event or its anticipation, should not be considered as
a symptom of mania or hypomania.
J. The behaviors do not occur exclusively during an episode of major depressive
disorder and are not better explained by another mental disorder (e.g., autism
spectrum disorder, posttraumatic stress disorder, separation anxiety disorder,
persistent depressive disorder).
Note: This diagnosis cannot coexist with oppositional defiant disorder,
intermittent explosive disorder, or bipolar disorder, though it can coexist with
others, including major depressive disorder, attention-deficit/hyperactivity
disorder, conduct disorder, and substance use disorders. Individuals whose
symptoms meet criteria for both disruptive mood dysregulation disorder and

oppositional defiant disorder should only be given the diagnosis of disruptive
mood dysregulation disorder. If an individual has ever experienced a manic or
hypomanic episode, the diagnosis of disruptive mood dysregulation disorder
should not be assigned.
K. The symptoms are not attributable to the physiological effects of a substance or
another medical or neurological condition.
Diagnostic Features
The core feature of disruptive mood dysregulation disorder is chronic severe, persistent
irritability. This severe irritability has two prominent clinical manifestations, the first of which is
frequent temper outbursts. These outbursts typically occur in response to frustration and can be
verbal or behavioral (the latter in the form of aggression against property, self, or others). They
must occur frequently (i.e., on average, three or more times per week) (Criterion C) over at least
1 year in at least two settings (Criteria E and F), such as in the home and at school, and they must
be developmentally inappropriate (Criterion B). The second manifestation of severe irritability
consists of chronic, persistently irritable or angry mood that is present between the severe temper
outbursts. This irritable or angry mood must be characteristic of the child, being present most of
the day, nearly every day, and noticeable by others in the child’s environment (Criterion D).
The clinical presentation of disruptive mood dysregulation disorder must be carefully
distinguished from presentations of other, related conditions, particularly pediatric bipolar
disorder. In fact, disruptive mood dysregulation disorder was added to DSM-5 to address the
considerable concern about the appropriate classification and treatment of children who present
with chronic, persistent irritability relative to children who present with classic (i.e., episodic)
bipolar disorder.
Some researchers view severe, nonepisodic irritability as characteristic of bipolar disorder in
children, although both DSM-IV and DSM-5 require that both children and adults have distinct
episodes of mania or hypomania to qualify for the diagnosis of bipolar I disorder. During the
latter decades of the twentieth century, this contention by researchers that severe, nonepisodic
irritability is a manifestation of pediatric mania coincided with an upsurge in the rates at which
clinicians assigned the diagnosis of bipolar disorder to their pediatric patients. This sharp
increase in rates appears to be attributable to clinicians combining at least two clinical
presentations into a single category. That is, both classic, episodic presentations of mania and
nonepisodic presentations of severe irritability have been labeled as bipolar disorder in children.
In DSM-5, the term bipolar disorder is explicitly reserved for episodic presentations of bipolar
symptoms. DSM-IV did not include a diagnosis designed to capture youths whose hallmark
symptoms consisted of very severe, nonepisodic irritability, whereas DSM-5, with the inclusion
of disruptive mood dysregulation disorder, provides a distinct category for such presentations.
Prevalence
Disruptive mood dysregulation disorder is common among children presenting to pediatric

Temperamental.
Environmental.
Genetic and physiological.
mental health clinics. Prevalence estimates of the disorder in the community are unclear. In a
population-based cohort study of Brazilian 11-year-olds that used a specific module for
disruptive mood dysregulation disorder, the prevalence was 2.5%.
Consistent gender differences in prevalence have not been reported in population samples,
although clinic samples report a male preponderance. For example, up to 80% of children
presenting to clinics in Turkey with features of disruptive mood dysregulation disorder in a chart
review were boys. Data suggest that the diagnosis may be more common in younger age groups
(e.g., 8.2% in a community sample of 6-year-olds in the United States).
Development and Course
The onset of disruptive mood dysregulation disorder must be before age 10 years, and the
diagnosis should not be applied to children with a developmental age of younger than 6 years. It
is unknown whether the condition presents only in this age-delimited fashion. Because the
symptoms of disruptive mood dysregulation disorder are likely to change as children mature, use
of the diagnosis should be restricted to age groups similar to those in which validity has been
established (6–18 years). Approximately half of children with disruptive mood dysregulation
disorder living in a predominantly rural area in a large U.S. study continue to have symptoms
that meet criteria for the condition 1 year later, although those children whose symptoms no
longer meet the threshold for the diagnosis often have persistent, clinically impairing irritability.
Rates of conversion from severe, nonepisodic irritability to bipolar disorder are very low.
Instead, children with disruptive mood dysregulation disorder are at increased risk to develop
unipolar depressive and/or anxiety disorders in adulthood.
Risk and Prognostic Factors
Children with chronic irritability typically exhibit complicated psychiatric
histories. In such children, a relatively extensive history of chronic irritability is common,
typically manifesting before full criteria for the syndrome are met. Such prediagnostic
presentations may have qualified for a diagnosis of oppositional defiant
disorder. Many children with disruptive mood dysregulation disorder have symptoms that also
meet criteria for attention-deficit/hyperactivity disorder (ADHD) and for an anxiety disorder,
with such diagnoses often being present from a relatively early age. For some children, the
criteria for major depressive disorder may also be met.
Factors associated with disrupted family life, such as psychological abuse or
neglect, parental psychiatric disorder, limited parental education, single-parent household, early
trauma, death of a parent, parental grief, divorce, and malnutrition (e.g., vitamin deficiency), are
associated with the core behaviors of disruptive mood dysregulation disorder.
Data suggest that a family history of depression may be a risk factor for
disruptive mood dysregulation disorder. Consistent with this, twin data suggest that the
association between early irritability and later unipolar depression and anxiety may be, in part,
genetically mediated.
Compared with children with pediatric bipolar disorder or other mental illnesses, those with

disruptive mood dysregulation disorder exhibit both commonalities and differences in
information-processing deficits. For example, face-emotion labeling deficits, as well as perturbed
decision-making and cognitive control, are present in children with bipolar disorder as well as
those with disruptive mood dysregulation disorder. Importantly, however, the same behavioral
deficit may be associated with different patterns of neural dysfunction. There is also evidence for
disorder-specific dysfunction, such as during tasks assessing attention deployment in response to
emotional stimuli, which has demonstrated unique signs of dysfunction in children with chronic
irritability.
Culture-Related Diagnostic Issues
Culture-related data on disruptive mood dysregulation disorder are limited. However,
sociocultural factors affect the presentation of core psychological features of the disorder,
including impulsivity as well as emotion, reward, threat, and behavior dysregulation, especially
in settings characterized by severe social disruption, such as postconflict zones or communities
affected by long-standing racism and discrimination. It is important to distinguish disruptive
mood dysregulation disorder from adaptive responses to adversity that are context-dependent and
transitory.
Sex- and Gender-Related Diagnostic Issues
There is some evidence from twin studies that while irritability has a strong genetic component
in both sexes, patterns differ for boys and girls. For boys, genetic factors appear to account for an
increasing amount of the variance of the phenotype of irritability throughout childhood. While
genetic factors account for a large proportion of the variance of the irritability phenotype in
school-age girls, this decreases into adolescence and young adulthood, with environmental
influences playing a greater role. How this genetic risk for irritability translates into risk and
prognosis for disruptive mood dysregulation disorder, per se, is not yet known.
Functional Consequences of Disruptive Mood Dysregulation Disorder
Chronic, severe irritability, such as is seen in disruptive mood dysregulation disorder, is
associated with marked disruption in a child’s family and peer relationships, as well as in school
performance. Because of their extremely low frustration tolerance, such children generally have
difficulty succeeding in school; they are often unable to participate in the activities typically
enjoyed by healthy children; their family life is severely disrupted by their outbursts and
irritability; and they have trouble initiating or sustaining friendships. Levels of dysfunction in
children with bipolar disorder and disruptive mood
dysregulation disorder are generally comparable. Both conditions cause severe disruption in the
lives of the affected individual and his or her family. In both disruptive mood dysregulation
disorder and pediatric bipolar disorder, aggression and psychiatric hospitalization are common.
Differential Diagnosis

Bipolar disorders.
Oppositional defiant disorder.
Because chronically irritable children and adolescents typically present with complex histories,
the diagnosis of disruptive mood dysregulation disorder must be made while considering the
presence or absence of multiple other conditions. Despite the need to consider many other
syndromes, differentiation of disruptive mood dysregulation disorder from bipolar disorder and
oppositional defiant disorder requires particularly careful assessment.
The central feature differentiating disruptive mood dysregulation disorder and
bipolar disorders in children involves the longitudinal course of the core symptoms. In children,
as in adults, bipolar I disorder and bipolar II disorder manifest as an episodic illness with discrete
episodes of mood perturbation that can be differentiated from the child’s typical presentation.
The mood perturbation that occurs during a manic episode is distinctly different from the child’s
usual mood. In addition, during a manic episode, the change in mood must be accompanied by
the onset, or worsening, of associated cognitive, behavioral, and physical symptoms (e.g.,
distractibility, increased goal-directed activity), which are also present to a degree that is
distinctly different from the child’s usual baseline. Thus, in the case of a manic episode, parents
(and, depending on developmental level, children) should be able to identify a distinct time
period during which the child’s mood and behavior were markedly different from usual. In
contrast, the irritability of disruptive mood dysregulation disorder is persistent and is present
over many months; while it may wax and wane to a certain degree, severe irritability is
characteristic of the child with disruptive mood dysregulation disorder. Thus, while bipolar
disorders are episodic conditions, disruptive mood dysregulation disorder is not. In fact, the
diagnosis of disruptive mood dysregulation disorder cannot be assigned to a child who has ever
experienced a full-duration hypomanic or manic episode (irritable or euphoric) or who has ever
had a manic or hypomanic episode lasting more than 1 day. Another central differentiating
feature between bipolar disorders and disruptive mood dysregulation disorder is the presence of
elevated or expansive mood and grandiosity. These symptoms are common features of mania but
are not characteristic of disruptive mood dysregulation disorder.
While symptoms of oppositional defiant disorder typically do occur
in children with disruptive mood dysregulation disorder, mood symptoms of disruptive mood
dysregulation disorder are relatively rare in children with oppositional defiant disorder. The key
features that warrant the diagnosis of disruptive mood dysregulation disorder in children whose
symptoms also meet criteria for oppositional defiant disorder are the presence of severe and
frequently recurrent outbursts and a persistent disruption in mood between outbursts. In addition,
the diagnosis of disruptive mood dysregulation disorder requires severe impairment in at least
one setting (i.e., home, school, or among peers) and mild to moderate impairment in a second
setting. For this reason, while most children whose symptoms meet criteria for disruptive mood
dysregulation disorder will also have a presentation that meets criteria for oppositional defiant
disorder, the reverse is not the case. That is, in only approximately 15% of individuals with
oppositional defiant disorder would criteria for disruptive mood dysregulation disorder be met.
Moreover, even for children in whom criteria for both disorders are met, only the diagnosis of
disruptive mood dysregulation disorder should be made. Finally, both the prominent mood
symptoms in disruptive mood dysregulation disorder and the high risk for depressive and anxiety
disorders in follow-up studies justify placement of disruptive mood dysregulation disorder
among the depressive disorders in DSM-5. (Oppositional defiant disorder is included in the
chapter “Disruptive, Impulse-Control, and Conduct

Attention-deficit/hyperactivity disorder, major depressive disorder, anxiety disorders, and
autism spectrum disorder.
Intermittent explosive disorder.
Disorders.”) This reflects the more prominent mood component among individuals with
disruptive mood dysregulation disorder, as compared with individuals with oppositional defiant
disorder. Nevertheless, it also should be noted that disruptive mood dysregulation disorder
appears to carry a high risk for behavioral problems as well as mood problems.
Unlike children diagnosed with bipolar disorder or oppositional defiant disorder—for whom a
diagnosis of disruptive mood dysregulation disorder cannot be given even if the symptoms meet
diagnostic criteria for that disorder—children whose symptoms meet criteria for disruptive mood
dysregulation disorder also can receive a comorbid diagnosis of ADHD, major depressive
disorder, and/or anxiety disorder. However, children whose irritability is present only in the
context of a major depressive episode or persistent depressive disorder should receive one of
those diagnoses rather than disruptive mood dysregulation disorder. Children with disruptive
mood dysregulation disorder may have symptoms that also meet criteria for an anxiety disorder
and can receive both diagnoses, but children whose irritability is manifest only in the context of
exacerbation of an anxiety disorder should receive the relevant anxiety disorder diagnosis rather
than disruptive mood dysregulation disorder. In addition, children with autism spectrum
disorders frequently present with temper outbursts when, for example, their routines are
disturbed. In that instance, the temper outbursts would be considered secondary to the autism
spectrum disorder, and the child should not receive the diagnosis of disruptive mood
dysregulation disorder.
Children with symptoms suggestive of intermittent explosive
disorder present with instances of severe temper outbursts, much like children with disruptive
mood dysregulation disorder. However, unlike disruptive mood dysregulation disorder,
intermittent explosive disorder does not require the individual’s mood to be persistently irritable
or angry between outbursts. In addition, a diagnosis of intermittent explosive disorder involving
verbal aggression or physical aggression that does not result in damage to property or physical
injury to animals or other individuals occurring at least twice weekly can be made after only 3
months of symptoms, in contrast to the 12-month requirement for disruptive mood dysregulation
disorder. Thus, these two diagnoses should not be made in the same child. For children with
outbursts and intercurrent, persistent irritability, only the diagnosis of disruptive mood
dysregulation disorder should be made.
Comorbidity
Rates of comorbidity in disruptive mood dysregulation disorder are extremely high. It is rare to
find individuals whose symptoms meet criteria for disruptive mood dysregulation disorder alone.
Comorbidity between disruptive mood dysregulation disorder and other DSM-defined
syndromes appears higher than for many other pediatric mental illnesses; the strongest overlap is
with oppositional defiant disorder. Not only is the overall rate of comorbidity high in disruptive
mood dysregulation disorder, but also the range of comorbid illnesses appears particularly
diverse. These children typically present to the clinic with a wide range of disruptive behavior,
mood, anxiety, and even autism spectrum symptoms and diagnoses. However, children with

disruptive mood dysregulation disorder should not have symptoms that meet criteria for bipolar
disorder, as in that context, only the bipolar disorder diagnosis should be made. If children have
symptoms that meet criteria for oppositional defiant disorder or intermittent explosive disorder
and disruptive mood dysregulation disorder, only the diagnosis of disruptive mood dysregulation
disorder should be assigned. Also, as noted earlier, the diagnosis of disruptive mood
dysregulation disorder should not be assigned if the symptoms occur only in an anxietyprovoking context, when the routines of a child with autism spectrum disorder or obsessivecompulsive disorder are disturbed, or in the context of a major depressive episode.
Major Depressive Disorder
Diagnostic Criteria
A. Five (or more) of the following symptoms have been present during the same 2week period and represent a change from previous functioning; at least one of
the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.
Note: Do not include symptoms that are clearly attributable to another medical
condition.
1. Depressed mood most of the day, nearly every day, as indicated by either
subjective report (e.g., feels sad, empty, hopeless) or observation made by
others (e.g., appears tearful). (Note: In children and adolescents, can be
irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most of
the day, nearly every day (as indicated by either subjective account or
observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of
more than 5% of body weight in a month), or decrease or increase in appetite
nearly every day. (Note: In children, consider failure to make expected weight
gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others,
not merely subjective feelings of restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be
delusional) nearly every day (not merely self-reproach or guilt about being
sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day
(either by subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation

without a specific plan, or a suicide attempt or a specific plan for committing
suicide.
B. The symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
C. The episode is not attributable to the physiological effects of a substance or
another medical condition.
Note: Criteria A–C represent a major depressive episode.
Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses
from a natural disaster, a serious medical illness or disability) may include the
feelings of intense sadness, rumination about the loss, insomnia, poor appetite,
and weight loss noted in Criterion A, which may resemble a depressive episode.
Although such symptoms may be understandable or considered appropriate to
the loss, the presence of a major depressive episode in addition to the normal
response to a significant loss should also be carefully considered. This decision
inevitably requires the exercise of clinical judgment based on the individual’s
history and the cultural norms for the expression of distress in the context of
loss.1
D. At least one major depressive episode is not better explained by schizoaffective
disorder and is not superimposed on schizophrenia, schizophreniform disorder,
delusional disorder, or other specified and unspecified schizophrenia spectrum
and other psychotic disorders.
E. There has never been a manic episode or a hypomanic episode.
Note: This exclusion does not apply if all of the manic-like or hypomanic-like
episodes are substance-induced or are attributable to the physiological effects of
another medical condition.
Coding and Recording Procedures
The diagnostic code for major depressive disorder is based on whether this is a
single or recurrent episode, current severity, presence of psychotic features, and
remission status. Current severity and psychotic features are only indicated if full
criteria are currently met for a major depressive episode. Remission specifiers are
only indicated if the full criteria are not currently met for a major depressive episode.
Codes are as follows:
Severity/course specifier
Single episode
Recurrent
episode*
Mild (p. 214)
F32.0
F33.0
Moderate (p. 214)
F32.1
F33.1
Severe (p. 214)
F32.2
F33.2
With psychotic features** (pp. 212–213)
F32.3
F33.3
In partial remission (p. 214)
F32.4
F33.41

In full remission (p. 214)
F32.5
F33.42
Unspecified
F32.9
F33.9
*For an episode to be considered recurrent, there must be an interval of at least 2 consecutive months between
separate episodes in which criteria are not met for a major depressive episode. The definitions of specifiers are
found on the indicated pages.
**If psychotic features are present, code the “with psychotic features” specifier irrespective of episode severity.
In recording the name of a diagnosis, terms should be listed in the following order:
major depressive disorder, single or recurrent episode, severity/psychotic/remission
specifiers, followed by as many of the following specifiers without codes that apply to
the current episode (or the most recent episode if the major depressive disorder is in
partial or full remission). Note: The specifier “with seasonal pattern” describes the
pattern of recurrent major depressive episodes.
Specify if:
With anxious distress (pp. 210–211)
With mixed features (p. 211)
With melancholic features (pp. 211–212)
With atypical features (p. 212)
With mood-congruent psychotic features (p. 213)
With mood-incongruent psychotic features (p. 213)
With catatonia (p. 213). Coding note: Use additional code F06.1.
With peripartum onset (p. 213)
With seasonal pattern (applies to pattern of recurrent major depressive
episodes) (p. 214)
Diagnostic Features
Major depressive disorder is defined by the presence of at least one major depressive episode
occurring in the absence of a history of manic or hypomanic episodes. The essential feature of a
major depressive episode is a period lasting at least 2 weeks during which there is either
depressed mood or the loss of interest or pleasure in all or nearly all activities for most of the day
nearly every day (Criterion A). The individual must also experience at least four additional
symptoms during the same 2-week period, drawn from a list that includes changes in appetite or
weight, sleep, and psychomotor activity; decreased energy; feelings of worthlessness or guilt;
difficulty thinking, concentrating, or making decisions; or thoughts of death, suicidal ideation, a
suicide attempt, or a specific plan for suicidal behavior. To count toward a diagnosis of a major
depressive episode, a symptom must either be newly present or have clearly worsened compared
with the individual’s pre-episode status. Moreover, the symptoms must occur nearly every day,
for at least 2 consecutive weeks, with the exception of thoughts of death and suicidal ideation,
which must be recurrent, and attempting suicide or making a specific plan, which only needs to

occur once. The episode must be accompanied by clinically significant distress or impairment in
social, occupational, or other important areas of functioning. For some individuals with milder
episodes, functioning may appear to be normal but requires markedly increased effort. The
presenting complaint is often insomnia or fatigue rather than depressed mood or loss of interest;
thus, the failure to probe for accompanying depressive symptoms can result in underdiagnosis.
Fatigue and sleep disturbance are present in a high proportion of cases; psychomotor
disturbances are much less common but are indicative of greater overall severity, as is the
presence of delusional or near-delusional guilt.
The mood in a major depressive episode is often described by the individual as depressed,
sad, hopeless, discouraged, or “down in the dumps” (Criterion A1). In some cases, sadness may
be denied at first but may subsequently be elicited by interview (e.g., by pointing out that the
individual looks as if he or she is about to cry). In some individuals who complain of feeling
“blah,” having no feelings, or feeling anxious, the presence of a depressed mood can be inferred
from the individual’s facial expression and demeanor. Some individuals emphasize somatic
complaints (e.g., bodily aches and pains) rather than reporting feelings of sadness. Many
individuals report or exhibit increased irritability (e.g., persistent anger, a tendency to respond to
events with angry outbursts or blaming others, an exaggerated sense of frustration over minor
matters). In children and adolescents, an irritable or cranky mood may develop rather than a sad
or dejected mood. This presentation should be differentiated from a pattern of irritability when
frustrated.
Diminished interest or pleasure in usual activities is nearly always present, at least to some
degree. Individuals may report feeling less interested in hobbies, “not caring anymore,” or not
feeling any enjoyment in activities that were previously considered pleasurable (Criterion A2).
Family members often notice social withdrawal or neglect of pleasurable avocations (e.g., a
formerly avid golfer no longer plays, a child who used to enjoy soccer finds excuses not to
practice). In some individuals, there is a significant reduction from previous levels of sexual
interest or desire.
Appetite change may involve either a reduction or an increase. Some depressed individuals
report that they have to force themselves to eat. Others may eat more and may crave specific
foods (e.g., sweets or other carbohydrates). When appetite changes are severe (in either
direction), there may be a significant loss or gain in weight, or, in children, a failure to make
expected weight gains may be noted (Criterion A3).
Sleep disturbance may take the form of either difficulty sleeping or sleeping excessively
(Criterion A4). When insomnia is present, it typically takes the form of middle insomnia (i.e.,
waking up during the night and then having difficulty returning to sleep) or terminal insomnia
(i.e., waking too early and being unable to return to sleep). Initial insomnia (i.e., difficulty falling
asleep) may also occur. Individuals who present with oversleeping (hypersomnia) may
experience prolonged sleep episodes at night or increased daytime sleep. Sometimes the reason
that the individual seeks treatment is for the disturbed sleep.
Psychomotor changes include agitation (e.g., the inability to sit still, pacing, hand-wringing;
or pulling or rubbing of the skin, clothing, or other objects) or retardation (e.g., slowed speech,
thinking, and body movements; increased pauses before answering; speech that is decreased in

volume, inflection, amount, or variety of content, or muteness) (Criterion A5). The psychomotor
agitation or retardation must be severe enough to be observable by others and not represent
merely subjective feelings. Individuals who display either psychomotor disturbance (i.e.,
psychomotor agitation or retardation) are likely to have histories of the other.
Decreased energy, tiredness, and fatigue are common (Criterion A6). An individual may
report sustained fatigue without physical exertion. Even the smallest tasks seem to require
substantial effort. The efficiency with which tasks are accomplished may be reduced. For
example, an individual may complain that washing and dressing in the morning are exhausting
and take twice as long as usual. This symptom accounts for much of the impairment resulting
from major depressive disorder, both during acute episodes and when remission is incomplete.
The sense of worthlessness or guilt associated with a major depressive episode may include
unrealistic negative evaluations of one’s worth or guilty preoccupations or ruminations over
minor past failings (Criterion A7). Such individuals often misinterpret neutral or trivial day-today events as evidence of personal defects and have an exaggerated sense of responsibility for
untoward events. The sense of worthlessness or guilt may be of delusional proportions (e.g., an
individual who is convinced that he or she is personally responsible for world poverty). Blaming
oneself for being sick and for failing to meet occupational or interpersonal responsibilities as a
result of the depression is very common and, unless delusional, is not considered sufficient to
meet this criterion.
Many individuals report impaired ability to think, concentrate, or make even minor decisions
(Criterion A8). They may appear easily distracted or complain of memory difficulties. Those
engaged in cognitively demanding pursuits are often unable to function. In children, a
precipitous drop in grades may reflect poor concentration. In elderly individuals, memory
difficulties may be the chief complaint and may be mistaken for early signs of a dementia
(“pseudodementia”). When the major depressive episode is successfully treated, the memory
problems often fully abate. However, in some individuals, particularly elderly persons, a major
depressive episode may sometimes be the initial presentation of an irreversible dementia.
Thoughts of death, suicidal ideation, or suicide attempts (Criterion A9) are common. They
may range from a passive wish not to awaken in the morning or a belief that others would be
better off if the individual were dead, to transient but recurrent thoughts of dying by suicide, to a
specific suicide plan. More severely suicidal individuals may have put their affairs in order (e.g.,
updated wills, settled debts), acquired needed materials (e.g., a rope or a gun), and chosen a
location and time to accomplish the suicide. Motivations for suicide may include a desire to give
up in the face of perceived insurmountable obstacles,
an intense wish to end what is perceived as an unending and excruciatingly painful emotional
state, an inability to foresee any enjoyment in life, or the wish to not be a burden to others. The
resolution of such thinking may be a more meaningful measure of diminished suicide risk than
denial of further plans for suicide.
The degree of impairment associated with a major depressive episode varies, but even in
milder cases, there must be either clinically significant distress or some interference in social,
occupational, or other important areas of functioning (Criterion B). If impairment is severe, the
individual may lose the ability to function socially or occupationally. In extreme cases, the

individual may be unable to perform minimal self-care (e.g., feeding and clothing self) or to
maintain minimal personal hygiene.
The individual’s report of symptoms may be compromised by difficulties in concentrating,
impaired memory, or a tendency to deny, discount, or explain away symptoms. Information from
additional informants can be especially helpful in clarifying the course of current or prior major
depressive episodes and in assessing whether there have been any manic or hypomanic episodes.
Because major depressive episodes can begin gradually, a review of clinical information that
focuses on the worst part of the current episode may be most likely to detect the presence of
symptoms.
The evaluation of the symptoms of a major depressive episode is especially difficult when
they occur in an individual who also has another medical condition (e.g., cancer, stroke,
myocardial infarction, diabetes, pregnancy). Some of the criterion signs and symptoms of a
major depressive episode are identical to those of another medical condition (e.g., weight loss
with untreated diabetes; fatigue with cancer; hypersomnia early in pregnancy; insomnia later in
pregnancy or the postpartum). Such symptoms count toward a major depressive diagnosis except
when they are clearly and fully attributable to another medical condition. Nonvegetative
symptoms of dysphoria, anhedonia, guilt or worthlessness, impaired concentration or indecision,
and suicidal thoughts should be assessed with particular care in such cases. Definitions of major
depressive episodes that have been modified to include only these nonvegetative symptoms
appear to identify nearly the same individuals as do the full criteria.
Associated Features
Major depressive disorder is associated with high mortality, much of which is accounted for by
suicide; however, it is not the only cause. For example, depressed individuals admitted to nursing
homes have a markedly increased likelihood of death in the first year. Individuals frequently
present with tearfulness, irritability, brooding, obsessive rumination, anxiety, phobias, excessive
worry over physical health, and complaints of pain (e.g., headaches; joint, abdominal, or other
pains). In children, separation anxiety may occur.
Although an extensive literature exists describing neuroanatomical, neuroendocrinological,
and neurophysiological correlates of major depressive disorder, no laboratory test has yielded
results of sufficient sensitivity and specificity to be used as a diagnostic tool for this disorder.
Until recently, hypothalamic-pituitary-adrenal axis hyperactivity had been the most extensively
investigated abnormality associated with major depressive episodes, and it appears to be
associated with melancholia (a particularly severe type of depression), psychotic features, and
risks for eventual suicide. Molecular studies have also implicated peripheral factors, including
genetic variants in neurotrophic factors and pro-inflammatory cytokines. Additionally,
volumetric and functional magnetic resonance imaging studies provide evidence for
abnormalities in specific neural systems supporting emotion processing, reward seeking, and
emotion regulation in adults with major depression.
Prevalence
Twelve-month prevalence of major depressive disorder in the United States is approximately
7%, with marked differences by age group such that the prevalence in 18- to 29-year-old

188
individuals is threefold higher than the prevalence in individuals age 60 years or older. The most
reproducible finding in the epidemiology of major depressive disorder has been a higher
prevalence in females, an effect that peaks in adolescence and then stabilizes. Women experience
approximately twofold higher rates than men, especially between menarche and menopause.
Women report more atypical symptoms of depression characterized by hypersomnia, increased
appetite, and leaden paralysis compared with men.
Systematic reviews show that the 12-month and point prevalence of major depressive
disorder vary eight- to ninefold across global geographic regions. In the United States,
prevalence increased from 2005 to 2015, with steeper rates of increase for youth compared with
older groups. After stratification by ethnoracial groups, non-Hispanic Whites showed a
significant increase in prevalence after adjustment for demographic characteristics, whereas no
significant change in rate of depression was observed among non-Hispanic Blacks or Hispanics.
Development and Course
Major depressive disorder may first appear at any age, but the likelihood of onset increases
markedly with puberty. In the United States, incidence appears to peak in the 20s; however, first
onset in late life is not uncommon.
The course of major depressive disorder is quite variable, such that some individuals rarely,
if ever, experience remission (a period of 2 or more months with no symptoms, or only one or
two symptoms to no more than a mild degree), while others experience many years with few or
no symptoms between discrete episodes. The course of depression may reflect social-structural
adversity associated with poverty, racism, and marginalization.
It is important to distinguish individuals who present for treatment during an exacerbation of
a chronic depressive illness from those whose symptoms developed recently. Chronicity of
depressive symptoms substantially increases the likelihood of underlying personality, anxiety,
and substance use disorders and decreases the likelihood that treatment will be followed by full
symptom resolution. It is therefore useful to ask individuals presenting with depressive
symptoms to identify the last period of at least 2 months during which they were entirely free of
depressive symptoms. Cases in which depressive symptoms are present for more days than not
might warrant an additional diagnosis of persistent depressive disorder.
Recovery from a major depressive episode begins within 3 months of onset for 40% of
individuals with major depression and within 1 year for 80% of individuals. Recency of onset is
a strong determinant of the likelihood of near-term recovery, and many individuals who have
been depressed for only several months can be expected to recover spontaneously. Features
associated with lower recovery rates, other than current episode duration, include psychotic
features, prominent anxiety, personality disorders, and symptom severity.
The risk of recurrence becomes progressively lower over time as the duration of remission
increases. The risk is higher in individuals whose preceding episode was severe, in younger
individuals, and in individuals who have already experienced multiple episodes. The persistence
of even mild depressive symptoms during remission is a powerful predictor of recurrence.
Many bipolar illnesses begin with one or more depressive episodes, and a substantial
proportion of individuals who initially appear to have major depressive disorder will prove, in

Temperamental.
Environmental.
Genetic and physiological.
Course modifiers.
time, to instead have a bipolar disorder. This is more likely in individuals with onset of the
illness in adolescence, those with psychotic features, and those with a family history of bipolar
illness. The presence of a “with mixed features” specifier also increases the risk for future manic
or hypomanic diagnosis. Major depressive disorder, particularly with psychotic features, may
also transition into schizophrenia, a change that is much more frequent than the reverse.
There are no clear effects of current age on the course or treatment response of major
depressive disorder. Some symptom differences exist, though, such that hypersomnia and
hyperphagia are more likely in younger individuals, and melancholic symptoms, particularly
psychomotor disturbances, are more common in older individuals. Depressions with earlier ages
at onset are more familial and more likely to involve personality disturbances. The course of
major depressive disorder within individuals does not generally change with aging. Mean times
to recovery do not change over multiple episodes, and the likelihood of being in an episode does
not generally increase or decrease with time.
Risk and Prognostic Factors
Negative affectivity (neuroticism) is a well-established risk factor for the onset
of major depressive disorder, and high levels appear to render individuals more likely to develop
depressive episodes in response to stressful life events.
Adverse childhood experiences, particularly when they are multiple and of
diverse types, constitute a set of potent risk factors for major depressive disorder. Women may
be disproportionately at risk for adverse childhood experiences, including sexual abuse, that may
contribute to the increased prevalence of depression in this group. Other social determinants of
mental health, such as low income, limited formal education, racism, and other forms of
discrimination, are associated with higher risk of major depressive disorder. Stressful life events
are well recognized as precipitants of major depressive episodes, but the presence or absence of
adverse life events near the onset of episodes does not appear to provide a useful guide to
prognosis or treatment selection. Etiologically, women are disproportionately affected by major
risk factors for depression across the life span, including interpersonal trauma.
First-degree family members of individuals with major depressive
disorder have a risk for major depressive disorder two- to fourfold higher than that of the general
population. Relative risks appear to be higher for early-onset and recurrent forms. Heritability is
approximately 40%, and the personality trait neuroticism accounts for a substantial portion of
this genetic liability.
Women may also be at risk for depressive disorders in relation to specific reproductive life
stages, including in the premenstrual period, postpartum, and in perimenopause.
Essentially all major nonmood disorders (i.e., anxiety, substance use, traumaand stressor-related, feeding and eating, and obsessive-compulsive and related disorders)
increase the risk of an individual developing depression. Major depressive episodes that develop
against the background of another disorder often follow a more refractory course. Substance use,
anxiety, and borderline personality disorders are among the most common of these, and the
presenting depressive symptoms may obscure and delay their recognition. However, sustained

clinical improvement in depressive symptoms may depend on the appropriate treatment of
underlying illnesses. Chronic or disabling medical conditions also increase risks for major
depressive episodes. Prevalent illnesses such as diabetes, morbid obesity, and cardiovascular
disease are often complicated by depressive episodes, and these episodes are more likely to
become chronic than are depressive episodes in medically healthy individuals.
Culture-Related Diagnostic Issues
Although there is substantial cross-cultural variation in the prevalence, course, and
symptomatology of depression, a syndrome similar to major depressive disorder can be
identified across diverse cultural contexts. Symptoms commonly associated with depression
across cultural contexts, not listed in the DSM criteria, include social isolation or loneliness,
anger, crying, and diffuse pain. A wide range of other somatic complaints are
common and vary by cultural context. Understanding the significance of these symptoms
requires exploring their meaning in local social contexts.
Symptoms of major depressive disorder may be underdetected or underreported, potentially
leading to misdiagnosis, including overdiagnosis of schizophrenia spectrum disorders in some
ethnic and racialized groups facing discrimination. Cross-nationally, higher levels of income
inequality in a society are associated with higher prevalence of major depressive disorder. In the
United States, the chronicity of major depressive disorder appears to be higher among African
Americans and Caribbean Blacks compared with non-Latinx Whites, possibly because of the
impact of racism, discrimination, greater sociostructural adversity, and lack of access to quality
mental health care.
Sex- and Gender-Related Diagnostic Issues
There are no clear differences between genders in treatment response or functional
consequences. There is some evidence for sex and gender differences in phenomenology and
course of illness. Women tend to experience more disturbances in appetite and sleep, including
atypical features such as hyperphagia and hypersomnia, and are more likely to experience
interpersonal sensitivity and gastrointestinal symptoms. Men with depression, however, may be
more likely than depressed women to report greater frequencies and intensities of maladaptive
self-coping and problem-solving strategies, including alcohol or other drug misuse, risk taking,
and poor impulse control.
Association With Suicidal Thoughts or Behavior
Age-adjusted rates of suicide in the United States have increased from 10.5 to 14.0 per 100,000
over the past two decades. An earlier review of the literature indicated that individuals with
depressive illness have a 17-fold increased risk for suicide over the age- and sex-adjusted general
population rate. The likelihood of suicide attempts lessens in middle and late life, although the
risk of death by suicide does not. The possibility of suicidal behavior exists at all times during
major depressive episodes. The most consistently described risk factor is a past history of suicide
attempts or threats, but it should be remembered that most deaths by suicide are not preceded by

Manic episodes with irritable mood or with mixed features.
Bipolar I disorder, bipolar II disorder, or other specified bipolar and related disorder.
Depressive disorder due to another medical condition.
nonfatal attempts. Anhedonia has a particularly strong association with suicidal ideation. Other
features associated with an increased risk for death by suicide include being single, living alone,
social disconnectedness, early life adversity, availability of lethal methods such as a firearm,
sleep disturbance, cognitive and decision-making deficits, and having prominent feelings of
hopelessness. Women attempt suicide at a higher rate than men, while men are more likely to
complete suicide. The difference in suicide rate between men and women with depressive
disorders is smaller than in the population as a whole, however. Comorbidities, including
aggressive-impulsive traits, borderline personality disorder, substance use disorder, anxiety,
other medical conditions, and functional impairment, increase risk for future suicidal behavior.
Functional Consequences of Major Depressive Disorder
Many of the functional consequences of major depressive disorder derive from individual
symptoms. Impairment can be very mild, such that many of those who interact with the affected
individual are unaware of depressive symptoms. Impairment may, however, range to complete
incapacity such that the depressed individual is unable to attend to basic self-care needs or is
mute or catatonic. For individuals seen in general medical settings, those with major depressive
disorder have more pain and physical illness and greater decreases in physical, social, and role
functioning. Depressed women report greater functional impairment in their relationships than
men.
Differential Diagnosis
Major depressive episodes with prominent
irritable mood may be difficult to distinguish from manic episodes with irritable mood or with
mixed features. This distinction requires a careful clinical evaluation of the presence of sufficient
manic symptoms to meet threshold criteria (i.e., three if mood is manic, four if mood is irritable
but not manic).
Major 
depressive
episodes along with a history of a manic or hypomanic episode preclude the diagnosis of major
depressive disorder. Major depressive episodes with a history of hypomanic episodes and
without a history of manic episodes indicate a diagnosis of bipolar II disorder, whereas major
depressive episodes with a history of manic episodes (with or without hypomanic episodes)
indicate a diagnosis of bipolar I disorder. On the other hand, presentations of major depressive
episodes with a history of periods of hypomania that do not meet criteria for a hypomanic
episode may be diagnosed as either other specified bipolar and related disorder or major
depressive disorder depending on where the clinician judges the presentation to best fall. For
example, the presentation may be best considered other specified bipolar and related disorder
because of the clinical significance of the subthreshold hypomanic symptoms, or the presentation
may be best considered a case of major depressive disorder with some subthreshold hypomanic
symptoms in between episodes.
A diagnosis of depressive disorder due to
another medical condition requires the presence of an etiological medical condition. Major

Substance/medication-induced depressive disorder.
Persistent depressive disorder.
Premenstrual dysphoric disorder.
Disruptive mood dysregulation disorder.
Major 
depressive 
episodes 
superimposed 
on 
schizophrenia, 
delusional 
disorder,
schizophreniform disorder, or other specified or unspecified schizophrenia spectrum and other
psychotic disorder.
Schizoaffective disorder.
Attention-deficit/hyperactivity disorder.
Adjustment disorder with depressed mood.
depressive disorder is not diagnosed if the major depressive–like episodes are all attributable to
the direct pathophysiological consequence of a specific medical condition (e.g., multiple
sclerosis, stroke, hypothyroidism).
This disorder is distinguished from major
depressive disorder by the fact that a substance (e.g., a drug of abuse, a medication, a toxin)
appears to be etiologically related to the mood disturbance. For example, depressed mood that
occurs only in the context of withdrawal from cocaine would be diagnosed as cocaine-induced
depressive disorder.
Persistent depressive disorder is characterized by depressed mood,
more days than not, for at least 2 years. If criteria are met for both major depressive disorder and
persistent depressive disorder, both can be diagnosed.
Premenstrual dysphoric disorder is characterized by dysphoric
mood that is present in the final week before the onset of menses, that starts to improve within a
few days after the onset of menses, and that becomes minimal or absent in the week postmenses.
By contrast, the episodes of major depressive disorder are not temporally connected to the
menstrual cycle.
Disruptive mood dysregulation disorder is characterized by
severe, recurrent temper outbursts manifested verbally and/or behaviorally, accompanied by
persistent or labile mood, most of the day, nearly every day, in between the outbursts. In
contrast, in major depressive disorder, irritability is confined to the major depressive episodes.
Depressive 
symptoms 
may 
be 
present 
during 
schizophrenia, 
delusional 
disorder,
schizophreniform disorder, or other specified or unspecified schizophrenia spectrum and other
psychotic disorder. Most commonly, such depressive symptoms can be considered associated
features of these disorders and do not merit a
separate diagnosis. However, when the depressive symptoms meet full criteria for a major
depressive episode, a diagnosis of other specified depressive disorder may be made in addition to
the diagnosis of the psychotic disorder.
Schizoaffective disorder differs from major depressive disorder, with
psychotic features, by the requirement that in schizoaffective disorder, delusions or
hallucinations are present for at least 2 weeks in the absence of a major depressive episode.
Distractibility and low frustration tolerance can occur in
both attention-deficit/hyperactivity disorder (ADHD) and a major depressive episode; if the
criteria are met for both, ADHD may be diagnosed in addition to the mood disorder. However,
the clinician must be cautious not to overdiagnose a major depressive episode in children with
ADHD whose disturbance in mood is characterized by irritability rather than by sadness or loss
of interest.
A major depressive episode that occurs in response to a
psychosocial stressor is distinguished from adjustment disorder, with depressed mood, by the

Bereavement.
Sadness.
F34.1
fact that the full criteria for a major depressive episode are not met in adjustment disorder.
Bereavement is the experience of losing a loved one to death. It generally triggers
a grief response that may be intense and may involve many features that overlap with symptoms
characteristic of a major depressive episode, such as sadness, difficulty sleeping, and poor
concentration. Features that help differentiate a bereavement-related grief response from a major
depressive episode include the following: the predominant affects in grief are feelings of
emptiness and loss, whereas in a major depressive episode they are persistent depressed mood
and a diminished ability to experience pleasure. Moreover, the dysphoric mood of grief is likely
to decrease in intensity over days to weeks and occurs in waves that tend to be associated with
thoughts or reminders of the deceased, whereas the depressed mood in a major depressive
episode is more persistent and not tied to specific thoughts or preoccupations. It is important to
note that in a vulnerable individual (e.g., someone with a past history of major depressive
disorder), bereavement may trigger not only a grief response but also the development of an
episode of depression or the worsening of an existing episode.
Finally, periods of sadness are inherent aspects of the human experience. These
periods should not be diagnosed as a major depressive episode unless criteria are met for severity
(i.e., five out of nine symptoms), duration (i.e., most of the day, nearly every day for at least 2
weeks), and clinically significant distress or impairment. The diagnosis other specified
depressive disorder may be appropriate for presentations of depressed mood with clinically
significant impairment that do not meet criteria for duration or severity.
Comorbidity
Other disorders with which major depressive disorder frequently co-occurs are substance-related
disorders, panic disorder, generalized anxiety disorder, posttraumatic stress disorder, obsessivecompulsive disorder, anorexia nervosa, bulimia nervosa, and borderline personality disorder.
While women are more likely than men to report comorbid anxiety disorders, bulimia
nervosa, and somatoform disorder (somatic symptom and related disorders), men are more likely
to report comorbid alcohol and substance abuse.
Persistent Depressive Disorder
Diagnostic Criteria
This disorder represents a consolidation of DSM-IV-defined chronic major
depressive disorder and dysthymic disorder.
A. Depressed mood for most of the day, for more days than not, as indicated by
either subjective account or observation by others, for at least 2 years.
Note: In children and adolescents, mood can be irritable and duration must be at
least 1 year.
B. Presence, while depressed, of two (or more) of the following:

1. Poor appetite or overeating.
2. Insomnia or hypersomnia.
3. Low energy or fatigue.
4. Low self-esteem.
5. Poor concentration or difficulty making decisions.
6. Feelings of hopelessness.
C. During the 2-year period (1 year for children or adolescents) of the disturbance,
the individual has never been without the symptoms in Criteria A and B for more
than 2 months at a time.
D. Criteria for a major depressive disorder may be continuously present for 2 years.
E. There has never been a manic episode or a hypomanic episode.
F. The disturbance is not better explained by a persistent schizoaffective disorder,
schizophrenia, 
delusional 
disorder, 
or 
other 
specified 
or 
unspecified
schizophrenia spectrum and other psychotic disorder.
G. The symptoms are not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication) or another medical condition (e.g.,
hypothyroidism).
H. The symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Note: If criteria are sufficient for a diagnosis of a major depressive episode at any
time during the 2-year period of depressed mood, then a separate diagnosis of major
depression should be made in addition to the diagnosis of persistent depressive
disorder along with the relevant specifier (e.g., with intermittent major depressive
episodes, with current episode).
Specify if:
With anxious distress (pp. 210–211)
With atypical features (p. 212)
Specify if:
In partial remission (p. 214)
In full remission (p. 214)
Specify if:
Early onset: If onset is before age 21 years.
Late onset: If onset is at age 21 years or older.
Specify if (for most recent 2 years of persistent depressive disorder):
With pure dysthymic syndrome: Full criteria for a major depressive episode
have not been met in at least the preceding 2 years.
With persistent major depressive episode: Full criteria for a major depressive
episode have been met throughout the preceding 2-year period.

With intermittent major depressive episodes, with current episode: Full
criteria for a major depressive episode are currently met, but there have been
periods of at least 8 weeks in at least the preceding 2 years with symptoms
below the threshold for a full major depressive episode.
With intermittent major depressive episodes, without current episode: Full
criteria for a major depressive episode are not currently met, but there has been
one or more major depressive episodes in at least the preceding 2 years.
Specify current severity:
Mild (p. 214)
Moderate (p. 214)
Severe (p. 214)
Diagnostic Features
The essential feature of persistent depressive disorder is a depressed mood that occurs for most
of the day, for more days than not, for at least 2 years, or at least 1 year for children and
adolescents (Criterion A). This disorder represents a consolidation of DSM-IV-defined chronic
major depressive disorder and dysthymic disorder. Major depression may precede persistent
depressive disorder, and major depressive episodes may occur during persistent depressive
disorder. Individuals whose symptoms meet major depressive disorder criteria for 2 years should
be given a diagnosis of persistent depressive disorder as well as major depressive disorder.
Individuals with persistent depressive disorder describe their mood as sad or “down in the
dumps.” During periods of depressed mood, at least two of the six symptoms from Criterion B
are present. Because these symptoms have become a part of the individual’s day-to-day
experience, particularly in the case of early onset (e.g., “I’ve always been this way”), they may
not be reported unless the individual is directly prompted. During the 2-year period (1 year for
children or adolescents), any symptom-free intervals that have occurred have lasted no longer
than 2 months (Criterion C).
Prevalence
Persistent depressive disorder is effectively an amalgam of DSM-IV dysthymic disorder and
chronic major depressive episode. The 12-month prevalence in the United States is
approximately 0.5% for dysthymic disorder and 1.5% for chronic major depressive disorder,
with prevalence among women approximately 1.5 and 2 times higher than prevalence among
men for each of these diagnoses, respectively. Based on studies using comparable ascertainment
procedures, the lifetime and 12-month estimates of DSM-IV dysthymia may be higher in highincome than in low- and middle-income countries. However, the disorder is associated with
elevated risk of suicidal outcomes and comparable levels of disability wherever it occurs.
Development and Course
Persistent depressive disorder often has an early and insidious onset (i.e., in childhood,
adolescence, or early adult life) and, by definition, a chronic course. Borderline personality
disorder is a particularly robust risk factor for persistent depressive disorder. When persistent

Temperamental.
Environmental.
Genetic and physiological.
depressive disorder and borderline personality disorder coexist, the covariance of the
corresponding features over time suggests the operation of a common mechanism. Early onset
(i.e., before age 21 years) is associated with a higher likelihood of comorbid personality
disorders and substance use disorders.
When symptoms rise to the level of a major depressive episode, they are likely to
subsequently revert to a lower level. However, depressive symptoms are much less likely to
resolve fully in a given period of time in the context of persistent depressive disorder than they
are in a nonchronic major depressive episode.
Risk and Prognostic Factors
Factors predictive of poorer long-term outcome include higher levels of negative
affectivity (neuroticism), greater symptom severity, poorer global functioning, and presence of
anxiety disorders or conduct disorder.
Childhood risk factors include parental loss or separation and childhood
adversity.
There are no clear differences in illness development, course, or family
history between DSM-IV dysthymic disorder and chronic major depressive disorder. Earlier
findings pertaining to either disorder are therefore likely to apply to persistent depressive
disorder. It is thus likely that individuals with persistent depressive disorder will have a higher
proportion of first-degree relatives with persistent depressive disorder than do individuals with
nonchronic major depressive disorder, and more depressive disorders in general.
A number of brain regions (e.g., prefrontal cortex, anterior cingulate, amygdala,
hippocampus) 
have 
been 
implicated 
in 
persistent 
depressive 
disorder. 
Possible
polysomnographic abnormalities exist as well.
Culture-Related Diagnostic Issues
The perceived abnormality or tolerance of chronic depressive symptoms may vary across
cultures, affecting symptom detection and treatment acceptability. For example, some social
groups or age cohorts may consider long-standing depressive symptoms to be normal reactions
to adversity.
Association With Suicidal Thoughts or Behavior
Persistent depressive disorder is associated with elevated risk of suicidal outcomes and
comparable levels of disability, whether the disorder occurs in high-, middle-, or low-income
countries.
Functional Consequences of Persistent Depressive Disorder
The degree to which persistent depressive disorder impacts social and occupational functioning
is likely to vary widely, but effects can be as great as or greater than those of major depressive
disorder.

Major depressive disorder.
Other specified depressive disorder.
Bipolar I and bipolar II disorders.
Cyclothymic disorder.
Differential Diagnosis
If there is a depressed mood for more days than not plus two or more
persistent depressive disorder Criterion B symptoms for 2 years or more, then the diagnosis of
persistent depressive disorder is made. If the symptom criteria are sufficient for a diagnosis of a
major depressive episode at any time during this period, then the additional diagnosis of major
depression should be made. The comorbid presence of major depressive episodes during this
period should also be noted by assigning the appropriate course specifier to the persistent
depressive disorder diagnosis as follows: If the individual’s symptoms currently meet full criteria
for a major depressive episode, and there have been periods of at least 8 weeks in at least the
preceding 2 years with symptoms below the threshold for a full major depressive episode, then
the specifier “with intermittent major depressive episodes, with current episode” would be
assigned. If full criteria for a major depressive episode are not currently met but there has been
one or more major depressive episodes in at least the preceding 2 years, then the specifier “with
intermittent major depressive episodes, without current episode” is assigned. If a major
depressive episode
has persisted for at least a 2-year duration and remains present, then the specifier “with persistent
major depressive episode” is used. If the individual has not experienced an episode of major
depression in the last 2 years, then the specifier “with pure dysthymic syndrome” is used.
Because the criteria for a major depressive episode include
symptoms (i.e., markedly diminished interest or pleasure in activities; psychomotor agitation or
retardation; recurrent thoughts of death, suicidal ideation, suicide attempt or plan) that are absent
from the symptom list for persistent depressive disorder (i.e., depressed mood and two out of six
Criterion B symptoms), a very limited number of individuals will have depressive symptoms that
have persisted longer than 2 years but that do not meet criteria for persistent depressive disorder.
If full criteria for a major depressive episode have been met at some point during the current
episode of illness, a diagnosis of major depressive disorder would apply. Otherwise, a diagnosis
of other specified depressive disorder or unspecified depressive disorder should be given.
A history of a manic or hypomanic episode precludes the
diagnosis of persistent depressive disorder. A history of manic episodes (with or without
hypomanic episodes) indicates a diagnosis of bipolar I disorder. A history of hypomanic episodes
(without any history of manic episodes in individuals with persistent depressive presentations
during which criteria have been met for a major depressive episode) warrants a diagnosis of
bipolar II disorder. Other specified bipolar disorder applies to individuals whose presentations
include a history of hypomanic episodes along with persistent depressive presentation that has
never met full criteria for a major depressive episode.
A diagnosis of cyclothymic disorder precludes the diagnosis of persistent
depressive disorder. Thus, if during the period lasting at least 2 years of depressed mood for most
of the day, for more days than not, 1) there are numerous periods with hypomanic symptoms that
do not meet criteria for a hypomanic episode, 2) there have not been any symptom-free periods
of more than 2 months at a time, and 3) criteria have never been met for a major depressive,
manic, or hypomanic episode, then the diag-nosis would be cyclothymic disorder instead of

Psychotic disorders.
Depressive or bipolar and related disorder due to another medical condition.
Substance/medication-induced depressive or bipolar and related disorder.
Personality disorders.
F32.81
persistent depressive disorder.
Depressive symptoms are a common associated feature of chronic psychotic
disorders (e.g., schizoaffective disorder, schizophrenia, delusional disorder). A separate
diagnosis of persistent depressive disorder is not made if the symptoms occur only during the
course of the psychotic disorder (including residual phases).
Persistent 
depressive
disorder must be distinguished from a depressive or bipolar and related disorder due to another
medical condition. The diagnosis is depressive or bipolar and related disorder due to another
medical condition if the mood disturbance is judged, based on history, physical examination, or
laboratory findings, to be attributable to the direct pathophysiological effects of a specific,
usually chronic, medical condition (e.g., multiple sclerosis). If it is judged that the depressive
symptoms are not attributable to the physiological effects of another medical condition, then the
primary mental disorder (e.g., persistent depressive disorder) is recorded, and the medical
condition is noted as a concomitant medical condition (e.g., diabetes mellitus).
A 
substance/medicationinduced depressive or bipolar and related disorder is distinguished from persistent depressive
disorder when a substance (e.g., a drug of abuse, a medication, a toxin) is judged to be
etiologically related to the mood disturbance.
A personality disorder is characterized by an enduring pattern of inner
experience and behavior that deviates markedly from the expectations of the
individual’s culture, with onset by adolescence or early adulthood. Personality disorders
commonly co-occur with persistent depressive disorder. If criteria are met for persistent
depressive disorder and a personality disorder, both may be diagnosed.
Comorbidity
In comparison to individuals with major depressive disorder, those with persistent depressive
disorder are at higher risk for psychiatric comorbidity in general, and for anxiety disorders,
substance use disorders, and personality disorders in particular. Early-onset persistent depressive
disorder is strongly associated with DSM-5 Cluster B and C personality disorders.
Premenstrual Dysphoric Disorder
Diagnostic Criteria
A. In the majority of menstrual cycles, at least five symptoms must be present in the
final week before the onset of menses, start to improve within a few days after
the onset of menses, and become minimal or absent in the week postmenses.
B. One (or more) of the following symptoms must be present:

1. Marked affective lability (e.g., mood swings; feeling suddenly sad or tearful, or
increased sensitivity to rejection).
2. Marked irritability or anger or increased interpersonal conflicts.
3. Marked depressed mood, feelings of hopelessness, or self-deprecating
thoughts.
4. Marked anxiety, tension, and/or feelings of being keyed up or on edge.
C. One (or more) of the following symptoms must additionally be present, to reach a
total of five symptoms when combined with symptoms from Criterion B above.
1. Decreased interest in usual activities (e.g., work, school, friends, hobbies).
2. Subjective difficulty in concentration.
3. Lethargy, easy fatigability, or marked lack of energy.
4. Marked change in appetite; overeating; or specific food cravings.
5. Hypersomnia or insomnia.
6. A sense of being overwhelmed or out of control.
7. Physical symptoms such as breast tenderness or swelling, joint or muscle
pain, a sensation of “bloating,” or weight gain.
Note: The symptoms in Criteria A–C must have been met for most menstrual
cycles that occurred in the preceding year.
D. The symptoms cause clinically significant distress or interference with work,
school, usual social activities, or relationships with others (e.g., avoidance of
social activities; decreased productivity and efficiency at work, school, or home).
E. The disturbance is not merely an exacerbation of the symptoms of another
disorder, such as major depressive disorder, panic disorder, persistent
depressive disorder, or a personality disorder (although it may co-occur with any
of these disorders).
F. Criterion A should be confirmed by prospective daily ratings during at least two
symptomatic cycles. (Note: The diagnosis may be made provisionally prior to
this confirmation.)
G. The symptoms are not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication, other treatment) or another medical
condition (e.g., hyperthyroidism).
Recording Procedures
If symptoms have not been confirmed by prospective daily ratings of at least two symptomatic
cycles, “provisional” should be noted after the name of the diagnosis (i.e., “premenstrual
dysphoric disorder, provisional”).
Diagnostic Features

The essential features of premenstrual dysphoric disorder are the expression of mood lability,
irritability, dysphoria, and anxiety symptoms that occur repeatedly during the premenstrual phase
of the cycle and remit around the onset of menses or shortly thereafter. These symptoms may be
accompanied by behavioral and physical symptoms. Symptoms must have occurred in most of
the menstrual cycles during the past year and must have an adverse effect on work or social
functioning. The intensity and/or expressivity of the accompanying symptoms may be closely
related to social and cultural background characteristics as well as religious beliefs, social
tolerance, attitude toward the female reproductive cycle, and female gender role issues more
generally.
Typically, symptoms peak around the time of the onset of menses. Although it is not
uncommon for symptoms to linger into the first few days of menses, the individual must have a
symptom-free period in the follicular phase after the menstrual period begins. While the core
symptoms include mood and anxiety symptoms, behavioral and somatic symptoms commonly
also occur. However, the presence of somatic and/or behavioral symptoms in the absence of
mood and/or anxious symptoms is not sufficient for a diagnosis. Symptoms are of comparable
severity (but not duration) to those of other mental disorders, such as a major depressive episode
or generalized anxiety disorder. In order to confirm a provisional diagnosis, daily prospective
symptom ratings are required for at least two symptomatic cycles.
Symptoms must cause clinically significant distress and/or an obvious and marked
impairment in the ability to function socially or occupationally in the week prior to menses.
Associated Features
Delusions and hallucinations have been described in the late luteal phase of the menstrual cycle
but are rare.
Prevalence
The 12-month prevalence of premenstrual dysphoric disorder in the community has been
estimated at 5.8% based on a large study from Germany. Another study that looked at prevalence
over two menstrual cycles found 1.3% of menstruating women with the disorder in the United
States. Estimates based on retrospective reports are often higher than those based on prospective
daily ratings. Yet, estimates based on a daily record of symptoms for 1–2 months may not be
fully representative, because those with the most severe symptoms may be unable to sustain the
rating process. The most rigorous estimate of premenstrual dysphoric disorder prevalence in the
United States using prospective ratings of two consecutive menstrual cycles was 1.3% for
women whose symptoms met diagnostic criteria, who experienced functional impairment, and
had no co-occurring mental disorder. The prevalence of premenstrual dysphoric disorder
symptoms in adolescent girls may be higher than that observed in adult women.
Development and Course
Onset of premenstrual dysphoric disorder can occur at any point after menarche. Incidence of
new cases over a 40-month follow-up period in Germany is 2.5% (95% confidence interval =
1.7–3.7). Symptoms cease after menopause, although cyclical hormone replacement can trigger
the re-expression of symptoms.

Environmental.
Genetic and physiological.
Premenstrual syndrome.
Risk and Prognostic Factors
Environmental factors associated with the expression of premenstrual dysphoric
disorder include stress, history of interpersonal trauma, seasonal changes, and sociocultural
aspects of female sexual behavior in general, and female gender roles in particular.
No studies have examined heritability in premenstrual dysphoric
disorder specifically. Estimates for heritability of premenstrual dysphoric symptoms range
between 30% and 80%, although it remains unclear whether the symptoms themselves are
heritable or whether they are simply associated with other heritable factors or traits.
Culture-Related Diagnostic Issues
Premenstrual dysphoric disorder has been observed in individuals in the United States, Europe,
India, Nigeria, Brazil, and Asia, with a broad prevalence range. Nevertheless, as with most
mental disorders, frequency, intensity, and expressivity of symptoms; perceived consequences;
help-seeking patterns; and management may be significantly influenced by social and cultural
factors, such as a history of sexual abuse or domestic violence, limited social support, and
cultural variations in attitudes toward menstruation.
Diagnostic Markers
As indicated earlier, the diagnosis of premenstrual dysphoric disorder is appropriately confirmed
by 2 months of prospective symptom ratings. A number of scales, including the Daily Rating of
Severity of Problems and the Visual Analogue Scales for Premenstrual Mood Symptoms, have
undergone validation and are commonly used in clinical trials for premenstrual dysphoric
disorder. The Premenstrual Tension Syndrome Rating Scale has a self-report and an observer
version, both of which have been validated and used widely to measure illness severity in women
who have premenstrual dysphoric disorder.
Association With Suicidal Thoughts or Behavior
The premenstrual phase has been considered by some to be a risk period for suicide.
Functional Consequences of Premenstrual Dysphoric Disorder
Impairment in social functioning may be manifested by discord in the intimate partner
relationship and problems with children, other family members, or friends that occur only in
association with the premenstrual dysphoric disorder (i.e., as opposed to chronic interpersonal
problems). Impairments in work and health-related quality of life are also prominent. There is
evidence that premenstrual dysphoric disorder can be associated with impairments in function
and health-related quality of life that are on par with those observed in major depressive disorder
and persistent depressive disorder.
Differential Diagnosis
Premenstrual syndrome differs from premenstrual dysphoric disorder in

Dysmenorrhea.
Bipolar disorder, major depressive disorder, and persistent depressive disorder.
Use of hormonal treatments.
Other medical conditions.
that premenstrual syndrome does not require a minimum of five symptoms nor mood-related
symptomatology, and it is generally considered to be less severe than premenstrual dysphoric
disorder. Premenstrual syndrome may be more common than premenstrual dysphoric disorder;
its estimated prevalence varies with numbers that hover at about 20%. While premenstrual
syndrome shares the feature of symptom expression during the premenstrual phase of the
menstrual cycle, the presence of somatic or
behavioral symptoms, without the required affective symptoms, likely meets criteria for
premenstrual syndrome and not for premenstrual dysphoric disorder.
Dysmenorrhea is a syndrome of painful menses, but this is distinct from a
syndrome characterized by affective changes. Moreover, symptoms of dysmenorrhea begin with
the onset of menses, whereas symptoms of premenstrual dysphoric disorder, by definition, begin
before the onset of menses, even if they linger into the first few days of menses.
Many 
women 
with
(either naturally occurring or substance/medication-induced) bipolar or major depressive disorder
or persistent depressive disorder believe that they have premenstrual dysphoric disorder.
However, when they chart symptoms, they realize that the symptoms do not follow a
premenstrual pattern. Because the onset of menses constitutes a memorable event, they may
report that symptoms occur only during the premenstruum or that symptoms worsen
premenstrually. This is one of the rationales for the requirement that symptoms be confirmed by
daily prospective ratings. The process of differential diagnosis, particularly if the clinician relies
on retrospective symptoms only, is made more difficult because of the overlap between
symptoms of premenstrual dysphoric disorder and some other diagnoses. The overlap of
symptoms is particularly salient for differentiating premenstrual dysphoric disorder from major
depressive episodes, persistent depressive disorder, bipolar disorders, and borderline personality
disorder.
Some women who present with moderate to severe premenstrual
symptoms may be using hormonal treatments, including hormonal contraceptives. If such
symptoms occur after initiation of exogenous hormone use, the symptoms may be attributable to
the use of hormones rather than to the underlying condition of premenstrual dysphoric disorder.
If the woman stops hormones and the symptoms disappear, then this is consistent with
substance/medication-induced depressive disorder.
Women with chronic medical conditions may experience symptoms of
premenstrual dysphoria. As with any depressive disorder, medical conditions that could better
account for the symptoms should be ruled out, such as thyroid deficiency and anemia.
Comorbidity
A major depressive episode is the most frequently reported previous disorder in individuals
presenting with premenstrual dysphoric disorder. A wide range of medical conditions (e.g.,
migraine, asthma, allergies, seizure disorders) or other mental disorders (e.g., depressive and
bipolar disorders, anxiety disorders, bulimia nervosa, substance use disorders) may worsen in the

premenstrual phase; however, the absence of a symptom-free period during the postmenstrual
interval obviates a diagnosis of premenstrual dysphoric disorder. These conditions are better
considered premenstrual exacerbation of a current mental disorder or medical condition.
Although the diagnosis of premenstrual dysphoric disorder should not be assigned in situations
in which an individual experiences only a premenstrual exacerbation of another mental or
physical disorder, it can be considered in addition to the diagnosis of another mental disorder or
medical condition if the individual experiences symptoms and changes in level of functioning
that are characteristic of premenstrual dysphoric disorder and markedly different from the
symptoms experienced as part of the ongoing disorder.
Substance/Medication-Induced Depressive Disorder
Diagnostic Criteria
A. A prominent and persistent disturbance in mood that predominates in the clinical
picture and is characterized by depressed mood or markedly diminished interest
or pleasure in all, or almost all, activities.
B. There is evidence from the history, physical examination, or laboratory findings
of both (1) and (2):
1. The symptoms in Criterion A developed during or soon after substance
intoxication or withdrawal or after exposure to or withdrawal from a
medication.
2. The involved substance/medication is capable of producing the symptoms in
Criterion A.
C. The disturbance is not better explained by a depressive disorder that is not
substance/medication-induced. Such evidence of an independent depressive
disorder could include the following:
The symptoms preceded the onset of the substance/medication use; the
symptoms persist for a substantial period of time (e.g., about 1 month) after the
cessation of acute withdrawal or severe intoxication; or there is other evidence
suggesting the existence of an independent non-substance/medication-induced
depressive disorder (e.g., a history of recurrent non-substance/medicationrelated episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Note: This diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the symptoms in Criterion A
predominate in the clinical picture and when they are sufficiently severe to warrant

clinical attention.
Coding note: The ICD-10-CM codes for the [specific substance/medication]-induced
depressive disorders are indicated in the table below. Note that the ICD-10-CM code
depends on whether or not there is a comorbid substance use disorder present for
the same class of substance. In any case, an additional separate diagnosis of a
substance use disorder is not given. If a mild substance use disorder is comorbid
with the substance-induced depressive disorder, the 4th position character is “1,”
and the clinician should record “mild [substance] use disorder” before the substanceinduced depressive disorder (e.g., “mild cocaine use disorder with cocaine-induced
depressive disorder”). If a moderate or severe substance use disorder is comorbid
with the substance-induced depressive disorder, the 4th position character is “2,”
and the clinician should record “moderate [substance] use disorder” or “severe
[substance] use disorder,” depending on the severity of the comorbid substance use
disorder. If there is no comorbid substance use disorder (e.g., after a one-time heavy
use of the substance), then the 4th position character is “9,” and the clinician should
record only the substance-induced depressive disorder.
ICD-10-CM
With mild use
disorder
With moderate or
severe use
disorder
Without use
disorder
Alcohol
F10.14
F10.24
F10.94
Phencyclidine
F16.14
F16.24
F16.94
Other hallucinogen
F16.14
F16.24
F16.94
Inhalant
F18.14
F18.24
F18.94
Opioid
F11.14
F11.24
F11.94
Sedative, hypnotic, or anxiolytic
F13.14
F13.24
F13.94
Amphetamine-type substance (or other
stimulant)
F15.14
F15.24
F15.94
Cocaine
F14.14
F14.24
F14.94
Other (or unknown) substance
F19.14
F19.24
F19.94
Specify (see Table 1 in the chapter “Substance-Related and Addictive Disorders,”
which indicates whether “with onset during intoxication” and/or “with onset during
withdrawal” applies to a given substance class; or specify “with onset after
medication use”):
With onset during intoxication: If criteria are met for intoxication with the
substance and the symptoms develop during intoxication.
With onset during withdrawal: If criteria are met for withdrawal from the
substance and the symptoms develop during, or shortly after, withdrawal.
With onset after medication use: If symptoms developed at initiation of
medication, with a change in use of medication, or during withdrawal of

medication.
Recording Procedures
The name of the substance/medication-induced depressive disorder begins with the specific
substance (e.g., cocaine, dexamethasone) that is presumed to be causing the depressive
symptoms. The diagnostic code is selected from the table included in the criteria set, which is
based on the drug class and presence or absence of a comorbid substance use disorder. For
substances that do not fit into any of the classes (e.g., dexamethasone), the code for “other (or
unknown) substance” should be used; and in cases in which a substance is judged to be an
etiological factor but the specific class of substance is unknown, the same code should also be
used.
When recording the name of the disorder, the comorbid substance use disorder (if any) is
listed first, followed by the word “with,” followed by the name of the substance-induced
depressive disorder, followed by the specification of onset (i.e., onset during intoxication, onset
during withdrawal). For example, in the case of depressive symptoms occurring during
withdrawal in a man with a severe cocaine use disorder, the diagnosis is F14.24 severe cocaine
use disorder with cocaine-induced depressive disorder, with onset during withdrawal. A separate
diagnosis of the comorbid severe cocaine use disorder is not given. If the substance-induced
depressive disorder occurs without a comorbid substance use disorder (e.g., after a one-time
heavy use of the substance), no accompanying substance use disorder is noted (e.g., F16.94
phencyclidine-induced depressive disorder, with onset during intoxication). When more than one
substance is judged to play a significant role in the development of depressive
mood symptoms, each should be listed separately (e.g., F15.24 severe methylphenidate use
disorder with methylphenidate-induced depressive disorder, with onset during withdrawal;
F19.94 dexamethasone-induced depressive disorder, with onset during intoxication).
Diagnostic Features
The essential feature of substance/medication-induced depressive disorder is a prominent and
persistent disturbance in mood that predominates in the clinical picture and is characterized by
depressed mood or markedly diminished interest or pleasure in all, or almost all, activities
(Criterion A) that is due to the direct physiological effects of a substance (e.g., a drug of abuse, a
medication, or a toxin exposure) (Criterion B). In order to meet criteria for the diagnosis, the
depressive symptoms must have developed during or soon after substance intoxication or
withdrawal or after exposure to or withdrawal from a medication, as evidenced by clinical
history, physical examination, or laboratory findings (Criterion B1), and the involved
substance/medication must be capable of producing the depressive symptoms (Criterion B2). In
addition, the depressed symptoms are not better explained by a non-substance/medicationinduced depressive disorder.
Evidence of an independent depressive disorder includes the observation that the depressive
symptoms preceded the onset of substance/medication use, the depressive symptoms persist
beyond a substantial period of time after the cessation of acute withdrawal or severe intoxication,

or there is other evidence that suggests the existence of an independent nonsubstance/medication-induced depressive disorder (Criterion C), such as a history of recurrent
non-substance-induced depressive episodes. This diagnosis should not be made when symptoms
occur exclusively during the course of a delirium (Criterion D). Finally, the diagnosis requires
that the substance/medication-induced depressive symptoms cause clinically significant distress
or impairment in social, occupational, or other important areas of functioning (Criterion E). The
substance-induced depressive disorder diagnosis should be made instead of a diagnosis of
substance intoxication or substance withdrawal only when the symptoms in Criterion A
predominate in the clinical picture and are sufficiently severe to warrant independent clinical
attention.
The two categories of drugs of abuse most likely to cause a substance/medication-induced
depressive disorder are depressants (e.g., intoxication with alcohol, benzodiazepines and other
sedative, hypnotic, or anxiolytic drugs) and stimulants (e.g., withdrawal from amphetamine-type
substances and cocaine). Some medications (e.g., steroids; antihypertensive medications such as
clonidine, guanethidine, methyldopoa, and reserpine; interferon; L-dopa) are especially likely to
cause 
substance/medication-induced 
depressive 
syndromes. 
Substances 
implicated 
in
medication-induced depressive disorder, with varying degrees of evidence, include antibiotics,
antiviral agents (efavirenz), cardiovascular agents (beta-blockers and calcium channel blockers,
retinoic acid derivatives (isotretinoin), antidepressants, anticonvulsants, antimigraine agents
(triptans), antipsychotics, hormonal agents (corticosteroids, oral contraceptives, gonadotropinreleasing hormone agonists, tamoxifen), chemotherapeutic drugs, and smoking cessation agents
(varenicline). This list is likely to grow as new compounds are synthesized.
Clear clinical histories and careful judgment are essential in determining whether the
substance of abuse or medication is truly associated with induced depressive symptoms or
whether the symptoms are better understood as constituting an independent depressive disorder.
A diagnosis of a substance/medication-induced depressive disorder is most likely if the
individual was taking high doses of a relevant drug of abuse or medication and there is no past
history of independent depressive episodes. For example, a depressive episode that developed in
the context of heavy use of a relevant substance of abuse or within the first several weeks of
beginning alpha-methyldopa (an antihypertensive agent) in an individual with no history of
major depressive disorder would qualify for the diagnosis of a substance- or medication-induced
depressive disorder. In some cases, a previously established condition (e.g., major depressive
disorder, recurrent) can recur while the individual is
coincidentally taking a drug or medication that has the capacity to cause depressive
symptoms (e.g., alcohol and/or stimulants in context of heavy use, L-dopa, oral contraceptives).
In all of these cases, the clinician must make a judgment as to whether the medication is
causative in this particular situation.
A substance/medication-induced depressive disorder is distinguished from an independent
depressive disorder by the onset or course, or by other factors associated with the substance or
medication use. There must be evidence from the history, physical examination, or laboratory
findings of use of a drug of abuse or a medication that is capable of producing depressive
symptoms after exposure to, withdrawal from, or intoxication with that substance prior to the

onset of the depressive disorder. The neurochemical changes associated with intoxication and
withdrawal states for some substances can be relatively protracted, and thus intense depressive
symptoms can last for a longer period after the cessation of substance use and still be consistent
with a diagnosis of a substance/medication-induced depressive disorder.
Prevalence
The lifetime rate of alcohol- and stimulant-induced depressive episodes has been reported to be
40% or higher among individuals with relevant substance use disorders. However, in a nationally
representative U.S. adult population, the lifetime prevalence of substance/medication-induced
depressive disorder in the absence of a lifetime history of non-substance-induced depressive
disorder was only 0.26%. These data indicate that special care must be taken to search for and
address substance-induced conditions in individuals with alcohol and stimulant use disorders.
Development and Course
A depressive disorder associated with the use of substances (e.g., alcohol, amphetamine-type
substances and/or cocaine, or a prescribed treatment for medical conditions) must have its onset
while the individual is using the substance or during withdrawal, if there is a withdrawal
syndrome associated with the substance. Most often, the depressive disorder has its onset within
the first few weeks or 1 month of heavy use of the substance. Once the substance is discontinued,
the depressive symptoms usually remit within days to several weeks, depending on the half-life
of the substance/medication and the presence of a withdrawal syndrome. If symptoms persist 4
weeks beyond the expected time course of withdrawal of a particular substance/medication, other
causes for the depressive mood symptoms should be considered.
There are several prospective controlled trials examining the association of depressive
symptoms with use of a prescribed medication, but most reports on this topic involve
retrospective series of individuals entering treatment, or participants in large cross-sectional
studies. More studies exist regarding the clinical course of alcohol- and illicit drug–induced
depressions, and most support the contention that the substance-induced conditions are very
likely to fade away within a relatively short time after abstinence. Equally important are
indications that individuals with significant residual depressive symptoms following treatment
for substance use disorders have a greater likelihood of relapse into their substance use.
Risk and Prognostic Factors
Risk factors for substance-induced depressive disorder include a history of antisocial personality
disorder, schizophrenia, and bipolar disorder; a history of stressful life events in the past 12
months; a history of prior drug-induced depressions; and a family history of substance use
disorders. In addition, neurochemical changes associated with alcohol and other drugs of abuse
often contribute to depressive and anxiety symptoms during withdrawal that subsequently
influence ongoing substance use and reduce the likelihood of remission of substance use
disorders. The course of substance-induced depressive disorder may be worsened by socialstructural adversity associated with poverty, racism, and marginalization.

Substance intoxication and withdrawal.
Independent depressive disorder.
Depressive disorder due to another medical condition.
Sex- and Gender-Related Diagnostic Issues
Among individuals with a substance use disorder, the risk for developing a substance-induced
depressive disorder appears to be similar in men and women.
Diagnostic Markers
Laboratory assays of the suspected substance in the blood or urine are of limited value in
identifying substance-induced depressive disorder because blood and urine levels are often
negative when an individual comes for evaluation, reflecting the fact that substance-induced
depressions can last for up to 4 weeks after use of the drug of abuse or medication has ceased.
Therefore, a positive test value only means that an individual has had recent experience with a
substance but by itself does not establish a time course or other characteristics that are likely to
be associated with substance-induced depressive disorder. However, as is true of most mental
disorders, the most important data in diagnosing these conditions come from a detailed clinical
history and the mental status examination.
Association With Suicidal Thoughts or Behavior
The risk of suicide attempts is higher among individuals with possible alcohol use disorder
experiencing depressive episodes, whether substance induced or independent of substances, as
compared with control subjects.
Differential Diagnosis
Depressive symptoms occur commonly in substance
intoxication and substance withdrawal. A diagnosis of substance-induced depressive disorder
should be made instead of a diagnosis of substance intoxication or substance withdrawal when
the mood symptoms are sufficiently severe to warrant independent clinical attention. For
example, dysphoric mood is a characteristic feature of cocaine withdrawal. Substance-induced
depressive disorder with onset during withdrawal should be diagnosed instead of cocaine
withdrawal only if the mood disturbance in Criterion A predominates in the clinical picture and
is sufficiently severe to be a separate focus of attention and treatment.
A 
substance/medication-induced 
depressive 
disorder 
is
distinguished from an independent depressive disorder by the fact that even though a substance is
taken in high enough amounts to be possibly etiologically related to the symptoms, if the
depressive syndrome is observed at times other than when the substance or medication is being
used, it should be diagnosed as an independent depressive disorder.
Because individuals with medical conditions
often take medications for those conditions, the clinician must consider the possibility that the
mood symptoms are caused by the physiological consequences of the medical condition rather
than the medication, in which case depressive disorder due to another medical condition is
diagnosed. The history often provides the primary basis for such a judgment. At times, a change
in the treatment for the medical condition (e.g., medication substitution or discontinuation) may
be needed to determine empirically whether the medication is the causative agent. If the clinician
has ascertained that the disturbance is a function of both another medical condition and substance
use or withdrawal, then both diagnoses (i.e., depressive disorder due to another medical

condition and substance/medication-induced depressive disorder) may be given. When there is
insufficient evidence to determine whether the depressive symptoms are associated with
substance (including a medication) ingestion or withdrawal or with another medical condition or
are independent (i.e., not a function of either a substance or another medical condition), a
diagnosis of other specified depressive disorder or unspecified depressive disorder is indicated.
Comorbidity
In one study using DSM-IV, comparing individuals with independent major depressive disorder
and no comorbid substance use disorder and individuals with substance/medication-induced
depressive disorder, those with substance/medication-induced depressive disorder had higher
rates of comorbidity with any DSM-IV mental disorder; were more likely to have specific
disorders of tobacco use disorder, gambling disorder, and antisocial personality disorder; and
were less likely to have persistent depressive disorder. Compared with individuals with major
depressive 
disorder 
and 
a 
comorbid 
substance 
use 
disorder, 
individuals 
with
substance/medication-induced depressive disorder are more likely to have alcohol or other
substance use disorder; however, they are less likely to have persistent depressive disorder.
Depressive Disorder Due to Another Medical Condition
Diagnostic Criteria
A. A prominent and persistent disturbance in mood that predominates in the clinical
picture and is characterized by depressed mood or markedly diminished interest
or pleasure in all, or almost all, activities.
B. There is evidence from the history, physical examination, or laboratory findings
that the disturbance is the direct pathophysiological consequence of another
medical condition.
C. The disturbance is not better explained by another mental disorder (e.g.,
adjustment disorder, with depressed mood, in which the stressor is a serious
medical condition).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Coding note: The ICD-10-CM code depends on the specifier (see below).
Specify if:
F06.31 With depressive features: Full criteria are not met for a major
depressive episode.
F06.32 With major depressive–like episode: Full criteria are met (except
Criterion C) for a major depressive episode.

F06.34 With mixed features: Symptoms of mania or hypomania are also
present but do not predominate in the clinical picture.
Coding note: Include the name of the other medical condition in the name of the
mental disorder (e.g., F06.31 depressive disorder due to hypothyroidism, with
depressive features). The other medical condition should also be coded and listed
separately immediately before the depressive disorder due to the medical condition
(e.g., E03.9 hypothyroidism; F06.31 depressive disorder due to hypothyroidism,
with depressive features).
Diagnostic Features
The essential feature of depressive disorder due to another medical condition is a prominent and
persistent period of depressed mood or markedly diminished interest or pleasure in all, or almost
all, activities that predominates in the clinical picture (Criterion A) and that is thought to be due
to the physiological effects of another medical condition (Criterion B). In determining whether
the mood disturbance is due to another medical condition, the clinician must first establish the
presence of another medical condition. Further, the clinician must establish that the mood
disturbance is etiologically related to another medical condition through a physiological
mechanism. A careful and comprehensive assessment of multiple factors is necessary to make
this judgment. Although there are no infallible guidelines for determining whether the
relationship between the mood disturbance and another medical condition is etiological, several
considerations provide some guidance in this area. One consideration is the presence of a
temporal association between the onset, exacerbation, or remission of another medical condition
and that of the mood disturbance. A second consideration is the presence of features that are
atypical of independent depressive disorders (e.g., atypical age at onset or course or absence of
family history). Evidence from the literature that suggests that there can be a direct association
between another medical condition in question and the development of mood symptoms can
provide a useful context in the assessment of a particular situation.
Associated Features
Etiology (i.e., a causal relationship to another medical condition based on best clinical evidence)
is the key variable in depressive disorder due to another medical condition. The listing of the
medical conditions that are said to be able to induce major depression is never complete, and the
clinician’s best judgment is the essence of this diagnosis.
There are clear associations, as well as some neuroanatomical correlates, of depression with
cerebrovascular accident (CVA), Huntington’s disease, Parkinson’s disease, and traumatic brain
injury (TBI). Among the neuroendocrine conditions most closely associated with depression are
Cushing’s syndrome and hypothyroidism. Autoimmune disorders, such systemic lupus
erythematosus, and deficiencies of certain vitamins, such as vitamin B12, have also been linked
to depression. There are numerous other conditions thought to be associated with depression,
such as multiple sclerosis. However, the literature’s support for a causal association is greater

with some conditions than with others. Currently, there is support for a direct pathophysiological
mechanism for depressive symptoms in focal lesions (CVA, TBI, neoplasm) affecting certain
brain regions, Parkinson’s disease, Huntington’s disease, hypothyroidism, Cushing’s syndrome,
and pancreatic cancer.
Prevalence
Sex differences in prevalence depend somewhat on the sex difference associated with the
medical condition (e.g., systemic lupus erythematosus is more common in women; stroke is
somewhat more common in middle-age men compared with women).
Development and Course
Following stroke, the onset of depression appears to be acute, occurring within a few days of the
CVA in the largest case series. However, in some cases, onset of the depression is weeks to
months following the CVA. In the largest series, the duration of the major depressive episode
following stroke was 9–11 months on average. With Parkinson’s disease and Huntington’s
disease, depression often precedes the major motor impairments and cognitive impairments
associated with each condition. This is more prominently the case for Huntington’s disease, in
which depression is considered to be the first neuropsychiatric symptom. There is some
observational evidence that depression is less common as the neurocognitive disorder due to
Huntington’s disease progresses. In some individuals with static brain injuries and other central
nervous system diseases, mood symptoms may be episodic (i.e., recurring) over the course of the
disorder. In Cushing’s syndrome and hypothyroidism, depression can be an early manifestation
of the disease. In pancreatic cancer, depression often precedes other features.
Risk and Prognostic Factors
The risk of acute onset of a major depressive disorder following a CVA (within 1 day to a week
of the event) appears to be strongly correlated with lesion location, with greatest risk associated
with left frontal strokes and least risk apparently associated with right frontal lesions
in those individuals who present within days of the stroke. The association with frontal regions
and laterality is not observed in depressive states that occur in the 2–6 months following stroke,
perhaps indicative of later depressive symptoms representing major depressive disorder,
adjustment disorder, or demoralization. In individuals with Parkinson’s disease, early age at
onset, greater burden of motor symptoms, and longer duration of the disease have been
associated with depression. Risk of depression after TBI has been associated with female gender,
prior depressive disorder, early psychiatric symptoms following injury, lower brain volume, and
unemployment.
Sex- and Gender-Related Diagnostic Issues
Women may be at differentially higher risk for developing depression in the setting of
cardiovascular disease, particularly poststroke.

Depressive disorders not due to another medical condition.
Medication-induced depressive disorder.
Delirium and major or mild neurocognitive disorder.
Adjustment disorders.
Diagnostic Markers
Diagnostic markers pertain to those associated with the medical condition (e.g., steroid levels in
blood or urine to help corroborate the diagnosis of Cushing’s disease, which can be associated
with manic or depressive syndromes).
Association With Suicidal Thoughts or Behavior
There are no epidemiological studies that provide evidence to differentiate the risk of suicide
from a major depressive episode due to another medical condition compared with the risk from a
major depressive episode in general. There are case reports of suicides in association with major
depressive episodes associated with another medical condition. There is a clear association
between serious medical illnesses and suicide, particularly shortly after onset or diagnosis of the
illness. Thus, it would be prudent to assume that the risk of suicide for major depressive episodes
associated with medical conditions is not less than that for other forms of major depressive
episode, and might even be greater.
Differential Diagnosis
Determination of whether a medical
condition accompanying a depressive disorder is causing the disorder depends on a) the absence
of an episode(s) of depressive episodes prior to the onset of the medical condition, b) the
probability that the associated medical condition has a potential to promote or cause a depressive
disorder, and c) a course of the depressive symptoms shortly after the onset or worsening of the
medical condition, especially if the depressive symptoms remit near the time that the medical
disorder is effectively treated or remits.
An important caveat is that some medical conditions are
treated with medications (e.g., steroids or alpha-interferon) that can induce depressive or manic
symptoms. In these cases, clinical judgment, based on all the evidence in hand, is the best way to
try to separate the most likely and/or the most important of two etiological factors (i.e.,
association with the medical condition vs. a substance-induced syndrome).
A separate diagnosis of depressive disorder due
to another medical condition is not given if the depressive disturbance occurs exclusively during
the course of a delirium. However, a diagnosis of depressive disorder due to another medical
condition may be given in addition to a diagnosis of major or mild neurocognitive disorder if the
depressive disturbance is judged to be a physiological consequence of the pathological process
causing the neurocognitive disorder and if symptoms of depression are a prominent part of the
clinical presentation.
It is important to differentiate a depressive episode from an adjustment
disorder, as the onset of the medical condition is in itself a life stressor that could
bring on either an adjustment disorder or an episode of major depression. The major
differentiating elements are the pervasiveness of the depressive picture and the number and
quality of the depressive symptoms that the individual reports or demonstrates on the mental

Demoralization.
status examination. The differential diagnosis of the associated medical conditions is relevant but
largely beyond the scope of the present manual.
Demoralization is a common reaction to chronic medical illness. It is marked by
a sense of subjective incompetence, helplessness, and hopelessness, and a desire to give up. It is
often accompanied by depressive symptoms such as low mood and fatigue. Demoralization
typically lacks the anhedonia associated with depressive disorder due to another medical
condition, and individuals will generally find pleasure in previously meaningful activities and be
able to experience moments of happiness.
Comorbidity
Conditions comorbid with depressive disorder due to another medical condition are those
associated with the medical conditions of etiological relevance. It has been noted that delirium
can occur before or along with depressive symptoms in individuals with a variety of medical
conditions, such as Cushing’s disease. The association of anxiety symptoms, usually generalized
symptoms, is common in depressive disorders, regardless of cause.
Other Specified Depressive Disorder
F32.89
This category applies to presentations in which symptoms characteristic of a
depressive disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the depressive disorders diagnostic class
and do not meet criteria for adjustment disorder with depressed mood or adjustment
disorder with mixed anxiety and depressed mood. The other specified depressive
disorder category is used in situations in which the clinician chooses to communicate
the specific reason that the presentation does not meet the criteria for any specific
depressive disorder. This is done by recording “other specified depressive disorder”
followed by the specific reason (e.g., “short-duration depressive episode”).
Examples of presentations that can be specified using the “other specified”
designation include the following:
1. Recurrent brief depression: Concurrent presence of depressed mood and at
least four other symptoms of depression for 2–13 days at least once per month
(not associated with the menstrual cycle) for at least 12 consecutive months in
an individual whose presentation has never met criteria for any other depressive
or bipolar disorder and does not currently meet active or residual criteria for any
psychotic disorder.
2. Short-duration depressive episode (4–13 days): Depressed affect and at least
four of the other eight symptoms of a major depressive episode associated with
clinically significant distress or impairment that persists for more than 4 days, but
less than 14 days, in an individual whose presentation has never met criteria for
any other depressive or bipolar disorder, does not currently meet active or

residual criteria for any psychotic disorder, and does not meet criteria for
recurrent brief depression.
3. Depressive episode with insufficient symptoms: Depressed affect and at
least one of the other eight symptoms of a major depressive episode associated
with clinically significant distress or impairment that persist for at least 2 weeks in
an individual whose presentation has never met criteria for any other depressive
or bipolar disorder, does not currently meet active or residual criteria for any
psychotic disorder, and does not meet criteria for mixed anxiety and depressive
disorder symptoms.
4. Major depressive episode superimposed on schizophrenia, schizophreniform
disorder, delusional disorder, or other specified and unspecified schizophrenia
spectrum and other psychotic disorder. Note: Major depressive episodes that are
part of schizoaffective disorder do not merit an additional diagnosis of other
specified depressive disorder.
Unspecified Depressive Disorder
F32.A
This category applies to presentations in which symptoms characteristic of a
depressive disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the depressive disorders diagnostic class
and do not meet criteria for adjustment disorder with depressed mood or adjustment
disorder with mixed anxiety and depressed mood. The unspecified depressive
disorder category is used in situations in which the clinician chooses not to specify
the reason that the criteria are not met for a specific depressive disorder, and
includes presentations for which there is insufficient information to make a more
specific diagnosis (e.g., in emergency room settings).
Unspecified Mood Disorder
F39
This category applies to presentations in which symptoms characteristic of a mood
disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not at the
time of the evaluation meet the full criteria for any of the disorders in either the
bipolar or the depressive disorders diagnostic classes and in which it is difficult to

choose between unspecified bipolar and related disorder and unspecified depressive
disorder (e.g., acute agitation).
Specifiers for Depressive Disorders
Specify if:
With anxious distress: Anxious distress is defined as the presence of at least
two of the following symptoms during the majority of days of the current major
depressive episode (or the most recent major depressive episode if major
depressive disorder is currently in partial or full remission) or current persistent
depressive disorder:
1. Feeling keyed up or tense.
2. Feeling unusually restless.
3. Difficulty concentrating because of worry.
4. Fear that something awful may happen.
5. Feeling that the individual might lose control of himself or herself.
Specify current severity:
Mild: Two symptoms.
Moderate: Three symptoms.
Moderate-severe: Four or five symptoms.
Severe: Four or five symptoms and with motor agitation.
Note: Anxious distress has been noted as a prominent feature of both bipolar
and major depressive disorder in both primary care and specialty mental
health
settings. High levels of anxiety have been associated with higher suicide risk,
longer duration of illness, and greater likelihood of treatment nonresponse. As
a result, it is clinically useful to specify accurately the presence and severity
levels of anxious distress for treatment planning and monitoring of response to
treatment.
With mixed features:
A. At least three of the following manic/hypomanic symptoms are present during
the majority of days of the current major depressive episode (or the most
recent major depressive episode if major depressive disorder is currently in
partial or full remission):
1. Elevated, expansive mood.
2. Inflated self-esteem or grandiosity.
3. More talkative than usual or pressure to keep talking.

4. Flight of ideas or subjective experience that thoughts are racing.
5. Increase in energy or goal-directed activity (either socially, at work or
school, or sexually).
6. Increased or excessive involvement in activities that have a high potential
for painful consequences (e.g., engaging in unrestrained buying sprees,
sexual indiscretions, or foolish business investments).
7. Decreased need for sleep (feeling rested despite sleeping less than usual;
to be contrasted with insomnia).
B. Mixed symptoms are observable by others and represent a change from the
person’s usual behavior.
C. For individuals whose symptoms meet full criteria for either mania or
hypomania, the diagnosis should be bipolar I or bipolar II disorder.
D. The mixed symptoms are not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication or other treatment).
Note: Mixed features associated with a major depressive episode have been
found to be a significant risk factor for the development of bipolar I or bipolar II
disorder. As a result, it is clinically useful to note the presence of this specifier
for treatment planning and monitoring of response to treatment.
With melancholic features:
A. One of the following is present during the most severe period of the current
major depressive episode (or the most recent major depressive episode if
major depressive disorder is currently in partial or full remission):
1. Loss of pleasure in all, or almost all, activities.
2. Lack of reactivity to usually pleasurable stimuli (does not feel much better,
even temporarily, when something good happens).
B. Three (or more) of the following:
1. A distinct quality of depressed mood characterized by profound
despondency, despair, and/or moroseness or by so-called empty mood.
2. Depression that is regularly worse in the morning.
3. Early-morning awakening (i.e., at least 2 hours before usual awakening).
4. Marked psychomotor agitation or retardation.
5. Significant anorexia or weight loss.
6. Excessive or inappropriate guilt.
Note: The specifier “with melancholic features” is applied if these features are
present at the most severe stage of the episode. There is a near-complete
absence of the
capacity for pleasure, not merely a diminution. A guideline for evaluating the lack

of reactivity of mood is that even highly desired events are not associated with
marked brightening of mood. Either mood does not brighten at all, or it brightens
only partially (e.g., up to 20%–40% of normal for only minutes at a time). The
“distinct quality” of mood that is characteristic of the “with melancholic features”
specifier is experienced as qualitatively different from that during a
nonmelancholic depressive episode. A depressed mood that is described as
merely more severe, longer lasting, or present without a reason is not considered
distinct in quality. Psychomotor changes are nearly always present and are
observable by others.
 Melancholic features exhibit only a modest tendency to repeat across episodes
in the same individual. They are more frequent in inpatients, as opposed to
outpatients; are less likely to occur in milder than in more severe major
depressive episodes; and are more likely to occur in individuals with psychotic
features.
With atypical features: This specifier is applied when these features
predominate during the majority of days of the current major depressive episode
(or the most recent major depressive episode if major depressive disorder is
currently in partial or full remission) or current persistent depressive disorder.
A. Mood reactivity (i.e., mood brightens in response to actual or potential positive
events).
B. Two (or more) of the following:
1. Significant weight gain or increase in appetite.
2. Hypersomnia.
3. Leaden paralysis (i.e., heavy, leaden feelings in arms or legs).
4. A long-standing pattern of interpersonal rejection sensitivity (not limited to
episodes of mood disturbance) that results in significant social or
occupational impairment.
C. Criteria are not met for “with melancholic features” or “with catatonia” during
the same episode.
Note: “Atypical depression” has historical significance (i.e., atypical in
contradistinction to the more classical agitated, “endogenous” presentations of
depression that were the norm when depression was rarely diagnosed in
outpatients and almost never in adolescents or younger adults) and today does
not connote an uncommon or unusual clinical presentation as the term might
imply.
 Mood reactivity is the capacity to be cheered up when presented with positive
events (e.g., a visit from children, compliments from others). Mood may become
euthymic (not sad) even for extended periods of time if the external
circumstances remain favorable. Increased appetite may be manifested by an
obvious increase in food intake or by weight gain. Hypersomnia may include
either an extended period of nighttime sleep or daytime napping that totals at
least 10 hours of sleep per day (or at least 2 hours more than when not

depressed). Leaden paralysis is defined as feeling heavy, leaden, or weighted
down, usually in the arms or legs. This sensation is generally present for at least
an hour a day but often lasts for many hours at a time. Unlike the other atypical
features, pathological sensitivity to perceived interpersonal rejection is a trait that
has an early onset and persists throughout most of adult life. Rejection sensitivity
occurs when the person is and is not depressed, though it may be exacerbated
during depressive periods.
With psychotic features: Delusions and/or hallucinations are present at any
time in the current major depressive episode (or the most recent major
depressive episode if major depressive disorder is currently in partial or full
remission). If psychotic features are present, specify if mood-congruent or moodincongruent:
With mood-congruent psychotic features: The content of all delusions and
hallucinations is consistent with the typical depressive themes of personal
inadequacy, guilt, disease, death, nihilism, or deserved punishment.
With mood-incongruent psychotic features: The content of the delusions or
hallucinations does not involve typical depressive themes of personal
inadequacy, guilt, disease, death, nihilism, or deserved punishment, or the
content is a mixture of mood-incongruent and mood-congruent themes.
With catatonia: This specifier is applied to the current major depressive episode
(or the most recent major depressive episode if major depressive disorder is
currently in partial or full remission) if catatonic features are present during most
of the episode. See criteria for catatonia associated with a mental disorder in the
chapter “Schizophrenia Spectrum and Other Psychotic Disorders.”
With peripartum onset: This specifier is applied to the current major depressive
episode (or the most recent major depressive episode if major depressive
disorder is currently in partial or full remission) if onset of mood symptoms
occurs during pregnancy or in the 4 weeks following delivery.
Note: Mood episodes can have their onset either during pregnancy or
postpartum. About 50% of postpartum major depressive episodes begin prior
to delivery. Thus, these episodes are referred to collectively as peripartum
episodes.
 Between conception and birth, about 9% of women will experience a major
depressive episode. The best estimate for prevalence of a major depressive
episode between birth and 12 months postpartum is just below 7%.
 Peripartum-onset mood episodes can present either with or without
psychotic features. Infanticide (a rare occurrence) is most often associated
with postpartum psychotic episodes that are characterized by command
hallucinations to kill the infant or delusions that the infant is possessed, but
psychotic symptoms can also occur in severe postpartum mood episodes

without such specific delusions or hallucinations.
 Postpartum mood (major depressive or manic) episodes with psychotic
features appear to occur in from 1 in 500 to 1 in 1,000 deliveries and may be
more common in primiparous women. The risk of postpartum episodes with
psychotic features is particularly increased for women with prior postpartum
psychotic mood episodes but is also elevated for those with a prior history of a
depressive or bipolar disorder (especially bipolar I disorder) and those with a
family history of bipolar disorders.
 Once a woman has had a postpartum episode with psychotic features, the
risk of recurrence with each subsequent delivery is between 30% and 50%.
Postpartum episodes must be differentiated from delirium occurring in the
postpartum period, which is distinguished by a fluctuating level of awareness
or attention.
 Peripartum-onset depressive disorders must be distinguished from the much
more common “maternity blues,” or what is known in lay terms as “baby
blues.” Maternity blues is not considered to be a mental disorder and is
characterized by sudden changes in mood (e.g., the sudden onset of
tearfulness in the absence of depression) that do not cause functional
impairment and that are likely caused by physiological changes occurring after
delivery. It is temporary and self-limited, typically improving quickly (within a
week) without the need for treatment. Other symptoms of maternity blues
include sleep disturbance and even confusion that can occur shortly after
delivery.
 Perinatal women may be at higher risk for depressive disorders due to
thyroid abnormalities as well as other medical conditions that can cause
depressive symptoms. If the depressive symptoms are judged to be due to
another medical condition related to the perinatal period, depressive disorder
due to another medical condition should be diagnosed instead of a major
depressive episode, with peripartum onset.
With seasonal pattern: This specifier applies to recurrent major depressive
disorder.
A. There has been a regular temporal relationship between the onset of major
depressive episodes in major depressive disorder and a particular time of the
year (e.g., in the fall or winter).
Note: Do not include cases in which there is an obvious effect of seasonally
related psychosocial stressors (e.g., regularly being unemployed every
winter).
B. Full remissions also occur at a characteristic time of the year (e.g., depression
disappears in the spring).
C. In the last 2 years, two major depressive episodes have occurred that

demonstrate the temporal seasonal relationships defined above and no
nonseasonal major depressive episodes have occurred during that same
period.
D. Seasonal major depressive episodes (as described above) substantially
outnumber the nonseasonal major depressive episodes that may have
occurred over the individual’s lifetime.
Note: The specifier “with seasonal pattern” can apply to the pattern of major
depressive episodes in major depressive disorder, recurrent. The essential
feature is the onset and remission of major depressive episodes at characteristic
times of the year. In most cases, the episodes begin in fall or winter and remit in
spring. Less commonly, there may be recurrent summer depressive episodes.
This pattern of onset and remission of episodes must have occurred during at
least a 2-year period, without any nonseasonal episodes occurring during this
period. In addition, the seasonal depressive episodes must substantially
outnumber any nonseasonal depressive episodes over the individual’s lifetime.
 This specifier does not apply to those situations in which the pattern is better
explained by seasonally linked psychosocial stressors (e.g., seasonal
unemployment or school schedule). Major depressive episodes that occur in a
seasonal pattern are often characterized by loss of energy, hypersomnia,
overeating, weight gain, and a craving for carbohydrates.
 The prevalence of winter-type seasonal pattern appears to vary with latitude,
age, and sex. Prevalence increases with higher latitudes. Age is also a strong
predictor of seasonality, with younger persons at higher risk for winter depressive
episodes.
Specify if:
In partial remission: Symptoms of the immediately previous major depressive
episode are present but full criteria are not met, or there is a period lasting less
than 2 months without any significant symptoms of a major depressive episode
following the end of such an episode.
In full remission: During the past 2 months, no significant signs or symptoms of
the disturbance were present.
Specify current severity:
Severity is based on the number of criterion symptoms, the severity of those
symptoms, and the degree of functional disability.
Mild: Few, if any, symptoms in excess of those required to make the diagnosis
are present, the intensity of the symptoms is distressing but manageable, and
the symptoms result in minor impairment in social or occupational functioning.
Moderate: The number of symptoms, intensity of symptoms, and/or functional
impairment are between those specified for “mild” and “severe.”
Severe: The number of symptoms is substantially in excess of that required to
make the diagnosis, the intensity of the symptoms is seriously distressing and
unmanageable, and the symptoms markedly interfere with social and

occupational functioning.
1In distinguishing grief from a major depressive episode (MDE), it is useful to consider that in grief the predominant affect is
feelings of emptiness and loss, while in an MDE it is persistent depressed mood and the inability to anticipate happiness or
pleasure. The dysphoria in grief is likely to decrease in intensity over days to weeks and occurs in waves, the so-called pangs of
grief. These waves tend to be associated with thoughts or reminders of the deceased. The depressed mood of an MDE is more
persistent and not tied to specific thoughts or preoccupations. The pain of grief may be accompanied by positive emotions and
humor that are uncharacteristic of the pervasive unhappiness and misery characteristic of an MDE. The thought content
associated with grief generally features a preoccupation with thoughts and memories of the deceased, rather than the self-critical
or pessimistic ruminations seen in an MDE. In grief, self-esteem is generally preserved, whereas in an MDE feelings of
worthlessness and self-loathing are common. If self-derogatory ideation is present in grief, it typically involves perceived failings
vis-à-vis the deceased (e.g., not visiting frequently enough, not telling the deceased how much he or she was loved). If a bereaved
individual thinks about death and dying, such thoughts are generally focused on the deceased and possibly about “joining” the
deceased, whereas in an MDE such thoughts are focused on ending one’s own life because of feeling worthless, undeserving of
life, or unable to cope with the pain of depression.

# 05 - Anxiety Disorders

# Anxiety Disorders

215

Anxiety Disorders
Anxiety disorders include disorders that share features of excessive fear and anxiety and
related behavioral disturbances. Fear is the emotional response to real or perceived imminent
threat, whereas anxiety is anticipation of future threat. Obviously, these two states overlap, but
they also differ, with fear more often associated with surges of autonomic arousal necessary for
fight or flight, thoughts of immediate danger, and escape behaviors, and anxiety more often
associated with muscle tension and vigilance in preparation for future danger and cautious or
avoidant behaviors. Sometimes the level of fear or anxiety is reduced by pervasive avoidance
behaviors. Panic attacks feature prominently within the anxiety disorders as a particular type of
fear response. Panic attacks are not limited to anxiety disorders but rather can be seen in other
mental disorders as well.
The anxiety disorders differ from one another in the types of objects or situations that induce
fear, anxiety, or avoidance behavior, and the associated cognition. Thus, while the anxiety
disorders tend to be highly comorbid with each other, they can be differentiated by close
examination of the types of situations that are feared or avoided and the content of the associated
thoughts or beliefs.
Anxiety disorders differ from developmentally normative fear or anxiety by being excessive
or persisting beyond developmentally appropriate periods. They differ from transient fear or
anxiety, often stress-induced, by being persistent (e.g., typically lasting 6 months or more),
although the criterion for duration is intended as a general guide with allowance for some degree
of flexibility and is sometimes of shorter duration in children (as in separation anxiety disorder
and selective mutism). Since individuals with anxiety disorders typically overestimate the danger
in situations they fear or avoid, the primary determination of whether the fear or anxiety is
excessive or out of proportion is made by the clinician, taking cultural contextual factors into
account. Many of the anxiety disorders develop in childhood and tend to persist if not treated.
Most occur more frequently in girls than in boys (approximately 2:1 ratio). Each anxiety disorder
is diagnosed only when the symptoms are not attributable to the physiological effects of a
substance/medication or to another medical condition or are not better explained by another
mental disorder.
The chapter is arranged developmentally, with disorders sequenced according to the typical
age at onset. The individual with separation anxiety disorder is fearful or anxious about
separation from attachment figures to a degree that is developmentally inappropriate. There is
persistent fear or anxiety about harm coming to attachment figures and events that could lead to
loss of or separation from attachment figures and reluctance to go away from attachment figures,
as well as nightmares and physical symptoms of distress. Although the symptoms often develop
in childhood, they can be expressed throughout adulthood as well in the absence of a history of
childhood separation anxiety disorder.
Selective mutism is characterized by a consistent failure to speak in social situations in which

there is an expectation to speak (e.g., school) even though the individual speaks in other
situations. The failure to speak has significant consequences on achievement in academic or
occupational settings or otherwise interferes with normal social communication.
Individuals with specific phobia are fearful or anxious about or avoidant of circumscribed
objects or situations. A specific cognition is not featured in this disorder, as it is in other anxiety
disorders. The fear, anxiety, or avoidance is almost always immediately induced by the phobic
situation, to a degree that is persistent and out of proportion to the actual risk posed. There are
various types of specific phobias: animal; natural environment; blood-injection-injury;
situational; and other situations.
In social anxiety disorder, the individual is fearful or anxious about or avoidant of social
interactions and situations that involve the possibility of being scrutinized. These include social
interactions such as meeting unfamiliar people, situations in which the individual may be
observed eating or drinking, and situations in which the individual performs in front of others.
The cognition is of being negatively evaluated by others, by being embarrassed, humiliated, or
rejected, or offending others.
In panic disorder, the individual experiences recurrent unexpected panic attacks and is
persistently concerned or worried about having more panic attacks or changes his or her behavior
in maladaptive ways because of the panic attacks (e.g., avoidance of exercise or of unfamiliar
locations). Panic attacks are abrupt surges of intense fear or intense discomfort that reach a peak
within minutes, accompanied by physical and/or cognitive symptoms. Limited-symptom panic
attacks include fewer than four symptoms. Panic attacks may be expected, such as in response to
a typically feared object or situation, or unexpected, meaning that the panic attack occurs for no
apparent reason. Panic attacks function as a marker and prognostic factor for severity of
diagnosis, course, and comorbidity across an array of disorders, including, but not limited to,
anxiety, substance use, depressive, and psychotic disorders. The specifier “with panic attacks”
may therefore be used for panic attacks that occur in the context of any anxiety disorder, as well
as other mental disorders (e.g., depressive disorders, posttraumatic stress disorder).
Individuals with agoraphobia are fearful and anxious in many different situations, and the
diagnostic criteria require symptoms in two or more of the following: using public transportation,
being in open spaces, being in enclosed places, standing in line or being in a crowd, or being
outside of the home alone in other situations. The individual fears these situations because of
thoughts that escape might be difficult or help might not be available in the event of developing
panic-like symptoms or other incapacitating or embarrassing symptoms. These situations
consistently induce fear or anxiety and are often avoided or require the presence of a companion.
The key features of generalized anxiety disorder are persistent and excessive anxiety and
worry about various domains, including work and school performance, that the individual finds
difficult to control. In addition, the individual experiences physical symptoms, including
restlessness or feeling keyed up or on edge; being easily fatigued; difficulty concentrating or
mind going blank; irritability; muscle tension; and sleep disturbance.
Substance/medication-induced anxiety disorder involves anxiety due to substance
intoxication or withdrawal or to a medication treatment. In anxiety disorder due to another
medical condition, anxiety symptoms are the physiological consequence of another medical

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condition.
Disorder-specific scales are available to better characterize the severity of each anxiety
disorder and to capture change in severity over time. For ease of use, particularly for individuals
with more than one anxiety disorder, these scales have been developed to have the same format
(but different focus) across the anxiety disorders, with ratings of behavioral symptoms, cognitive
symptoms, and physical symptoms relevant to each disorder.
Individuals with anxiety may be more likely to have suicidal thoughts, attempt suicide, and
die by suicide than those without anxiety. Panic disorder, generalized anxiety disorder, and
specific phobia have been identified as the anxiety disorders most strongly associated with a
transition from suicidal thoughts to suicide attempt.
Separation Anxiety Disorder
Diagnostic Criteria
A. Developmentally inappropriate and excessive fear or anxiety concerning
separation from those to whom the individual is attached, as evidenced by at
least three of the following:
1. Recurrent excessive distress when anticipating or experiencing separation
from home or from major attachment figures.
2. Persistent and excessive worry about losing major attachment figures or
about possible harm to them, such as illness, injury, disasters, or death.
3. Persistent and excessive worry about experiencing an untoward event (e.g.,
getting lost, being kidnapped, having an accident, becoming ill) that causes
separation from a major attachment figure.
4. Persistent reluctance or refusal to go out, away from home, to school, to
work, or elsewhere because of fear of separation.
5. Persistent and excessive fear of or reluctance about being alone or without
major attachment figures at home or in other settings.
6. Persistent reluctance or refusal to sleep away from home or to go to sleep
without being near a major attachment figure.
7. Repeated nightmares involving the theme of separation.
8. Repeated complaints of physical symptoms (e.g., headaches, stomachaches,
nausea, vomiting) when separation from major attachment figures occurs or
is anticipated.
B. The fear, anxiety, or avoidance is persistent, lasting at least 4 weeks in children
and adolescents and typically 6 months or more in adults.
C. The disturbance causes clinically significant distress or impairment in social,
academic, occupational, or other important areas of functioning.

D. The disturbance is not better explained by another mental disorder, such as
refusing to leave home because of excessive resistance to change in autism
spectrum disorder; delusions or hallucinations concerning separation in
psychotic disorders; refusal to go outside without a trusted companion in
agoraphobia; worries about ill health or other harm befalling significant others in
generalized anxiety disorder; or concerns about having an illness in illness
anxiety disorder.
Diagnostic Features
The essential feature of separation anxiety disorder is excessive fear or anxiety concerning
separation from home or attachment figures. The anxiety exceeds what may be expected given
the individual’s developmental level (Criterion A). Individuals with separation anxiety disorder
have symptoms that meet at least three of the following criteria: They experience recurrent
excessive distress when separation from home or major attachment figures is anticipated or
occurs (Criterion A1). They worry about the well-being or death of attachment figures,
particularly when separated from them, and they need to know the whereabouts of their
attachment figures and want to stay in touch with them (Criterion A2). They also worry about
untoward events to themselves, such as getting lost, being kidnapped, or having an accident, that
would keep them from ever being reunited with their major attachment figure (Criterion A3).
Individuals with separation anxiety disorder are reluctant or refuse to go out by themselves
because of separation fears (Criterion A4). They have
persistent and excessive fear or reluctance about being alone or without major attachment figures
at home or in other settings. Children with separation anxiety disorder may be unable to stay or
go in a room by themselves and may display “clinging” behavior, staying close to or
“shadowing” the parent around the house, or requiring someone to be with them when going to
another room in the house (Criterion A5). They have persistent reluctance or refusal to go to
sleep without being near a major attachment figure or to sleep away from home (Criterion A6).
Children with this disorder often have difficulty at bedtime and may insist that someone stay
with them until they fall asleep. During the night, they may make their way to their parents’ bed
(or that of a significant other, such as a sibling). Children may be reluctant or refuse to attend
camp, to sleep at friends’ homes, or to go on errands. Adults may be uncomfortable when
traveling independently (e.g., sleeping in a hotel room away from home or attachment figures).
There may be repeated nightmares in which the content expresses the individual’s separation
anxiety (e.g., destruction of the family through fire, murder, or other catastrophe) (Criterion A7).
Physical symptoms (e.g., headaches, abdominal complaints, nausea, vomiting) are common in
children when separation from major attachment figures occurs or is anticipated (Criterion A8).
Cardiovascular symptoms such as palpitations, dizziness, and feeling faint are rare in younger
children but may occur in adolescents and adults.
The disturbance must last for a period of at least 4 weeks in children and adolescents younger
than 18 years and is typically 6 months or longer in adults (Criterion B). However, the duration
criterion for adults should be used as a general guide, with allowance for some degree of

flexibility. The disturbance must cause clinically significant distress or impairment in social,
academic, occupational, or other important areas of functioning (Criterion C).
Associated Features
When separated from major attachment figures, children and adults with separation anxiety
disorder may exhibit social withdrawal, apathy, sadness, or difficulty concentrating on work or
play. Depending on their age, individuals may have fears of animals, monsters, the dark,
muggers, burglars, kidnappers, car accidents, plane travel, and other situations that are perceived
as presenting danger to the family or themselves. Some individuals become homesick and
extremely uncomfortable when away from home. Separation anxiety disorder in children may
lead to school refusal, which in turn may lead to academic difficulties and social isolation. When
extremely upset at the prospect of separation, children may show anger or occasionally
aggression toward someone who is forcing separation. When alone, especially in the evening or
the dark, young children may report unusual perceptual experiences (e.g., seeing people peering
into their room, frightening creatures reaching for them, feeling eyes staring at them). Children
with this disorder may be described as demanding, intrusive, and in need of constant attention,
and, as adults, may appear dependent and overprotective as parents. Adults with the disorder are
likely to text or phone their major attachment figures throughout the day and repeatedly check on
their whereabouts. The individual’s excessive demands often become a source of frustration for
family members, leading to resentment and conflict within the family.
Prevalence
The 6- to 12-month prevalence of separation anxiety disorder in children is estimated to be
approximately 4%. In a community sample of toddlers, separation anxiety disorder appears to be
equally represented among girls and boys; however, school-age girls appear to have higher
prevalence rates than school-age boys. In adolescents in the United States, the 12-month
prevalence is 1.6%. Separation anxiety disorder decreases in prevalence from childhood through
adolescence and adulthood. In clinical samples of children, the disorder is equally common in
boys and girls in contrast to community samples, where the
disorder is more frequent in girls. Reports from children tend to yield higher rates of separation
anxiety disorder than parent reports of the child’s symptoms.
For adults, the 12-month prevalence of separation anxiety disorder in the United States
ranges from 0.9% to 1.9%. Among adults with separation anxiety disorder, women tend to have
higher prevalence rates of the disorder in both clinical and community studies. Across 18
countries, the mean 12-month prevalence in adults is 1.0%, with a range of < 0.1% to 2.7% (e.g.,
0.3% in Romania, 2.7% in Colombia). A higher prevalence was observed in women compared
with men in this total sample (1.3% compared with 0.8%).
Development and Course
Periods of heightened separation anxiety from attachment figures are part of normal early
development and may indicate the development of secure attachment relationships (e.g., around

Environmental.
Genetic and physiological.
age 1 year, when infants may experience stranger anxiety). Onset of separation anxiety disorder
may be as early as preschool age and may occur at any time during childhood and in
adolescence. Across 18 countries, median age at onset reported by adults (age 18 years and
older) with the disorder is in late adolescence in high- and upper-middle-income countries and in
the mid-20’s in low- and lower-middle-income countries. Most adults report a fluctuating course
of the disorder over their lifetime, and they may report some symptoms in childhood.
Typically there are periods of exacerbation and remission. In some cases, both the anxiety
about possible separation and the avoidance of situations involving separation from the home or
nuclear family (e.g., going away to college, moving away from attachment figures) may persist
through adulthood. However, the majority of children with separation anxiety disorder are free of
impairing anxiety disorders over their lifetimes.
The manifestations of separation anxiety disorder vary with age. Younger children are more
reluctant to go to school or may avoid school altogether. Younger children may not express
worries or specific fears of definite threats to parents, home, or themselves, and the anxiety is
manifested only when separation is experienced. As children age, worries emerge; these are often
worries about specific dangers (e.g., accidents, kidnapping, mugging, death) or vague concerns
about not being reunited with attachment figures. In adults, separation anxiety disorder may limit
their ability to cope with changes in circumstances (e.g., moving, getting married). Adults with
the disorder are typically overconcerned about their offspring, spouses, parents, and pets and
experience marked discomfort when separated from them. They may also experience significant
disruption in work or social experiences because of needing to continuously check on the
whereabouts of a significant other.
Risk and Prognostic Factors
Separation anxiety disorder often develops after life stress, especially a loss (e.g.,
the death of a relative or pet; an illness of the individual or a relative; a change of schools;
parental divorce; a move to a new neighborhood; immigration; a disaster that involved periods of
separation from attachment figures). Being bullied during childhood has been shown to be a risk
factor for the development of separation anxiety disorder. In young adults, other examples of life
stress include leaving the parental home, entering into a romantic relationship, and becoming a
parent. A history of parental overprotection and intrusiveness may be associated with separation
anxiety disorder in both childhood and adulthood.
There is evidence that separation anxiety disorder may be heritable.
Heritability was estimated at 73% in a community sample of 6-year-old twins, with higher rates
found in girls. Children with separation anxiety disorder display particularly enhanced sensitivity
to respiratory stimulation using CO2-enriched air. Separation anxiety disorder also appears to
aggregate in families.
Culture-Related Diagnostic Issues
There are cultural variations in the degree to which it is considered desirable to tolerate
separation, so that demands and opportunities for separation between parents and children are
avoided in some cultural contexts. For example, there is wide variation across countries and

Generalized anxiety disorder.
Panic disorder.
Agoraphobia.
cultural contexts with respect to the age at which it is expected that offspring should leave the
parental home. Youth vary in their self-reports of separation anxiety symptoms; for instance,
Taiwanese youth endorse higher symptoms of separation anxiety compared with U.S. youth. It is
important to differentiate separation anxiety disorder from the high value some cultural
communities place on strong interdependence among family members.
Association With Suicidal Thoughts or Behavior
Separation anxiety disorder in children and adolescents may be associated with an increased risk
for suicide, although this association is not specific to separation anxiety disorder and is found in
other anxiety disorders where there is significant comorbidity. A large twin study showed that
being bullied during childhood was a risk factor for suicidal thoughts during young adulthood.
Functional Consequences of Separation Anxiety Disorder
Individuals with separation anxiety disorder often limit independent activities away from home
or attachment figures (e.g., in children, avoiding school, not going to camp, having difficulty
sleeping alone; in adolescents, not going away to college; in adults, not leaving the parental
home, not traveling long distances without their close attachments, not working outside the
home). Symptoms in adults are often debilitating and affect multiple areas of their lives. For
example, adults with separation anxiety disorder may deliberately reorganize their work
schedules and other activities because of their anxieties about possible separations from close
attachment figures; they may often express frustration with the limitations on their lives because
of their need to maintain proximity to, or at least virtual contact with, their key attachment
figures (e.g., by texting or phoning them repeatedly throughout the day). Separation anxiety
disorder is associated with greater reported impairment in individuals from high- and uppermiddle-income countries compared with those from low- and lower-middle-income countries.
Differential Diagnosis
Separation anxiety disorder is distinguished from generalized anxiety
disorder in that the anxiety in separation anxiety disorder predominantly concerns real or
imagined separation from attachment figures. Furthermore, if other worries occur, they are not
excessive.
In separation anxiety disorder, threats of separation from close attachments may
lead to extreme anxiety and panic attacks. In contrast to panic disorder, where panic attacks
occur unexpectedly and are usually accompanied by fears of dying or going “crazy,” the panic
attacks in separation anxiety disorder occur in anticipation of real or imagined separations from
attachment figures or places of safety and security, or from worries that untoward events will
befall the individual’s close attachments.
Unlike individuals with agoraphobia, those with separation anxiety disorder are not
anxious about being trapped or incapacitated in situations from which escape is perceived as
difficult in the event of panic-like symptoms or other incapacitating symptoms. Instead, they fear
being away from places of safety associated with their major attachment figures.

Conduct disorder.
Social anxiety disorder.
Posttraumatic stress disorder.
Illness anxiety disorder.
Prolonged grief disorder.
Depressive and bipolar disorders.
Oppositional defiant disorder.
Psychotic disorders.
Personality disorders.
School avoidance (truancy) is common in conduct disorder, but anxiety about
separation is not responsible for school absences, and the child or adolescent usually stays away
from, rather than returns to, the home.
School refusal may be attributable to social anxiety disorder. In such
instances, the school avoidance is due to fear of being judged negatively by others rather than
due to worries about being separated from attachment figures.
Fear of separation from loved ones is common after a traumatic
event such as a major disaster, particularly when periods of separation from loved ones are
experienced during the traumatic event. In posttraumatic stress disorder (PTSD), the central
symptoms concern intrusions about, and avoidance of, memories associated with the traumatic
event itself, whereas in separation anxiety disorder, the worries and avoidance concern the wellbeing of attachment figures and separation from them.
Separation anxiety disorder concerns worries about the health and wellbeing of close attachments. In contrast, individuals with illness anxiety disorder worry about
specific medical illnesses they themselves may have, not about them being separated from their
close attachments.
Intense yearning or longing for the deceased, intense sorrow and
emotional pain, and preoccupation with the deceased or the circumstances of the death are
expected responses occurring in prolonged grief disorder, whereas fear of possible separation
from key attachment figures is central in separation anxiety disorder.
These disorders may be associated with reluctance to leave
home, but the main concern is not worry or fear of untoward events befalling attachment figures,
but rather low motivation for engaging with the outside world. However, individuals with
separation anxiety disorder may become depressed while being separated or in anticipation of
separation.
Children and adolescents with separation anxiety disorder may be
oppositional in the context of being forced to separate from attachment figures. Oppositional
defiant disorder should be considered only when there is persistent oppositional behavior
unrelated to the anticipation or occurrence of separation from attachment figures.
Unlike the hallucinations in psychotic disorders, the unusual perceptual
experiences that may occur in separation anxiety disorder are usually based on a misperception
of an actual stimulus, occur only in certain situations (e.g., nighttime), and are reversed by the
presence of an attachment figure.
Dependent personality disorder is characterized by an indiscriminate
tendency to rely on others, whereas separation anxiety disorder involves concern about the
proximity and safety of key attachment figures. Borderline personality disorder is characterized
by fear of abandonment by loved ones, but problems in identity, self-direction, interpersonal
functioning, and impulsivity are additionally central to that disorder, whereas they are not central
to separation anxiety disorder.
Comorbidity
In children, separation anxiety disorder is highly comorbid with generalized anxiety disorder and

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specific phobia. In adults, common comorbidities include specific phobia, PTSD, panic disorder,
generalized anxiety disorder, social anxiety disorder, agoraphobia, obsessive-compulsive
disorder, prolonged grief disorder, and personality disorders. Among the personality disorders,
dependent, avoidant, and obsessive-compulsive (Cluster C) personality disorders may be
comorbid with separation anxiety disorder. Depressive and bipolar disorders are also comorbid
with separation anxiety disorder in adults.
Selective Mutism
Diagnostic Criteria
A. Consistent failure to speak in specific social situations in which there is an
expectation for speaking (e.g., at school) despite speaking in other situations.
B. The disturbance interferes with educational or occupational achievement or with
social communication.
C. The duration of the disturbance is at least 1 month (not limited to the first month
of school).
D. The failure to speak is not attributable to a lack of knowledge of, or comfort with,
the spoken language required in the social situation.
E. The disturbance is not better explained by a communication disorder (e.g.,
childhood-onset fluency disorder) and does not occur exclusively during the
course of autism spectrum disorder, schizophrenia, or another psychotic
disorder.
Diagnostic Features
When encountering other individuals in social interactions, children with selective mutism do not
initiate speech or reciprocally respond when spoken to by others. Lack of speech occurs in social
interactions with children or adults. Children with selective mutism will speak in their home in
the presence of immediate family members but often not even in front of close friends or seconddegree relatives, such as grandparents or cousins. The disturbance is most often marked by high
social anxiety. Children with selective mutism often refuse to speak at school, leading to
academic or educational impairment, as teachers often find it difficult to assess skills such as
reading. The lack of speech may interfere with social communication, although children with this
disorder sometimes use nonspoken or nonverbal means (e.g., grunting, pointing, writing) to
communicate and may be willing or eager to perform or engage in social encounters when
speech is not required (e.g., nonverbal parts in school plays).
Associated Features
Associated features of selective mutism may include excessive shyness, fear of social

Temperamental.
Environmental.
Genetic and physiological.
embarrassment, social isolation and withdrawal, clinging, compulsive traits, negativism, temper
tantrums, or mild oppositional behavior. Although children with this disorder generally have
normal language skills, there may occasionally be an associated communication disorder,
although no particular association with a specific communication disorder has been identified.
Even when these disorders are present, anxiety is present as well. In clinical settings, children
with selective mutism are almost always given an additional diagnosis of another anxiety
disorder—most commonly, social anxiety disorder.
Prevalence
Selective mutism is a relatively rare disorder and has not been included as a diagnostic category
in epidemiological studies of prevalence of childhood disorders. Point prevalence using various
clinic or school samples in the United States, Europe, and Israel ranges between 0.03% and 1.9%
depending on the setting and ages of the sample. Studies in community-based and treatmentseeking samples suggest an equal gender distribution for selective mutism, although there is also
evidence that selective mutism is more common among girls than boys. Prevalence does not
seem to vary by race/ethnicity, but individuals who need to speak in a non-native language (e.g.,
children of immigrant families) run greater risk for developing the disorder. The disorder is more
likely to manifest in young children than in adolescents and adults.
Development and Course
The onset of selective mutism is usually before age 5 years, but the disturbance may not come to
clinical attention until entry into school, where there is an increase in social interaction and
performance tasks, such as reading aloud. The persistence of the disorder is variable. Although
clinical reports suggest that many individuals “outgrow” selective mutism, the longitudinal
course of the disorder is largely unknown. In most cases, selective mutism may fade, but
symptoms of social anxiety disorder often remain.
Risk and Prognostic Factors
Temperamental risk factors for selective mutism are not well identified.
Negative affectivity (neuroticism) or behavioral inhibition may play a role, as may parental
history of shyness, social isolation, and social anxiety. Children with selective mutism may have
subtle receptive language difficulties compared with their peers, although receptive language is
still within the normal range.
Social inhibition on the part of parents may serve as a model for social reticence
and selective mutism in children. Furthermore, parents of children with selective mutism have
been described as overprotective or more controlling than parents of children with other anxiety
disorders or no disorder.
Because of the significant overlap between selective mutism and social
anxiety disorder, there may be shared genetic factors between these conditions. There is also
evidence for increased abnormalities in the auditory efferent neural activity during vocalization
in individuals with selective mutism, which could lead to peculiarities in the perception of their

Silent period in immigrant children learning a second language.
Communication disorders.
Neurodevelopmental disorders and schizophrenia and other psychotic disorders.
Social anxiety disorder.
own voice and hence a reticence to speak.
Culture-Related Diagnostic Issues
Children in families who have migrated to a country where a different language is spoken may
appear to have selective mutism because they may refuse to speak the new language because of
lack of knowledge of the language. Such children would not qualify for the diagnosis because
such cases are explicitly excluded from the diagnosis.
Functional Consequences of Selective Mutism
Selective mutism may result in social impairment, as children may be too anxious to engage in
reciprocal social interaction with other children. As children with selective mutism mature, they
may face increasing social isolation. In school settings, these children may suffer academic
impairment, because often they do not communicate with teachers regarding their academic or
personal needs (e.g., not understanding a class assignment, not asking to use the restroom).
Severe impairment in school and social functioning, including that resulting from teasing by
peers, is common. In certain instances, selective mutism may serve as a compensatory strategy to
decrease anxious arousal in social encounters.
Differential Diagnosis
Selective 
mutism 
must 
be
distinguished from the typical “silent period” associated with the acquisition of a new language
in young children. If comprehension of the new language is adequate but refusal to speak persists
in both languages, in several unfamiliar settings, and for a prolonged period, a diagnosis of
selective mutism may be warranted.
Selective mutism should be distinguished from speech disturbances
that are better explained by a communication disorder, such as language disorder, speech sound
disorder (previously phonological disorder), childhood-onset
fluency disorder (stuttering), or social (pragmatic) communication disorder. Unlike selective
mutism, the speech disturbance in these conditions is not restricted to a specific social situation.
Individuals with an
autism spectrum disorder, schizophrenia or another psychotic disorder, or severe intellectual
developmental disorder (intellectual disability) may have problems in social communication and
be unable to speak appropriately in social situations. In contrast, selective mutism should be
diagnosed only when a child has an established capacity to speak in some social situations (e.g.,
typically at home).
The social anxiety and social avoidance in social anxiety disorder may be
associated with selective mutism. In such cases, both diagnoses may be given.
Comorbidity
The most common comorbid conditions are other anxiety disorders, most often social anxiety

disorder, followed by separation anxiety disorder and specific phobia. In clinical settings,
selective mutism and autism spectrum disorder have also been noted as frequently co-occurring
conditions. Oppositional behaviors can be observed in a substantial minority of children with
selective mutism, although this oppositional behavior may be limited to situations requiring
speech. Communication delays or disorders also may appear in some children with selective
mutism.
Specific Phobia
Diagnostic Criteria
A. Marked fear or anxiety about a specific object or situation (e.g., flying, heights,
animals, receiving an injection, seeing blood).
Note: In children, the fear or anxiety may be expressed by crying, tantrums,
freezing, or clinging.
B. The phobic object or situation almost always provokes immediate fear or anxiety.
C. The phobic object or situation is actively avoided or endured with intense fear or
anxiety.
D. The fear or anxiety is out of proportion to the actual danger posed by the specific
object or situation and to the sociocultural context.
E. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or
more.
F. The fear, anxiety, or avoidance causes clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
G. The disturbance is not better explained by the symptoms of another mental
disorder, including fear, anxiety, and avoidance of situations associated with
panic-like symptoms or other incapacitating symptoms (as in agoraphobia);
objects or situations related to obsessions (as in obsessive-compulsive
disorder); reminders of traumatic events (as in posttraumatic stress disorder);
separation from home or attachment figures (as in separation anxiety disorder);
or social situations (as in social anxiety disorder).
Specify if:
Code based on the phobic stimulus:
F40.218 Animal (e.g., spiders, insects, dogs).
F40.228 Natural environment (e.g., heights, storms, water).
F40.23x Blood-injection-injury (e.g., needles, invasive medical procedures).
Coding note: Select specific ICD-10-CM code as follows: F40.230 fear of
blood; F40.231 fear of injections and transfusions; F40.232 fear of other

medical care; or F40.233 fear of injury.
F40.248 Situational (e.g., airplanes, elevators, enclosed places).
F40.298 Other (e.g., situations that may lead to choking or vomiting; in children,
e.g., loud sounds or costumed characters).
Coding note: When more than one phobic stimulus is present, code all ICD-10-CM
codes that apply (e.g., for fear of snakes and flying, F40.218 specific phobia, animal,
and F40.248 specific phobia, situational).
Specifiers
It is common for individuals to have multiple specific phobias. The average individual with
specific phobia fears three objects or situations, and approximately 75% of individuals with
specific phobia fear more than one situation or object. In such cases, multiple specific phobia
diagnoses, each with its own diagnostic code reflecting the phobic stimulus, would need to be
given. For example, if an individual fears thunderstorms and flying, then two diagnoses would be
given: specific phobia, natural environment, and specific phobia, situational.
Diagnostic Features
A key feature of this disorder is that the fear or anxiety is circumscribed to the presence of a
particular situation or object (Criterion A), which may be termed the phobic stimulus. The
categories of feared situations or objects are provided as specifiers. Many individuals fear objects
or situations from more than one category, or phobic stimulus. For the diagnosis of specific
phobia, the response must differ from normal, transient fears that commonly occur in the
population. To meet the criteria for a diagnosis, the fear or anxiety must be intense or severe (i.e.,
“marked”) (Criterion A). The amount of fear experienced may vary with proximity to the feared
object or situation and may occur in anticipation of or in the actual presence of the object or
situation. Also, the fear or anxiety may take the form of a full or limited symptom panic attack
(i.e., expected panic attack). Another characteristic of specific phobias is that fear or anxiety is
evoked nearly every time the individual comes into contact with the phobic stimulus (Criterion
B). Thus, an individual who becomes anxious only occasionally upon being confronted with the
situation or object (e.g., becomes anxious when flying only on one out of every five airplane
flights) would not be diagnosed with specific phobia. However, the degree of fear or anxiety
expressed may vary (from anticipatory anxiety to a full panic attack) across different occasions
of encountering the phobic object or situation because of various contextual factors such as the
presence of others, duration of exposure, and other threatening elements such as turbulence on a
flight for individuals who fear flying. Fear and anxiety are often expressed differently between
children and adults. Also, the fear or anxiety occurs as soon as the phobic object or situation is
encountered (i.e., immediately rather than being delayed).
The individual actively avoids the situation, or if he or she either is unable or decides not to
avoid it, the situation or object evokes intense fear or anxiety (Criterion C). Active avoidance
means the individual intentionally behaves in ways that are designed to prevent or minimize
contact with phobic objects or situations (e.g., takes tunnels instead of bridges on daily commute
to work for fear of heights; avoids entering a dark room for fear of spiders; avoids accepting a
job in a locale where a phobic stimulus is more common). Avoidance behaviors are often

obvious (e.g., an individual who fears blood refusing to go to the doctor) but are sometimes less
obvious (e.g., an individual who fears snakes refusing to look at pictures that resemble the form
or shape of snakes). Many individuals with specific phobias have suffered over many years and
have changed their living circumstances in
ways designed to avoid the phobic object or situation as much as possible (e.g., an individual
diagnosed with specific phobia, animal, who moves to reside in an area devoid of the particular
feared animal). Therefore, they no longer experience fear or anxiety in their daily life. In such
instances, avoidance behaviors or ongoing refusal to engage in activities that would involve
exposure to the phobic object or situation (e.g., repeated refusal to accept offers for work-related
travel because of fear of flying) may be helpful in confirming the diagnosis in the absence of
overt anxiety or panic.
The fear or anxiety is out of proportion to the actual danger that the object or situation poses,
or more intense than is deemed necessary (Criterion D). Although individuals with specific
phobia often recognize their reactions as disproportionate, they tend to overestimate the danger
in their feared situations, and thus the judgment of being out of proportion is made by the
clinician. The individual’s sociocultural context should also be considered. For example, fears of
the dark may be reasonable in a context of ongoing violence, and the degree of fear of insects
considered to be disproportionate would be higher in settings where insects are consumed in the
diet. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more
(Criterion E), which helps distinguish the disorder from transient fears that are common in the
population, particularly among children. The specific phobia must cause clinically significant
distress or impairment in social, occupational, or other important areas of functioning in order for
the disorder to be diagnosed (Criterion F).
Associated Features
Individuals with specific phobia typically experience an increase in physiological arousal in
anticipation of or during exposure to a phobic object or situation. However, the physiological
response to the feared situation or object varies. Whereas individuals with situational, natural
environment, and animal specific phobias are likely to show sympathetic nervous system arousal,
individuals with blood-injection-injury specific phobia often demonstrate a vasovagal fainting or
near-fainting response that is marked by initial brief acceleration of heart rate and elevation of
blood pressure followed by a deceleration of heart rate and a drop in blood pressure.
Additionally, specific phobia is most consistently associated with abnormal activity in the
amygdala, anterior cingulate cortex, thalamus, and insula in response to the phobic
object/situation.
Prevalence
In the United States, the 12-month community prevalence estimate for specific phobia is
approximately 8%–12%. Prevalence rates in European countries are largely similar to those in
the United States (e.g., about 6%), but rates are generally lower in Asian, African, and Latin
American countries (2%–4%). Prevalence estimates in children average approximately 5%

across various countries, with a range of 3%–9%, and are approximately 16% in adolescents ages
13–17 years in the United States. Prevalence estimates are lower in older individuals (about 3%–
5%), possibly reflecting diminishing severity to subclinical levels. Women are more frequently
affected than men across subtypes, at a rate of approximately 2:1.
Development and Course
Specific phobia sometimes develops following a traumatic event (e.g., being attacked by an
animal or stuck in an elevator), observation of others going through a traumatic event (e.g.,
watching someone drown), an unexpected panic attack in the to be feared situation (e.g., an
unexpected panic attack while on the subway), or informational transmission (e.g., extensive
media coverage of a plane crash). However, many individuals with specific phobia are unable to
recall the specific reason for the onset of their phobias. Specific phobia usually develops in early
childhood, with the majority of cases developing prior to age 10 years. Median age at onset is
between 7 and 11 years, with the mean at about 10 years.
Situational specific phobias tend to have a later age at onset than natural environment, animal, or
blood-injection-injury specific phobias. Specific phobias that develop in childhood and
adolescence are likely to wax and wane during that period. However, phobias that do persist into
adulthood are unlikely to remit for the majority of individuals.
When specific phobia is being diagnosed in children, two issues should be considered. First,
young children may express their fear and anxiety by crying, tantrums, freezing, or clinging.
Second, young children typically are not able to understand the concept of avoidance. Therefore,
the clinician should assemble additional information from parents, teachers, or others who know
the child well. Excessive fears are quite common in young children but are usually transitory and
only mildly impairing and thus considered developmentally appropriate. In such cases a
diagnosis of specific phobia would not be made. When the diagnosis of specific phobia is being
considered in a child, it is important to assess the degree of impairment and the duration of the
fear, anxiety, or avoidance, and whether it is typical for the child’s particular developmental
stage.
Although the prevalence of specific phobia is lower in older populations, it remains one of
the more commonly experienced disorders in late life. Several issues should be considered when
diagnosing specific phobia in older populations. First, older individuals may be more likely to
endorse natural environment specific phobias, as well as phobias of falling. Second, specific
phobia (like all anxiety disorders) tends to co-occur with medical concerns in older individuals,
including coronary heart disease, chronic obstructive pulmonary disease, and Parkinson’s
disease. Third, older individuals may be more likely to attribute the symptoms of anxiety to
medical conditions. Fourth, older individuals may be more likely to manifest anxiety in an
atypical manner (e.g., involving symptoms of both anxiety and depression) and thus be more
likely to warrant a diagnosis of unspecified anxiety disorder. Additionally, the presence of
specific phobia in older adults is associated with decreased quality of life and may serve as a risk
factor for major neurocognitive disorder.
Although most specific phobias develop in childhood and adolescence, it is possible for a

Temperamental.
Environmental.
Genetic and physiological.
specific phobia to develop at any age, often as the result of experiences that are traumatic. For
example, phobias of choking almost always follow a near-choking event at any age.
Risk and Prognostic Factors
Temperamental risk factors for specific phobia, such as negative affectivity
(neuroticism) or behavioral inhibition, are risk factors for other anxiety disorders as well.
Environmental 
risk 
factors 
for 
specific 
phobias, 
such 
as 
parental
overprotectiveness, parental loss and separation, and physical and sexual abuse, tend to predict
other anxiety disorders as well. As noted earlier, negative or traumatic encounters with the feared
object or situation sometimes (but not always) precede the development of specific phobia.
There may be a genetic susceptibility to a certain category of specific
phobia (e.g., an individual with a first-degree relative with a specific phobia of animals is
significantly more likely to have the same type of specific phobia than any other category of
phobia). Twin studies have examined the heritability of individual subtypes of fears and phobias,
suggesting that animal phobia has approximately 32% heritability, blood-injury-injection phobia
has 33%, and situational phobia has 25%.
Culture-Related Diagnostic Issues
In the United States, individuals of Asian and Latinx descent report lower prevalence of specific
phobia than non-Latinx Whites and African Americans. The prevalence of specific phobia
subtypes varies cross-nationally.
Sex- and Gender-Related Diagnostic Issues
Animal, natural environment, and situational specific phobias are predominantly experienced by
women, whereas blood-injection-injury phobia is experienced nearly equally among women and
men. The average age at onset of specific phobia during childhood does not differ between
girls/women and boys/men.
Association With Suicidal Thoughts or Behavior
Specific phobia is associated with both suicidal thoughts and suicide attempts based on national
U.S. survey data. Specific phobia is also associated with a transition from ideation to attempt.
For individuals in the community ages 14–24 years, a large prospective study over a 10-year
period in Germany found that 30% of first suicide attempts could be attributable to specific
phobia.
Functional Consequences of Specific Phobia
Individuals with specific phobia show similar patterns of impairment in psychosocial functioning
and decreased quality of life as individuals with other anxiety disorders and alcohol and
substance use disorders, including impairments in occupational and interpersonal functioning. In
older adults, impairment may be seen in caregiving duties and volunteer activities. Also, fear of

Agoraphobia.
Social anxiety disorder.
Separation anxiety disorder.
Panic disorder.
Obsessive-compulsive disorder.
falling in older adults can lead to reduced mobility and reduced physical and social functioning,
and may lead to receiving formal or informal home support. The distress and impairment caused
by specific phobias tend to increase with the number of feared objects and situations. Thus, an
individual who fears four objects or situations is likely to have more impairment in his or her
occupational and social roles and a lower quality of life than an individual who fears only one
object or situation. Individuals with blood-injection-injury specific phobia are often reluctant to
obtain medical care even when a medical concern is present. Additionally, fear of vomiting and
choking may substantially reduce dietary intake.
Differential Diagnosis
Situational specific phobia may resemble agoraphobia in its clinical presentation,
given the overlap in feared situations (e.g., flying, enclosed places, elevators). If an individual
fears only one of the agoraphobic situations, then specific phobia, situational, may be diagnosed.
If two or more agoraphobic situations are feared, a diagnosis of agoraphobia is likely warranted.
For example, an individual who fears airplanes and elevators (which overlap with the “public
transportation” agoraphobic situation) but does not fear other agoraphobic situations would be
diagnosed with specific phobia, situational, whereas an individual who fears airplanes, elevators,
and crowds (which overlap with two agoraphobic situations, “using public transportation” and
“standing in line or being in a crowd”) would be diagnosed with agoraphobia. Criterion B of
agoraphobia (the situations are feared or avoided “because of thoughts that escape might be
difficult or help might not be available in the event of developing panic-like symptoms or other
incapacitating or embarrassing symptoms”) can also be useful in differentiating agoraphobia
from specific phobia. If the situations are feared for reasons other than not being able to escape
or get help, such as fear of being harmed directly by the object or situation (e.g., fear of the plane
crashing, fear of the animal biting), a specific phobia diagnosis may be more appropriate.
If the situations are feared because of negative evaluation, social anxiety
disorder should be diagnosed instead of specific phobia.
If the situations are feared because of separation from a primary
caregiver or attachment figure, separation anxiety disorder should be diagnosed instead of
specific phobia.
Individuals with specific phobia may experience panic attacks when confronted
with their feared situation or object. A diagnosis of specific phobia would be given if the panic
attacks only occurred in response to the specific object or situation, whereas a diagnosis of panic
disorder would be given if the individual also experienced panic attacks that were unexpected
(i.e., not in response to the specific phobia object or situation).
If an individual’s primary fear or anxiety is of an object or
situation as a result of obsessions (e.g., fear of blood due to obsessive thoughts about
contamination from blood-borne pathogens [i.e., HIV]; fear of driving due to obsessive images
of harming others), and if other diagnostic criteria for obsessive-compulsive disorder are met,
then obsessive-compulsive disorder should be diagnosed.

Trauma- and stressor-related disorders.
Eating disorders.
Schizophrenia spectrum and other psychotic disorders.
F40.10
If the phobia develops following a traumatic event,
posttraumatic stress disorder (PTSD) should be considered as a diagnosis. However, traumatic
events can precede the onset of PTSD and specific phobia. In this case, a diagnosis of specific
phobia would be assigned only if all of the criteria for PTSD are not met.
A diagnosis of specific phobia is not given if the avoidance behavior is
exclusively limited to avoidance of food and food-related cues, in which case a diagnosis of
anorexia nervosa or bulimia nervosa should be considered.
When the fear and avoidance are attributable
to delusional thinking (as in schizophrenia or other schizophrenia spectrum and other psychotic
disorders), a diagnosis of specific phobia is not warranted.
Comorbidity
Specific phobia is rarely seen in medical-clinical settings in the absence of other
psychopathology and is more frequently seen in nonmedical mental health settings. Specific
phobia is frequently associated with a range of other disorders. Because of early onset, specific
phobia is typically the temporally primary disorder. Individuals with specific phobia are at
increased risk for the development of other disorders, including other anxiety disorders,
depressive and bipolar disorders, substance-related disorders, somatic symptom and related
disorders, and personality disorders (particularly dependent personality disorder).
Social Anxiety Disorder
Diagnostic Criteria
A. Marked fear or anxiety about one or more social situations in which the individual
is exposed to possible scrutiny by others. Examples include social interactions
(e.g., having a conversation, meeting unfamiliar people), being observed (e.g.,
eating or drinking), and performing in front of others (e.g., giving a speech).
Note: In children, the anxiety must occur in peer settings and not just during
interactions with adults.
B. The individual fears that he or she will act in a way or show anxiety symptoms
that will be negatively evaluated (i.e., will be humiliating or embarrassing; will
lead to rejection or offend others).
C. The social situations almost always provoke fear or anxiety.
Note: In children, the fear or anxiety may be expressed by crying, tantrums,
freezing, clinging, shrinking, or failing to speak in social situations.
D. The social situations are avoided or endured with intense fear or anxiety.
E. The fear or anxiety is out of proportion to the actual threat posed by the social
situation and to the sociocultural context.

F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or
more.
G. The fear, anxiety, or avoidance causes clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
H. The fear, anxiety, or avoidance is not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication) or another medical condition.
I. The fear, anxiety, or avoidance is not better explained by the symptoms of
another mental disorder, such as panic disorder, body dysmorphic disorder, or
autism spectrum disorder.
J. If another medical condition (e.g., Parkinson’s disease, obesity, disfigurement
from burns or injury) is present, the fear, anxiety, or avoidance is clearly
unrelated or is excessive.
Specify if:
Performance only: If the fear is restricted to speaking or performing in public.
Specifiers
Individuals with the performance only type of social anxiety disorder have performance fears
that are typically most impairing in their professional lives (e.g., musicians, dancers, performers,
athletes) or in roles that require regular public speaking. Performance fears may also manifest in
work, school, or academic settings in which regular public presentations are required. Individuals
with performance only social anxiety disorder do not fear or avoid nonperformance social
situations.
Diagnostic Features
The essential feature of social anxiety disorder is a marked, or intense, fear or anxiety of social
situations in which the individual may be scrutinized by others. In children the fear or anxiety
must occur in peer settings and not just during interactions with adults (Criterion A). When
exposed to such social situations, the individual fears that he or she will be negatively evaluated.
The individual is concerned that he or she will be judged as anxious, weak, crazy, stupid, boring,
intimidating, dirty, or unlikable. The individual fears that he or she will act or appear in a certain
way or show anxiety symptoms, such as blushing, trembling, sweating, stumbling over one’s
words, or staring, that will be negatively evaluated by others (Criterion B). Some individuals fear
offending others or being rejected as a result. Fear of offending others—for example, by a gaze
or by showing anxiety symptoms—may be the predominant fear in individuals from cultures
with strong collectivistic orientations. An individual with fear of trembling of the hands may
avoid drinking, eating, writing, or pointing in public; an individual with fear of sweating may
avoid shaking hands or eating spicy foods; and an individual with fear of blushing may avoid
public performance, bright lights, or discussion about intimate topics. Some individuals fear and
avoid urinating in public restrooms when other individuals are present (i.e., paruresis, or “shy
bladder syndrome”).
The social situations almost always provoke fear or anxiety (Criterion C). Thus, an individual
who becomes anxious only occasionally in the social situation(s) would not be diagnosed with

social anxiety disorder. However, the degree and type of fear and anxiety may vary (e.g.,
anticipatory anxiety, a panic attack) across different occasions. The anticipatory anxiety may
occur sometimes far in advance of upcoming situations (e.g., worrying every day for weeks
before attending a social event, repeating a speech for days in advance). In children, the fear or
anxiety may be expressed by crying, tantrums, freezing, clinging, or shrinking in social
situations. The individual will often avoid the feared social situations. Alternatively, the
situations are endured with intense fear or anxiety (Criterion D). Avoidance can be extensive
(e.g., not going to parties, refusing school) or subtle (e.g., overpreparing the text of a speech,
diverting attention to others, limiting eye contact).
The fear or anxiety is judged to be out of proportion to the actual risk of being negatively
evaluated or to the consequences of such negative evaluation (Criterion E).
Sometimes, the anxiety may not be judged to be excessive, because it is related to an actual
danger (e.g., being bullied or tormented by others). However, individuals with social anxiety
disorder often overestimate the negative consequences of social situations, and thus the judgment
of being out of proportion is made by the clinician. The individual’s sociocultural context needs
to be taken into account when this judgment is being made. For example, in certain cultures,
behavior that might otherwise appear socially anxious may be considered appropriate in social
situations (e.g., might be seen as a sign of respect).
The duration of the disturbance is typically at least 6 months (Criterion F). This duration
threshold helps distinguish the disorder from transient social fears that are common, particularly
among children and in the community. The fear, anxiety, and avoidance must interfere
significantly with the individual’s normal routine, occupational or academic functioning, or
social activities or relationships, or must cause clinically significant distress (Criterion G). For
example, an individual who is afraid to speak in public would not receive a diagnosis of social
anxiety disorder if this activity is not routinely encountered on the job or in classroom work, and
if the individual is not significantly distressed about it. However, if the individual avoids, or is
passed over for, the job or education he or she really wants because of social anxiety symptoms,
Criterion G is met.
Associated Features
Individuals with social anxiety disorder may be inadequately assertive or excessively submissive
or, less commonly, highly controlling of the conversation. They may show overly rigid body
posture or inadequate eye contact, or speak with an overly soft voice. These individuals may be
shy or withdrawn, and they may be less open in conversations and disclose little about
themselves. They may seek employment in jobs that do not require social contact, although this
is not the case for individuals with social anxiety disorder, performance only. They may live at
home longer. Men may be delayed in marrying and having a family, whereas women who would
want to work outside the home may live a life without ever doing so. Self-medication with
substances is common (e.g., drinking before going to a party). Social anxiety among older adults
may also include exacerbation of symptoms of medical illnesses, such as increased tremor or
tachycardia. Blushing is a hallmark physical response of social anxiety disorder.

Prevalence
The 12-month prevalence estimate of social anxiety disorder for the United States is
approximately 7%. Lower 12-month prevalence estimates are seen in much of the world using
the same diagnostic instrument, clustering around 0.5%–2.0%; median prevalence in Europe is
2.3%. Prevalence appears to be increasing in the United States and East Asian countries. Twelvemonth prevalence rates in young adolescents (ages 13–17 years) are roughly half those in adults.
Twelve-month prevalence rates decrease after age 65. The 12-month prevalence for older adults
in North America, Europe, and Australia ranges from 2% to 5%. In general, higher rates of social
anxiety disorder are found in women than in men in the general population (with odds ratios
ranging from 1.5 to 2.2), and the gender difference in prevalence is more pronounced in
adolescents and young adults. Gender rates are equivalent or slightly higher for men in clinical
samples, and it is assumed that gender roles and social expectations play a significant role in
explaining the heightened help-seeking behavior in men. Prevalence in the United States has
been found to be lower in individuals of Asian, Latinx, African American, and Caribbean Black
descent compared with non-Hispanic Whites.
Development and Course
Median age at onset of social anxiety disorder in the United States is 13 years, and 75% of
individuals have an age at onset between 8 and 15 years. The disorder sometimes emerges
out of a childhood history of social inhibition or shyness in U.S. and European studies. Onset can
also occur in early childhood. Onset of social anxiety disorder may follow a stressful or
humiliating experience (e.g., being bullied, vomiting during a public speech), or it may be
insidious, developing slowly. First onset in adulthood is relatively rare and is more likely to
occur after a stressful or humiliating event or after life changes that require new social roles (e.g.,
marrying someone from a different social class, receiving a job promotion). Social anxiety
disorder may diminish after an individual with fear of dating marries and may reemerge after
divorce. Among individuals presenting to clinical care, the disorder tends to be particularly
persistent.
Adolescents endorse a broader pattern of fear and avoidance, including of dating, compared
with younger children. Older adults express social anxiety at lower levels but across a broader
range of situations, whereas younger adults express higher levels of social anxiety for specific
situations. In older adults, social anxiety may concern disability due to declining sensory
functioning (hearing, vision) or embarrassment about one’s appearance (e.g., tremor as a
symptom of Parkinson’s disease) or functioning due to medical conditions, incontinence, or
cognitive impairment (e.g., forgetting people’s names). Detection of social anxiety disorder in
older adults may be challenging because of several factors, including a focus on somatic
symptoms, comorbid medical illness, limited insight, changes to social environment or roles that
may obscure impairment in social functioning, or reticence about describing psychological
distress. There is large variation in rates of remission for social anxiety disorder, suggestive of
different trajectories (short, fluctuating, and chronic).

Temperamental.
Environmental.
Genetic and physiological.
Risk and Prognostic Factors
Underlying traits that predispose individuals to social anxiety disorder include
behavioral inhibition and fear of negative evaluation, as well as harm avoidance. Personality
traits consistently associated with social anxiety disorder are high negative affectivity
(neuroticism) and low extraversion.
There is evidence that negative social experiences, particularly peer victimization,
are associated with the development of social anxiety disorder, although causal pathways remain
unknown. Childhood maltreatment and adversity are risk factors for social anxiety disorder.
Among African Americans and Caribbean Blacks in the United States, everyday forms of ethnic
discrimination and racism are associated with social anxiety disorder.
Traits predisposing individuals to social anxiety disorder, such as
behavioral inhibition, are strongly genetically influenced. The genetic influence is subject to
gene-environment interaction; that is, children with high behavioral inhibition are more
susceptible to environmental influences, such as socially anxious modeling by parents. Also,
social anxiety disorder is heritable. First-degree relatives have a two to six times greater chance
of having social anxiety disorder, and liability to the disorder involves the interplay of disorderspecific (e.g., fear of negative evaluation) and nonspecific (e.g., negative affectivity
[neuroticism]) genetic factors. Genetic contribution to social anxiety disorder has been found to
be higher for social anxiety disorder in children than social anxiety disorder in adults and higher
for social anxiety symptoms than a clinical diagnosis of social anxiety disorder.
Culture-Related Diagnostic Issues
The nature and types of social situations that precipitate symptoms of social anxiety disorder are
similar across U.S. ethnoracial groups, including fear of performance/public speaking, social
interaction, and being observed. U.S. non-Latinx Whites report an earlier age at onset of social
anxiety disorder than U.S. Latinx, yet the latter describe greater impairment across home, work,
and relationship domains associated with the disorder.
Immigrant status is associated with lower rates of social anxiety disorder in both Latinx and nonLatinx White groups. The syndrome of taijin kyofusho (e.g., in Japan and Korea) is often
characterized by social-evaluative concerns, fulfilling criteria for social anxiety disorder, which
are associated with the fear that the individual makes other people uncomfortable (e.g., “My gaze
upsets people so they look away and avoid me”), a fear that is at times experienced with
delusional intensity. Other presentations of taijin kyofusho may fulfill criteria for body
dysmorphic disorder or delusional disorder.
Sex- and Gender-Related Diagnostic Issues
Age at onset of social anxiety disorder does not differ by gender. Women with social anxiety
disorder report a greater number of social fears and comorbid major depressive disorder and
other anxiety disorders, whereas men are more likely to fear dating; have oppositional defiant
disorder, conduct disorder, or antisocial personality disorder; and use alcohol and illicit drugs to

Normative shyness.
Agoraphobia.
Panic disorder.
Generalized anxiety disorder.
relieve symptoms of the disorder. Paruresis is more common in men.
Association With Suicidal Thoughts or Behavior
Among U.S. adolescents, social anxiety disorder has been reported to increase the risk for active
suicidal thoughts and suicide attempts in Latinx but not in non-Latinx Whites, independently of
the effect of major depression and family income.
Functional Consequences of Social Anxiety Disorder
Social anxiety disorder is associated with elevated rates of school dropout and with decreased
well-being, employment, workplace productivity, socioeconomic status, and quality of life.
Social anxiety disorder is also associated with being single, unmarried, or divorced and with not
having children, particularly among men, whereas women are more likely to be unemployed.
Social anxiety disorder is also negatively associated with friendship quality, such that individuals
with social anxiety disorder report having friendships that are less close and less supportive than
persons without the disorder. In older adults, there may be impairment in caregiving duties and
volunteer activities. Social anxiety disorder also impedes leisure activities. Despite the extent of
distress and social impairment associated with social anxiety disorder, only about half of
individuals with the disorder in high-income societies ever seek treatment, and they tend to do so
only after 15–20 years of experiencing symptoms. Not being employed is a strong predictor for
the persistence of social anxiety disorder.
Differential Diagnosis
Shyness (i.e., social reticence) is a common personality trait and is not by
itself pathological. In some societies, shyness is even evaluated positively. However, when there
is a significant adverse impact on social, occupational, and other important areas of functioning,
a diagnosis of social anxiety disorder should be considered, and when full diagnostic criteria for
social anxiety disorder are met, the disorder should be diagnosed. Only a minority (12%) of selfidentified shy individuals in the United States have symptoms that meet diagnostic criteria for
social anxiety disorder.
Individuals with agoraphobia may fear and avoid social situations (e.g., going to a
movie) because escape might be difficult or help might not be available in the event of
incapacitation or panic-like symptoms, whereas individuals with social anxiety disorder are most
fearful of scrutiny by others. Moreover, individuals with social anxiety disorder are likely to be
calm when left entirely alone, which is often not the case in agoraphobia.
Individuals with social anxiety disorder may have panic attacks, but the panic
attacks are always cued by social situations and do not occur “out of the blue.” Additionally,
individuals with social anxiety disorder are more likely to be distressed by fear of negative
evaluation stemming from a panic attack than by the panic attacks themselves.
Social worries are common in generalized anxiety disorder, but the
focus is more on the nature of ongoing relationships rather than on fear of negative evaluation.

Separation anxiety disorder.
Specific phobias.
Selective mutism.
Major depressive disorder.
Body dysmorphic disorder.
Delusional disorder.
Autism spectrum disorder.
Personality disorders.
Individuals with generalized anxiety disorder, particularly children, may have excessive worries
about the quality of their social performance, but these worries also pertain to nonsocial
performance and when the individual is not being evaluated by others. In social anxiety disorder,
the worries focus on social performance and others’ evaluation.
Individuals with separation anxiety disorder may avoid social settings
(including school refusal) because of concerns about being separated from attachment figures or,
in children, about requiring the presence of a parent when it is not developmentally appropriate.
Individuals with separation anxiety disorder are usually comfortable in social settings when their
attachment figure is present or when they are at home, whereas those with social anxiety disorder
may be uncomfortable when social situations occur at home or in the presence of attachment
figures.
Individuals with specific phobias may fear embarrassment or humiliation (e.g.,
embarrassment about fainting when they have their blood drawn), but they do not generally fear
negative evaluation in other social situations.
Individuals with selective mutism may fail to speak because of fear of negative
evaluation, but they do not fear negative evaluation in social situations where no speaking is
required (e.g., nonverbal play).
Individuals with major depressive disorder may be concerned about
being negatively evaluated by others because they feel they are bad or not worthy of being liked.
In contrast, individuals with social anxiety disorder are worried about being negatively evaluated
because of certain social behaviors or physical symptoms.
Individuals with body dysmorphic disorder are preoccupied with one
or more perceived defects or flaws in their physical appearance that are not observable or appear
slight to others; this preoccupation often causes social anxiety and avoidance. If their social fears
and avoidance are caused only by their beliefs about their appearance, a separate diagnosis of
social anxiety disorder is not warranted.
Individuals with delusional disorder may have nonbizarre delusions and/or
hallucinations related to the delusional theme that focus on being rejected by or offending others.
Although extent of insight into beliefs about social situations may vary, many individuals with
social anxiety disorder have good insight that their beliefs are out of proportion to the actual
threat posed by the social situation.
Social anxiety and social communication deficits are hallmarks of
autism spectrum disorder. Individuals with social anxiety disorder typically have adequate ageappropriate social relationships and social communication capacity, although they may appear to
have impairment in these areas when first interacting with unfamiliar peers or adults.
Given its frequent onset in childhood and its persistence into and through
adulthood, social anxiety disorder may resemble a personality disorder. The most apparent
overlap is with avoidant personality disorder. Individuals with avoidant personality disorder have
a broader avoidance pattern and higher rates of impairment than those individuals with social
anxiety disorder. Moreover, individuals with avoidant personality disorder have a strong and
pervasively negative self-concept, a view of rejection as equating to a global evaluation of the
self as being of little worth, and a sense of not fitting in

Other mental disorders.
Other medical conditions.
Oppositional defiant disorder.
F41.0
socially that dates from early childhood. Nonetheless, social anxiety disorder is typically more
comorbid with avoidant personality disorder than with any other personality disorder, and
avoidant personality disorder is more comorbid with social anxiety disorder than with any other
anxiety disorder.
Social fears and discomfort can occur as part of schizophrenia, but other
evidence for psychotic symptoms is usually present. In individuals with an eating disorder, it is
important to determine that fear of negative evaluation about eating disorder symptoms or
behaviors (e.g., purging and vomiting) is not the sole source of social anxiety before applying a
diagnosis of social anxiety disorder. Similarly, obsessive-compulsive disorder may be associated
with social anxiety, but the additional diagnosis of social anxiety disorder is used only when
social fears and avoidance are independent of the foci of the obsessions and compulsions.
Medical conditions may produce symptoms that may be embarrassing
(e.g., trembling in Parkinson’s disease). When the fear of negative evaluation due to other
medical conditions is judged to be excessive, a diagnosis of social anxiety disorder should be
considered.
Refusal to speak because of opposition to authority figures should be
differentiated from failure to speak because of fear of negative evaluation.
Comorbidity
Social anxiety disorder is often comorbid with other anxiety disorders, major depressive
disorder, and substance use disorders, and the onset of social anxiety disorder generally precedes
that of the other disorders, except for specific phobia and separation anxiety disorder. Chronic
social isolation in the course of social anxiety disorder may result in major depressive disorder.
Comorbidity with depression is high also in older adults. Substances may be used as selfmedication for social fears, but the symptoms of substance intoxication or withdrawal, such as
trembling, may also be a source of (further) social fear. Social anxiety disorder is frequently
comorbid with body dysmorphic disorder, and generalized social anxiety disorder is often
comorbid with avoidant personality disorder. In children, comorbidities with high-functioning
autism spectrum disorder and selective mutism are common.
Panic Disorder
Diagnostic Criteria
A. Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense
fear or intense discomfort that reaches a peak within minutes, and during which
time four (or more) of the following symptoms occur:
Note: The abrupt surge can occur from a calm state or an anxious state.
1. Palpitations, pounding heart, or accelerated heart rate.

2. Sweating.
3. Trembling or shaking.
4. Sensations of shortness of breath or smothering.
5. Feelings of choking.
6. Chest pain or discomfort.
7. Nausea or abdominal distress.
8. Feeling dizzy, unsteady, light-headed, or faint.
9. Chills or heat sensations.
10. Paresthesias (numbness or tingling sensations).
11. Derealization (feelings of unreality) or depersonalization (being detached from
oneself).
12. Fear of losing control or “going crazy.”
13. Fear of dying.
Note: Culture-specific symptoms (e.g., tinnitus, neck soreness, headache,
uncontrollable screaming or crying) may be seen. Such symptoms should not
count as one of the four required symptoms.
B. At least one of the attacks has been followed by 1 month (or more) of one or
both of the following:
1. Persistent concern or worry about additional panic attacks or their
consequences (e.g., losing control, having a heart attack, “going crazy”).
2. A significant maladaptive change in behavior related to the attacks (e.g.,
behaviors designed to avoid having panic attacks, such as avoidance of
exercise or unfamiliar situations).
C. The disturbance is not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication) or another medical condition (e.g.,
hyperthyroidism, cardiopulmonary disorders).
D. The disturbance is not better explained by another mental disorder (e.g., the
panic attacks do not occur only in response to feared social situations, as in
social anxiety disorder; in response to circumscribed phobic objects or situations,
as in specific phobia; in response to obsessions, as in obsessive-compulsive
disorder; in response to reminders of traumatic events, as in posttraumatic stress
disorder; or in response to separation from attachment figures, as in separation
anxiety disorder).
Diagnostic Features
Panic disorder is characterized by recurrent unexpected panic attacks (Criterion A). (For a
detailed description of symptoms and course characterizing a panic attack, see Panic Attack

Specifier, “Features” section, following this text on panic disorder.) A panic attack is an abrupt
surge of intense fear or intense discomfort that reaches a peak within minutes, and during which
time 4 or more of a list of 13 physical and cognitive symptoms occur. The term recurrent means
more than one unexpected panic attack. The term unexpected refers to a panic attack for which
there is no obvious cue or trigger at the time of occurrence—that is, the attack appears to occur
from out of the blue, such as when the individual is relaxing or emerging from sleep (nocturnal
panic attack). In contrast, expected panic attacks are those for which there is an obvious cue or
trigger, such as a situation in which panic attacks have typically occurred. The determination of
whether panic attacks are expected or unexpected is made by the clinician, who makes this
judgment based on a combination of careful questioning as to the sequence of events preceding
or leading up to the attack and the individual’s own judgment of whether the attack seemed to
occur for no apparent reason. Cultural interpretations may influence the assignment of panic
attacks as expected or unexpected (see section “Culture-Related Diagnostic Issues” for this
disorder). In the United States and Europe, approximately one-half of individuals with panic
disorder have expected panic attacks as well as unexpected panic attacks. Thus, the presence of
expected panic attacks does not rule out the diagnosis of panic disorder.
The frequency and severity of panic attacks vary widely. In terms of frequency, there may be
moderately frequent attacks (e.g., one per week) for months at a time, or short bursts of more
frequent attacks (e.g., daily) separated by weeks or months without any attacks or with less
frequent attacks (e.g., two per month) over many years. Individuals who have infrequent panic
attacks resemble those with more frequent panic attacks in terms of panic attack symptoms,
demographic characteristics, comorbidity with other disorders, family
history, and biological data. In terms of severity, individuals with panic disorder may have
both full-symptom (four or more symptoms) and limited-symptom (fewer than four symptoms)
attacks, and the number and type of panic attack symptoms frequently differ from one panic
attack to the next. However, more than one unexpected full-symptom panic attack is required for
the diagnosis of panic disorder.
A nocturnal panic attack (i.e., waking from sleep in a state of panic) differs from panicking
after fully waking from sleep. In the United States, nocturnal panic attack has been estimated to
occur at least one time in roughly one-quarter to one-third of individuals with panic disorder, of
whom the majority also have daytime panic attacks. Individuals with both daytime and nocturnal
panic attacks tend to have more severe panic disorder overall.
The worries about panic attacks or their consequences usually pertain to physical concerns,
such as worry that panic attacks reflect the presence of life-threatening illnesses (e.g., cardiac
disease, seizure disorder); social concerns, such as embarrassment or fear of being judged
negatively by others because of visible panic symptoms; and concerns about mental functioning,
such as “going crazy” or losing control (Criterion B). Individuals who report fears of dying in
their panic attacks tend to have more severe presentations of panic disorder (e.g., panic attacks
involving more symptoms). The maladaptive changes in behavior represent attempts to minimize
or avoid panic attacks or their consequences. Examples include avoiding physical exertion,
reorganizing daily life to ensure that help is available in the event of a panic attack, restricting
usual daily activities, and avoiding agoraphobia-type situations, such as leaving home, using

public transportation, or shopping. If agoraphobia is present, a separate diagnosis of agoraphobia
is given.
Associated Features
In addition to worry about panic attacks and their consequences, many individuals with panic
disorder report constant or intermittent feelings of anxiety that are more broadly related to health
and mental health concerns. For example, individuals with panic disorder often anticipate a
catastrophic outcome from a mild physical symptom or medication side effect (e.g., thinking that
they may have heart disease or that a headache means presence of a brain tumor). Such
individuals often are relatively intolerant of medication side effects. In addition, there may be
pervasive concerns about abilities to complete daily tasks or withstand daily stressors, excessive
use of drugs (e.g., alcohol, prescribed medications or illicit drugs) to control panic attacks, or
extreme behaviors aimed at controlling panic attacks (e.g., severe restrictions on food intake or
avoidance of specific foods or medications because of concerns about physical symptoms that
provoke panic attacks).
Prevalence
In the general population, the 12-month prevalence estimate for panic disorder across the United
States and several European countries is about 2%–3% in adults and adolescents. The global
lifetime prevalence is estimated at 1.7%, with a 2.7% projected lifetime risk in the World Mental
Health Surveys. In the United States, significantly lower prevalence estimates of panic disorder
are reported among Latinx, African Americans, Caribbean Blacks, and Asian Americans,
compared with non-Latinx Whites. Prevalence estimates of panic disorder in American Indians
range from 2.6% to 4.1%. Lower estimates have been reported for Asian, African, and Latin
American countries, ranging from 0.1% to 0.8%. Women are more frequently affected than men,
at a rate of approximately 2:1. The gender differentiation occurs in adolescence and is already
observable before age 14 years. Although panic attacks occur in children, the overall prevalence
of panic disorder is low before age 14 years (<0.4%). The rates of panic disorder show a gradual
increase during adolescence and possibly following the onset of puberty, and peak during
adulthood. The prevalence declines in older individuals (i.e., 1.2% in adults older than age 55,
0.7% in adults older than age 64), possibly reflecting diminishing severity to subclinical levels.
Development and Course
The median age at onset for panic disorder in the United States is 20–24 years, and crossnationally is 32 years. The mean age at onset is 34.7 years. A small number of cases begin in
childhood, and onset after age 55 years is unusual but can occur. The usual course, if the disorder
is untreated, is chronic but waxing and waning. Some individuals may have episodic outbreaks
with years of remission in between, and others may have continuous severe symptomatology.
According to a longitudinal study in the Netherlands, about one-quarter of the individuals with
panic disorder experienced recurrence of symptoms within the initial 2-year follow-up period.
Only a minority of individuals have full remission without subsequent relapse within a few
years. The course of panic disorder typically is complicated by a range of other disorders, in

Temperamental.
Environmental.
particular other anxiety disorders, depressive disorders, and substance use disorders (see section
“Comorbidity” for this disorder). African American adults have been reported to have a more
chronic course of panic disorder compared with non-Latinx White adults, possibly because of the
enduring impact of racism and discrimination, stigma due to mental illness, and limited access to
adequate care.
Although panic disorder is very rare in childhood, first occurrence of “fearful spells” is often
dated retrospectively back to childhood. As in adults, panic disorder in adolescents tends to have
a chronic course and is frequently comorbid with other anxiety, depressive, and bipolar
disorders. To date, no differences in the clinical presentation between adolescents and adults
have been found. However, adolescents may be less worried about additional panic attacks than
are young adults. Lower prevalence of panic disorder in older adults appears to be attributable to
age-related “dampening” of the autonomic nervous system response. Many older individuals
with “panicky feelings” are observed to have a “hybrid” of limited-symptom panic attacks and
generalized anxiety. Also, older adults tend to attribute their panic attacks to certain stressful
situations, such as a medical procedure or social setting. Older individuals may retrospectively
endorse explanations for the panic attack (which would preclude the diagnosis of panic disorder),
even if an attack might actually have been unexpected in the moment (and thus qualify as the
basis for a panic disorder diagnosis). This may result in under-endorsement of unexpected panic
attacks in older individuals. Thus, careful questioning of older adults is required to assess
whether panic attacks were expected before entering the situation, so that unexpected panic
attacks and the diagnosis of panic disorder are not overlooked.
While the low rate of panic disorder in children could relate to difficulties in symptom
reporting, this seems unlikely given that children are capable of reporting intense fear or panic in
relation to separation and to phobic objects or phobic situations. Adolescents might be less
willing than adults to openly discuss panic attacks. Therefore, clinicians should be aware that
unexpected panic attacks do occur in adolescents, much as they do in adults, and be attuned to
this possibility when encountering adolescents presenting with episodes of intense fear or
distress.
Risk and Prognostic Factors
Negative affectivity (neuroticism) (i.e., proneness to experiencing negative
emotions), anxiety sensitivity (i.e., the disposition to believe that symptoms of anxiety are
harmful), behavioral inhibition, and harm avoidance are risk factors for the onset of panic attacks
and panic disorder. History of “fearful spells” (i.e., limited-symptom attacks that do not meet full
criteria for a panic attack) may be a risk factor for later panic attacks and panic disorder,
particularly when the first panic experience is appraised as negative. Although separation anxiety
in childhood, especially when severe, may precede the later development of panic disorder, it is
not a consistent risk factor.
Most individuals report identifiable stressors in the months before their first panic
attack (e.g., interpersonal stressors and stressors related to physical well-being,
such as negative experiences with illicit or prescription drugs, disease, or death in the family).

Genetic and physiological.
Furthermore, more chronic life stress is associated with greater panic disorder severity. Between
10% and 60% of individuals with panic disorder endorse a history of trauma, and stressful life
experiences and childhood adversities are associated with more severe panic pathology. Parental
overprotection and low emotional warmth are also risk factors for panic disorder. Individuals
with few economic resources are more likely to have symptoms that meet criteria for panic
disorder. Smoking is a risk factor for panic attacks and panic disorder.
Multiple genes likely confer vulnerability to panic disorder; however,
the exact genes, gene products, or functions related to the genetic regions implicated remain
unknown. There is an increased risk for panic disorder among offspring of parents with anxiety,
depressive, and bipolar disorders.
Individuals with panic disorder display particularly enhanced sensitivity to respiratory
stimulation using CO2-enriched air. Respiratory disturbance, such as asthma, may be associated
with panic disorder, in terms of past history, comorbidity, and family history.
Culture-Related Diagnostic Issues
The rate of fears about mental and somatic symptoms of anxiety appears to vary across cultural
contexts and may influence the rate of panic attacks and panic disorder. Also, cultural
expectations may influence the classification of panic attacks as expected or unexpected. For
example, a Vietnamese individual who has a panic attack after walking out into a windy
environment (trúng gió; “hit by the wind”) may attribute the panic attack to exposure to wind as
a result of the cultural syndrome that links these two experiences, resulting in classification of
the panic attack as expected. Various other cultural concepts of distress are associated with panic
disorder, including ataque de nervios (“attack of nerves”) among Latin Americans and khyâl
attacks and “soul loss” among Cambodians. Ataque de nervios may involve trembling,
uncontrollable screaming or crying, aggressive or suicidal behavior, and depersonalization or
derealization, which may be experienced longer than the few minutes typical of panic attacks.
Some clinical presentations of ataque de nervios fulfill criteria for conditions other than panic
attack (e.g., functional neurological symptom disorder). These concepts of distress have an
impact on the symptoms and frequency of panic disorder, including the individual’s attribution
of unexpectedness, as cultural concepts of distress may create fear of certain situations, ranging
from interpersonal arguments (associated with ataque de nervios), to types of exertion
(associated with khyâl attacks), to atmospheric wind (associated with trúng gió attacks).
Clarification of the details of cultural attributions may aid in distinguishing expected and
unexpected panic attacks. For more information regarding cultural concepts of distress, refer to
the “Culture and Psychiatric Diagnosis” chapter in Section III.
The specific worries about panic attacks or their consequences are likely to vary across
ethnoracial groups and cultural contexts (and across different age groups and gender). Among
Asian Americans, Hispanic Americans, and African Americans in the United States, panic
disorder is associated with reports of ethnic discrimination and racism, after the effect of
demographic factors is taken into account. For panic disorder, U.S. community samples of nonLatinx Whites have significantly less functional impairment than African Americans. There are
also higher rates of objectively defined severity in non-Latinx Caribbean Blacks with panic
disorder, and lower reported rates of panic disorder overall in both African Americans and
Caribbean Blacks, suggesting that among U.S. community samples of African descent, panic

disorder criteria may be endorsed only when there is substantial severity and impairment. The
rate of mental health service use for panic disorder varies across ethnoracial groups.
Sex- and Gender-Related Diagnostic Issues
The rate of panic disorder is nearly twofold higher in women compared with men. Relapse from
panic disorder also occurs more frequently in adult women compared with men,
suggesting that women have a more unstable illness course. Gender differences in clinical course
are also found among adolescents. Panic disorder has a larger impact on health-related quality of
life in women than in men, which may be attributable to greater anxiety sensitivity among some
women or greater comorbidity with agoraphobia and depression. There is some evidence for
sexual dimorphism, with high expression of MAOA-uVNTR alleles potentially acting as a
female-specific risk factor for panic disorder.
Diagnostic Markers
Individuals with panic disorder exhibit an attentional bias to threatening stimuli. Panic attacks
may be provoked by agents with disparate mechanisms of action, such as sodium lactate,
caffeine, isoproterenol, yohimbine, CO2, and cholecystokinin, to a much greater extent in
individuals with panic disorder than in those without it. There is considerable interest in the
relationship between panic disorder and sensitivity to these panic-provoking agents. While none
of the data suggest diagnostic utility, data for sensitivity to respiratory stimulation reflect some
level of specificity for panic disorder and related conditions, such as separation anxiety disorder.
Chronically higher baseline hyperventilation and rate of sighing may occur among individuals
with panic disorder. However, none of these laboratory findings are considered diagnostic of
panic disorder.
Association With Suicidal Thoughts or Behavior
Panic attacks and a diagnosis of panic disorder in the past 12 months are related to a higher rate
of suicidal behavior and suicidal thoughts in the past 12 months even when comorbidity and a
history of childhood abuse and other suicide risk factors are taken into account. Approximately
25% of primary care patients with panic disorder report suicidal thoughts. Panic disorder may
increase risk for future suicidal behaviors but not deaths.
Epidemiological survey data of panic attack symptoms show that the cognitive symptoms of
panic (e.g., derealization) may be associated with suicidal thoughts, whereas physical symptoms
(e.g., dizziness, nausea) may be associated with suicidal behaviors.
Functional Consequences of Panic Disorder
Panic disorder is associated with high levels of social, occupational, and physical disability;
considerable economic costs; and the highest number of medical visits among the anxiety
disorders, although the effects are strongest with the presence of agoraphobia. Individuals with
panic disorder may be frequently absent from work or school for doctor and emergency room

Only limited-symptom panic attacks.
Anxiety disorder due to another medical condition.
Substance/medication-induced anxiety disorder.
Other mental disorders with panic attacks as an associated feature (e.g., other anxiety disorders
and psychotic disorders).
visits, which can lead to unemployment or dropping out of school. In older adults, impairment
may be seen in caregiving duties or volunteer activities, and panic disorder is related to lower
health-related quality of life and greater receipt of emergency department services. Full-symptom
panic attacks typically are associated with greater morbidity (e.g., greater health care utilization,
more disability, poorer quality of life) than limited-symptom attacks.
Differential Diagnosis
Panic disorder should not be diagnosed if full-symptom
(unexpected) panic attacks have never been experienced. In the case of only limited-symptom
unexpected panic attacks, an other specified anxiety disorder or unspecified anxiety disorder
diagnosis should be considered.
Panic disorder is not diagnosed if the panic
attacks are judged to be a direct physiological consequence of another medical condition.
Examples of medical conditions that can cause panic attacks include hyperthyroidism,
hyperparathyroidism, pheochromocytoma, vestibular dysfunctions, seizure
disorders, and cardiopulmonary conditions (e.g., arrhythmias, supraventricular tachycardia,
asthma, chronic obstructive pulmonary disease [COPD]). Appropriate laboratory tests (e.g.,
serum calcium levels for hyperparathyroidism; Holter monitor for arrhythmias) or physical
examinations (e.g., for cardiac conditions) may be helpful in determining the etiological role of
another medical condition. Features such as onset after age 45 years or the presence of atypical
symptoms during a panic attack (e.g., vertigo, loss of consciousness, loss of bladder or bowel
control, slurred speech, amnesia) suggest the possibility that another medical condition or a
substance may be causing the panic attack symptoms.
Panic disorder is not diagnosed if the panic attacks
are judged to be a direct physiological consequence of a substance. Intoxication with central
nervous system stimulants (e.g., cocaine, amphetamine-type substances, caffeine) or cannabis
and withdrawal from central nervous system depressants (e.g., alcohol, barbiturates) can
precipitate a panic attack.
However, if panic attacks continue to occur outside of the context of substance use (e.g., long
after the effects of intoxication or withdrawal have ended), a diagnosis of panic disorder should
be considered. In addition, because panic disorder may precede substance use in some
individuals and may be associated with increased substance use, especially for purposes of selfmedication, a detailed history should be taken to determine if the individual had panic attacks
prior to excessive substance use. If this is the case, a diagnosis of panic disorder should be
considered in addition to a diagnosis of substance use disorder. Features such as onset after age
45 years or the presence of atypical symptoms during a panic attack (e.g., vertigo, loss of
consciousness, loss of bladder or bowel control, slurred speech, amnesia) suggest the possibility
that another medical condition or a substance may be causing the panic attack symptoms.
Panic attacks that occur as a symptom of other anxiety disorders are expected (e.g., triggered by

social situations in social anxiety disorder, by phobic objects or situations in specific phobia or
agoraphobia, by worry in generalized anxiety disorder, by separation from home or attachment
figures in separation anxiety disorder) and thus would not meet criteria for panic disorder. (Note:
Sometimes an unexpected panic attack is associated with the onset of another anxiety disorder,
but then the attacks become expected, whereas panic disorder is characterized by recurrent
unexpected panic attacks.) If the panic attacks occur only in response to specific triggers, then
only the relevant anxiety disorder is assigned. However, if the individual experiences unexpected
panic attacks as well and shows persistent concern and worry or behavioral change because of
the attacks, then an additional diagnosis of panic disorder should be considered.
Comorbidity
Panic disorder infrequently occurs in clinical settings in the absence of other psychopathology. In
the general population, 80% of individuals with panic disorder had a lifetime comorbid mental
diagnosis. The prevalence of panic disorder is elevated in individuals with other disorders,
particularly other anxiety disorders (and especially agoraphobia), major depressive disorder,
bipolar I and bipolar II disorder, and possibly mild alcohol use disorder. While panic disorder
occasionally has an earlier age at onset than the comorbid disorder(s), onset often occurs after the
comorbid disorder and may be seen as a severity marker of the comorbid illness.
Reported lifetime rates of comorbidity between major depressive disorder and panic disorder
vary widely, ranging from 10% to 65% in individuals with panic disorder. In approximately onethird of individuals with both disorders, the depression precedes the onset of panic disorder. In
the remaining two-thirds, depression occurs coincident with or following the onset of panic
disorder. A subset of individuals with panic disorder develop a
substance-related disorder, which for some represents an attempt to treat their anxiety with
alcohol or medications. Comorbidity with other anxiety disorders and illness anxiety disorder is
also common.
Panic disorder is significantly comorbid with numerous general medical symptoms and
conditions, including, but not limited to, dizziness, cardiac arrhythmias, hyperthyroidism,
asthma, COPD, and irritable bowel syndrome. However, the nature of the association (e.g., cause
and effect) between panic disorder and these conditions remains unclear. Although mitral valve
prolapse and thyroid disease are more common among individuals with panic disorder than in the
general population, the increases in prevalence are not consistent.
Panic Attack Specifier
Note: Symptoms are presented for the purpose of identifying a panic attack;
however, panic attack is not a mental disorder and cannot be coded. Panic attacks
can occur in the context of any anxiety disorder as well as other mental disorders
(e.g., depressive disorders, posttraumatic stress disorder, substance use disorders)
and some medical conditions (e.g., cardiac, respiratory, vestibular, gastrointestinal).
When the presence of a panic attack is identified, it should be noted as a specifier

(e.g., “posttraumatic stress disorder with panic attacks”). For panic disorder, the
presence of panic attack is contained within the criteria for the disorder and panic
attack is not used as a specifier.
An abrupt surge of intense fear or intense discomfort that reaches a peak within
minutes, and during which time four (or more) of the following symptoms occur:
Note: The abrupt surge can occur from a calm state or an anxious state.
1. 
1. Palpitations, pounding heart, or accelerated heart rate.
2. Sweating.
3. Trembling or shaking.
4. Sensations of shortness of breath or smothering.
5. Feelings of choking.
6. Chest pain or discomfort.
7. Nausea or abdominal distress.
8. Feeling dizzy, unsteady, light-headed, or faint.
9. Chills or heat sensations.
10. Paresthesias (numbness or tingling sensations).
11. Derealization (feelings of unreality) or depersonalization (being detached from
oneself).
12. Fear of losing control or “going crazy.”
13. Fear of dying.
Note: Culture-specific symptoms (e.g., tinnitus, neck soreness, headache,
uncontrollable screaming or crying) may be seen. Such symptoms should not count
as one of the four required symptoms.
Features
The essential feature of a panic attack is an abrupt surge of intense fear or intense discomfort that
reaches a peak within minutes and during which time 4 or more of 13 physical and cognitive
symptoms occur. Eleven of these 13 symptoms are physical (e.g., palpitations, sweating), while 2
are cognitive (i.e., fear of losing control or going crazy, fear of dying). “Fear of going crazy” is a
colloquialism often used by individuals with panic attacks and is not intended as a pejorative or
diagnostic term. The term within minutes means that the time to peak intensity is literally only a
few minutes. A panic attack can arise from either a calm state or an
anxious state, and time to peak intensity should be assessed independently of any preceding
anxiety. That is, the start of the panic attack is the point at which there is an abrupt increase in
discomfort rather than the point at which anxiety first developed. Likewise, a panic attack can
return to either an anxious state or a calm state and possibly peak again. A panic attack is
distinguished from ongoing anxiety by its time to peak intensity, which occurs within minutes;
its discrete nature; and its typically greater severity. Attacks that meet all other criteria but have
fewer than four physical and/or cognitive symptoms are referred to as limited-symptom attacks.

There are two characteristic types of panic attacks: expected and unexpected. Expected panic
attacks are attacks for which there is an obvious cue or trigger, such as situations in which panic
attacks have typically occurred. Unexpected panic attacks are those for which there is no obvious
cue or trigger at the time of occurrence (e.g., when relaxing or out of sleep [nocturnal panic
attack]). The determination of whether panic attacks are expected or unexpected is made by the
clinician, who makes this judgment based on a combination of careful questioning as to the
sequence of events preceding or leading up to the attack and the individual’s own judgment of
whether the attack seemed to occur for no apparent reason. Panic attacks can occur in the context
of any mental disorder (e.g., anxiety disorders, depressive disorders, bipolar disorders, eating
disorders, obsessive-compulsive and related disorders, personality disorders, psychotic disorders,
substance use disorders) and some medical conditions (e.g., cardiac, respiratory, vestibular,
gastrointestinal), with the majority of presentations never meeting criteria for panic disorder.
Recurrent unexpected panic attacks are required for a diagnosis of panic disorder.
Associated Features
One type of unexpected panic attack is a nocturnal panic attack (i.e., waking from sleep in a
state of panic), which differs from panicking after fully waking from sleep.
Prevalence
In the general population, 12-month prevalence estimates for panic attacks in Spain and in the
United States range from 9.5% to 11.2% in adults. Twelve-month prevalence estimates do not
appear to differ significantly among African Americans, Asian Americans, and Latinx.
Approximately 8.5% of American Indians report a lifetime history of panic attacks. Lifetime
prevalence rates of panic attacks cross-nationally are 13.2%. Women are more frequently
affected than men, although this gender difference is more pronounced for panic disorder. Panic
attacks can occur in children but are relatively rare until the age of puberty, when the prevalence
rates increase. The prevalence declines in older individuals, possibly reflecting diminishing
severity to subclinical levels.
Development and Course
The mean age at onset for panic attacks in the United States is approximately 22–23 years among
adults. However, the course of panic attacks is likely influenced by the course of any cooccurring mental disorder(s) and stressful life events. Panic attacks are uncommon, and
unexpected panic attacks are rare, in preadolescent children. Adolescents might be less willing
than adults to openly discuss panic attacks, even though they present with episodes of intense
fear or discomfort. Lower prevalence of panic attacks in older individuals may be related to a
weaker autonomic response to emotional states relative to younger individuals. Older individuals
may be less inclined to use the word “fear” and more inclined to use the word “discomfort” to
describe panic attacks. Older individuals with “panicky feelings” may have a hybrid of limitedsymptom attacks and generalized anxiety. In addition, older individuals tend to attribute panic
attacks to certain situations that are stressful (e.g., medical procedures, social settings) and may
retrospectively endorse explanations for the panic attack even if it was unexpected in the
moment. This may result in under-endorsement of unexpected panic attacks in older individuals.

Temperamental.
Environmental.
Genetic and physiological.
Risk and Prognostic Factors
Negative affectivity (neuroticism) (i.e., proneness to experiencing negative
emotions), anxiety sensitivity (i.e., the disposition to believe that symptoms of anxiety are
harmful), behavioral inhibition, and harm avoidance are risk factors for the onset of panic
attacks. History of “fearful spells” (i.e., limited-symptom attacks that do not meet full criteria for
a panic attack) may be a risk factor for later panic attacks.
Smoking is a risk factor for panic attacks. Most individuals report identifiable
stressors in the months before their first panic attack (e.g., interpersonal stressors and stressors
related to physical well-being, such as negative experiences with illicit or prescription drugs,
disease, or death in the family). Separation from parents, overprotective parenting, and parental
rejection are risk factors for panic attacks.
Individuals with chronic obstructive pulmonary disease who report low
perceptions of control over the disease and negative beliefs about the consequences of
unpredictable breathless attacks are more likely to have panic symptoms.
Culture-Related Diagnostic Issues
Cultural interpretations may influence the determination of panic attacks as expected or
unexpected. Culture-specific symptoms (e.g., tinnitus, neck soreness, headache, and
uncontrollable screaming or crying) may be seen; however, such symptoms should not count as
one of the four required symptoms. Frequency of each of the 13 symptoms varies crossculturally (e.g., higher rates of paresthesias in African Americans, of dizziness in several Asian
groups, and of trembling in non-Latinx Whites). Cultural concepts of distress also influence the
cross-cultural presentation of panic attacks, resulting in different symptom profiles across
different cultural groups. Examples include khyâl (wind) attacks, a Cambodian cultural
syndrome involving dizziness, tinnitus, and neck soreness; and trúng gió (wind-related) attacks,
a Vietnamese cultural syndrome associated with headaches. Cultural explanatory models can
heighten the salience of specific panic symptoms. For example, traditional Cambodian views
about the abnormal circulation of khyâl in the body are associated with the perceived
dangerousness of some symptoms (e.g., neck soreness), which can trigger catastrophic
cognitions and panic attacks. Ataque de nervios (attack of nerves) is a cultural syndrome among
Latin Americans that may involve trembling, uncontrollable screaming or crying, aggressive or
suicidal behavior, and depersonalization or derealization, and which may be experienced for
longer than only a few minutes. Some clinical presentations of ataque de nervios fulfill criteria
for conditions other than panic attack (e.g., other specified dissociative disorder). Also, cultural
expectations may influence the classification of panic attacks as expected or unexpected, as
cultural syndromes may create fear of certain situations, ranging from interpersonal arguments
(associated with ataque de nervios), to types of exertion (associated with khyâl attacks), to
atmospheric wind (associated with trúng gió attacks). Clarification of the details of cultural
attributions may aid in distinguishing expected and unexpected panic attacks. For more
information about cultural concepts of distress, see the “Culture and Psychiatric Diagnosis”
chapter in Section III.

Other paroxysmal episodes (e.g., “anger attacks”).
Anxiety disorder due to another medical condition.
Sex- and Gender-Related Diagnostic Issues
Panic attacks are more common in women than in men. Among those who report panic attacks,
women are more likely to endorse symptoms of shortness of breath and nausea but less likely to
endorse sweating than are men.
Diagnostic Markers
Physiological recordings of naturally occurring panic attacks in individuals with panic disorder
indicate abrupt surges of arousal, usually of heart rate, that reach a peak within
minutes and subside within minutes, and for a proportion of these individuals the panic attack
may be preceded by cardiorespiratory instabilities. Panic attacks are characterized by heart rate
and tidal volume increases and a drop in pCO2.
Association With Suicidal Thoughts or Behavior
Panic attacks are related to a higher rate of suicide attempts and suicidal thoughts even when
comorbidity and other suicide risk factors are taken into account.
Functional Consequences of Panic Attacks
In the context of co-occurring mental disorders, including anxiety disorders, depressive
disorders, bipolar disorder, substance use disorders, psychotic disorders, and personality
disorders, panic attacks are associated with increased symptom severity, higher rates of
comorbidity, and poorer treatment response. Recurrent panic attacks in particular are associated
with increased odds of many mental health diagnoses. Furthermore, more severe panic attacks
are associated with a greater likelihood of developing panic disorder and a variety of other
mental health conditions, as well as greater persistence of mental illness and impaired
functioning. Also, full-symptom panic attacks typically are associated with greater morbidity
(e.g., greater health care utilization, more disability, poorer quality of life) than limited-symptom
attacks.
Differential Diagnosis
Panic attacks should not be diagnosed if the
episodes do not involve the essential feature of an abrupt surge of intense fear or intense
discomfort, but rather other emotional states (e.g., anger, grief).
Medical conditions that can cause or be
misdiagnosed 
as 
panic 
attacks 
include 
hyperthyroidism, 
hyperparathyroidism,
pheochromocytoma, vestibular dysfunctions, seizure disorders, and cardiopulmonary conditions
(e.g., arrhythmias, supraventricular tachycardia, asthma, chronic obstructive pulmonary disease).
Appropriate laboratory tests (e.g., serum calcium levels for hyperparathyroidism; Holter monitor
for arrhythmias) or physical examinations (e.g., for cardiac conditions) may be helpful in
determining the etiological role of another medical condition.

Substance/medication-induced anxiety disorder.
Panic disorder.
F40.00
Intoxication with central nervous system stimulants
(e.g., cocaine, amphetamine-type substances, caffeine) or cannabis and withdrawal from central
nervous system depressants (e.g., alcohol, barbiturates) can precipitate a panic attack. A detailed
history should be taken to determine if the individual had panic attacks prior to excessive
substance use. Features such as onset after age 45 years or the presence of atypical symptoms
during a panic attack (e.g., vertigo, loss of consciousness, loss of bladder or bowel control,
slurred speech, or amnesia) suggest the possibility that a medical condition or a substance may
be causing the panic attack symptoms.
Repeated unexpected panic attacks are required but are not sufficient for the
diagnosis of panic disorder (i.e., full diagnostic criteria for panic disorder must be met).
Comorbidity
Panic attacks are associated with increased likelihood of various comorbid mental disorders,
including anxiety disorders, depressive disorders, bipolar disorders, impulse-control disorders,
and substance use disorders. Panic attacks are associated with increased likelihood of later
developing anxiety disorders, depressive disorders, bipolar disorders, alcohol use disorder, and
possibly other disorders.
Agoraphobia
Diagnostic Criteria
A. Marked fear or anxiety about two (or more) of the following five situations:
1. Using public transportation (e.g., automobiles, buses, trains, ships, planes).
2. Being in open spaces (e.g., parking lots, marketplaces, bridges).
3. Being in enclosed places (e.g., shops, theaters, cinemas).
4. Standing in line or being in a crowd.
5. Being outside of the home alone.
B. The individual fears or avoids these situations because of thoughts that escape
might be difficult or help might not be available in the event of developing paniclike symptoms or other incapacitating or embarrassing symptoms (e.g., fear of
falling in the elderly; fear of incontinence).
C. The agoraphobic situations almost always provoke fear or anxiety.
D. The agoraphobic situations are actively avoided, require the presence of a
companion, or are endured with intense fear or anxiety.
E. The fear or anxiety is out of proportion to the actual danger posed by the
agoraphobic situations and to the sociocultural context.
F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or

more.
G. The fear, anxiety, or avoidance causes clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
H. If another medical condition (e.g., inflammatory bowel disease, Parkinson’s
disease) is present, the fear, anxiety, or avoidance is clearly excessive.
I. The fear, anxiety, or avoidance is not better explained by the symptoms of
another mental disorder—for example, the symptoms are not confined to specific
phobia, situational type; do not involve only social situations (as in social anxiety
disorder); and are not related exclusively to obsessions (as in obsessivecompulsive disorder), perceived defects or flaws in physical appearance (as in
body dysmorphic disorder), reminders of traumatic events (as in posttraumatic
stress disorder), or fear of separation (as in separation anxiety disorder).
Note: Agoraphobia is diagnosed irrespective of the presence of panic disorder. If an
individual’s presentation meets criteria for panic disorder and agoraphobia, both
diagnoses should be assigned.
Diagnostic Features
The essential feature of agoraphobia is marked fear or anxiety triggered by the real or anticipated
exposure to a wide range of situations (Criterion A). The diagnosis requires endorsement of
symptoms occurring in at least two of the following five situations: 1) using public
transportation, such as automobiles, buses, trains, ships, or planes; 2) being in open spaces, such
as parking lots, marketplaces, or bridges; 3) being in enclosed spaces, such as shops, theaters, or
cinemas; 4) standing in line or being in a crowd; or 5) being outside of the home alone. The
examples for each situation are not exhaustive; other situations may be feared. When
experiencing fear and anxiety cued by such situations, individuals typically experience thoughts
that something terrible might happen (Criterion B). Individuals frequently believe that escape
from such situations might be difficult (e.g., “can’t get out of here”) or that help might be
unavailable (e.g., “there is nobody to help me”) when panic-like symptoms or other
incapacitating or embarrassing symptoms occur. “Panic-like symptoms” refer to any of the 13
symptoms included in the criteria for panic attack, such as dizziness, faintness, and fear of dying.
“Other incapacitating or embarrassing symptoms” include
symptoms such as vomiting and inflammatory bowel symptoms, as well as, in older adults, a fear
of falling or, in children, a sense of disorientation and getting lost.
The amount of fear experienced may vary with proximity to the feared situation and may
occur in anticipation of or in the actual presence of the agoraphobic situation. Also, the fear or
anxiety may take the form of a full- or limited-symptom panic attack (i.e., an expected panic
attack). Fear or anxiety is evoked nearly every time the individual comes into contact with the
feared situation (Criterion C). Thus, an individual who becomes anxious only occasionally in an
agoraphobic situation (e.g., becomes anxious when standing in line on only one out of every five
occasions) would not be diagnosed with agoraphobia. The individual actively avoids the

situation, requires the presence of a companion, or, if he or she either is unable or decides not to
avoid it, the situation evokes intense fear or anxiety (Criterion D). Active avoidance means the
individual is currently behaving in ways that are intentionally designed to prevent or minimize
contact with agoraphobic situations. Avoidance can be behavioral (e.g., changing daily routines,
choosing a job nearby to avoid using public transportation, arranging for food delivery to avoid
entering shops and supermarkets) as well as cognitive (e.g., using distraction to get through
agoraphobic situations) in nature. The avoidance can become so severe that the individual is
completely homebound. Often, an individual is better able to confront a feared situation when
accompanied by a companion, such as a partner, friend, or health professional. Also, the
individual may employ safety behaviors (e.g., sitting near exits when taking public transportation
or at the movies) to better endure such situations.
The fear, anxiety, or avoidance must be out of proportion to the actual danger posed by the
agoraphobic situations and to the sociocultural context (Criterion E). Differentiating
disproportionate, clinically significant agoraphobic fears from reasonable fears (e.g., not wanting
to leave the house during a bad storm) or from situations that are deemed dangerous (e.g.,
walking in a parking lot or using public transportation in a high-crime area) is important for a
number of reasons. First, what constitutes avoidance may be difficult to judge across cultures and
sociocultural contexts (e.g., it is socioculturally appropriate for orthodox Muslim women in
certain parts of the world to avoid leaving the house alone, and thus such avoidance would not be
considered indicative of agoraphobia). Second, older adults are likely to overattribute their fears
to age-related constraints and are less likely to judge their fears as being out of proportion to the
actual risk. Third, individuals with agoraphobia are likely to overestimate danger in relation to
panic-like or other bodily symptoms. Agoraphobia should be diagnosed only if the fear, anxiety,
or avoidance is persistent (Criterion F) and if it causes clinically significant distress or
impairment in social, occupational, or other important areas of functioning (Criterion G). The
duration of “typically lasting for 6 months or more” is meant to exclude individuals with shortlived, transient problems.
Associated Features
In its most severe forms, agoraphobia can cause individuals to become completely homebound,
unable to leave their home and dependent on others for services or assistance to provide even for
basic needs. Demoralization and depressive symptoms, as well as abuse of alcohol and sedative
medication as inappropriate self-medication strategies, are common.
Prevalence
Every year approximately 1%–1.7% of adolescents and adults worldwide have symptoms that
meet diagnostic criteria for agoraphobia. Women are twice as likely as men to experience
agoraphobia. Agoraphobia may occur in childhood, but incidence peaks in late adolescence and
early adulthood. Studies have shown the 12-month prevalence in individuals living in the United
States who are older than 65 years is 0.4% and 0.5% among individuals in Europe and North
America older than 55 years. Approximately 0.2%–0.8% of

Temperamental.
the adult population in various countries has a past 12-month diagnosis of agoraphobia without
panic disorder.
Development and Course
The percentage of individuals with agoraphobia reporting panic attacks or panic disorder
preceding the onset of agoraphobia ranges from 30% in community samples to more than 50% in
clinical samples.
In two-thirds of all cases of agoraphobia, initial onset is before age 35 years, with 21 years
the mean age at onset, although age at onset of agoraphobia without preceding panic attacks or
panic disorder is 25–29 years. First onset in childhood is rare. There is a substantial incidence
risk in adolescence and early adulthood, with indications for a second high incidence risk phase
after age 40 years. Approximately 10% of older adults with agoraphobia reported their first
episode of agoraphobia occurring after age 65.
The course of agoraphobia is typically persistent and chronic. Complete remission is rare
(10%), unless the agoraphobia is treated. Individuals with comorbid panic disorder and
agoraphobia are more likely to experience recurrence of symptoms after a period of remission if
they had an earlier age at onset (< 20 years old). With more severe agoraphobia, rates of full
remission decrease, whereas rates of relapse and chronicity increase. Approximately 36% of
individuals with agoraphobia who achieve remission eventually experience relapse. A range of
other disorders, in particular other anxiety disorders, depressive disorders, substance use
disorders, and personality disorders, may complicate the course of agoraphobia. The long-term
course and outcome of agoraphobia are associated with substantially elevated risk of secondary
major depressive disorder, persistent depressive disorder, and substance use disorders.
The clinical features of agoraphobia are relatively consistent across the life span, although
the type of agoraphobic situations triggering fear, anxiety, or avoidance, as well as the type of
cognitions, may vary. For example, in children, being outside of the home alone is the most
frequent situation feared, whereas in older adults, being in shops, standing in line, and being in
open spaces are most often feared. Also, cognitions often pertain to becoming lost (in children),
to experiencing panic-like symptoms (in adults), to falling (in older adults).
The apparent low prevalence of agoraphobia in children could reflect difficulties in symptom
reporting, and thus assessments in young children may require solicitation of information from
multiple sources, including parents or teachers. Adolescents, particularly boys, may be less
willing than adults to openly discuss agoraphobic fears and avoidance; however, agoraphobia
can occur before adulthood and should be assessed in children and adolescents. In older adults,
comorbid somatic symptom disorder, having medical complications, and motor disturbances
(e.g., a sense of falling) are frequently mentioned by individuals as the reason for their fear and
avoidance. In these instances, care is to be taken in evaluating whether the fear and avoidance are
out of proportion to the real danger involved.
Risk and Prognostic Factors
Behavioral inhibition, negative affectivity (neuroticism), anxiety sensitivity, and
trait anxiety are closely associated with agoraphobia but are relevant to most anxiety disorders
(specific phobia, social anxiety disorder, panic disorder, generalized anxiety disorder). Anxiety
sensitivity (the disposition to believe that symptoms of anxiety are harmful) is also characteristic

Environmental.
Genetic and physiological.
Specific phobia, situational type.
of individuals with agoraphobia.
Negative events in childhood (e.g., separation, death of parent) and other stressful
events, such as being attacked or mugged, are associated with the onset of agoraphobia.
Furthermore, individuals with agoraphobia describe the family climate and child-rearing
behavior as being characterized by reduced warmth and increased overprotection.
Heritability for agoraphobia is 61%. Of the various phobias,
agoraphobia has the strongest and most specific association with the genetic factor that
represents proneness to phobias. Family history of anxiety disorders is associated with an earlier
age at onset of agoraphobia (< 27 years old), and family history of panic disorder in particular is
associated with agoraphobia.
Sex- and Gender-Related Diagnostic Issues
Women have different patterns of comorbid disorders than men. Consistent with gender
differences in the prevalence of mental disorders, men have higher rates of comorbid substance
use disorders.
Association With Suicidal Thoughts or Behavior
Approximately 15% of individuals with agoraphobia report suicidal thoughts or behavior. For
individuals with panic disorder, symptoms of agoraphobia may be a risk factor for suicidal
thoughts.
Functional Consequences of Agoraphobia
Like most other anxiety disorders, agoraphobia is associated with considerable impairment and
disability in terms of role functioning, work productivity, and disability days. Agoraphobia
severity is a strong determinant of the degree of disability, irrespective of the presence of
comorbid panic disorder, panic attacks, and other comorbid conditions. Individuals with
agoraphobia can be completely homebound or unable to work. Individuals with panic disorder
with agoraphobia who have an early course of onset (< age 20 years) are less likely to be
married.
Differential Diagnosis
Differentiating agoraphobia from situational specific phobia can
be challenging in some cases, because these conditions share several symptom characteristics
and criteria. Specific phobia, situational type, should be diagnosed versus agoraphobia if the fear,
anxiety, or avoidance is limited to one of the agoraphobic situations. Requiring fears from two or
more of the agoraphobic situations is a robust means for differentiating agoraphobia from
specific phobias, particularly the situational subtype. Additional differentiating features include
the content of the individual’s cognitions. Thus, if the situation is feared for reasons other than
panic-like symptoms or other incapacitating or embarrassing symptoms (e.g., fears of being
directly harmed by the situation itself, such as fear of the plane crashing for individuals who fear

Separation anxiety disorder.
Social anxiety disorder.
Panic disorder.
Acute stress disorder and posttraumatic stress disorder.
Major depressive disorder.
Avoidance related to other medical conditions.
flying), then a diagnosis of specific phobia may be more appropriate.
Separation anxiety disorder can be best differentiated from
agoraphobia by examining the individual’s cognitions. In separation anxiety disorder, the
thoughts are about detachment from significant others and the home environment (i.e., parents or
other attachment figures), whereas in agoraphobia the focus is on panic-like symptoms or other
incapacitating or embarrassing symptoms in the feared situations.
Agoraphobia should be differentiated from social anxiety disorder based
primarily on the situational clusters that trigger fear, anxiety, or avoidance and the individual’s
cognitions. In social anxiety disorder, the focus is on fear of being negatively evaluated.
When criteria for panic disorder are met, agoraphobia should not be diagnosed if
the avoidance behaviors associated with the panic attacks do not extend to avoidance of two or
more agoraphobic situations.
Acute stress disorder and posttraumatic
stress disorder (PTSD) can be differentiated from agoraphobia by examining whether the fear,
anxiety, or avoidance is related only to situations that remind the individual of a traumatic event.
If the fear, anxiety, or avoidance is restricted to trauma reminders, and if the avoidance behavior
does not extend to two or more agoraphobic situations, then a diagnosis of agoraphobia is not
warranted.
In major depressive disorder, the individual may avoid leaving home
because of apathy, loss of energy, low self-esteem, and anhedonia. If the avoidance is unrelated
to fears of panic-like or other incapacitating or embarrassing symptoms, then agoraphobia should
not be diagnosed.
Individuals with certain medical conditions may
avoid situations because of realistic concerns about being incapacitated (e.g., fainting in an
individual with transient ischemic attacks) or being embarrassed (e.g., diarrhea in an individual
with Crohn’s disease). The diagnosis of agoraphobia should be given only when the fear or
avoidance is clearly in excess of that usually associated with these medical conditions.
Comorbidity
About 90% of individuals with agoraphobia also have other mental disorders. The most frequent
additional diagnoses are other anxiety disorders (e.g., specific phobias, panic disorder, social
anxiety disorder), depressive disorders (major depressive disorder), PTSD, and alcohol use
disorder. Whereas other anxiety disorders (e.g., separation anxiety disorder, specific phobias,
panic disorder) frequently precede onset of agoraphobia, depressive disorders and substance use
disorders typically occur secondary to agoraphobia. In some individuals, a substance use disorder
precedes agoraphobia. Individuals with comorbid agoraphobia and major depressive disorder
tend to have a more treatment-resistant course of agoraphobia relative to individuals with
agoraphobia alone.

F41.1
Generalized Anxiety Disorder
Diagnostic Criteria
A. Excessive anxiety and worry (apprehensive expectation), occurring more days
than not for at least 6 months, about a number of events or activities (such as
work or school performance).
B. The individual finds it difficult to control the worry.
C. The anxiety and worry are associated with three (or more) of the following six
symptoms (with at least some symptoms having been present for more days
than not for the past 6 months):
Note: Only one item is required in children.
1. Restlessness or feeling keyed up or on edge.
2. Being easily fatigued.
3. Difficulty concentrating or mind going blank.
4. Irritability.
5. Muscle tension.
6. Sleep disturbance (difficulty falling or staying asleep, or restless, unsatisfying
sleep).
D. The anxiety, worry, or physical symptoms cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
E. The disturbance is not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication) or another medical condition (e.g.,
hyperthyroidism).
F. The disturbance is not better explained by another mental disorder (e.g., anxiety
or worry about having panic attacks in panic disorder, negative evaluation in
social anxiety disorder, contamination or other obsessions in obsessivecompulsive disorder, separation from attachment figures in separation anxiety
disorder, reminders of traumatic events in posttraumatic stress disorder, gaining
weight in anorexia nervosa, physical complaints in somatic symptom disorder,
perceived appearance flaws in body dysmorphic disorder, having a serious
illness in illness anxiety disorder, or the content of delusional beliefs in
schizophrenia or delusional disorder).
Diagnostic Features
The essential feature of generalized anxiety disorder is excessive anxiety and worry
(apprehensive expectation) about a number of events or activities. The intensity, duration, or

frequency of the anxiety and worry is out of proportion to the actual likelihood or impact of the
anticipated event. The individual finds it difficult to control the worry and to keep worrisome
thoughts from interfering with attention to tasks at hand. Adults with generalized anxiety
disorder often worry about everyday, routine life circumstances, such as possible job
responsibilities, health and finances, the health of family members, misfortune to their children,
or minor matters (e.g., doing household chores or being late for appointments). Children with
generalized anxiety disorder tend to worry excessively about their competence or the quality of
their performance. During the course of the disorder, the focus of worry may shift from one
concern to another.
Several features distinguish generalized anxiety disorder from nonpathological anxiety. First,
the worries associated with generalized anxiety disorder are excessive and typically interfere
significantly with psychosocial functioning, whereas the worries of everyday life are not
excessive and are perceived as more manageable and may be put off when more pressing matters
arise. Second, the worries associated with generalized anxiety disorder are more pervasive,
pronounced, and distressing; have longer duration; and frequently occur without precipitants.
The greater the range of life circumstances about which a person worries (e.g., finances,
children’s safety, job performance), the more likely his or her symptoms are to meet criteria for
generalized anxiety disorder. Third, everyday worries are much less likely to be accompanied by
physical symptoms (e.g., restlessness or feeling keyed up or on edge). Individuals with
generalized anxiety disorder report subjective distress as a result of constant worry and related
impairment in social, occupational, or other important areas of functioning.
The anxiety and worry are accompanied by at least three of the following additional
symptoms: restlessness or feeling keyed up or on edge, being easily fatigued, difficulty
concentrating or mind going blank, irritability, muscle tension, and disturbed sleep, although
only one additional symptom is required in children.
Associated Features
Associated with muscle tension, there may be trembling, twitching, feeling shaky, and muscle
aches or soreness. Many individuals with generalized anxiety disorder also experience somatic
symptoms (e.g., sweating, nausea, diarrhea) and an exaggerated startle response. Symptoms of
autonomic hyperarousal (e.g., accelerated heart rate, shortness of breath, dizziness) are less
prominent in generalized anxiety disorder than in other anxiety disorders, such as panic disorder.
Other conditions that may be associated with stress (e.g., irritable bowel syndrome, headaches)
frequently accompany generalized anxiety disorder.
Prevalence
The 12-month prevalence of generalized anxiety disorder is 0.9% among adolescents and 2.9%
among adults in the general community of the United States. The mean 12-month
prevalence for the disorder around the world is 1.3%, with a range of 0.2% to 4.3%. The lifetime
morbid risk in the United States is 9.0%. Women and adolescent girls are at least twice as likely
as men and adolescent boys to experience generalized anxiety disorder. The 12-month

Temperamental.
Environmental.
prevalence in older adults including individuals age 75 years and older ranges from 2.8% to
3.1% in the United States, Israel, and European countries.
Individuals of European descent tend to have symptoms that meet criteria for generalized
anxiety disorder more frequently than do individuals of Asian and African descent. Furthermore,
individuals from high-income countries are more likely than individuals from low- and middleincome countries to report that they have experienced symptoms that meet criteria for
generalized anxiety disorder in their lifetime.
Development and Course
Many individuals with generalized anxiety disorder report that they have felt anxious and
nervous all their lives. The mean age at onset for generalized anxiety disorder in North America
is 35 years, later than that for the other anxiety disorders; the disorder rarely occurs prior to
adolescence. However, age at onset is spread over a very broad range and tends to be older in
lower-income countries worldwide. The symptoms of excessive worry and anxiety may occur
early in life but are then manifested as an anxious temperament. Generalized anxiety disorder
symptoms tend to be chronic and wax and wane across the life span, fluctuating between
syndromal and subsyndromal forms of the disorder. Course is more persistent in lower-income
countries, but impairment tends to be higher in high-income countries. Rates of full remission are
very low.
The earlier in life individuals have symptoms that meet criteria for generalized anxiety
disorder, the more comorbidity and impairment they tend to have. Younger adults experience
greater severity of symptoms than do older adults.
The clinical expression of generalized anxiety disorder is relatively consistent across the life
span. The primary difference across age groups is in the content of the individual’s worry; thus,
the content of an individual’s worry tends to be age appropriate.
In children and adolescents with generalized anxiety disorder, the anxieties and worries often
concern the quality of their performance or competence at school or in sporting events, even
when their performance is not being evaluated by others. There may be excessive concerns about
punctuality. They may also worry about catastrophic events, such as earthquakes or nuclear war.
Children with the disorder may be overly conforming, perfectionistic, and unsure of themselves
and may tend to redo tasks because of excessive dissatisfaction with less-than-perfect
performance. They may be overzealous in seeking reassurance and approval and require
excessive reassurance about their performance and other things they are worried about.
In the elderly, the advent of chronic physical disease can be a potent issue for excessive
worry. In the frail elderly, worries about safety—and especially about falling—may limit
activities.
Risk and Prognostic Factors
Behavioral inhibition, negative affectivity (neuroticism), harm avoidance,
reward dependence, and attentional bias to threat have been associated with generalized anxiety
disorder.
Childhood adversities and parenting practices (e.g., overprotection, overcontrol,
reinforcement of avoidance) have been associated with generalized anxiety disorder.

Genetic and physiological. One-third of the risk of experiencing generalized anxiety disorder is
genetic, and these genetic factors overlap with the risk of negative affectivity (neuroticism) and
are shared with other anxiety and mood disorders, particularly major depressive disorder.
Culture-Related Diagnostic Issues
There is considerable cultural variation in the expression of generalized anxiety disorder. For
example, in some cultural contexts, somatic symptoms predominate in the expression of the
disorder, whereas in other cultural contexts cognitive symptoms tend to predominate. This
difference may be more evident on initial presentation than subsequently, as more symptoms are
reported over time. There is no information as to whether the propensity for excessive worrying
is related to cultural background, although the topic being worried about can be culturally
specific. It is important to consider the social and cultural context when evaluating whether
worries about certain situations are excessive. In the United States, higher prevalence is
associated with exposure to racism and ethnic discrimination and, for some ethnoracial groups,
with being born in the United States.
Sex- and Gender-Related Diagnostic Issues
In clinical settings, generalized anxiety disorder is diagnosed somewhat more frequently in
women than in men (about 55%–60% of those presenting with the disorder are women). In
epidemiological studies, approximately two-thirds are women. Women and men who experience
generalized anxiety disorder appear to have similar symptoms but demonstrate different patterns
of comorbidity consistent with gender differences in the prevalence of disorders. In women,
comorbidity is largely confined to the anxiety disorders and unipolar depression, whereas in
men, comorbidity is more likely to extend to the substance use disorders as well.
Association With Suicidal Thoughts or Behavior
Generalized anxiety disorder is associated with increased suicidal thoughts and behavior, even
after adjustment for comorbid disorders and stressful life events. Psychological autopsy studies
show that generalized anxiety disorder is the most frequent anxiety disorder diagnosed in
suicides. Both subthreshold and threshold generalized anxiety disorder occurring in the past year
may be associated with suicidal thoughts.
Functional Consequences of Generalized Anxiety Disorder
Excessive worrying impairs the individual’s capacity to do things quickly and efficiently,
whether at home or at work. The worrying takes time and energy; the associated symptoms of
muscle tension and feeling keyed up or on edge, tiredness, difficulty concentrating, and disturbed
sleep contribute to the impairment. Importantly the excessive worrying may impair the ability of
individuals with generalized anxiety disorder to encourage confidence in their children.
Generalized anxiety disorder is associated with significant disability and distress that is
independent of comorbid disorders, and most non-institutionalized adults with the disorder are
moderately to seriously disabled. Generalized anxiety disorder accounts for 110 million

Anxiety disorder due to another medical condition.
Substance/medication-induced anxiety disorder.
Social anxiety disorder.
Separation anxiety disorder.
Panic disorder.
Illness anxiety disorder and somatic symptom disorder.
Obsessive-compulsive disorder.
Posttraumatic stress disorder and adjustment disorders.
disability days per annum in the U.S. population. Generalized anxiety disorder is also linked to
decreased work performance, increased medical resource use, and increased risk for coronary
morbidity.
Differential Diagnosis
The diagnosis of anxiety disorder due to another
medical condition should be assigned if the individual’s anxiety and worry are judged, based on
history, laboratory findings, or physical examination, to be a physiological effect of another
specific medical condition (e.g., pheochromocytoma, hyperthyroidism).
A substance/medication-induced anxiety disorder is
distinguished from generalized anxiety disorder by the fact that a substance or medication (e.g., a
drug of abuse, exposure to a toxin) is judged to be etiologically related to the anxiety. For
example, severe anxiety that occurs only in the context of heavy coffee consumption would be
diagnosed as caffeine-induced anxiety disorder.
Individuals with social anxiety disorder often have anticipatory anxiety
that is focused on upcoming social situations in which they must perform or be evaluated by
others, whereas individuals with generalized anxiety disorder worry, whether or not they are
being evaluated.
Individuals with separation anxiety disorder worry excessively only
about separation from attachment figures, whereas individuals with generalized anxiety disorder
may worry about separation but present other excessive worry concerns as well.
Panic attacks that are triggered by worry in generalized anxiety disorder would
not qualify for panic disorder. However, if the individual experiences unexpected panic attacks
as well and shows persistent concern and worry or behavioral change because of the attacks, then
an additional diagnosis of panic disorder should be considered.
Individuals with generalized anxiety disorder
worry about multiple events, situations, or activities, only one of which may involve their health.
If the individual’s only fear is his or her own illness, then illness anxiety disorder should be
diagnosed. Worry focusing on somatic symptoms is characteristic for somatic symptom disorder.
Several features distinguish the excessive worry of generalized
anxiety disorder from the obsessional thoughts of obsessive-compulsive disorder. In generalized
anxiety disorder the focus of the worry is about forthcoming problems, and it is the
excessiveness of the worry about future events that is abnormal. In obsessive-compulsive
disorder, the obsessions are inappropriate ideas that take the form of intrusive and unwanted
thoughts, urges, or images.
Anxiety 
is 
invariably 
present 
in
posttraumatic stress disorder. Generalized anxiety disorder is not diagnosed if the anxiety and
worry are better explained by symptoms of posttraumatic stress disorder. Although anxiety may
manifest in adjustment disorder, this residual category should be used only when the criteria are
not met for any other mental disorder (including generalized anxiety disorder). Moreover, in

Depressive, bipolar, and psychotic disorders.
adjustment disorders, the anxiety occurs in response to an identifiable stressor within 3 months
of the onset of the stressor and does not persist for more than 6 months after the termination of
the stressor or its consequences.
Although generalized anxiety/worry is a common
associated feature of depressive, bipolar, and psychotic disorders, generalized anxiety disorder
may be diagnosed comorbidly if the anxiety/worry is sufficiently severe to warrant clinical
attention.
Comorbidity
Individuals whose presentation meets criteria for generalized anxiety disorder are likely to have
met, or currently meet, criteria for other anxiety and unipolar depressive disorders. The negative
affectivity (neuroticism) or emotional liability that underpins this pattern of comorbidity is
associated with temperamental antecedents and genetic and environmental risk factors shared
between these disorders, although independent pathways are also possible. Comorbidity with
substance use, conduct, psychotic, neurodevelopmental, and neurocognitive disorders is less
common.
Substance/Medication-Induced Anxiety Disorder
Diagnostic Criteria
A. Panic attacks or anxiety is predominant in the clinical picture.
B. There is evidence from the history, physical examination, or laboratory findings
of both (1) and (2):
1. The symptoms in Criterion A developed during or soon after substance
intoxication or withdrawal or after exposure to or withdrawal from a
medication.
2. The involved substance/medication is capable of producing the symptoms in
Criterion A.
C. The disturbance is not better explained by an anxiety disorder that is not
substance/medication-induced. Such evidence of an independent anxiety
disorder could include the following:
The symptoms precede the onset of the substance/medication use; the
symptoms persist for a substantial period of time (e.g., about 1 month) after
the cessation of acute withdrawal or severe intoxication; or there is other
evidence 
suggesting 
the 
existence 
of 
an 
independent 
nonsubstance/medication-induced anxiety disorder (e.g., a history of recurrent
non-substance/medication-related episodes).
D. The disturbance does not occur exclusively during the course of a delirium.

E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Note: This diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the symptoms in Criterion A
predominate in the clinical picture and they are sufficiently severe to warrant clinical
attention.
Coding note: The ICD-10-CM codes for the [specific substance/medication]-induced
anxiety disorders are indicated in the table below. Note that the ICD-10-CM code
depends on whether or not there is a comorbid substance use disorder present for
the same class of substance. In any case, an additional separate diagnosis of a
substance use disorder is not given. If a mild substance use disorder is comorbid
with the substance-induced anxiety disorder, the 4th position character is “1,” and
the clinician should record “mild [substance] use disorder” before the substanceinduced anxiety disorder (e.g., “mild cocaine use disorder with cocaine-induced
anxiety disorder”). If a moderate or severe substance use disorder is comorbid with
the substance-induced anxiety disorder, the 4th position character is “2,” and the
clinician should record “moderate [substance] use disorder” or “severe [substance]
use disorder,” depending on the severity of the comorbid substance use disorder. If
there is no comorbid substance use disorder (e.g., after a one-time heavy use of the
substance), then the 4th position character is “9,” and the clinician should record
only the substance-induced anxiety disorder.
ICD-10-CM
With mild use
disorder
With moderate or
severe use disorder
Without use
disorder
Alcohol
F10.180
F10.280
F10.980
Caffeine
NA
NA
F15.980
Cannabis
F12.180
F12.280
F12.980
Phencyclidine
F16.180
F16.280
F16.980
Other hallucinogen
F16.180
F16.280
F16.980
Inhalant
F18.180
F18.280
F18.980
Opioid
F11.188
F11.288
F11.988
Sedative, hypnotic, or anxiolytic
F13.180
F13.280
F13.980
Amphetamine-type substance (or other
stimulant)
F15.180
F15.280
F15.980
Cocaine
F14.180
F14.280
F14.980
Other (or unknown) substance
F19.180
F19.280
F19.980
Specify (see Table 1 in the chapter “Substance-Related and Addictive Disorders,”
which indicates whether “with onset during intoxication” and/or “with onset during
withdrawal” applies to a given substance class; or specify “with onset after
medication use”):
With onset during intoxication: If criteria are met for intoxication with the

substance and the symptoms develop during intoxication.
With onset during withdrawal: If criteria are met for withdrawal from the
substance and the symptoms develop during, or shortly after, withdrawal.
With onset after medication use: If symptoms developed at initiation of
medication, with a change in use of medication, or during withdrawal of
medication.
Recording Procedures
The name of the substance/medication-induced anxiety disorder begins with the specific
substance (e.g., cocaine, salbutamol) that is presumed to be causing the anxiety symptoms. The
diagnostic code is selected from the table included in the criteria set, which is based on the drug
class and presence or absence of a comorbid substance use disorder. For substances that do not
fit into any of the classes (e.g., salbutamol), the code for “other (or unknown) substance” should
be used; and in cases in which a substance is judged to be an etiological factor but the specific
class of substance is unknown, the same code should also be used.
To record the name of the disorder, the comorbid substance use disorder (if any) is listed
first, followed by “with substance/medication-induced anxiety disorder” (incorporating the name
of the specific etiological substance/medication), followed by the specification of onset (i.e.,
onset during intoxication, onset during withdrawal, with onset after medication use). For
example, in the case of anxiety symptoms occurring during withdrawal in a man with a severe
lorazepam use disorder, the diagnosis is F13.280 severe lorazepam use disorder with lorazepaminduced anxiety disorder, with onset during withdrawal. A separate diagnosis of the comorbid
severe lorazepam use disorder is not given. If the substance-induced anxiety disorder occurs
without a comorbid substance use disorder (e.g., after a one-time
heavy use of the substance), no accompanying substance use disorder is noted (e.g., F16.980
psilocybin-induced anxiety disorder, with onset during intoxication). When more than one
substance is judged to play a significant role in the development of anxiety symptoms, each
should be listed separately (e.g., F15.280 severe methylphenidate use disorder with
methylphenidate-induced anxiety disorder, with onset during intoxication; F19.980 salbutamolinduced anxiety disorder, with onset after medication use).
Diagnostic Features
The essential features of substance/medication-induced anxiety disorder are prominent
symptoms of panic or anxiety (Criterion A) that are judged to be due to the effects of a substance
(e.g., a drug of abuse, a medication, or a toxin exposure). The panic or anxiety symptoms must
have developed during or soon after substance intoxication or withdrawal or after exposure to or
withdrawal from a medication, and the substances or medications must be capable of producing
the symptoms (Criterion B2). Substance/medication-induced anxiety disorder due to a prescribed
treatment for a mental disorder or another medical condition must have its onset while the
individual is receiving the medication (or during withdrawal, if a withdrawal is associated with

Substance intoxication and substance withdrawal.
the medication). Once the treatment is discontinued, the panic or anxiety symptoms will usually
improve or remit within days to several weeks to a month (depending on the half-life of the
substance/medication and the presence of withdrawal). The diagnosis of substance/medicationinduced anxiety disorder should not be given if the onset of the panic or anxiety symptoms
precedes the substance/medication intoxication or withdrawal, or if the symptoms persist for a
substantial period of time (i.e., usually longer than 1 month) from the time of severe intoxication
or withdrawal. If the panic or anxiety symptoms persist for substantial periods of time, other
causes for the symptoms should be considered.
The substance/medication-induced anxiety disorder diagnosis should be made instead of a
diagnosis of substance intoxication or substance withdrawal only when the symptoms in
Criterion A are predominant in the clinical picture and are sufficiently severe to warrant
independent clinical attention.
Associated Features
Panic or anxiety can occur in association with intoxication with the following classes of
substances: alcohol, caffeine, cannabis, phencyclidine, other hallucinogens, inhalants, stimulants
(including cocaine), and other (or unknown) substances. Panic or anxiety can occur in
association with withdrawal from the following classes of substances: alcohol; opioids;
sedatives, hypnotics, and anxiolytics; stimulants (including cocaine); and other (or unknown)
substances. Some medications that evoke anxiety symptoms include anesthetics and analgesics,
sympathomimetics or other bronchodilators, anticholinergics, insulin, thyroid preparations, oral
contraceptives, antihistamines, antiparkinsonian medications, corticosteroids, antihypertensive
and cardiovascular medications, anticonvulsants, lithium carbonate, antipsychotic medications,
and antidepressant medications. Heavy metals and toxins (e.g., organophosphate insecticide,
nerve gases, carbon monoxide, CO2, volatile substances such as gasoline and paint) may also
cause panic or anxiety symptoms.
Prevalence
The prevalence of substance/medication-induced anxiety disorder is not clear. General
population data suggest that it may be rare, with a 12-month prevalence in the United States of
approximately 0.002%. However, in clinical populations, the prevalence is likely to be higher.
Diagnostic Markers
Laboratory assessments (e.g., urine toxicology) may be useful to measure substance intoxication
as part of an assessment for substance/medication-induced anxiety disorder.
Differential Diagnosis
Anxiety symptoms commonly occur in substance
intoxication and substance withdrawal. The diagnosis of the substance-specific intoxication or
substance-specific withdrawal will usually suffice to categorize the symptom presentation. A
diagnosis of substance/medication-induced anxiety disorder either with onset during intoxication

Independent anxiety disorder (i.e., not induced by a substance/medication).
Delirium.
Anxiety disorder due to another medical condition.
F06.4
or with onset during withdrawal should be made instead of a diagnosis of substance intoxication
or substance withdrawal when the panic or anxiety symptoms are predominant in the clinical
picture and are sufficiently severe to warrant clinical attention. For example, panic or anxiety
symptoms are characteristic of alcohol withdrawal.
An 
independent 
anxiety
disorder 
co-occurring 
with 
substance/medication 
use 
is 
distinguished 
from 
a
substance/medication-induced 
anxiety 
disorder 
by 
the 
fact 
that 
even 
though 
a
substance/medication may be taken in high enough amounts to be possibly etiologically related
to the anxiety symptoms, the anxiety symptoms are observed at times other than during
substance/medication use (i.e., preceding the onset of substance/medication use or persisting for
a substantial period of time after substance intoxication, substance withdrawal, or medication
use) and would warrant the diagnosis of an independent anxiety disorder.
If panic or anxiety symptoms occur exclusively during the course of delirium, they are
considered to be an associated feature of the delirium and are not diagnosed separately.
If the panic or anxiety symptoms are attributed to
the physiological consequences of another medical condition (i.e., rather than to the medication
taken for the medical condition), anxiety disorder due to another medical condition should be
diagnosed. The history often provides the basis for such a judgment. At times, a change in the
treatment for the other medical condition (e.g., medication substitution or discontinuation) may
be needed to determine whether the medication is the causative agent (in which case the
symptoms may be better explained by substance/medication-induced anxiety disorder). If the
disturbance is attributable to both another medical condition and substance use, both diagnoses
(i.e., anxiety disorder due to another medical condition and substance/medication-induced
anxiety disorder) may be given. When there is insufficient evidence to determine whether the
panic or anxiety symptoms are attributable to a substance/medication or to another medical
condition or are primary (i.e., not attributable to either a substance or another medical condition),
a diagnosis of other specified or unspecified anxiety disorder would be indicated.
Anxiety Disorder Due to Another Medical Condition
Diagnostic Criteria
A. Panic attacks or anxiety is predominant in the clinical picture.
B. There is evidence from the history, physical examination, or laboratory findings
that the disturbance is the direct pathophysiological consequence of another
medical condition.
C. The disturbance is not better explained by another mental disorder.
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Coding note: Include the name of the other medical condition within the name of the

mental disorder (e.g., F06.4 anxiety disorder due to pheochromocytoma). The other
medical condition should be coded and listed separately immediately before the
anxiety disorder due to the medical condition (e.g., D35.00 pheochromocytoma;
F06.4 anxiety disorder due to pheochromocytoma).
Diagnostic Features
The essential feature of anxiety disorder due to another medical condition is clinically significant
anxiety that is judged to be best explained as a physiological effect of another medical condition.
Symptoms can include prominent anxiety symptoms or panic attacks (Criterion A). The
judgment that the symptoms are best explained by the associated physical condition must be
based on evidence from the history, physical examination, or laboratory findings (Criterion B).
Additionally, it must be judged that the symptoms are not better accounted for by another mental
disorder (Criterion C)—in particular, adjustment disorder with anxiety, in which the stressor is
the medical condition. In this case, an individual with adjustment disorder is especially distressed
about the meaning or the consequences of the associated medical condition. By contrast, there is
often a prominent physical component to the anxiety (e.g., shortness of breath) when the anxiety
is due to another medical condition. The diagnosis is not made if the anxiety symptoms occur
only during the course of a delirium (Criterion D). The anxiety symptoms must cause clinically
significant distress or impairment in social, occupational, or other important areas of functioning
(Criterion E).
In determining whether the anxiety symptoms are attributable to another medical condition,
the clinician must first establish the presence of the medical condition. Furthermore, it must be
established that anxiety symptoms can be etiologically related to the medical condition through a
physiological mechanism before making a judgment that this is the best explanation for the
symptoms in a specific individual. A careful and comprehensive assessment of multiple factors is
necessary to make this judgment. Several aspects of the clinical presentation should be
considered: 1) the presence of a clear temporal association between the onset, exacerbation, or
remission of the medical condition and the anxiety symptoms; 2) the presence of features that are
atypical of an independent anxiety disorder (e.g., atypical age at onset or course); and 3)
evidence in the literature that a known physiological mechanism (e.g., hyperthyroidism) causes
anxiety. In addition, the disturbance must not be better explained by an independent anxiety
disorder, a substance/medication-induced anxiety disorder, or another mental disorder (e.g.,
adjustment disorder).
A number of medical conditions are known to include anxiety as a symptomatic
manifestation. Examples include endocrine disease (e.g., hyperthyroidism, pheochromocytoma,
hypoglycemia, hyperadrenocortisolism), cardiovascular disorders (e.g., congestive heart failure,
pulmonary embolism, arrhythmia such as atrial fibrillation), respiratory illness (e.g., chronic
obstructive pulmonary disease, asthma, pneumonia), metabolic disturbances (e.g., vitamin B12
deficiency, porphyria), and neurological illness (e.g., neoplasms, vestibular dysfunction,
encephalitis, seizure disorders).

Delirium and major or mild neurocognitive disorder.
Mixed presentation of symptoms (e.g., mood and anxiety).
Substance/medication-induced anxiety disorder.
Prevalence
The prevalence of anxiety disorder due to another medical condition is unclear. There appears to
be an elevated prevalence of anxiety disorders among individuals with a variety of medical
conditions, including asthma, hypertension, ulcers, and arthritis. However, this increased
prevalence may be due to reasons other than the anxiety disorder directly causing the medical
condition.
Development and Course
The development and course of anxiety disorder due to another medical condition generally
follows the course of the underlying illness. This diagnosis is not meant to include primary
anxiety disorders that arise in the context of chronic medical illness. This is
important to consider with older adults, who may experience chronic medical illness and then
develop independent anxiety disorders secondary to the chronic medical illness.
Diagnostic Markers
Laboratory assessments and/or medical examinations are necessary to confirm the diagnosis of
the associated medical condition.
Differential Diagnosis
A separate diagnosis of anxiety disorder due to
another medical condition is not given if the anxiety disturbance occurs exclusively during the
course of a delirium. However, a diagnosis of anxiety disorder due to another medical condition
may be given in addition to a diagnosis of major or mild neurocognitive disorder if the anxiety is
judged to be a physiological consequence of the pathological process causing the neurocognitive
disorder and if anxiety is a prominent part of the clinical presentation.
If the presentation includes a mix of
different types of symptoms, the specific mental disorder due to another medical condition
depends on which symptoms predominate in the clinical picture.
If there is evidence of recent or prolonged substance
use (including medications with psychoactive effects), withdrawal from a substance, or exposure
to a toxin, a substance/medication-induced anxiety disorder should be considered. Certain
medications are known to increase anxiety (e.g., corticosteroids, estrogens, metoclopramide), and
when this is the case, the medication may be the most likely etiology, although it may be difficult
to distinguish whether the anxiety is attributable to the medications or to the medical illness
itself. When a diagnosis of substance-induced anxiety is being made in relation to recreational or
nonprescribed drugs, it may be useful to obtain a urine or blood drug screen or other appropriate
laboratory evaluation. Symptoms that develop during or soon after substance intoxication or
withdrawal or after medication use may be especially indicative of a substance/medicationinduced anxiety disorder, depending on the type, duration, or amount of the substance used. If
the disturbance is associated with both another medical condition and substance use, both

Anxiety disorder (not due to a known medical condition).
Illness anxiety disorder.
Adjustment disorders.
diagnoses (i.e., anxiety disorder due to another medical condition and substance/medicationinduced anxiety disorder) can be given. Features such as onset after age 45 years or the presence
of atypical symptoms during a panic attack (e.g., vertigo, loss of consciousness, loss of bladder
or bowel control, slurred speech, amnesia) suggest the possibility that another medical condition
or a substance may be causing the panic attack symptoms.
Anxiety disorder due to another medical
condition should be distinguished from other anxiety disorders (especially panic disorder and
generalized anxiety disorder). In other anxiety disorders, no specific and direct causative
physiological mechanisms associated with another medical condition can be demonstrated. Late
age at onset, atypical symptoms, and the absence of a personal or family history of anxiety
disorders suggest the need for a thorough assessment to rule out the diagnosis of anxiety disorder
due to another medical condition. Anxiety disorders can exacerbate or pose increased risk for
medical conditions such as cardiovascular events and myocardial infarction and should not be
diagnosed as anxiety disorder due to another medical condition in these cases.
Anxiety disorder due to another medical condition should be
distinguished from illness anxiety disorder. Illness anxiety disorder is characterized by worry
about illness, concern about pain, and bodily preoccupations. In the case of illness anxiety
disorder, individuals may or may not have diagnosed medical conditions. Although
an individual with illness anxiety disorder and a diagnosed medical condition is likely to
experience anxiety about the medical condition, the medical condition is not physiologically
related to the anxiety symptoms.
Anxiety disorder due to another medical condition should be distinguished
from adjustment disorders with anxiety or adjustment disorders with anxiety and depressed
mood. Adjustment disorder is warranted when individuals experience a maladaptive response to
the stress of being diagnosed with or having to manage the medical condition. The reaction to
stress usually concerns the meaning or consequences of the medical condition, in contrast with
the experience of anxiety or mood symptoms that occur as a physiological consequence of the
medical condition. In adjustment disorder, the anxiety symptoms are typically related to coping
with the stress of having the medical condition, whereas in anxiety disorder due to another
medical condition, individuals are more likely to have prominent physical symptoms and to be
focused on issues other than the stress of the illness itself.
Other Specified Anxiety Disorder
F41.8
This category applies to presentations in which symptoms characteristic of an
anxiety disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the anxiety disorders diagnostic class, and

do not meet criteria for adjustment disorder with anxiety or adjustment disorder with
mixed anxiety and depressed mood. The other specified anxiety disorder category is
used in situations in which the clinician chooses to communicate the specific reason
that the presentation does not meet the criteria for any specific anxiety disorder. This
is done by recording “other specified anxiety disorder” followed by the specific
reason (e.g., “generalized anxiety occurring less often than ‘more days than not’ ”).
Examples of presentations that can be specified using the “other specified”
designation include the following:
1. Limited-symptom attacks.
2. Generalized anxiety occurring less often than “more days than not.”
3. Khyâl cap (wind attacks): See “Culture and Psychiatric Diagnosis” in Section
III.
4. Ataque de nervios (attack of nerves): See “Culture and Psychiatric Diagnosis”
in Section III.
Unspecified Anxiety Disorder
F41.9
This category applies to presentations in which symptoms characteristic of an
anxiety disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the anxiety disorders diagnostic class, and
do not meet criteria for adjustment disorder with anxiety or adjustment disorder with
mixed anxiety and depressed mood. The unspecified anxiety disorder category is
used in situations in which the clinician chooses not to specify the reason that the
criteria are not met for a specific anxiety disorder and includes presentations in
which there is insufficient information to make a more specific diagnosis (e.g., in
emergency room settings).

# 06 - Obsessive Compulsive and Related Disorders

# Obsessive-Compulsive and Related Disorders

263

Obsessive-Compulsive and Related Disorders
Obsessive-compulsive and related disorders include obsessivecompulsive disorder (OCD), body dysmorphic disorder, hoarding disorder, trichotillomania
(hair-pulling disorder), excoriation (skin-picking) disorder, substance/medication-induced
obsessive-compulsive and related disorder, obsessive-compulsive and related disorder due to
another medical condition, other specified obsessive-compulsive and related disorder (e.g., nail
biting, lip biting, cheek chewing, obsessional jealousy, olfactory reference disorder [olfactory
reference syndrome]), and unspecified obsessive-compulsive and related disorder.
OCD is characterized by the presence of obsessions and/or compulsions. Obsessions are
recurrent and persistent thoughts, urges, or images that are experienced as intrusive and
unwanted, whereas compulsions are repetitive behaviors or mental acts that an individual feels
driven to perform in response to an obsession or according to rules that must be applied rigidly.
Some other obsessive-compulsive and related disorders are also characterized by preoccupations
and by repetitive behaviors or mental acts in response to the preoccupations. Other obsessivecompulsive and related disorders are characterized primarily by recurrent body-focused
repetitive behaviors (e.g., hair pulling, skin picking) and repeated attempts to decrease or stop the
behaviors.
The inclusion of a chapter on obsessive-compulsive and related disorders in DSM-5 reflects
the increasing evidence of these disorders’ relatedness to one another in terms of a range of
diagnostic validators as well as the clinical utility of grouping these disorders in the same
chapter. Clinicians are encouraged to screen for these conditions in individuals who present with
one of them and be aware of overlaps among these conditions. At the same time, there are
important differences in diagnostic validators and treatment approaches across these disorders.
Moreover, there are close relationships between the anxiety disorders and some of the obsessivecompulsive and related disorders (e.g., OCD), which is reflected in the sequence of DSM-5
chapters, with obsessive-compulsive and related disorders following anxiety disorders.
The obsessive-compulsive and related disorders differ from developmentally normative
preoccupations and rituals by being excessive or persisting beyond developmentally appropriate
periods. The distinction between the presence of subclinical symptoms and a clinical disorder
requires assessment of a number of factors, including the individual’s level of distress and
impairment in functioning.
The chapter begins with OCD. It then covers body dysmorphic disorder and hoarding
disorder, which are characterized by cognitive symptoms such as perceived defects or flaws in
physical appearance or the perceived need to save possessions, respectively. The chapter then
covers trichotillomania and excoriation disorder, which are characterized by recurrent bodyfocused repetitive behaviors. Finally, it covers substance/medication-induced obsessivecompulsive and related disorder, obsessive-compulsive and related disorder due to another
medical condition, other specified obsessive-compulsive and related disorder, and unspecified

obsessive-compulsive and related disorder.
While the specific content of obsessions and compulsions varies among individuals, certain
symptom dimensions are common in OCD, including those of cleaning (contamination
obsessions and cleaning compulsions); symmetry (symmetry obsessions and repeating, ordering,
and counting compulsions); forbidden or taboo thoughts (e.g., aggressive, sexual, and religious
obsessions and related compulsions); and harm (e.g., fears of harm to self or others and related
checking compulsions). The tic-related specifier of OCD is used when an individual has a
current or past history of a tic disorder.
Body dysmorphic disorder is characterized by preoccupation with one or more perceived
defects or flaws in physical appearance that are not observable or appear only slight to others,
and by repetitive behaviors (e.g., mirror checking, excessive grooming, skin picking, or
reassurance seeking) or mental acts (e.g., comparing one’s appearance with that of other people)
in response to the appearance concerns. The appearance preoccupations are not better explained
by concerns with body fat or weight in an individual with an eating disorder. Muscle dysmorphia
is a form of body dysmorphic disorder that is characterized by the belief that one’s body build is
too small or is insufficiently muscular.
Hoarding disorder is characterized by persistent difficulty discarding or parting with
possessions, regardless of their actual value, as a result of a strong perceived need to save the
items and distress associated with discarding them. Hoarding disorder differs from normal
collecting. For example, symptoms of hoarding disorder result in the accumulation of a large
number of possessions that congest and clutter active living areas to the extent that their intended
use is substantially compromised. The excessive acquisition form of hoarding disorder, which
characterizes most but not all individuals with hoarding disorder, consists of excessive
collecting, buying, or stealing of items that are not needed or for which there is no available
space.
Trichotillomania is characterized by recurrent pulling out of one's hair resulting in hair loss,
and repeated attempts to decrease or stop hair pulling. Excoriation disorder is characterized by
recurrent picking of one’s skin resulting in skin lesions and repeated attempts to decrease or stop
skin picking. The body-focused repetitive behaviors that characterize these two disorders are not
triggered by obsessions or preoccupations; however, they may be preceded or accompanied by
various emotional states, such as feelings of anxiety or boredom. They may also be preceded by
an increasing sense of tension or may lead to gratification, pleasure, or a sense of relief when the
hair is pulled out or the skin is picked. Individuals with these disorders may have varying
degrees of conscious awareness of the behavior while engaging in it, with some individuals
displaying more focused attention on the behavior (with preceding tension and subsequent relief)
and other individuals displaying more automatic behavior (with the behaviors seeming to occur
without full awareness).
Substance/medication-induced obsessive-compulsive and related disorder consists of
symptoms characteristic of the obsessive-compulsive and related disorders developed in the
context of substance intoxication or withdrawal or after exposure to or withdrawal from a
medication. Obsessive-compulsive and related disorder due to another medical condition
involves symptoms characteristic of obsessive-compulsive and related disorders that are the

F42.2
direct pathophysiological consequence of another medical condition.
Other specified obsessive-compulsive and related disorder (e.g., nail biting, lip biting, cheek
chewing, obsessional jealousy, olfactory reference disorder [olfactory reference syndrome]) and
unspecified obsessive-compulsive and related disorder consist of symptoms that cause clinically
significant distress or impairment that do not meet criteria for a specific obsessive-compulsive
and related disorder in DSM-5 because of atypical presentation or uncertain etiology. These
categories are also used for other specific syndromes that are not listed in Section II and when
insufficient information is available to diagnose the presentation as another obsessivecompulsive and related disorder.
Those obsessive-compulsive and related disorders that have a cognitive component (i.e.,
OCD, body dysmorphic disorder, and hoarding disorder) include a specifier for
indicating the individual’s degree of insight with respect to disorder-related beliefs, which
ranges from “good or fair insight” to “poor insight” to “absent insight/delusional beliefs.” Those
individuals whose degree of insight is in the “absent insight/delusional beliefs” range should not
be given an additional diagnosis of a psychotic disorder unless their delusional beliefs involve
content that extends beyond what is characteristic of their obsessive-compulsive and related
disorder (e.g., an individual with body dysmorphic disorder who is convinced that his or her food
has been poisoned).
Obsessive-Compulsive Disorder
Diagnostic Criteria
A. Presence of obsessions, compulsions, or both:
Obsessions are defined by (1) and (2):
1. Recurrent and persistent thoughts, urges, or images that are experienced, at
some time during the disturbance, as intrusive and unwanted, and that in
most individuals cause marked anxiety or distress.
2. The individual attempts to ignore or suppress such thoughts, urges, or
images, or to neutralize them with some other thought or action (i.e., by
performing a compulsion).
Compulsions are defined by (1) and (2):
1. Repetitive behaviors (e.g., hand washing, ordering, checking) or mental acts
(e.g., praying, counting, repeating words silently) that the individual feels
driven to perform in response to an obsession or according to rules that must
be applied rigidly.
2. The behaviors or mental acts are aimed at preventing or reducing anxiety or
distress, or preventing some dreaded event or situation; however, these

behaviors or mental acts are not connected in a realistic way with what they
are designed to neutralize or prevent, or are clearly excessive.
Note: Young children may not be able to articulate the aims of these
behaviors or mental acts.
B. The obsessions or compulsions are time-consuming (e.g., take more than 1 hour
per day) or cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
C. The obsessive-compulsive symptoms are not attributable to the physiological
effects of a substance (e.g., a drug of abuse, a medication) or another medical
condition.
D. The disturbance is not better explained by the symptoms of another mental
disorder (e.g., excessive worries, as in generalized anxiety disorder;
preoccupation with appearance, as in body dysmorphic disorder; difficulty
discarding or parting with possessions, as in hoarding disorder; hair pulling, as in
trichotillomania [hair-pulling disorder]; skin picking, as in excoriation [skinpicking] disorder; stereotypies, as in stereotypic movement disorder; ritualized
eating behavior, as in eating disorders; preoccupation with substances or
gambling, as in substance-related and addictive disorders; preoccupation with
having an illness, as in illness anxiety disorder; sexual urges or fantasies, as in
paraphilic disorders; impulses, as in disruptive, impulse-control, and conduct
disorders; guilty ruminations, as in major depressive disorder; thought insertion
or delusional preoccupations, as in schizophrenia spectrum and other psychotic
disorders; or repetitive patterns of behavior, as in autism spectrum disorder).
Specify if:
With good or fair insight: The individual recognizes that obsessive-compulsive
disorder beliefs are definitely or probably not true or that they may or may not be
true.
With poor insight: The individual thinks obsessive-compulsive disorder beliefs
are probably true.
With absent insight/delusional beliefs: The individual is completely convinced
that obsessive-compulsive disorder beliefs are true.
Specify if:
Tic-related: The individual has a current or past history of a tic disorder.
Specifiers
Individuals with obsessive-compulsive disorder (OCD) vary in the degree of insight they have
about the accuracy of the beliefs that underlie their obsessive-compulsive symptoms. Many
individuals have good or fair insight (e.g., the individual believes that the house definitely will
not, probably will not, or may or may not burn down if the stove is not checked 30 times). Some

have poor insight (e.g., the individual believes that the house will probably burn down if the
stove is not checked 30 times), and a few (4% or less) have absent insight/delusional beliefs
(e.g., the individual is convinced that the house will burn down if the stove is not checked 30
times). Insight can vary within an individual over the course of the illness. Poorer insight has
been linked to worse long-term outcome.
Up to 30% of individuals with OCD have a lifetime tic disorder. This is most common in
men with onset of OCD in childhood. These individuals tend to differ from those without a
history of tic disorders in the themes of their OCD symptoms, comorbidity, course, and pattern
of familial transmission.
Diagnostic Features
The characteristic symptoms of OCD are the presence of obsessions and compulsions (Criterion
A). Obsessions are repetitive and persistent thoughts (e.g., of contamination), images (e.g., of
violent or horrific scenes), or urges (e.g., to stab someone). Importantly, obsessions are not
pleasurable or experienced as voluntary: they are intrusive and unwanted and cause marked
distress or anxiety in most individuals. The individual attempts to ignore or suppress these
obsessions (e.g., avoiding triggers or using thought suppression) or to neutralize them with
another thought or action (e.g., performing a compulsion). Compulsions (or rituals) are repetitive
behaviors (e.g., washing, checking) or mental acts (e.g., counting, repeating words silently) that
the individual feels driven to perform in response to an obsession or according to rules that must
be applied rigidly. Most individuals with OCD have both obsessions and compulsions.
Obsessions and compulsions are typically thematically related (e.g., thoughts of contamination
associated with washing rituals; thoughts of harm associated with repeated checking).
Individuals often report that they perform compulsions to reduce the distress triggered by
obsessions or to prevent a feared event (e.g., becoming ill). However, these compulsions either
are not connected in a realistic way to the feared event (e.g., arranging items symmetrically to
prevent harm to a loved one) or are clearly excessive (e.g., showering for hours each day).
Compulsions are not done for pleasure, although individuals may experience temporary relief
from anxiety or distress.
The specific content of obsessions and compulsions varies between individuals. However,
certain themes, or dimensions, are common, including those of cleaning (contamination
obsessions and cleaning compulsions); symmetry (symmetry obsessions and repeating, ordering,
and counting compulsions); forbidden or taboo thoughts (e.g., aggressive, sexual, or religious
obsessions and related compulsions); and harm (e.g., fears of harm to self or others and checking
compulsions). Some individuals also have difficulties discarding and accumulate objects as a
consequence of typical obsessions and
compulsions (e.g., fears of harming others); such compulsions must be distinguished from
the primary accumulation behaviors seen in hoarding disorder, discussed later in this chapter.
These themes occur across different cultures, are relatively consistent over time in adults with the
disorder, and may be associated with different neural substrates. Importantly, individuals often
have symptoms in more than one dimension.

Criterion B emphasizes that obsessions and compulsions must be time-consuming (e.g., more
than 1 hour per day) or cause clinically significant distress or impairment to warrant a diagnosis
of OCD. This criterion helps to distinguish the disorder from the occasional intrusive thoughts or
repetitive behaviors that are common in the general population (e.g., double-checking that a door
is locked). The frequency and severity of obsessions and compulsions vary across individuals
with OCD (e.g., some have mild to moderate symptoms, spending 1–3 hours per day obsessing
or doing compulsions, whereas others have nearly constant intrusive thoughts or compulsions
that can be incapacitating).
Associated Features
Sensory phenomena, defined as physical experiences (e.g., physical sensations, just-right
sensations, and feelings of incompleteness) that precede compulsions, are common in OCD. Up
to 60% of individuals with OCD report these phenomena.
Individuals with OCD experience a range of affective responses when confronted with
situations that trigger obsessions and compulsions. For example, many individuals experience
marked anxiety that can include recurrent panic attacks. Others report strong feelings of disgust.
While performing compulsions, some individuals report a distressing sense of “incompleteness”
or uneasiness until things look, feel, or sound “just right.”
It is common for individuals with the disorder to avoid people, places, and things that trigger
obsessions and compulsions. For example, individuals with contamination concerns might avoid
public situations (e.g., restaurants, public restrooms) to reduce exposure to feared contaminants;
individuals with intrusive thoughts about causing harm might avoid social interactions.
Many individuals with OCD have dysfunctional beliefs. These beliefs can include an inflated
sense of responsibility and the tendency to overestimate threat; perfectionism and intolerance of
uncertainty; and overimportance of thoughts (e.g., believing that having a forbidden thought is as
bad as acting on it) and the need to control thoughts. These beliefs, however, are not specific to
OCD. The involvement of family or friends in compulsive rituals, termed accommodation, can
exacerbate or maintain symptoms and is an important target in treatment, especially in children.
Prevalence
The 12-month prevalence of OCD in the United States is 1.2%, with a similar prevalence
internationally (including Canada, Puerto Rico, Germany, Taiwan, Korea, and New Zealand;
1.1%–1.8%). Women are affected at a slightly higher rate than men in adulthood, although men
are more commonly affected in childhood.
Development and Course
In the United States, the mean age at onset of OCD is 19.5 years, and 25% of cases start by age
14 years. Onset after age 35 years is unusual but does occur. Men have an earlier age at onset
than women: nearly 25% of men have onset before age 10 years. The onset of symptoms is
typically gradual; however, acute onset can also occur.
If OCD is untreated, the course is usually chronic, often with waxing and waning symptoms.
Some individuals have an episodic course, and a minority have a deteriorating course. Without
treatment, remission rates in adults are low (e.g., 20% for those reevaluated 40 years later). Onset

Temperamental.
Environmental.
Genetic and physiological.
in childhood or adolescence can lead to a lifetime of OCD.
However, 40% of individuals with onset of OCD in childhood or adolescence may
experience remission by early adulthood. The course of OCD is often complicated by the cooccurrence of other disorders (see section “Comorbidity” for this disorder).
Compulsions are more easily diagnosed in children than obsessions are because compulsions
are usually observable. However, most children have both obsessions and compulsions (as do
most adults). The pattern of symptoms in adults can be stable over time, but it is more variable in
children. Some differences in the content of obsessions and compulsions have been reported
when children and adolescent samples are compared with adult samples. These differences likely
reflect content appropriate to different developmental stages (e.g., higher rates of sexual and
religious obsessions in adolescents than in children; higher rates of harm obsessions [e.g., fears
of catastrophic events, such as death or illness to self or loved ones] in children and adolescents
than in adults).
Risk and Prognostic Factors
Greater internalizing symptoms, higher negative emotionality, and behavioral
inhibition in childhood are possible temperamental risk factors.
Different environmental factors may increase the risk for OCD. These include
adverse perinatal events, premature birth, maternal tobacco use during pregnancy, physical and
sexual abuse in childhood, and other stressful or traumatic events. Some children may develop
the sudden onset of obsessive-compulsive symptoms, which has been associated with different
environmental factors, including various infectious agents and a postinfectious autoimmune
syndrome.
The rate of OCD among first-degree relatives of adults with OCD is
approximately two times that among first-degree relatives of those without the disorder;
however, among first-degree relatives of individuals with onset of OCD in childhood or
adolescence, the rate is increased 10-fold. Familial transmission is due in part to genetic factors
(e.g., a concordance rate of 0.57 for monozygotic vs. 0.22 for dizygotic twins). Twin studies
suggest that additive genetic effects account for ~40% of the variance in obsessive-compulsive
symptoms. Dysfunction in the orbitofrontal cortex, anterior cingulate cortex, and striatum have
been most strongly implicated; alterations in frontolimbic, frontoparietal, and cerebellar
networks have also been reported.
Culture-Related Diagnostic Issues
OCD occurs across the world. There is substantial similarity across cultures in the gender
distribution, age at onset, and comorbidity of OCD. Moreover, around the globe, there is a
similar symptom structure involving cleaning, symmetry, hoarding, taboo thoughts, and fear of
harm. However, regional variation in symptom expression exists, and cultural factors may shape
the content of obsessions and compulsions. For example, obsessions related to sexual content
may be reported less frequently in some religious and cultural groups, and obsessions related to
violence and aggression may be more common in settings with higher prevalence of urban

violence. Attributions of OCD symptoms vary cross-culturally, including physical, social,
spiritual, and supernatural causes; specific compulsions and help-seeking options may be
reinforced by these cultural attributions.
Sex- and Gender-Related Diagnostic Issues
Men have an earlier age at onset of OCD than women, often in childhood, and are more likely to
have comorbid tic disorders. Onset in girls is more typically in adolescence; among adults, OCD
is slightly more common in women than in men. Gender differences in the pattern of symptom
dimensions have been reported, with, for example, women more likely to have symptoms in the
cleaning dimension and men more likely to have
symptoms in the forbidden thoughts and symmetry dimensions. Onset or exacerbation of OCD,
as well as symptoms that can interfere with the mother-infant relationship (e.g., aggressive
obsessions such as intrusive violent thoughts of harming the infant, leading to avoidance of the
infant), has been reported in the peripartum period. Some women also report exacerbation of
OCD symptoms premenstrually.
Association With Suicidal Thoughts or Behavior
A systematic literature review of suicidal ideation and suicide attempts in clinical samples with
OCD from multiple countries found a mean rate of lifetime suicide attempts of 14.2%, a mean
rate of lifetime suicidal ideation of 44.1%, and a mean rate of current suicidal ideation of 25.9%.
Predictors of greater suicide risk were severity of OCD, the symptom dimension of unacceptable
thoughts, severity of comorbid depressive and anxiety symptoms, and past history of suicidality.
Another international systematic review of 48 studies found a moderate to high significant
association between suicidal ideation/suicide attempts and OCD.
A cross-sectional study of 582 outpatients with OCD from Brazil found that 36% reported
lifetime suicidal thoughts, 20% had made suicide plans, 11% had already attempted suicide, and
10% presented with current suicidal thoughts. The sexual/religious dimension of OCD and
comorbid substance use disorders were associated with suicidal thoughts and suicide plans,
impulse-control disorders were associated with current suicidal thoughts and with suicide plans
and attempts, and lifetime comorbid major depressive disorder and posttraumatic stress disorder
(PTSD) were associated with all aspects of suicidal behaviors.
In a study using Swedish national registry data involving 36,788 individuals with OCD and
matched general population control subjects, individuals with OCD had a higher risk of suicide
death (OR = 9.8) and suicide attempt (OR = 5.5), and the increased risk for both outcomes
remained substantial even after adjusting for psychiatric comorbidities. Comorbid personality or
substance use disorder increased suicide risk, whereas female gender, higher parental education,
and a comorbid anxiety disorder were protective factors.
Functional Consequences of Obsessive-Compulsive Disorder
OCD is associated with reduced quality of life as well as high levels of social and occupational
impairment. Impairment occurs across many different domains of life and is associated with

Anxiety disorders.
Major depressive disorder.
Other obsessive-compulsive and related disorders.
symptom severity. Impairment can be caused by the time spent obsessing and performing
compulsions. Avoidance of situations that can trigger obsessions or compulsions can also
severely impair functioning. In addition, specific symptoms can create specific obstacles. For
example, obsessions about harm can make relationships with family and friends feel hazardous;
the result can be avoidance of these relationships. Obsessions about symmetry can derail the
timely completion of school or work projects because the project never feels “just right,”
potentially resulting in school failure or job loss. Health consequences can also occur. For
example, individuals with contamination concerns may avoid doctors’ offices and hospitals (e.g.,
because of fears of exposure to germs) or develop dermatological problems (e.g., skin lesions
due to excessive washing). Sometimes the symptoms of the disorder interfere with its own
treatment (e.g., when medications are considered contaminated). When the disorder starts in
childhood or adolescence, individuals may experience developmental difficulties. For example,
adolescents may avoid socializing with peers; young adults may struggle when they leave home
to live independently. The result can be few significant relationships outside the family and a
lack of autonomy and financial independence from their family of origin. In addition, some
individuals with OCD try to impose rules and prohibitions on family members because of their
obsessions
(e.g., no one in the family can have visitors to the house for fear of contamination), and this can
lead to family dysfunction.
Differential Diagnosis
Recurrent thoughts, avoidant behaviors, and repetitive requests for reassurance
can also occur in anxiety disorders. However, the recurrent thoughts that are present in
generalized anxiety disorder (i.e., worries) are usually about real-life concerns, whereas the
obsessions of OCD usually do not involve real-life concerns and can include content that is odd,
irrational, or of a seemingly magical nature; moreover, compulsions are usually present and
usually linked to the obsessions. Like individuals with OCD, individuals with specific phobia
can have a fear reaction to specific objects or situations; however, in specific phobia the feared
object is usually much more circumscribed, and rituals are not present. In social anxiety disorder,
the feared objects or situations are limited to social interactions or performance situations, and
avoidance or reassurance seeking is focused on reducing feelings of embarrassment.
OCD needs to be distinguished from the rumination of major
depressive disorder, in which thoughts are usually mood-congruent and not necessarily
experienced as intrusive or distressing; moreover, ruminations are not linked to compulsions, as
is typical in OCD.
In body dysmorphic disorder, the obsessions and
compulsions are limited to concerns about physical appearance; and in trichotillomania (hairpulling disorder), the compulsive behavior is limited to hair pulling in the absence of obsessions.
Hoarding disorder symptoms focus exclusively on the persistent difficulty discarding or parting
with possessions, marked distress associated with discarding items, and excessive accumulation
of objects. However, if an individual has obsessions that are typical of OCD (e.g., concerns about

Eating disorders.
Tics (in tic disorder) and stereotyped movements.
Psychotic disorders.
Other compulsive-like behaviors.
Obsessive-compulsive personality disorder.
incompleteness or harm), and these obsessions lead to compulsive accumulation (e.g., acquiring
all objects in a set to attain a sense of completeness or not discarding old newspapers because
they may contain information that could prevent harm), a diagnosis of OCD should be given
instead.
OCD can be distinguished from anorexia nervosa in that in OCD the obsessions
and compulsions are not limited to concerns about weight and food.
A tic is a sudden, rapid, recurrent, nonrhythmic
motor movement or vocalization (e.g., eye blinking, throat clearing). A stereotyped movement is
a repetitive, seemingly driven, nonfunctional motor behavior (e.g., head banging, body rocking,
self-biting). Tics and stereotyped movements are typically less complex than compulsions and
are not aimed at neutralizing obsessions. However, distinguishing between complex tics and
compulsions can be difficult. Whereas compulsions are usually preceded by obsessions, tics are
often preceded by premonitory sensory urges. Some individuals have symptoms of both OCD
and a tic disorder, in which case both diagnoses may be warranted.
Some individuals with OCD have poor insight or even delusional OCD
beliefs. However, they have obsessions and compulsions (distinguishing their condition from
delusional disorder) and do not have other features of schizophrenia or schizoaffective disorder
(e.g., hallucinations or disorganized speech). For individuals whose OCD symptoms warrant the
“with absent insight/delusional beliefs” specifier, these symptoms should not be diagnosed as a
psychotic disorder.
Certain behaviors are sometimes described as “compulsive,”
including sexual behavior (in the case of paraphilias), gambling (i.e., gambling disorder), and
substance use (e.g., alcohol use disorder). However, these behaviors differ
from the compulsions of OCD in that the person usually derives pleasure from the activity and
may wish to resist it only because of its deleterious consequences.
Although obsessive-compulsive personality disorder
and OCD have similar names, the clinical manifestations of these disorders are quite different.
Obsessive-compulsive personality disorder is not characterized by intrusive thoughts, images, or
urges or by repetitive behaviors that are performed in response to these intrusive symptoms;
instead, it involves an enduring and pervasive maladaptive pattern of excessive perfectionism
and rigid control. If an individual manifests symptoms of both OCD and obsessive-compulsive
personality disorder, both diagnoses can be given.
Comorbidity
Individuals with OCD often have other psychopathology. Many adults with the disorder in the
United States have a lifetime diagnosis of an anxiety disorder (76%; e.g., panic disorder, social
anxiety disorder, generalized anxiety disorder, specific phobia) or a depressive or bipolar
disorder (63% for any depressive or bipolar disorder, with the most common being major
depressive disorder [41%]); a lifetime diagnosis of an impulse-control disorder (56%) or a
substance use disorder (39%) is also common. Onset of OCD is usually later than for most

F45.22
comorbid anxiety disorders (with the exception of separation anxiety disorder) and PTSD but
often precedes that of depressive disorders. In a study of 214 treatment-seeking adults in the
United States with DSM-IV OCD at intake, comorbid obsessive-compulsive personality disorder
was found in 23%–32% of individuals followed longitudinally.
Up to 30% of individuals with OCD also have a lifetime tic disorder. A comorbid tic disorder
is most common in men with onset of OCD in childhood. These individuals tend to differ from
those without a history of tic disorders in the themes of their OCD symptoms, comorbidity,
course, and pattern of familial transmission. A triad of OCD, tic disorder, and attentiondeficit/hyperactivity disorder can also be seen in children.
Several obsessive-compulsive and related disorders, including body dysmorphic disorder,
trichotillomania, and excoriation (skin-picking) disorder, also occur more frequently in
individuals with OCD than in those without OCD.
OCD is also much more common in individuals with certain other disorders than would be
expected based on its prevalence in the general population; when one of those other disorders is
diagnosed, the individual should be assessed for OCD as well. For example, in individuals with
schizophrenia or schizoaffective disorder, the prevalence of OCD is approximately 12%. Rates
of OCD are also elevated in bipolar disorder; eating disorders, such as anorexia nervosa and
bulimia nervosa; body dysmorphic disorder; and Tourette’s disorder.
Body Dysmorphic Disorder
Diagnostic Criteria
A. Preoccupation with one or more perceived defects or flaws in physical
appearance that are not observable or appear slight to others.
B. At some point during the course of the disorder, the individual has performed
repetitive behaviors (e.g., mirror checking, excessive grooming, skin picking,
reassurance seeking) or mental acts (e.g., comparing his or her appearance with
that of others) in response to the appearance concerns.
C. The preoccupation causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
D. The appearance preoccupation is not better explained by concerns with body fat
or weight in an individual whose symptoms meet diagnostic criteria for an eating
disorder.
Specify if:
With muscle dysmorphia: The individual is preoccupied with the idea that his
or her body build is too small or insufficiently muscular. This specifier is used
even if the individual is preoccupied with other body areas, which is often the
case.

Specify if:
Indicate degree of insight regarding body dysmorphic disorder beliefs (e.g., “I look
ugly” or “I look deformed”).
With good or fair insight: The individual recognizes that the body dysmorphic
disorder beliefs are definitely or probably not true or that they may or may not be
true.
With poor insight: The individual thinks that the body dysmorphic disorder
beliefs are probably true.
With absent insight/delusional beliefs: The individual is completely convinced
that the body dysmorphic disorder beliefs are true.
Specifiers
Muscle dysmorphia, a form of body dysmorphic disorder occurring almost exclusively in men
and adolescent boys, consists of preoccupation with the idea that one’s body is too small or
insufficiently lean or muscular. Individuals with this form of the disorder actually have a normallooking body or are even very muscular. They may also be preoccupied with other body areas,
such as skin or hair. A majority (but not all) diet, exercise, and/or lift weights excessively,
sometimes causing bodily damage. Some use potentially dangerous anabolic-androgenic steroids
and other substances to try to make their body bigger and more muscular.
Individuals with body dysmorphic disorder vary in the degree of insight they have about the
accuracy of their body dysmorphic disorder beliefs (e.g., “I look ugly,” “I look deformed”).
Insight regarding body dysmorphic disorder beliefs can range from good to absent/delusional
(i.e., delusional beliefs consisting of complete conviction that the individual’s view of his or her
appearance is accurate and undistorted). On average, insight is poor, and one-third or more of
individuals currently have absent insight/delusional body dysmorphic disorder beliefs.
Individuals with delusional body dysmorphic disorder tend to have greater morbidity in some
areas (e.g., suicidal thoughts or behavior), but this appears to be accounted for by their tendency
to have more severe body dysmorphic disorder symptoms.
Diagnostic Features
Individuals with body dysmorphic disorder (formerly known as dysmorphophobia) are
preoccupied with one or more perceived defects or flaws in their physical appearance, which
they believe look ugly, unattractive, abnormal, or deformed (Criterion A). The perceived flaws
are not observable or appear only slight to other individuals. Concerns range from looking
“unattractive” or “not right” to looking “hideous” or “like a monster.” Preoccupations can focus
on one or many body areas, most commonly the skin (e.g., perceived acne, scars, lines, wrinkles,
paleness), hair (e.g., “thinning” hair or “excessive” body or facial hair), or nose (e.g., size or
shape). However, any body area can be the focus of concern (e.g., eyes, teeth, weight, stomach,
breasts, legs, face size or shape, lips, chin, eyebrows, genitals). Some individuals are concerned
about perceived asymmetry of body areas. The preoccupations are intrusive, unwanted, timeconsuming (occurring, on average, 3–8 hours per day), and usually difficult to resist or control.
Excessive repetitive behaviors or mental acts (e.g., comparing) are performed in response to

the preoccupation (Criterion B). The individual feels driven to perform these
behaviors, which are not pleasurable and may increase anxiety and dysphoria. They are
typically time-consuming and difficult to resist or control. Common behaviors are comparing
one’s appearance with that of other individuals; repeatedly checking perceived defects in mirrors
or other reflecting surfaces or examining them directly; taking excessive “selfies”; excessively
grooming (e.g., combing, styling, shaving, plucking or pulling hair); seeking reassurance about
how the perceived flaws look; touching disliked areas to check them; excessively exercising or
weight lifting; and seeking cosmetic procedures. Some individuals excessively tan (e.g., to
darken “pale” skin or diminish perceived acne), repeatedly change their clothes (e.g., to
camouflage perceived defects), or compulsively shop (e.g., for beauty products). Compulsive
skin picking intended to improve perceived skin defects is common and can cause skin damage,
infections, or ruptured blood vessels. Camouflaging (i.e., hiding or covering) perceived defects, a
very common behavior in individuals with body dysmorphic disorder, may involve repetitive
behaviors (e.g., repeatedly applying makeup, adjusting a hat or clothing, rearranging head hair to
cover the forehead or eyes). The preoccupation must cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning (Criterion C); usually
both are present. Body dysmorphic disorder must be differentiated from an eating disorder. Body
dysmorphic disorder by proxy is a form of body dysmorphic disorder in which individuals are
preoccupied with defects they perceive in another person’s appearance, most often a significant
other (e.g., spouse or partner), but sometimes a parent, child, sibling, or stranger.
Associated Features
Many individuals with body dysmorphic disorder have ideas or delusions of reference, believing
that other people take special notice of them or mock them because of how they look. Body
dysmorphic disorder is associated with high levels of anxiety, social anxiety, social avoidance,
depressed mood, negative affectivity (neuroticism), rejection sensitivity, and perfectionism as
well as low extroversion and low self-esteem. Body dysmorphic disorder is also associated with
elevated hostility and aggressive behavior. Many individuals are ashamed of their appearance
and their excessive focus on how they look and are reluctant to reveal their concerns to others. A
majority of individuals receive cosmetic treatment to try to improve their perceived defects.
Dermatological treatment and surgery are most common, but any type (e.g., dental, electrolysis)
may be received. Some individuals perform surgery on themselves. Body dysmorphic disorder
appears to respond poorly to such treatments and sometimes becomes worse. Some individuals
take legal action or are violent toward the clinician (e.g., surgeon) because they are dissatisfied
with the cosmetic outcome.
Body dysmorphic disorder has been associated with abnormalities in emotion recognition,
attention, and executive function, as well as information-processing biases and inaccuracies in
interpretation of information and social situations. For example, individuals with this disorder
tend to have a bias for negative and threatening interpretations of facial expressions and
ambiguous scenarios. Body dysmorphic disorder is also characterized by visual processing
abnormalities, with a bias for analyzing and encoding details rather than holistic or configural

Environmental.
Genetic and physiological.
aspects of visual stimuli.
Prevalence
The point prevalence in a nationwide epidemiological study among U.S. adults was 2.4% (2.5%
in women and 2.2% in men). Outside the United States (e.g., Germany), similar studies indicate
that the point prevalence is 1.7%–2.9%, with a gender distribution similar to that in the United
States. Globally, the point prevalence is 11%–13% among dermatology patients, 13%–15%
among general cosmetic surgery patients, 20% in rhinoplasty surgery patients, 11% among adult
jaw correction surgery patients, and 5%–10% among adult orthodontia/cosmetic dentistry
patients. Among adolescents and college students, point prevalence rates are relatively higher in
girls/young women compared with boys/young men.
Development and Course
The mean age at disorder onset is 16–17 years, the median age at onset is 15 years, and the most
common age at onset is 12–13 years; in two-thirds of individuals, onset is before age 18.
Subclinical body dysmorphic disorder symptoms begin, on average, at age 12 or 13 years.
Subclinical concerns usually evolve gradually to the full disorder, although some individuals
experience abrupt onset of body dysmorphic disorder. The disorder appears to usually be
chronic, although improvement is likely when evidence-based treatment is received. The
disorder’s clinical features appear largely similar in children/adolescents and adults. Body
dysmorphic disorder occurs in the elderly, but little is known about the disorder in this age
group. Individuals with disorder onset before age 18 years have more comorbidity and are more
likely to have gradual (rather than acute) disorder onset than those with adult-onset body
dysmorphic disorder.
Risk and Prognostic Factors
Body dysmorphic disorder has been associated with high rates of childhood
neglect, abuse, and trauma, as well as elevated rates of teasing.
The prevalence of body dysmorphic disorder is elevated in first-degree
relatives of individuals with obsessive-compulsive disorder (OCD). Heritability of body
dysmorphic disorder symptoms is estimated at 37%–49% in studies of adolescent and young
adult twins and may be higher in women. There is shared genetic vulnerability with OCD as well
as genetic influences that are specific to body dysmorphic disorder symptoms.
Culture-Related Diagnostic Issues
Body dysmorphic disorder has been reported internationally. Certain features of the disorder
appear cross-culturally, such as gender ratio, body areas that are the object of concern, types of
repetitive behaviors, and levels of associated distress and impairment. Other features may vary
(e.g., in some cultural contexts with a collectivistic focus, such as Japan, body dysmorphic
concerns might emphasize the fear of offending others because of the perceived deformity).
Varying cultural standards may be associated with specific body image concerns, such as

eyelids in Japan and muscle dysmorphia in Western countries. Taijin kyofusho, included in the
traditional Japanese diagnostic system, has a subtype similar to body dysmorphic disorder:
shubo-kyofu (“the phobia of a deformed body”). For more information regarding cultural
concepts of distress, refer to the “Culture and Psychiatric Diagnosis” chapter.
Sex- and Gender-Related Diagnostic Issues
Muscle dysmorphia occurs almost exclusively in men, and men are more likely to have a
comorbid substance use disorder, whereas women are more likely to have a comorbid eating
disorder. Women and men appear to have more similarities than differences in terms of most
clinical features— for example, disliked body areas, types of repetitive behaviors, symptom
severity, suicidality, comorbidity, illness course, and receipt of cosmetic procedures for body
dysmorphic disorder. However, there are some differences. For example, men are more likely to
have preoccupations with their genitals, body build (thinking they are too small or inadequately
muscular), and thinning hair, whereas women are more likely to be preoccupied with weight
(usually thinking that they weigh too much), breasts/chest, buttocks, legs, hips, and excessive
body/facial hair.
Association With Suicidal Thoughts or Behavior
In a systematic review and meta-analysis of 17 studies that examined suicidal thoughts and
behaviors across several countries, individuals with body dysmorphic disorder were
four times more likely to have experienced suicidal thoughts (pooled OR = 3.87) and 2.6 times
more likely to have made suicide attempts (pooled OR = 2.57) when compared with healthy
control subjects and individuals diagnosed with eating disorders, OCD, or any anxiety disorder.
Two general population studies in Germany found higher rates of suicidal thoughts—19% vs.
3%; 31.0% vs. 3.5%—and behaviors—7% vs. 1%; 22.2% vs. 2.1%—in individuals diagnosed
with body dysmorphic disorder than in those without the diagnosis.
Severity of body dysmorphic disorder strengthens the association of body dysmorphic
disorder with suicidal thoughts and behaviors. The relationship between body dysmorphic
disorder and elevated suicidal thoughts and behaviors is independent of comorbidity, but certain
comorbidities may further strengthen this relationship. A substantial proportion of individuals
with body dysmorphic disorder attribute suicidal thoughts or suicide attempts primarily to their
appearance concerns.
Individuals with body dysmorphic disorder have many demographic and clinical risk factors
that more generally predict suicide death, such as high rates of suicidal thoughts and suicide
attempts, unemployment, perceived abuse, poor self-esteem, and high rates of comorbid major
depressive disorder, eating disorders, and substance use disorders.
Functional Consequences of Body Dysmorphic Disorder
Nearly all individuals with body dysmorphic disorder experience impaired psychosocial
functioning because of their appearance concerns. Impairment can range from moderate (e.g.,
avoidance of some social situations) to extreme and incapacitating (e.g., being completely

Normal appearance concerns and clearly noticeable physical defects.
Eating disorders.
Other obsessive-compulsive and related disorders.
Illness anxiety disorder.
Major depressive disorder.
Anxiety disorders.
housebound).
On average, psychosocial functioning and quality of life are markedly poor. More severe
body dysmorphic disorder symptoms are associated with poorer functioning and quality of life.
Most individuals experience impairment in their job, academic, or role functioning (e.g., as a
parent or caregiver), which is often severe (e.g., performing poorly, missing school or work, not
working). About 20% of youths with body dysmorphic disorder report dropping out of school
primarily because of their body dysmorphic disorder symptoms. A high proportion of adults and
adolescents have been psychiatrically hospitalized.
Differential Diagnosis
Body 
dysmorphic 
disorder
differs from normal appearance concerns in being characterized by excessive appearance-related
preoccupations and repetitive behaviors that are time-consuming, are usually difficult to resist or
control, and cause clinically significant distress or impairment in functioning. Physical defects
that are clearly noticeable (i.e., not slight) are not diagnosed as body dysmorphic disorder.
However, skin picking as a symptom of body dysmorphic disorder can cause noticeable skin
lesions and scarring; in such cases, body dysmorphic disorder should be diagnosed.
In an individual with an eating disorder, concerns about being fat or overweight
are considered a symptom of the eating disorder rather than body dysmorphic disorder. However,
weight concerns may occur in body dysmorphic disorder. Eating disorders and body dysmorphic
disorder can be comorbid, in which case both should be diagnosed.
The preoccupations and repetitive behaviors of
body dysmorphic disorder differ from obsessions and compulsions in OCD in that the former
focus only on physical appearance. These disorders have other differences, such as poorer
insight, more frequent depression, and higher rates of suicidal
ideation in body dysmorphic disorder. When skin picking is intended to improve the appearance
of perceived skin defects, body dysmorphic disorder, rather than excoriation (skin-picking)
disorder, is diagnosed. When hair removal (plucking, pulling, or other types of removal) is
intended to improve perceived defects in the appearance of facial, head, or body hair, body
dysmorphic disorder is diagnosed rather than trichotillomania (hair-pulling disorder).
Individuals with body dysmorphic disorder are not preoccupied with
having or acquiring a serious illness and in clinical samples do not have particularly elevated
levels of somatization.
The prominent preoccupation with appearance and excessive repetitive
behaviors in body dysmorphic disorder differentiate it from major depressive disorder. However,
major depressive disorder and depressive symptoms are common in individuals with body
dysmorphic disorder, often appearing to be secondary to the distress and impairment that body
dysmorphic disorder causes. Body dysmorphic disorder should be diagnosed in depressed
individuals if diagnostic criteria for body dysmorphic disorder are met.
Social anxiety and avoidance are common in body dysmorphic disorder.

Psychotic disorders.
Other disorders and symptoms.
However, unlike social anxiety disorder, agoraphobia, and avoidant personality disorder, body
dysmorphic disorder includes prominent appearance-related preoccupation, which may be
delusional, and repetitive behaviors. In addition, the social anxiety and avoidance that are
characteristic of body dysmorphic disorder are attributable to concerns about perceived
appearance defects and the belief or fear that other people will consider these individuals ugly,
ridicule them, or reject them because of their physical features. Unlike generalized anxiety
disorder, anxiety and worry in body dysmorphic disorder focus on perceived appearance flaws.
Many individuals with body dysmorphic disorder have delusional
appearance beliefs (i.e., complete conviction that their view of their perceived defects is
accurate), which is diagnosed as body dysmorphic disorder, with absent insight/delusional
beliefs, not as delusional disorder. Appearance-related ideas or delusions of reference are
common in body dysmorphic disorder (i.e., thinking that other people take special notice in a
negative way because of the individual’s appearance). However, unlike schizophrenia or
schizoaffective 
disorder, 
body 
dysmorphic 
disorder 
involves 
prominent 
appearance
preoccupations and related repetitive behaviors; disorganized behavior and other psychotic
symptoms are absent (except for appearance beliefs, which may be delusional). For individuals
whose obsessive-compulsive and related disorder symptoms warrant the “with absent
insight/delusional beliefs” specifier, these symptoms should not be diagnosed as a psychotic
disorder.
Body dysmorphic disorder should not be diagnosed if the
preoccupation is limited to discomfort with or a desire to be rid of one’s primary and/or
secondary sex characteristics in an individual with gender dysphoria. Nor should body
dysmorphic disorder be diagnosed if the preoccupation focuses on the belief that one emits a foul
or offensive body odor as in olfactory reference disorder (olfactory reference syndrome), which
is an example of an other specified obsessive-compulsive and related disorder in DSM-5. Body
integrity dysphoria (which is included in ICD-11 but not DSM-5) involves a persistent desire to
become an amputee in order to correct a mismatch between the individual’s sense of how his or
her body should be configured and his or her actual anatomical configuration. In contrast to body
dysmorphic disorder, the individual does not feel that the limb to be amputated is ugly or
defective in any way, just that it should not be there. Koro, a culturally related disorder that
usually occurs in epidemics in Southeastern Asia, consists of a fear that the penis (labia, nipples,
or breasts in females) is shrinking or retracting and will disappear into the abdomen, often
accompanied by a belief that death
will result. Koro differs from body dysmorphic disorder in several ways, including a focus on
death rather than preoccupation with perceived ugliness. Dysmorphic concern (which is not a
DSM-5 disorder) is a broader construct that is similar to, but not equivalent to, body dysmorphic
disorder. It involves symptoms reflecting an overconcern with slight or imagined flaws in
appearance.
Comorbidity
Major depressive disorder is the most common comorbid disorder, with onset usually after that

F42.3
of body dysmorphic disorder. Comorbid social anxiety disorder, OCD, and substance-related
disorders (including use of anabolic-androgenic steroids in the muscle dysmorphia form of body
dysmorphic disorder) are also common.
Hoarding Disorder
Diagnostic Criteria
A. Persistent difficulty discarding or parting with possessions, regardless of their
actual value.
B. This difficulty is due to a perceived need to save the items and to distress
associated with discarding them.
C. The difficulty discarding possessions results in the accumulation of possessions
that congest and clutter active living areas and substantially compromises their
intended use. If living areas are uncluttered, it is only because of the
interventions of third parties (e.g., family members, cleaners, authorities).
D. The hoarding causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning (including maintaining a
safe environment for self and others).
E. The hoarding is not attributable to another medical condition (e.g., brain injury,
cerebrovascular disease, Prader-Willi syndrome).
F. The hoarding is not better explained by the symptoms of another mental disorder
(e.g., obsessions in obsessive-compulsive disorder, decreased energy in major
depressive disorder, delusions in schizophrenia or another psychotic disorder,
cognitive deficits in major neurocognitive disorder, restricted interests in autism
spectrum disorder).
Specify if:
With excessive acquisition: If difficulty discarding possessions is accompanied
by excessive acquisition of items that are not needed or for which there is no
available space.
Specify if:
With good or fair insight: The individual recognizes that hoarding-related
beliefs and behaviors (pertaining to difficulty discarding items, clutter, or
excessive acquisition) are problematic.
With poor insight: The individual is mostly convinced that hoarding-related
beliefs and behaviors (pertaining to difficulty discarding items, clutter, or
excessive acquisition) are not problematic despite evidence to the contrary.
With absent insight/delusional beliefs: The individual is completely convinced
that hoarding-related beliefs and behaviors (pertaining to difficulty discarding
items, clutter, or excessive acquisition) are not problematic despite evidence to
the contrary.

With excessive acquisition.
Specifiers
Approximately 80%–90% of individuals with hoarding disorder
display excessive acquisition. The most frequent form of acquisition is excessive buying,
followed by acquisition of free items (e.g., leaflets, items discarded by others). Stealing is less
common. Some individuals may deny excessive acquisition when first assessed, yet it may
appear later during the course of treatment. Individuals with hoarding disorder typically
experience distress if they are unable to or are prevented from acquiring items.
Diagnostic Features
The essential feature of hoarding disorder is persistent difficulty discarding or parting with
possessions, regardless of their actual value (Criterion A). The term persistent indicates a longstanding difficulty rather than more transient life circumstances that may lead to excessive
clutter, such as inheriting property. The difficulty in discarding possessions noted in Criterion A
refers to any form of discarding, including throwing away, selling, giving away, or recycling.
The main reasons given for this difficulty are the perceived utility or aesthetic value of the items
or strong sentimental attachment to the possessions. Some individuals feel responsible for the
fate of their possessions and often go to great lengths to avoid being wasteful. Fears of losing
important information are also common. The most commonly saved items are newspapers,
magazines, clothing, bags, books, mail, and papers, but virtually any item can be saved. The
nature of items is not limited to possessions that most other people would define as useless or of
limited value. Many individuals collect and save large numbers of valuable things as well, which
are often found in piles mixed with other less valuable items.
Individuals with hoarding disorder purposefully save possessions and experience distress
(e.g., anxiety, frustration, regret, sadness, guilt) when facing the prospect of discarding them
(Criterion B). This criterion emphasizes that the saving of possessions is intentional, which
discriminates hoarding disorder from other forms of psychopathology that are characterized by
the passive accumulation of items or the absence of distress when possessions are removed.
Individuals accumulate large numbers of items that fill up and clutter active living areas to
the extent that their intended use is no longer possible (Criterion C). For example, the individual
may not be able to cook in the kitchen, sleep in his or her bed, or sit in a chair. If the space can
be used, it is only with great difficulty. Clutter is defined as a large group of usually unrelated or
marginally related objects piled together in a disorganized fashion in spaces designed for other
purposes (e.g., tabletops, floor, hallway). Criterion C emphasizes the “active” living areas of the
home, rather than more peripheral areas, such as garages, attics, or basements, that are sometimes
cluttered in homes of individuals without hoarding disorder. However, individuals with hoarding
disorder often have possessions that spill beyond the active living areas and can occupy and
impair the use of other spaces, such as vehicles, yards, the workplace, and friends’ and relatives’
houses. In some cases, living areas may be uncluttered only because of the intervention of third
parties (e.g., family members, cleaners, local authorities). Individuals who have been forced to
clear their homes still have a symptom picture that meets criteria for hoarding disorder because

the lack of clutter is attributable to a third-party intervention. Hoarding disorder contrasts with
normative collecting behavior, which is organized and selective, although in some cases the
actual amount of possessions may be similar to the amount accumulated by an individual with
hoarding disorder. Normative collecting does not produce the clutter, distress, or impairment
typical of hoarding disorder.
Symptoms (i.e., difficulty discarding and/or clutter) must cause clinically significant distress
or impairment in social, occupational, or other important areas of functioning, including
maintaining a safe environment for self and others (Criterion D). In some cases, particularly
when there is poor insight, the individual may not report distress, and the
impairment may be apparent only to those around the individual. However, any attempts to
discard or clear the possessions by third parties result in high levels of distress.
Associated Features
Other common features of hoarding disorder include indecisiveness, perfectionism, avoidance,
procrastination, difficulty planning and organizing tasks, and distractibility. Some individuals
with hoarding disorder live in unsanitary conditions that may be a logical consequence of
severely cluttered spaces and/or that are related to planning and organizing difficulties. Animal
hoarding can be defined as the accumulation of a large number of animals and a failure to
provide minimal standards of nutrition, sanitation, and veterinary care, as well as failure to act on
the deteriorating condition of the animals (including disease, starvation, or death) and the
environment (e.g., severe overcrowding, extremely unsanitary conditions). Animal hoarding may
be a special manifestation of hoarding disorder. Many individuals who hoard animals also hoard
inanimate objects. The most prominent differences between animal and object hoarding are the
extent of unsanitary conditions and the poorer insight in animal hoarding.
Prevalence
Nationally representative prevalence studies of hoarding disorder are not available. Community
surveys estimate the point prevalence of clinically significant hoarding in the United States and
Europe to range between 1.5% and 6%. In a meta-analysis of 12 studies across high-income
countries, a prevalence of 2.5% was found, with no gender difference identified. This contrasts
with clinical samples, which are predominantly women. In one population-based study in the
Netherlands, hoarding symptoms appeared to be almost three times more prevalent in older
adults (older than 65 years) compared with younger adults (ages 30–40 years).
Development and Course
Hoarding appears to begin early in life and spans well into the late stages. Hoarding symptoms
may first emerge around ages 15–19 years, start interfering with the individual’s everyday
functioning by the mid-20s, and cause clinically significant impairment by the mid-30s.
Participants in clinical research studies are usually in their 50s. Thus, the severity of hoarding
increases with each decade of life, especially after age 30. Once symptoms begin, the course of
hoarding is often chronic, with few individuals reporting a waxing and waning course.

Temperamental.
Environmental.
Genetic and physiological.
Pathological hoarding in children appears to be easily distinguished from developmentally
adaptive saving and collecting behaviors. Because children and adolescents typically do not
control their living environment and discarding behaviors, the possible intervention of third
parties (e.g., parents keeping the spaces usable and thus reducing interference) should be
considered when making the diagnosis.
Risk and Prognostic Factors
Indecisiveness is a prominent feature of individuals with hoarding disorder and
their first-degree relatives.
Individuals with hoarding disorder often retrospectively report stressful and
traumatic life events preceding the onset of the disorder or causing an exacerbation.
Hoarding behavior is familial; more than 50% of individuals who hoard
report having a relative who also hoards. Twin studies indicate that approximately 50% of the
variability in hoarding behavior is attributable to additive genetic factors and the rest to
nonshared environmental factors.
Culture-Related Diagnostic Issues
While most of the research has been done in Western, industrialized countries and urban
communities, the available data from low- and middle-income countries suggest that hoarding
has consistent clinical features cross-culturally, including similarities in severity at clinical
presentation and associated cognitions and behaviors. In cultural contexts in which a high value
is placed on thrift and storing of possessions, the presence of distress and functional impairment
should be the basis for the diagnosis.
Sex- and Gender-Related Diagnostic Issues
The key features of hoarding disorder (i.e., difficulty discarding, excessive amount of clutter) are
generally comparable in men and women, but women tend to display more excessive acquisition,
particularly excessive buying, than do men.
Functional Consequences of Hoarding Disorder
Clutter impairs basic activities, such as moving through the house, cooking, cleaning,
maintaining personal hygiene, and even sleeping. Appliances may be broken, and utilities such
as water and electricity may be disconnected, as access for repair work may be difficult. Quality
of life is often considerably impaired. In severe cases, hoarding can put individuals at risk for
fire, falling (especially elderly individuals), poor sanitation, and other health risks. Hoarding
disorder is associated with occupational impairment, poor physical health, and high social
service utilization. Family relationships are frequently under great strain. Conflict with neighbors
and local authorities is common, and a substantial proportion of individuals with severe hoarding
disorder have been involved in legal eviction proceedings, and some have a history of eviction.
Differential Diagnosis

Other medical conditions.
Neurodevelopmental disorders.
Schizophrenia spectrum and other psychotic disorders.
Major depressive episode.
Obsessive-compulsive disorder.
Neurocognitive disorders.
Hoarding disorder is not diagnosed if the symptoms are judged to be a
direct consequence of another medical condition (Criterion E), such as traumatic brain injury,
surgical resection for treatment of a tumor or seizure control, cerebrovascular disease, infections
of the central nervous system (e.g., herpes simplex encephalitis), or neurogenetic conditions such
as Prader-Willi syndrome. Damage to the anterior ventromedial prefrontal and cingulate cortices
has been particularly associated with the excessive accumulation of objects. In these individuals,
the hoarding behavior is not present prior to the onset of the brain damage and appears shortly
after the brain damage occurs. Some of these individuals appear to have little interest in the
accumulated items and are able to discard them easily or do not care if others discard them,
whereas others appear to be very reluctant to discard anything.
Hoarding disorder is not diagnosed if the accumulation of objects
is judged to be a direct consequence of a neurodevelopmental disorder, such as autism spectrum
disorder or intellectual developmental disorder (intellectual disability).
Hoarding disorder is not diagnosed if the
accumulation of objects is judged to be a direct consequence of delusions or negative symptoms
in schizophrenia spectrum and other psychotic disorders.
Hoarding disorder is not diagnosed if the accumulation of objects is
judged to be a direct consequence of psychomotor retardation, fatigue, or loss of energy during a
major depressive episode.
Hoarding disorder is not diagnosed if the symptoms are judged to
be a direct consequence of typical obsessions or compulsions, such as fears of contamination,
harm, or feelings of incompleteness in obsessive-compulsive disorder
(OCD). Feelings of incompleteness (e.g., losing one’s identity, or having to document and
preserve all life experiences) are the most frequent OCD symptoms associated with this form of
hoarding. The accumulation of objects can also be the result of persistently avoiding onerous
rituals (e.g., not discarding objects in order to avoid endless washing or checking rituals).
In OCD, the behavior is generally unwanted and highly distressing, and the individual
experiences no pleasure or reward from it. Excessive acquisition is usually not present; if
excessive acquisition is present, items are acquired because of a specific obsession (e.g., the need
to buy items that have been accidentally touched in order to avoid contaminating other people),
not because of a genuine desire to possess the items. Individuals who hoard in the context of
OCD are also more likely to accumulate bizarre items, such as trash, feces, urine, fingernail and
toenail cuttings, hair, used diapers, or rotten food. Accumulation of such items is very unusual in
hoarding disorder.
When severe hoarding appears concurrently with other typical symptoms of OCD but is
judged to be independent from these symptoms, both hoarding disorder and OCD may be
diagnosed.
Hoarding disorder is not diagnosed if the accumulation of objects is
judged to be a direct consequence of a degenerative disorder, such as neurocognitive disorder
associated with frontotemporal degeneration or Alzheimer’s disease. Typically, onset of the
accumulating behavior is gradual and follows onset of the neurocognitive disorder. The

F63.3
accumulating behavior may be accompanied by self-neglect and severe domestic squalor,
alongside other neuropsychiatric symptoms, such as disinhibition, gambling, rituals/stereotypies,
tics, and self-injurious behaviors.
Comorbidity
Approximately 75% of individuals with hoarding disorder have a comorbid mood or anxiety
disorder. The most common comorbid conditions are major depressive disorder (30%–50%),
social anxiety disorder, and generalized anxiety disorder. Approximately 20% of individuals
with hoarding disorder also have symptoms that meet diagnostic criteria for OCD. These
comorbidities may often be the main reason for consultation, because individuals are unlikely to
spontaneously report hoarding symptoms, and hoarding symptoms are often not asked about in
routine clinical interviews.
Trichotillomania (Hair-Pulling Disorder)
Diagnostic Criteria
A. Recurrent pulling out of one’s hair, resulting in hair loss.
B. Repeated attempts to decrease or stop hair pulling.
C. The hair pulling causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
D. The hair pulling or hair loss is not attributable to another medical condition (e.g.,
a dermatological condition).
E. The hair pulling is not better explained by the symptoms of another mental
disorder (e.g., attempts to improve a perceived defect or flaw in appearance in
body dysmorphic disorder).
Diagnostic Features
The essential feature of trichotillomania (hair-pulling disorder) is the recurrent pulling out of
one’s own hair (Criterion A). Hair pulling may occur from any region of the body in
which hair grows; the most common sites are the scalp, eyebrows, and eyelids, while less
common sites are axillary, facial, pubic, and perirectal regions. Hair-pulling sites may vary over
time. Hair pulling may occur in brief episodes scattered throughout the day or during less
frequent but more sustained periods that can continue for hours, and such hair pulling may
endure for months or years. Criterion A requires that hair pulling lead to hair loss, although
individuals with this disorder may pull hair in a widely distributed pattern (i.e., pulling single
hairs from all over a site) such that hair loss may not be clearly visible. In addition, individuals
may attempt to conceal or camouflage hair loss (e.g., by using makeup, scarves, or wigs).

Individuals with trichotillomania have made repeated attempts to decrease or stop hair pulling
(Criterion B). Criterion C indicates that hair pulling causes clinically significant distress or
impairment in social, occupational, or other important areas of functioning. The term distress
includes negative affects that may be experienced by individuals with hair pulling, such as
feeling a loss of control, embarrassment, and shame. Significant impairment may occur in
several different areas of functioning (e.g., social, occupational, academic, and leisure), in part
because of avoidance of work, school, or other public situations.
Associated Features
Hair pulling may be accompanied by a range of behaviors or rituals involving hair. Thus,
individuals may search for a particular kind of hair to pull (e.g., hairs with a specific texture or
color), may try to pull out hair in a specific way (e.g., so that the root comes out intact), or may
visually examine or tactilely or orally manipulate the hair after it has been pulled (e.g., rolling the
hair between the fingers, pulling the strand between the teeth, biting the hair into pieces, or
swallowing the hair).
Hair pulling may also be preceded or accompanied by various emotional states; it may be
triggered by feelings of anxiety or boredom, may be preceded by an increasing sense of tension
(either immediately before pulling out the hair or when attempting to resist the urge to pull), or
may lead to gratification, pleasure, or a sense of relief when the hair is pulled out. Hair-pulling
behavior may involve varying degrees of conscious awareness, with some individuals displaying
more focused attention on the hair pulling (with preceding tension and subsequent relief), and
other individuals displaying more automatic behavior (in which the hair pulling seems to occur
without full awareness). Many individuals report a mix of both behavioral styles. Some
individuals experience an “itch-like” or tingling sensation in the scalp that is alleviated by the act
of pulling hair. Pain does not usually accompany hair pulling.
Patterns of hair loss are highly variable. Areas of complete alopecia, as well as areas of
thinned hair density, are common. When the scalp is involved, there may be a predilection for
pulling out hair in the crown or parietal regions. There may be a pattern of nearly complete
baldness except for a narrow perimeter around the outer margins of the scalp, particularly at the
nape of the neck (“tonsure trichotillomania”). Eyebrows and eyelashes may be completely
absent.
Hair pulling does not usually occur in the presence of other individuals, except immediate
family members. Some individuals have urges to pull hair from other individuals and may
sometimes try to find opportunities to do so surreptitiously. Some individuals may pull hairs
from pets, dolls, and other fibrous materials (e.g., sweaters or carpets). Some individuals may
deny their hair pulling to others. The majority of individuals with trichotillomania also have one
or more other body-focused repetitive behaviors, including skin picking, nail biting, and lip
chewing.
Prevalence
In the general population, data from nonrepresentative U.S. samples have suggested that the 12month prevalence estimate for trichotillomania in adults and adolescents may be in

Genetic and physiological.
the range of 1% to 2%. Women are more frequently affected than men in self-identified or
clinical samples, at a ratio estimated at 10:1 or greater, but the gender ratio may be closer to 2:1
in community samples. Among children with trichotillomania, boys and girls are more equally
represented. An online survey of more than 10,000 adults ages 18–69 years, representative of the
general U.S. population, found that 1.7% identified as having current trichotillomania and that
rates did not differ significantly based on gender (1.8% of men and 1.7% of women).
Development and Course
Hair pulling may be seen in infants, and this behavior typically resolves during early
development. Onset of hair pulling in trichotillomania most commonly coincides with, or follows
the onset of, puberty. Sites of hair pulling may vary over time. The usual course of
trichotillomania is chronic, with some waxing and waning if the disorder is untreated. Symptoms
may worsen in females premenstrually but not consistently during pregnancy. For some
individuals, the disorder may come and go for weeks, months, or years at a time. A minority of
individuals remit without subsequent relapse within a few years of onset.
Risk and Prognostic Factors
There is evidence for a genetic vulnerability to trichotillomania. The
disorder is more common in individuals with obsessive-compulsive disorder (OCD) and their
first-degree relatives than in the general population.
Culture-Related Diagnostic Issues
Trichotillomania appears to manifest similarly across cultures and ethnicities, although there is a
paucity of data from non-Western regions.
Diagnostic Markers
Most individuals with trichotillomania admit to hair pulling; thus, dermatopathological diagnosis
is rarely required. Skin biopsy and dermoscopy (or trichoscopy) of trichotillomania are able to
differentiate the disorder from other causes of alopecia. In trichotillomania, dermoscopy shows a
range of characteristic features, including decreased hair density, short vellus hair, and broken
hairs with different shaft lengths.
Functional Consequences of Trichotillomania (Hair-Pulling Disorder)
Trichotillomania is associated with distress as well as with social and occupational impairment.
There may be irreversible damage to hair growth and hair quality. Infrequent medical
consequences of trichotillomania include digit purpura, musculoskeletal injury (e.g., carpal
tunnel syndrome; back, shoulder and neck pain), blepharitis, and dental damage (e.g., worn or
broken teeth resulting from hair biting). Swallowing of hair (trichophagia) may lead to
trichobezoars, with subsequent anemia, abdominal pain, hematemesis, nausea and vomiting,
bowel obstruction, and even bowel perforation.
Differential Diagnosis

Normative hair removal/manipulation.
Other obsessive-compulsive and related disorders.
Stereotypic movement disorder.
Psychotic disorder.
Another medical condition.
Substance-related disorders.
F42.4
Trichotillomania should not be diagnosed when hair removal
is performed solely for cosmetic reasons (i.e., to improve physical appearance). Many
individuals twist and play with their hair, but this behavior does not usually qualify for a
diagnosis of trichotillomania. Some individuals may bite rather than pull hair; again, this does
not qualify for a diagnosis of trichotillomania.
Individuals with OCD and symmetry concerns
may pull out hairs as part of their symmetry rituals, and individuals with body dysmorphic
disorder may remove body hair that they perceive as ugly, asymmetrical, or abnormal; in such
cases a diagnosis of trichotillomania is not given.
Stereotypic movement disorder can sometimes involve hairpulling behavior. For example, a child with intellectual developmental disorder (intellectual
disability) or autism spectrum disorder may engage in stereotypic head banging, hand or arm
biting, and hair pulling when frustrated or angry, and sometimes when excited. This behavior, if
impairing, would be diagnosed as stereotypic movement disorder (co-occurring with intellectual
developmental disorder or autism spectrum disorder) rather than trichotillomania.
Individuals with a psychotic disorder may remove hair in response to a
delusion or hallucination. Trichotillomania is not diagnosed in such cases.
Trichotillomania is not diagnosed if the hair pulling or hair loss is
attributable to another medical condition (e.g., inflammation of the skin or other dermatological
conditions). Other causes of noncicatricial (nonscarring) alopecia (e.g., alopecia areata,
androgenic alopecia, telogen effluvium) or cicatricial (scarring) (e.g., chronic discoid lupus
erythematosus, lichen planopilaris, central centrifugal cicatricial alopecia, pseudopelade,
folliculitis decalvans, dissecting folliculitis, acne keloidalis nuchae) should be considered in
individuals with hair loss who deny hair pulling. Skin biopsy or dermoscopy can be used to
differentiate individuals with trichotillomania from those with dermatological disorders.
Hair-pulling symptoms may be exacerbated by certain substances—
for example, stimulants—but it is less likely that substances are the primary cause of persistent
hair pulling.
Comorbidity
Trichotillomania is often accompanied by other mental disorders, most commonly major
depressive disorder and excoriation (skin-picking) disorder. Repetitive body-focused symptoms
other than hair pulling or skin picking (e.g., nail biting) occur in the majority of individuals with
trichotillomania and may deserve an additional diagnosis of other specified obsessivecompulsive and related disorder (i.e., other body-focused repetitive behavior disorder).
Excoriation (Skin-Picking) Disorder
Diagnostic Criteria

A. Recurrent skin picking resulting in skin lesions.
B. Repeated attempts to decrease or stop skin picking.
C. The skin picking causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
D. The skin picking is not attributable to the physiological effects of a substance
(e.g., cocaine) or another medical condition (e.g., scabies).
E. The skin picking is not better explained by symptoms of another mental disorder
(e.g., delusions or tactile hallucinations in a psychotic disorder, attempts to
improve a perceived defect or flaw in appearance in body dysmorphic disorder,
stereotypies in stereotypic movement disorder, or intention to harm oneself in
nonsuicidal self-injury).
Diagnostic Features
The essential feature of excoriation (skin-picking) disorder is recurrent picking at one’s own skin
(Criterion A). The most commonly picked sites are the face, arms, and hands, but many
individuals pick from multiple body sites. Individuals may pick at healthy skin, at minor skin
irregularities, at lesions such as pimples or calluses, or at scabs from previous picking. Most
individuals pick with their fingernails, although many use tweezers, pins, or other objects. In
addition to skin picking, there may be skin rubbing, squeezing, lancing, and biting. Individuals
with excoriation disorder often spend significant amounts of time on their picking behavior,
sometimes several hours per day, and such skin picking may endure for months or years.
Criterion A requires that skin picking lead to skin lesions, although individuals with this disorder
often attempt to conceal or camouflage such lesions (e.g., with makeup or clothing). Individuals
with excoriation disorder have made repeated attempts to decrease or stop skin picking (Criterion
B).
Criterion C indicates that skin picking causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning. The term distress includes negative
affects that may be experienced by individuals with skin picking, such as feeling a loss of
control, embarrassment, and shame. Significant impairment may occur in several different areas
of functioning (e.g., social, occupational, academic, and leisure), in part because of avoidance of
social situations.
Associated Features
Skin picking may be accompanied by a range of behaviors or rituals involving skin or scabs.
Thus, individuals may search for a particular kind of scab to pull, and they may examine, play
with, or mouth or swallow the skin after it has been pulled. Skin picking may also be preceded or
accompanied by various emotional states. Skin picking may be triggered by feelings of anxiety
or boredom, may be preceded by an increasing sense of tension (either immediately before
picking the skin or when attempting to resist the urge to pick), and may lead to gratification,
pleasure, or a sense of relief when the skin or scab has been picked. Some individuals report

Genetic and physiological.
picking in response to a minor skin irregularity or to relieve an uncomfortable bodily sensation.
Pain is not routinely reported to accompany skin picking. Some individuals engage in skin
picking that is more focused (i.e., with preceding tension and subsequent relief), whereas others
engage in more automatic picking (i.e., when skin picking occurs without preceding tension and
without full awareness), and many have a mix of both behavioral styles. Skin picking does not
usually occur in the presence of other individuals, except immediate family members. Some
individuals report picking the skin of others.
Prevalence
An online survey of more than 10,000 adults, ages 18–69 years, age- and gender-matched to the
U.S. population, found that 2.1% identified as having current excoriation disorder and 3.1%
reported lifetime excoriation disorder. Three-quarters or more of individuals with the disorder are
women in community samples.
Development and Course
Although individuals with excoriation disorder may present at various ages, the skin picking
most often has onset during adolescence, commonly coinciding with or following the onset of
puberty. The disorder frequently begins with a dermatological condition, such as acne. Sites of
skin picking may vary over time. The usual course is chronic, with some waxing and waning if
untreated. For some individuals, the disorder may come and go for weeks, months, or years at a
time.
Risk and Prognostic Factors
There is evidence for a genetic vulnerability to excoriation disorder.
The disorder is more common in individuals with obsessive-compulsive disorder (OCD) and
their first-degree family members than in the general population.
Culture-Related Diagnostic Issues
There are limited data on the prevalence and clinical characteristics of excoriation disorder
across cultures. However, clinical features appear similar in studies of individuals in the United
States and other countries.
Diagnostic Markers
Most individuals with excoriation disorder admit to skin picking; therefore, dermatopathological
diagnosis is rarely required. However, the disorder may have characteristic features on
histopathology.
Functional Consequences of Excoriation (Skin-Picking) Disorder
Excoriation disorder is associated with social and occupational impairment. The majority of
individuals with this condition spend at least 1 hour per day picking, thinking about picking, and
resisting urges to pick. Many individuals report avoiding social or entertainment events as well

Psychotic disorder.
Other obsessive-compulsive and related disorders.
Neurodevelopmental disorders.
Dermatitis artefacta.
Other disorders.
Other medical conditions.
as going out in public. A majority of individuals with the disorder also report experiencing work
interference from skin picking on at least a daily or weekly basis. A significant proportion of
students with excoriation disorder report having missed school, having experienced difficulties
managing responsibilities at school, or having had difficulties studying because of skin picking.
Medical complications of skin picking include tissue damage, scarring, and infection and can be
life-threatening. Rarely, synovitis of the wrists resulting from chronic picking has been reported.
Skin picking often results in significant tissue damage and scarring. It frequently requires
antibiotic treatment for infection, and on occasion it may require surgery.
Differential Diagnosis
Skin picking may occur in response to a delusion (i.e., parasitosis) or tactile
hallucination (i.e., formication) in a psychotic disorder. In such cases, excoriation disorder
should not be diagnosed.
Excessive washing compulsions in response to
contamination obsessions in individuals with OCD may lead to skin lesions, and skin picking
may occur in individuals with body dysmorphic disorder who pick their skin because of
appearance concerns; in such cases, excoriation disorder should not be diagnosed. The
description of other body-focused repetitive behavior disorder in other specified obsessivecompulsive and related disorder excludes individuals whose symptoms meet diagnostic criteria
for excoriation disorder.
While stereotypic movement disorder may be characterized by
repetitive self-injurious behavior, onset is in the early developmental period. For example,
individuals with the neurogenetic condition Prader-Willi syndrome may have early onset of skin
picking, and their symptoms may meet criteria for stereotypic movement disorder. While tics in
individuals with Tourette’s disorder may lead to self-injury, the behavior is not tic-like in
excoriation disorder.
Dermatitis artefacta (also referred to as “factitious dermatitis”) is a term used
in dermatology to refer to medically unexplained, presumably self-induced skin lesions that the
individual denies any role in creating. Cases in which there is evidence of deception on the
individual’s part concerning the skin lesions can be diagnosed as either malingering (if the skin
picking is motivated by external incentives) or factitious disorder (if the skin picking occurs in
the absence of obvious external rewards). In the absence of deception, excoriation disorder can
be diagnosed if there are repeated attempts to decrease or stop skin picking.
Excoriation disorder is not diagnosed if the skin picking is primarily attributable
to the intention to harm oneself that is characteristic of nonsuicidal self-injury.
Excoriation disorder is not diagnosed if the skin picking is primarily
attributable to another medical condition. For example, scabies is a dermatological condition
invariably associated with severe itching and scratching. However, excoriation disorder may be
precipitated or exacerbated by an underlying dermatological condition. For example, acne may
lead to some scratching and picking, which may also be associated with comorbid excoriation

Substance/medication-induced disorders.
disorder (so-called acne excoriée). The differentiation between these two clinical situations (acne
with some scratching and picking vs. acne with comorbid excoriation disorder) requires an
assessment of the extent to which the individual’s skin picking has become independent of the
underlying dermatological condition.
Skin-picking symptoms may also be induced by certain
substances (e.g., cocaine), in which case excoriation disorder should not be diagnosed. If such
skin picking is clinically significant, then a diagnosis of substance/medication-induced
obsessive-compulsive and related disorder should be considered.
Comorbidity
Excoriation disorder is often accompanied by other mental disorders. Such disorders include
OCD and trichotillomania (hair-pulling disorder), as well as major depressive disorder.
Depression comorbidity seems to be more common in women. Repetitive body-focused
symptoms other than skin picking and hair pulling (e.g., nail biting) occur in many individuals
with excoriation disorder and may deserve an additional diagnosis of other specified obsessivecompulsive and related disorder (i.e., other body-focused repetitive behavior disorder).
Substance/Medication-Induced Obsessive-Compulsive
and Related Disorder
Diagnostic Criteria
A. Obsessions, compulsions, skin picking, hair pulling, other body-focused
repetitive behaviors, or other symptoms characteristic of the obsessivecompulsive and related disorders predominate in the clinical picture.
B. There is evidence from the history, physical examination, or laboratory findings
of both (1) and (2):
1. The symptoms in Criterion A developed during or soon after substance
intoxication or withdrawal or after exposure to or withdrawal from a
medication.
2. The involved substance/medication is capable of producing the symptoms in
Criterion A.
C. The disturbance is not better explained by an obsessive-compulsive and related
disorder that is not substance/medication-induced. Such evidence of an
independent obsessive-compulsive and related disorder could include the
following:
The symptoms precede the onset of the substance/medication use; the
symptoms persist for a substantial period of time (e.g., about 1 month) after

the cessation of acute withdrawal or severe intoxication; or there is other
evidence 
suggesting 
the 
existence 
of 
an 
independent 
nonsubstance/medication-induced obsessive-compulsive and related disorder
(e.g., a history of recurrent non-substance/medication-related episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Note: This diagnosis should be made in addition to a diagnosis of substance
intoxication or substance withdrawal only when the symptoms in Criterion A
predominate in the clinical picture and are sufficiently severe to warrant clinical
attention.
Coding note: The ICD-10-CM codes for the [specific substance/medication]-induced
obsessive-compulsive and related disorders are indicated in the table below. Note
that the ICD-10-CM code depends on whether or not there is a comorbid substance
use disorder present for the same class of substance. In any case, an additional
separate diagnosis of a substance use disorder is not given. If a mild substance use
disorder is comorbid with the substance-induced obsessive-compulsive and related
disorder, the 4th position character is “1,” and the clinician should record “mild
[substance] use disorder” before the substance-induced obsessive-compulsive and
related disorder (e.g., “mild cocaine use disorder with cocaine-induced obsessivecompulsive and related disorder”). If a moderate or severe substance use disorder is
comorbid with the substance-induced obsessive-compulsive and related disorder,
the 4th position character is “2,” and the clinician should record “moderate
[substance] use disorder” or “severe [substance] use disorder,” depending on the
severity of the comorbid substance use disorder. If there is no comorbid substance
use disorder (e.g., after a one-time heavy use of the substance), then the 4th
position character is “9,” and the clinician should record only the substance-induced
obsessive-compulsive and related disorder.
ICD-10-CM
With mild use
disorder
With moderate or
severe use disorder
Without use
disorder
Amphetamine-type substance (or other
stimulant)
F15.188
F15.288
F15.988
Cocaine
F14.188
F14.288
F14.988
Other (or unknown) substance
F19.188
F19.288
F19.988
Specify (see Table 1 in the chapter “Substance-Related and Addictive Disorders,”
which indicates whether “with onset during intoxication” and/or “with onset during
withdrawal” applies to a given substance class; or specify “with onset after
medication use”):
With onset during intoxication: If criteria are met for intoxication with the
substance and the symptoms develop during intoxication.

289
With onset during withdrawal: If criteria are met for withdrawal from the
substance and the symptoms develop during, or shortly after, withdrawal.
With onset after medication use: If symptoms developed at initiation of
medication, with a change in use of medication, or during withdrawal of
medication.
Recording Procedures
The name of the substance/medication-induced obsessive-compulsive and related disorder begins
with the specific substance (e.g., cocaine) that is presumed to be causing the obsessivecompulsive and related symptoms. The diagnostic code is selected from the table included in the
criteria set, which is based on the drug class and presence or absence of a comorbid substance
use disorder. For substances that do not fit into any of the classes (e.g., ropinirole), the code for
“other (or unknown) substance” should be used; and in cases in which a substance is judged to
be an etiological factor but the specific class of substance is unknown, the same code should also
be used.
To record the name of the disorder, the comorbid substance use disorder (if any) is listed
first, followed by “with substance/medication-induced obsessive-compulsive and related
disorder” (incorporating the name of the specific etiological substance/medication), followed by
the specification of onset (i.e., onset during intoxication, onset during withdrawal, with onset
after medication use). For example, in the case of repetitive skin-picking occurring during
intoxication in a man with a severe cocaine use disorder, the diagnosis is F14.288 severe cocaine
use disorder with cocaine-induced obsessive-compulsive and related disorder, with onset during
intoxication. A separate diagnosis of the comorbid severe cocaine use disorder is not given. If the
substance-induced obsessive-compulsive and related disorder occurs without a comorbid
substance use disorder (e.g., after a one-time heavy use of the substance), no accompanying
substance use disorder is noted (e.g., F15.988 amphetamine-induced obsessive-compulsive and
related disorder, with onset during intoxication). When more than one substance is judged to play
a significant role in the development of the obsessive-compulsive and related disorder, each
should be listed separately.
Diagnostic Features
The essential features of substance/medication-induced obsessive-compulsive and related
disorder are prominent symptoms of an obsessive-compulsive and related disorder (Criterion A)
that are judged to be attributable to the effects of a substance (e.g., drug of abuse, medication).
The obsessive-compulsive and related disorder symptoms must have developed during or soon
after substance intoxication or withdrawal or after exposure to or withdrawal from a medication
or toxin, and the substance/medication must be capable of producing the symptoms (Criterion
B). Substance/medication-induced obsessive-compulsive and related disorder due to a prescribed
treatment for a mental disorder or other medical condition must have its onset while the
individual is receiving the medication. Once the treatment is discontinued, the obsessivecompulsive and related disorder symptoms will usually improve or remit within days to weeks

Substance intoxication and substance withdrawal.
Obsessive-compulsive and related disorder (i.e., not induced by a substance).
(depending on the half-life of the substance/medication and the presence of withdrawal). The
diagnosis of substance/medication-induced obsessive-compulsive and related disorder should not
be given if onset of the obsessive-compulsive and related disorder symptoms precedes the
substance/medication use, or if the symptoms persist for a substantial period of time, usually
longer than 1 month, from the time of severe intoxication or withdrawal. The
substance/medication-induced obsessive-compulsive and related disorder diagnosis should be
made instead of a diagnosis of substance intoxication or substance withdrawal only when the
symptoms in Criterion A predominate in the clinical picture and are sufficiently severe to
warrant independent clinical attention.
Associated Features
Obsessions, compulsions, hair pulling, skin picking, or other body-focused repetitive behaviors
can occur in association with intoxication with the following classes of substances: stimulants
(including cocaine) and other (or unknown) substances. Heavy metals and toxins may also cause
obsessive-compulsive and related disorder symptoms.
Prevalence
In the U.S. general population, the very limited data that are available indicate that
substance/medication-induced obsessive-compulsive and related disorder is very rare.
Differential Diagnosis
Obsessive-compulsive 
and 
related 
disorder
symptoms may occur in the context of substance intoxication and substance withdrawal. The
diagnosis of the substance-specific intoxication or substance-specific withdrawal will usually
suffice to categorize the symptom presentation. A diagnosis of substance/medication-induced
obsessive-compulsive and related disorder either with onset during intoxication or with onset
during withdrawal should be made instead of a diagnosis of substance intoxication or substance
withdrawal if the obsessive-compulsive and related disorder symptoms are judged to be in excess
of those usually associated with intoxication or withdrawal and are sufficiently severe to warrant
clinical attention.
Substance/medicationinduced obsessive-compulsive and related disorder is distinguished from a primary obsessivecompulsive and related disorder by considering the onset, course, and other factors with respect
to substances/medications. For drugs of abuse, there must be evidence from the history, physical
examination, or laboratory findings for use or intoxication. Substance/medication-induced
obsessive-compulsive and related disorder arises only in association with intoxication, whereas a
primary 
obsessive-compulsive 
and 
related 
disorder 
may 
precede 
the 
onset 
of
substance/medication use. The presence of features that are atypical of a primary obsessivecompulsive and related disorder, such as atypical age at onset of symptoms, may suggest a
substance-induced etiology. A primary obsessive-compulsive and related disorder diagnosis is
warranted if the symptoms persist for a substantial period of time (about 1 month or longer) after

Obsessive-compulsive and related disorder due to another medical condition.
Delirium.
F06.8
the end of the substance intoxication or the individual has a history of an obsessive-compulsive
and related disorder.
If 
the 
obsessivecompulsive and related symptoms are attributable to another medical condition (i.e., rather than
to the medication taken for the other medical condition), obsessive-compulsive and related
disorder due to another medical condition should be diagnosed. The history often provides the
basis for judgment. At times, a change in the treatment for the other medical condition (e.g.,
medication substitution or discontinuation) may be needed to determine whether the medication
is the causative agent (in which case the symptoms may be better explained by
substance/medication-induced obsessive-compulsive and related disorder). If the disturbance is
attributable to both another medical condition and substance use, both diagnoses (i.e., obsessivecompulsive and related disorder due to another medical condition and substance/medicationinduced obsessive-compulsive and related disorder) may be given. When there is insufficient
evidence to determine whether the symptoms are attributable to a substance/medication or to
another medical condition or are primary (i.e., attributable to neither a substance/medication nor
another medical condition), a diagnosis of other specified or unspecified obsessive-compulsive
and related disorder would be indicated.
If obsessive-compulsive and related disorder symptoms occur exclusively during the
course of delirium, they are considered to be an associated feature of the delirium and are not
diagnosed separately.
Obsessive-Compulsive and Related Disorder Due to
Another Medical Condition
Diagnostic Criteria
A. Obsessions, compulsions, preoccupations with appearance, hoarding, skin
picking, hair pulling, other body-focused repetitive behaviors, or other symptoms
characteristic of obsessive-compulsive and related disorder predominate in the
clinical picture.
B. There is evidence from the history, physical examination, or laboratory findings
that the disturbance is the direct pathophysiological consequence of another
medical condition.
C. The disturbance is not better explained by another mental disorder.
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Specify if:

With 
obsessive-compulsive 
disorder–like 
symptoms: 
If 
obsessivecompulsive disorder–like symptoms predominate in the clinical presentation.
With appearance preoccupations: If preoccupation with perceived appearance
defects or flaws predominates in the clinical presentation.
With hoarding symptoms: If hoarding predominates in the clinical presentation.
With hair-pulling symptoms: If hair pulling predominates in the clinical
presentation.
With skin-picking symptoms: If skin picking predominates in the clinical
presentation.
Coding note: Include the name of the other medical condition in the name of the
mental disorder (e.g., F06.8 obsessive-compulsive and related disorder due to
cerebral infarction). The other medical condition should be coded and listed
separately immediately before the obsessive-compulsive and related disorder due
to the medical condition (e.g., I69.398 cerebral infarction; F06.8 obsessivecompulsive and related disorder due to cerebral infarction).
Diagnostic Features
The essential feature of obsessive-compulsive and related disorder due to another medical
condition is clinically significant obsessive-compulsive and related symptoms that are judged to
be best explained as the direct pathophysiological consequence of another medical condition.
Symptoms can include prominent obsessions, compulsions, preoccupations with appearance,
hoarding, hair pulling, skin picking, or other body-focused repetitive behaviors (Criterion A).
The judgment that the symptoms are best explained by the associated medical condition must be
based on evidence from the history, physical examination, or laboratory findings (Criterion B).
Additionally, it must be judged that the symptoms are not better explained by another mental
disorder (Criterion C). The diagnosis is not made if the obsessive-compulsive and related
symptoms occur only during the course of a delirium (Criterion D). The obsessive-compulsive
and related symptoms must cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning (Criterion E).
In determining whether the obsessive-compulsive and related symptoms are attributable to
another medical condition, a medical condition must be present at the time of the onset of the
obsessive-compulsive and related symptoms. Furthermore, it must be established that obsessivecompulsive and related symptoms can be etiologically related to the medical condition through a
pathophysiological mechanism and that this best explains the symptoms in the individual.
Although there are no infallible guidelines for determining whether the relationship between the
obsessive-compulsive and related symptoms and the medical condition is etiological,
considerations that may provide some guidance in making this diagnosis include the presence of
a clear temporal association between the onset, exacerbation, or remission of the medical
condition and the obsessive-compulsive and related symptoms; the presence of features that are
atypical of a primary obsessive-compulsive and related disorder (e.g., atypical age at onset or

Delirium.
course); and evidence in the literature that a known physiological mechanism (e.g., striatal
damage due to a cerebral infarction) causes obsessive-compulsive and related symptoms. In
addition, the disturbance cannot be better explained by a primary obsessive-compulsive and
related disorder, a substance/medication-induced obsessive-compulsive and related disorder, or
another mental disorder.
There has been considerable attention to the question of whether obsessive-compulsive and
related disorders can be attributed to Group A streptococcal infection. Sydenham’s chorea is the
neurological manifestation of rheumatic fever, which is in turn due to Group A streptococcal
infection. Sydenham’s chorea is characterized by a combination of motor and nonmotor
symptoms. Nonmotor features include obsessions, compulsions, attention deficit, and emotional
lability. Although individuals with Sydenham’s chorea may present with non-neuropsychiatric
features of acute rheumatic fever, such as carditis and arthritis, they may present with obsessivecompulsive disorder–like symptoms; such individuals should be diagnosed with obsessivecompulsive and related disorder due to another medical condition.
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections
(PANDAS) has been identified as another postinfectious autoimmune disorder characterized by
the sudden onset of obsessions, compulsions, and/or tics accompanied by a variety of acute
neuropsychiatric symptoms in the absence of chorea, carditis, or arthritis, after Group A
streptococcal infection. However, given that such acute-onset symptoms may be due to a range
of other infections or insults, the term pediatric acute-onset neuropsychiatric syndrome (PANS)
has been used. PANS is characterized by abrupt, dramatic onset of obsessive-compulsive
symptoms or severely restricted food intake, together with a range of additional neuropsychiatric
symptoms. Assessment guidelines for this syndrome are available.
Associated Features
A number of other medical conditions are known to include obsessive-compulsive and related
symptoms as a manifestation. Examples include disorders leading to striatal damage, such as
cerebral infarction or Huntington’s disorder.
Development and Course
The development and course of obsessive-compulsive and related disorder due to another
medical condition generally follows the course of the underlying illness.
Diagnostic Markers
Laboratory assessments and/or medical examinations are necessary to confirm the diagnosis of
another medical condition.
Differential Diagnosis
A separate diagnosis of obsessive-compulsive and related disorder due to another
medical condition is not given if the disturbance occurs exclusively during the course of a
delirium. However, a diagnosis of obsessive-compulsive and related disorder due to

Mixed presentation of symptoms (e.g., mood and obsessive-compulsive and related symptoms)
judged to be due to another medical condition.
Substance/medication-induced obsessive-compulsive and related disorders.
Obsessive-compulsive and related disorders (primary).
Illness anxiety disorder.
Associated feature of another mental disorder.
Other specified obsessive-compulsive and related disorder or unspecified obsessivecompulsive and related disorder.
another medical condition may be given in addition to a diagnosis of major neurocognitive
disorder (dementia) if the etiology of the obsessive-compulsive symptoms is judged to be a
physiological consequence of the pathological process causing the dementia and if obsessivecompulsive symptoms are a prominent part of the clinical presentation.
If the presentation includes a mix of different types of symptoms, the specific mental disorder
due to another medical condition depends on which symptoms predominate in the clinical
picture.
If there is evidence of
recent or prolonged substance use (including medications with psychoactive effects), withdrawal
from a substance, or exposure to a toxin, a substance/medication-induced obsessive-compulsive
and related disorder should be considered. When a substance/medication-induced obsessivecompulsive and related disorder is being diagnosed in relation to drugs of abuse, it may be useful
to obtain a urine or blood drug screen or other appropriate laboratory evaluation. Symptoms that
occur during or shortly after (i.e., within 4 weeks of) substance intoxication or withdrawal or
after medication use may be especially indicative of a substance/medication-induced obsessivecompulsive and related disorder, depending on the type, duration, or amount of the substance
used.
Obsessive-compulsive and related disorder
due to another medical condition should be distinguished from a primary obsessive-compulsive
and related disorder. In primary mental disorders, no specific and direct causative physiological
mechanisms associated with a medical condition can be demonstrated. Acute-onset symptoms,
late age at onset, or atypical symptoms suggest the need for a thorough assessment to rule out the
diagnosis of obsessive-compulsive and related disorder due to another medical condition.
Illness anxiety disorder is characterized by a preoccupation with having
or acquiring a serious illness. In the case of illness anxiety disorder, individuals may or may not
have diagnosed medical conditions.
Obsessive-compulsive and related symptoms may be
an associated feature of another mental disorder (e.g., schizophrenia, anorexia nervosa).
These diagnoses are given if it is unclear whether the obsessive-compulsive and related
symptoms are primary, substance-induced, or due to another medical condition.
Other Specified Obsessive-Compulsive and Related
Disorder
F42.8
This category applies to presentations in which symptoms characteristic of an
obsessive-compulsive and related disorder that cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning

predominate but do not meet the full criteria for any of the disorders in the
obsessive-compulsive and related disorders diagnostic class. The other specified
obsessive-compulsive and related disorder category is used in situations in which
the clinician chooses to communicate the specific reason that the presentation does
not meet the criteria for any specific obsessive-compulsive and related disorder. This
is done by recording “other specified obsessive-compulsive and related disorder”
followed by the specific reason (e.g., “obsessional jealousy”).
Examples of presentations that can be specified using the “other specified”
designation include the following:
1. Body dysmorphic–like disorder with actual flaws: This is similar to body
dysmorphic disorder except that the defects or flaws in physical appearance are
clearly observable by others (i.e., they are more noticeable than “slight”). In such
cases, the preoccupation with these flaws is clearly excessive and causes
significant impairment or distress.
2. Body dysmorphic–like disorder without repetitive behaviors: Presentations
that meet body dysmorphic disorder except that the individual has never
performed repetitive behaviors or mental acts in response to the appearance
concerns.
3. Other body-focused repetitive behavior disorder: Presentations involving
recurrent body-focused repetitive behaviors other than hair pulling and skin
picking (e.g., nail biting, lip biting, cheek chewing) that are accompanied by
repeated attempts to decrease or stop the behaviors and that cause clinically
significant distress or impairment in social, occupational, or other important areas
of functioning.
4. Obsessional jealousy: This is characterized by nondelusional preoccupation
with a partner’s perceived infidelity. The preoccupations may lead to repetitive
behaviors or mental acts in response to the infidelity concerns; they cause
clinically significant distress or impairment in social, occupational, or other
important areas of functioning; and they are not better explained by another
mental disorder such as delusional disorder, jealous type, or paranoid personality
disorder.
5. Olfactory reference disorder (olfactory reference syndrome): This is
characterized by the individual’s persistent preoccupation with the belief that he
or she emits a foul or offensive body odor that is unnoticeable or only slightly
noticeable to others; in response to this preoccupation, these individuals often
engage in repetitive and excessive behaviors such as repeatedly checking for
body odor, excessive showering, or seeking reassurance, as well as excessive
attempts to camouflage the perceived odor. These symptoms cause clinically
significant distress or impairment in social, occupational, or other important areas
of functioning. In traditional Japanese psychiatry, this disorder is known as
jikoshu-kyofu, a variant of taijin kyofusho (see “Culture and Psychiatric
Diagnosis” in Section III).

6. Shubo-kyofu: A variant of taijin kyofusho (see “Culture and Psychiatric
Diagnosis” in Section III) that is similar to body dysmorphic disorder and is
characterized by excessive fear of having a bodily deformity.
7. Koro: Related to dhat syndrome (see “Culture and Psychiatric Diagnosis” in
Section III), an episode of sudden and intense anxiety that the penis in males (or
the vulva and nipples in females) will recede into the body, possibly leading to
death.
Unspecified Obsessive-Compulsive and Related Disorder
F42.9
This category applies to presentations in which symptoms characteristic of an
obsessive-compulsive and related disorder that cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning
predominate but do not meet the full criteria for any of the disorders in the
obsessive-compulsive and related disorders diagnostic class. The unspecified
obsessive-compulsive and related disorder category is used in situations in which
the clinician chooses not to specify the reason that the criteria are not met for a
specific obsessive-compulsive and related disorder and includes presentations in
which there is insufficient information to make a more specific diagnosis (e.g., in
emergency room settings).

# 07 - Trauma and Stressor Related Disorders

# Trauma- and Stressor-Related Disorders

295

F94.1
Trauma- and Stressor-Related Disorders
Trauma- and stressor-related disorders include disorders in which
exposure to a traumatic or stressful event is listed explicitly as a diagnostic criterion. These
include reactive attachment disorder, disinhibited social engagement disorder, posttraumatic
stress disorder (PTSD), acute stress disorder, adjustment disorders, and prolonged grief disorder.
Placement of this chapter reflects the close relationship between these diagnoses and disorders in
the surrounding chapters on anxiety disorders, obsessive-compulsive and related disorders, and
dissociative disorders.
Psychological distress following exposure to a traumatic or stressful event is quite variable.
In some cases, symptoms can be well understood within an anxiety- or fear-based context. It is
clear, however, that many individuals who have been exposed to a traumatic or stressful event
exhibit a phenotype in which, rather than anxiety- or fear-based symptoms, the most prominent
clinical characteristics are anhedonic and dysphoric symptoms, externalizing angry and
aggressive symptoms, or dissociative symptoms. Because of these variable expressions of
clinical distress following exposure to catastrophic or aversive events, the aforementioned
disorders are grouped under a separate category: trauma- and stressor-related disorders.
Furthermore, it is not uncommon for the clinical picture to include some combination of the
above symptoms (with or without anxiety- or fear-based symptoms). Such a heterogeneous
picture has long been recognized in adjustment disorders, as well. Social neglect—that is, the
absence of adequate caregiving during childhood—is a diagnostic requirement of both reactive
attachment disorder and disinhibited social engagement disorder. Although the two disorders
share a common etiology, the former is expressed as an internalizing disorder with depressive
symptoms and withdrawn behavior, while the latter is marked by disinhibition and externalizing
behavior. Finally, it has long been recognized that whereas grief, despair, and general dysphoria
can be a part of the normal grieving process after the death of a loved one, the expression of such
emotions is sometimes abnormally excessive in duration and/or intensity. The diagnosis of
prolonged grief disorder has been introduced in this chapter to meet this clinical concern.
Reactive Attachment Disorder
Diagnostic Criteria
A. A consistent pattern of inhibited, emotionally withdrawn behavior toward adult
caregivers, manifested by both of the following:
1. The child rarely or minimally seeks comfort when distressed.
2. The child rarely or minimally responds to comfort when distressed.

B. A persistent social and emotional disturbance characterized by at least two of
the following:
1. Minimal social and emotional responsiveness to others.
2. Limited positive affect.
3. Episodes of unexplained irritability, sadness, or fearfulness that are evident
even during nonthreatening interactions with adult caregivers.
C. The child has experienced a pattern of extremes of insufficient care as
evidenced by at least one of the following:
1. Social neglect or deprivation in the form of persistent lack of having basic
emotional needs for comfort, stimulation, and affection met by caregiving
adults.
2. Repeated changes of primary caregivers that limit opportunities to form stable
attachments (e.g., frequent changes in foster care).
3. Rearing in unusual settings that severely limit opportunities to form selective
attachments (e.g., institutions with high child-to-caregiver ratios).
D. The care in Criterion C is presumed to be responsible for the disturbed behavior
in Criterion A (e.g., the disturbances in Criterion A began following the lack of
adequate care in Criterion C).
E. The criteria are not met for autism spectrum disorder.
F. The disturbance is evident before age 5 years.
G. The child has a developmental age of at least 9 months.
Specify if:
Persistent: The disorder has been present for more than 12 months.
Specify current severity:
Reactive attachment disorder is specified as severe when a child exhibits all
symptoms of the disorder, with each symptom manifesting at relatively high
levels.
Diagnostic Features
Reactive attachment disorder is characterized by a pattern of markedly disturbed and
developmentally inappropriate attachment behaviors, in which a child rarely or minimally turns
preferentially to an attachment figure for comfort, support, protection, and nurturance. The
essential feature is absent or grossly underdeveloped attachment between the child and putative
caregiving adults. Children with reactive attachment disorder are believed to have the capacity to
form selective attachments. However, because of limited opportunities during early development,
they fail to show the behavioral manifestations of selective attachments. That is, when distressed,
they show no consistent effort to obtain comfort, support, nurturance, or protection from
caregivers. Furthermore, when distressed, children with this disorder do not respond more than

Environmental.
minimally to comforting efforts of caregivers. Thus, the disorder is associated with the absence
of expected comfort seeking and response to comforting behaviors. As such, children with
reactive attachment disorder show diminished or absent expression of positive emotions during
routine interactions with caregivers. In addition, their emotion regulation capacity is
compromised, and they display episodes of negative emotions of fear, sadness, or irritability that
are not readily explained. A diagnosis of reactive attachment disorder should not be made in
children who are developmentally unable to form selective attachments. For this reason, the child
must have a developmental age of at least 9 months. Diagnostic assessment is enhanced by
multiple sources of input, supporting that the symptoms are apparent across contexts.
Associated Features
Because of the shared etiological association with social neglect, reactive attachment disorder
often co-occurs with developmental delays, especially in delays in cognition and language. Other
associated features include stereotypies and other signs of severe neglect (e.g., malnutrition or
signs of poor care).
Prevalence
The prevalence of reactive attachment disorder is unknown, but the disorder is seen relatively
rarely in clinical settings. The disorder has been found in young children exposed to severe
neglect before being placed in foster care or raised in institutions. The disorder is uncommon,
usually occurring in less than 10% of neglected children, even in cases of severe neglect.
Development and Course
Conditions of social neglect are often present in the first months of life in children diagnosed
with reactive attachment disorder, even before the disorder is diagnosed. The clinical features of
the disorder manifest in a similar fashion between the ages of 9 months and 5 years. That is,
signs of absent-to-minimal attachment behaviors and associated emotionally aberrant behaviors
are evident in children throughout this age range, although differing cognitive and motor abilities
may affect how these behaviors are expressed. Remediation and symptomatic recovery may
occur through normative caregiving environments; however, in the absence of enhanced
caregiving, the signs of the disorder may persist, at least for several years. Persistent signs of
reactive attachment disorder in early adolescence may be associated with problems in social
functioning. Less is known about the clinical presentation of reactive attachment disorder in
older children, and the diagnosis should be made with caution in children older than 5 years.
Risk and Prognostic Factors
Serious social neglect is a diagnostic requirement for reactive attachment disorder
and is also the only known risk factor for the disorder. However, the majority of severely
neglected children do not develop the disorder. Prognosis for children with the disorder appears
to depend on the quality of the caregiving environment following serious neglect.

Autism spectrum disorder.
Culture-Related Diagnostic Issues
There is limited information on reactive attachment behavior in young children from diverse
cultural backgrounds around the world. Cultural expectations of attachment behaviors and
caregiving practices may influence development of and concern about these patterns of behaviors
and their presentations in different settings. Caution should be exercised in making the diagnosis
of reactive attachment disorder in cultural contexts in which attachment has not been studied.
Symptoms of reactive attachment disorder may be more common in situations where attachment
figures have experienced extensive trauma, such as war-zone settings; attachment styles may also
vary among migrant and refugee children during the resettlement period. Variations in nurturing
care practices may influence risk of reactive attachment disorder.
Functional Consequences of Reactive Attachment Disorder
Reactive attachment disorder significantly impairs young children’s abilities to relate
interpersonally to adults or peers and is associated with functional impairment across many
domains of early childhood.
Differential Diagnosis
Aberrant social behaviors manifest in young children with reactive
attachment disorder, but they also are key features of autism spectrum disorder. Specifically,
young children with either condition can manifest dampened expression of positive emotions,
cognitive and language delays, and impairments in social reciprocity. As a result, reactive
attachment disorder must be differentiated from autism spectrum disorder. These
two disorders can be distinguished based on differential histories of neglect and on the presence
of restricted interests or ritualized behaviors, specific deficit in social communication, and
selective attachment behaviors. Children with reactive attachment disorder have experienced a
history of severe social neglect, although it is not always possible to obtain detailed histories
about the precise nature of their experiences, especially in initial evaluations. Children with
autism spectrum disorder will only rarely have a history of social neglect. The restricted interests
and repetitive behaviors characteristic of autism spectrum disorder are not a feature of reactive
attachment disorder. These clinical features manifest as excessive adherence to rituals and
routines; restricted, fixated interests; and unusual sensory reactions. However, it is important to
note that children with either condition can exhibit stereotypic behaviors such as rocking or
flapping. Children with either disorder also may exhibit a range of intellectual functioning, but
only children with autism spectrum disorder exhibit selective impairments in social
communicative behaviors, such as intentional communication (i.e., impairment in
communication that is deliberate, goal-directed, and aimed at influencing the behavior of the
recipient). Children with reactive attachment disorder show social communicative functioning
comparable to their overall level of intellectual functioning. Finally, children with autism
spectrum disorder regularly show attachment behavior typical for their developmental level. In
contrast, children with reactive attachment disorder do so only rarely or inconsistently, if at all.
Structured observations can help discriminate between the two disorders.

Intellectual developmental disorder (intellectual disability).
Depressive disorders.
F94.2
Developmental delays often accompany
reactive attachment disorder, but they should not be confused with the disorder. Children with
intellectual developmental disorder should exhibit social and emotional skills comparable to their
cognitive skills and do not demonstrate the profound reduction in positive affect and emotion
regulation difficulties evident in children with reactive attachment disorder. In addition,
developmentally delayed children who have reached a cognitive age of 7–9 months should
demonstrate selective attachments regardless of their chronological age. In contrast, children
with reactive attachment disorder show lack of preferred attachment despite having attained a
developmental age of at least 9 months.
Depression in young children is also associated with reductions in positive
affect. There is limited evidence, however, to suggest that children with depressive disorders
have impairments in attachment. That is, young children who have been diagnosed with
depressive disorders still should seek and respond to comforting efforts by caregivers.
Comorbidity
Conditions associated with neglect, including cognitive delays, language delays, and
stereotypies, often co-occur with reactive attachment disorder. Medical conditions, such as
severe malnutrition, may accompany signs of the disorder. Internalizing symptoms also may cooccur with reactive attachment disorder. A relationship between reactive attachment disorder and
externalizing behavior problems or attention-deficit/hyperactivity disorder (ADHD) has been
suggested but not clearly established.
Disinhibited Social Engagement Disorder
Diagnostic Criteria
A. A pattern of behavior in which a child actively approaches and interacts with
unfamiliar adults and exhibits at least two of the following:
1. Reduced or absent reticence in approaching and interacting with unfamiliar
adults.
2. Overly familiar verbal or physical behavior (that is not consistent with
culturally sanctioned and with age-appropriate social boundaries).
3. Diminished or absent checking back with adult caregiver after venturing
away, even in unfamiliar settings.
4. Willingness to go off with an unfamiliar adult with minimal or no hesitation.
B. The behaviors in Criterion A are not limited to impulsivity (as in attentiondeficit/hyperactivity disorder) but include socially disinhibited behavior.
C. The child has experienced a pattern of extremes of insufficient care as

evidenced by at least one of the following:
1. Social neglect or deprivation in the form of persistent lack of having basic
emotional needs for comfort, stimulation, and affection met by caregiving
adults.
2. Repeated changes of primary caregivers that limit opportunities to form stable
attachments (e.g., frequent changes in foster care).
3. Rearing in unusual settings that severely limit opportunities to form selective
attachments (e.g., institutions with high child-to-caregiver ratios).
D. The care in Criterion C is presumed to be responsible for the disturbed behavior
in Criterion A (e.g., the disturbances in Criterion A began following the
pathogenic care in Criterion C).
E. The child has a developmental age of at least 9 months.
Specify if:
Persistent: The disorder has been present for more than 12 months.
Specify current severity:
Disinhibited social engagement disorder is specified as severe when the child
exhibits all symptoms of the disorder, with each symptom manifesting at
relatively high levels.
Diagnostic Features
The essential feature of disinhibited social engagement disorder is a pattern of behavior that
involves culturally inappropriate, overly familiar behavior with relative strangers (Criterion A).
This overly familiar behavior violates the social boundaries of the culture. A diagnosis of
disinhibited social engagement disorder should not be made before children are developmentally
able to form selective attachments. For this reason, the child must have a developmental age of at
least 9 months.
Associated Features
Because of the shared etiological association with social neglect, disinhibited social engagement
disorder may co-occur with developmental delays, especially cognitive and language delays,
stereotypies, and other signs of severe neglect, such as malnutrition or poor care. However, signs
of the disorder often persist even after these other signs of neglect are no longer present.
Therefore, it is not uncommon for children with the disorder to present with no current signs of
neglect. Moreover, the condition can present in children who show no signs of disordered
attachment. Thus, disinhibited social engagement disorder may be seen in children with a history
of neglect who lack attachments or whose attachments to their caregivers range from disturbed to
secure.
Prevalence
The prevalence of disinhibited social engagement disorder is unknown. Nevertheless, the
disorder appears to be rare, occurring in a minority of children, even those who have experienced

Temperamental.
Environmental.
severe early deprivation. In low-income community populations in the United Kingdom, the
prevalence is up to 2%.
Development and Course
Conditions of social neglect are often present in the first months of life in children diagnosed
with disinhibited social engagement disorder, even before the disorder is diagnosed. As noted by
research among children with a history of institutional care, if neglect occurs early and signs of
the disorder appear, clinical features of the disorder are moderately stable over time, particularly
if conditions of neglect persist.
Signs of disinhibited social engagement disorder have been described from the second year
of life through adolescence among children raised in institutional settings, and even into young
adulthood. There are some differences in manifestations of the disorder from early childhood to
older ages. At the youngest ages, across many cultures, children typically show reticence when
interacting with strangers, which is nonpathological, even if they are raised in institutions and
foster care. Young children with the disorder, however, fail to show reticence to approach and
are found to engage with, and even accompany, unfamiliar adults without hesitation, as shown
by research among children with a history of institutionalized care. In preschool children raised
in institutional settings in the United Kingdom or the United States, verbal and social
intrusiveness appeared most prominent, often accompanied by attention-seeking behavior;
preschool children raised in institutional settings across several countries have displayed a
pattern of engaging in physical contact with strangers. Verbal and physical overfamiliarity
continued through middle childhood, sometimes accompanied by inauthentic expressions of
emotion. In adolescence, indiscriminate behavior may extend to peers. Relative to healthy
adolescents, adolescents with the disorder have more “superficial” peer relationships and more
peer conflicts. Adult manifestations of the disorder appear to be similar but may include
excessive self-disclosure and reduced stranger awareness.
Risk and Prognostic Factors
There is some evidence from research with international adoptees in the United
States that both blunted reward sensitivity and decreased inhibitory control are associated with
indiscriminate social behavior.
Serious social neglect is a diagnostic requirement for disinhibited social
engagement disorder. The rationale for this requirement includes research finding a strong
association between neglect and features of the disorder. Other factors also have been implicated,
such as multiple placement disruptions, borderline personality disorder in the mother, and
aberrant caregiving behaviors and low quality of care. All of these contribute to the insufficient
care criterion. Still, the majority of severely neglected children do not develop the disorder. The
disorder has not been identified in children who experience social neglect only after age 2 years.
Prognosis is only modestly associated with quality of the caregiving environment following
serious neglect. In many cases, the disorder persists, even in children whose caregiving
environment becomes markedly improved.

Genetic and physiological.
Course modifiers.
Attention-deficit/hyperactivity disorder.
F43.10
Various neurobiological factors have been associated with symptoms of
the disorder, but findings concerning the nature of such factors and their specific tie to the
disorder remain preliminary.
Caregiving quality seems to moderate the course of disinhibited social
engagement disorder, at least in young children. Nevertheless, even after placement in normative
caregiving environments, some children show persistent signs of the disorder, through
adolescence and into adulthood.
Culture-Related Diagnostic Issues
There is limited cross-cultural information on disinhibited social engagement disorder. Cultural
expectations of children’s social behaviors may affect their level of disinhibition
toward strangers. The absence of reticence that is characteristic of disinhibited social engagement
disorder should exceed culturally accepted norms.
Functional Consequences of Disinhibited Social Engagement Disorder
Disinhibited social engagement disorder significantly impairs young children’s abilities to relate
interpersonally to adults and peers. Both general social functioning and social competence may
be impaired, along with increased risk for peer conflicts and victimization.
Differential Diagnosis
Children with disinhibited social engagement disorder can
be distinguished from those with ADHD accompanied by social impulsivity, as the former do not
show difficulties with attention or hyperactivity.
Comorbidity
Conditions associated with neglect, including cognitive delays, language delays, and
stereotypies, may co-occur with disinhibited social engagement disorder. Autism spectrum
disorder may also co-occur. In younger children and in middle childhood, disinhibited social
engagement disorder often co-occurs with ADHD and externalizing disorders; this co-occurrence
has been proposed to relate to common impairments in cognitive inhibitory control.
Posttraumatic Stress Disorder
Diagnostic Criteria
Posttraumatic Stress Disorder in Individuals Older Than 6 Years
Note: The following criteria apply to adults, adolescents, and children older than 6

years. For children 6 years and younger, see corresponding criteria below.
A. Exposure to actual or threatened death, serious injury, or sexual violence in one
(or more) of the following ways:
1. Directly experiencing the traumatic event(s).
2. Witnessing, in person, the event(s) as it occurred to others.
3. Learning that the traumatic event(s) occurred to a close family member or
close friend. In cases of actual or threatened death of a family member or
friend, the event(s) must have been violent or accidental.
4. Experiencing repeated or extreme exposure to aversive details of the
traumatic event(s) (e.g., first responders collecting human remains; police
officers repeatedly exposed to details of child abuse).
Note: Criterion A4 does not apply to exposure through electronic media,
television, movies, or pictures, unless this exposure is work related.
B. Presence of one (or more) of the following intrusion symptoms associated with
the traumatic event(s), beginning after the traumatic event(s) occurred:
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic
event(s).
Note: In children older than 6 years, repetitive play may occur in which
themes or aspects of the traumatic event(s) are expressed.
2. Recurrent distressing dreams in which the content and/or affect of the dream
are related to the traumatic event(s).
Note: In children, there may be frightening dreams without recognizable
content.
3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts
as if the traumatic event(s) were recurring. (Such reactions may occur on a
continuum, with the most extreme expression being a complete loss of
awareness of present surroundings.)
Note: In children, trauma-specific reenactment may occur in play.
4. Intense or prolonged psychological distress at exposure to internal or external
cues that symbolize or resemble an aspect of the traumatic event(s).
5. Marked physiological reactions to internal or external cues that symbolize or
resemble an aspect of the traumatic event(s).
C. Persistent avoidance of stimuli associated with the traumatic event(s), beginning
after the traumatic event(s) occurred, as evidenced by one or both of the
following:
1. Avoidance of or efforts to avoid distressing memories, thoughts, or feelings
about or closely associated with the traumatic event(s).
2. Avoidance of or efforts to avoid external reminders (people, places,

conversations, activities, objects, situations) that arouse distressing
memories, thoughts, or feelings about or closely associated with the traumatic
event(s).
D. Negative alterations in cognitions and mood associated with the traumatic
event(s), beginning or worsening after the traumatic event(s) occurred, as
evidenced by two (or more) of the following:
1. Inability to remember an important aspect of the traumatic event(s) (typically
due to dissociative amnesia and not to other factors such as head injury,
alcohol, or drugs).
2. Persistent and exaggerated negative beliefs or expectations about oneself,
others, or the world (e.g., “I am bad,” “No one can be trusted,” “The world is
completely dangerous,” “My whole nervous system is permanently ruined”).
3. Persistent, distorted cognitions about the cause or consequences of the
traumatic event(s) that lead the individual to blame himself/herself or others.
4. Persistent negative emotional state (e.g., fear, horror, anger, guilt, or shame).
5. Markedly diminished interest or participation in significant activities.
6. Feelings of detachment or estrangement from others.
7. Persistent inability to experience positive emotions (e.g., inability to
experience happiness, satisfaction, or loving feelings).
E. Marked alterations in arousal and reactivity associated with the traumatic
event(s), beginning or worsening after the traumatic event(s) occurred, as
evidenced by two (or more) of the following:
1. Irritable behavior and angry outbursts (with little or no provocation) typically
expressed as verbal or physical aggression toward people or objects.
2. Reckless or self-destructive behavior.
3. Hypervigilance.
4. Exaggerated startle response.
5. Problems with concentration.
6. Sleep disturbance (e.g., difficulty falling or staying asleep or restless sleep).
F. Duration of the disturbance (Criteria B, C, D, and E) is more than 1 month.
G. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
H. The disturbance is not attributable to the physiological effects of a substance
(e.g., medication, alcohol) or another medical condition.
Specify whether:
With dissociative symptoms: The individual’s symptoms meet the criteria for
posttraumatic stress disorder, and in addition, in response to the stressor, the
individual experiences persistent or recurrent symptoms of either of the

following:
1. Depersonalization: Persistent or recurrent experiences of feeling detached
from, and as if one were an outside observer of, one’s mental processes or
body (e.g., feeling as though one were in a dream; feeling a sense of unreality
of self or body or of time moving slowly).
2. Derealization: Persistent or recurrent experiences of unreality of surroundings
(e.g., the world around the individual is experienced as unreal, dreamlike,
distant, or distorted).
Note: To use this subtype, the dissociative symptoms must not be attributable to
the physiological effects of a substance (e.g., blackouts, behavior during alcohol
intoxication) or another medical condition (e.g., complex partial seizures).
Specify if:
With delayed expression: If the full diagnostic criteria are not met until at least
6 months after the event (although the onset and expression of some symptoms
may be immediate).
Posttraumatic Stress Disorder in Children 6 Years and Younger
A. In children 6 years and younger, exposure to actual or threatened death, serious
injury, or sexual violence in one (or more) of the following ways:
1. Directly experiencing the traumatic event(s).
2. Witnessing, in person, the event(s) as it occurred to others, especially primary
caregivers.
3. Learning that the traumatic event(s) occurred to a parent or caregiving figure.
B. Presence of one (or more) of the following intrusion symptoms associated with
the traumatic event(s), beginning after the traumatic event(s) occurred:
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic
event(s).
Note: Spontaneous and intrusive memories may not necessarily appear
distressing and may be expressed as play reenactment.
2. Recurrent distressing dreams in which the content and/or affect of the dream
are related to the traumatic event(s).
Note: It may not be possible to ascertain that the frightening content is
related to the traumatic event.
3. Dissociative reactions (e.g., flashbacks) in which the child feels or acts as if
the traumatic event(s) were recurring. (Such reactions may occur on a
continuum, with the most extreme expression being a complete loss of
awareness of present surroundings.) Such trauma-specific reenactment may
occur in play.
4. Intense or prolonged psychological distress at exposure to internal or external
cues that symbolize or resemble an aspect of the traumatic event(s).

5. Marked physiological reactions to reminders of the traumatic event(s).
C. One (or more) of the following symptoms, representing either persistent
avoidance of stimuli associated with the traumatic event(s) or negative
alterations in cognitions and
mood associated with the traumatic event(s), must be present, beginning after
the event(s) or worsening after the event(s):
Persistent Avoidance of Stimuli
1. Avoidance of or efforts to avoid activities, places, or physical reminders that
arouse recollections of the traumatic event(s).
2. Avoidance of or efforts to avoid people, conversations, or interpersonal
situations that arouse recollections of the traumatic event(s).
Negative Alterations in Cognitions
3. Substantially increased frequency of negative emotional states (e.g., fear,
guilt, sadness, shame, confusion).
4. Markedly diminished interest or participation in significant activities, including
constriction of play.
5. Socially withdrawn behavior.
6. Persistent reduction in expression of positive emotions.
D. Alterations in arousal and reactivity associated with the traumatic event(s),
beginning or worsening after the traumatic event(s) occurred, as evidenced by
two (or more) of the following:
1. Irritable behavior and angry outbursts (with little or no provocation) typically
expressed as verbal or physical aggression toward people or objects
(including extreme temper tantrums).
2. Hypervigilance.
3. Exaggerated startle response.
4. Problems with concentration.
5. Sleep disturbance (e.g., difficulty falling or staying asleep or restless sleep).
E. The duration of the disturbance is more than 1 month.
F. The disturbance causes clinically significant distress or impairment in
relationships with parents, siblings, peers, or other caregivers or with school
behavior.
G. The disturbance is not attributable to the physiological effects of a substance
(e.g., medication or alcohol) or another medical condition.
Specify whether:
With dissociative symptoms: The individual’s symptoms meet the criteria for
posttraumatic stress disorder, and the individual experiences persistent or
recurrent symptoms of either of the following:

1. Depersonalization: Persistent or recurrent experiences of feeling detached
from, and as if one were an outside observer of, one’s mental processes or
body (e.g., feeling as though one were in a dream; feeling a sense of unreality
of self or body or of time moving slowly).
2. Derealization: Persistent or recurrent experiences of unreality of surroundings
(e.g., the world around the individual is experienced as unreal, dreamlike,
distant, or distorted).
Note: To use this subtype, the dissociative symptoms must not be attributable to
the physiological effects of a substance (e.g., blackouts) or another medical
condition (e.g., complex partial seizures).
Specify if:
With delayed expression: If the full diagnostic criteria are not met until at least
6 months after the event (although the onset and expression of some symptoms
may be immediate).
Diagnostic Features
The essential feature of posttraumatic stress disorder (PTSD) is the development of characteristic
symptoms following exposure to one or more traumatic events. The clinical presentation of
PTSD varies. In some individuals, fear-based reexperiencing, emotional, and behavioral
symptoms may predominate. In others, anhedonic or dysphoric mood states and negative
cognitions may be most prominent. In some other individuals, arousal and reactive-externalizing
symptoms are prominent, while in yet others, dissociative symptoms predominate. Finally, some
individuals exhibit combinations of these symptom patterns.
The following discussion of specific criteria for PTSD refers to specific criteria for adults;
criteria for children 6 years or younger may differ in criterion numbering given differences in
applicable criteria for this age group.
The traumatic events in Criterion A all involve actual or threatened death, serious injury, or
sexual violence in some way but differ in how the individual is exposed to them, which can be
through directly experiencing the traumatic event (Criterion A1), witnessing in person the event
as it occurred to others (Criterion A2), learning that the event occurred to a family member or a
close friend (Criterion A3), or indirect exposure in the course of occupational duties, through
being exposed to grotesque details of an event (Criterion A4). The disorder may be especially
severe or long-lasting when the stressor is interpersonal and intentional (e.g., torture, sexual
violence).
The directly experienced traumatic events in Criterion A include, but are not limited to,
exposure to war as a combatant or civilian, actual or threatened physical assault in which the
threat is perceived as imminent and realistic (e.g., physical attack, robbery, mugging, childhood
physical abuse), being kidnapped, being taken hostage, terrorist attack, torture, incarceration as a
prisoner of war, natural or human-made disasters, and severe motor vehicle accidents.
Sexual trauma includes, but is not limited to, actual or threatened sexual violence or coercion

(e.g., forced sexual penetration; alcohol/drug-facilitated nonconsensual sexual penetration; other
unwanted sexual contact; and other unwanted sexual experiences not involving contact, such as
being forced to watch pornography, exposure to the display of genitals by an exhibitionist, or
being the victim of unwanted photography or videotaping of a sexual nature or the unwanted
dissemination of these photographs or videos).
Being bullied may qualify as a Criterion A1 experience when there is a credible threat of
serious harm or sexual violence. For children, sexually violent events may include
developmentally inappropriate sexual experiences without physical violence or injury.
A life-threatening illness or debilitating medical condition is not necessarily considered a
traumatic event. Qualifying events of this type include life-threatening medical emergencies
(e.g., an acute myocardial infarction, anaphylactic shock) or a particular event in treatment that
evokes catastrophic feelings of terror, pain, helplessness, or imminent death (e.g., waking during
surgery, debridement of severe burn wounds, emergency cardioversion).
Witnessed events (Criterion A2) include, but are not limited to, observing threatened or
serious injury, unnatural death, physical or sexual abuse of another person due to violent assault,
domestic violence, accident, war, or disaster. For example, this would include parents witnessing
their child in an acute life-endangering incident (e.g., a diving accident) or a medical catastrophe
during the course of their child’s illness or ongoing treatment (e.g., a life-threatening
hemorrhage).
Indirect exposure through learning about an event (Criterion A3) is limited to events
affecting close relatives or friends that were violent or accidental (i.e., death from natural causes
does not qualify). Such events include murder, violent personal assault, combat, terrorist attack,
sexual violence, suicide, and serious accident or injury.
The indirect exposure of professionals to the grotesque effects of war, rape, genocide, or
abusive violence inflicted on others occurring in the context of their work duties can also result
in PTSD and thus is considered to be a qualifying trauma (Criterion A4). Examples
include first responders exposed to serious injury or death and military personnel collecting
human remains. Indirect exposure can also occur through photos, videos, verbal accounts, or
written accounts (e.g., police officers reviewing crime reports or conducting interviews with
crime victims, drone operators, members of the news media covering traumatic events, and
psychotherapists exposed to details of their patients’ traumatic experiences).
Exposure to multiple traumatic events is common and can take many forms. Some
individuals experience different types of traumatic events at different times (e.g., sexual violence
during childhood and natural disaster as adults). Others experience the same type of traumatic
event at different times or in a series committed by the same person/people over an extended
period (e.g., child sexual or physical assault; physical or sexual assault by an intimate partner).
Others may experience numerous traumatic events that are the same or different during an
extended hazardous period such as deployment or living in a conflict zone. When one is
assessing the PTSD criteria in individuals who have experienced multiple traumatic events
across their lives, it may be useful to determine if there is a specific, discrete example that the
individual considers to be the worst given that the symptomatic expressions of PTSD Criterion B
and Criterion C specifically refer to the traumatic event (e.g., recurrent, involuntary, and

intrusive distressing recollections of the traumatic event). However, if it is difficult for the
individual to identify a worst example, it is appropriate to consider the entire exposure as
meeting Criterion A. In addition, some discrete events may incorporate several traumatic event
types (e.g., an individual involved in a mass casualty incident sustains a major injury, witnesses
someone else being injured, and then learns that a family member was killed in the incident).
The traumatic event can be reexperienced in various ways. Commonly, the individual has
recurrent, involuntary, and intrusive recollections of the event (Criterion B1). Intrusive
recollections in PTSD are distinguished from depressive rumination in that they apply only to
involuntary and intrusive distressing memories. The emphasis is on recurrent memories of the
event that usually include intrusive, vivid, sensory, and emotional components that are
distressing and not merely ruminative. A common reexperiencing symptom is distressing dreams
that replay the event itself or that are representative or thematically related to the major threats
involved in the traumatic event (Criterion B2). The individual may experience dissociative states
that typically last a few seconds and rarely are of a longer duration, during which components of
the event are relived and the individual behaves as if the event were occurring at that moment
(Criterion B3). Such events occur on a continuum, ranging from brief visual or other sensory
intrusions about part of the traumatic event without loss of reality orientation to a partial loss of
awareness of present surroundings to a complete loss of awareness. These episodes, often
referred to as “flashbacks,” are typically brief but can be associated with prolonged distress and
heightened arousal. For young children, reenactment of events related to trauma may be
expressed behaviorally in play or in dissociative states. Intense psychological distress (Criterion
B4) or physiological reactivity (Criterion B5) often occurs when the individual is exposed to
triggering events or somatic reactions that resemble or symbolize an aspect of the traumatic
event (e.g., windy days after a hurricane, seeing someone who resembles one’s perpetrator). The
triggering cue could also be a physical sensation (e.g., dizziness for survivors of head trauma,
rapid heartbeat for a previously traumatized child), particularly for individuals with highly
somatic presentations.
Stimuli associated with the trauma are persistently avoided. The individual commonly makes
deliberate efforts to avoid thoughts, memories, or feelings (e.g., by utilizing distraction or
suppression techniques, including substance use, to avoid internal reminders) (Criterion C1), and
to avoid activities, conversations, objects, situations, or people who arouse recollections of it
(Criterion C2).
Negative alterations in cognitions or mood associated with the traumatic event begin or
worsen after exposure to the event. These negative alterations can take various forms, including
an inability to remember key and emotionally painful aspects of the traumatic
event. Such memory loss is typically attributable to dissociative amnesia and is not
attributable to head injury or impaired encoding of the memory due to drug or alcohol use
(Criterion D1). Individuals with PTSD often report that the traumatic event has irrevocably
altered their lives and their view of the world. This is characterized by persistent and exaggerated
negative beliefs and expectations regarding important aspects of life applied to themselves,
others, the world, or the future (Criterion D2) (e.g., “Bad things will always happen to me”; “The
world is dangerous, and I can never be adequately protected”; “I can’t trust anyone ever again”;

“My life is permanently ruined”; “I have lost any chance for future happiness”; “My life will be
cut short”). Individuals with PTSD may have persistent erroneous cognitions about the causes of
the traumatic event that lead them to blame themselves or others (e.g., “It’s all my fault that my
uncle abused me”) (Criterion D3). A persistent negative mood state (e.g., fear, dysphoria, horror,
anger, guilt, shame) either began or worsened after exposure to the event (Criterion D4). The
individual may experience markedly diminished interest or participation in previously enjoyed
activities (Criterion D5), may feel detached or estranged from other people (Criterion D6), or
may experience a persistent inability to feel positive emotions (especially happiness, joy,
satisfaction, or emotions associated with intimacy, tenderness, and sexuality) (Criterion D7).
Negative alterations in arousal and reactivity also begin or get worse after exposure to the
event. Individuals with PTSD may exhibit irritable or angry behavior and may engage in
aggressive verbal or physical behavior with little or no provocation (e.g., yelling at people,
getting into fights, destroying objects) (Criterion E1). They may also engage voluntarily in
reckless or self-destructive behavior that is dangerous, that shows a disregard for the physical
safety of themselves or others, and that could directly result in serious physical harm or death
(Criterion E2). Examples include, but are not limited to, dangerous driving (e.g., drunk driving,
driving at dangerously high speeds), excessive alcohol or drug use, having risky sex (e.g.,
unprotected sex with a partner whose HIV status is unknown, high number of sexual partners), or
self-directed violence including suicidal behaviors. Criterion E2 does not include circumstances
in which individuals must engage in dangerous situations as a part of their job (e.g., armed forces
members in combat situations or first responders in emergency situations) and take reasonable
safety precautions to reduce their risk or when individuals engage in behaviors that may be
unwise, unhealthy, or financially harmful but pose no direct risk of immediate serious physical
harm or death (e.g., pathological gambling, poor financial decisions, binge eating, unhealthy
lifestyles). PTSD is often characterized by a heightened vigilance for potential threats, including
those that are related to the traumatic experience (e.g., following a motor vehicle accident, being
especially sensitive to the threat potentially caused by cars or trucks) and those not related to the
traumatic event (e.g., being fearful of suffering a heart attack) (Criterion E3). Individuals with
PTSD may be very reactive to unexpected stimuli, displaying a heightened startle response, or
jumpiness, to loud noises or unexpected movements (e.g., jumping markedly in response to a
telephone ringing) (Criterion E4). Startle responses are involuntary and reflexive (automatic,
instantaneous), and stimuli that evoke exaggerated startle responses (Criterion E4) need not be
related at all to the traumatic event. Startle responses are distinguished from the cued
physiological arousal responses in Criterion B5, for which there needs to be at least some level
of conscious appraisal that the stimulus producing physiological responses is related to the
trauma. Concentration difficulties, including difficulty remembering daily events (e.g., forgetting
one’s telephone number) or attending to focused tasks (e.g., following a conversation for a
sustained period of time), are commonly reported (Criterion E5). Problems with sleep onset and
maintenance are common and may be associated with nightmares and safety concerns or with
generalized elevated arousal that interferes with adequate sleep (Criterion E6).
The diagnosis of PTSD requires that the duration of the symptoms in Criteria B, C, D, and E
be more than 1 month (Criterion F). For a current diagnosis of PTSD, Criteria B, C, D, and E
must all be met for more than 1 month, for at least the past month. For a lifetime

diagnosis of PTSD, there must be a period of time lasting more than 1 month during which
Criteria B, C, D, and E have all been met for the same 1-month period of time.
A significant subgroup of individuals with PTSD experience persistent dissociative
symptoms of either depersonalization (detachment from their bodies) or derealization
(detachment from the world around them). This can be indicated by using the “with dissociative
symptoms” specifier.
Associated Features
Developmental regression, such as loss of language in young children, may occur. Auditory
pseudo-hallucinations, such as having the sensory experience of hearing one’s thoughts spoken
in one or more different voices, as well as paranoid ideation, can be present. Following
prolonged, repeated, and severe traumatic events (e.g., childhood abuse, torture), the individual
may additionally experience difficulties in regulating emotions or maintaining stable
interpersonal relationships, or dissociative symptoms. When the traumatic event involves the
violent death of someone with whom the individual had a close relationship, symptoms of both
prolonged grief disorder and PTSD may be present.
Prevalence
The national lifetime prevalence estimate for PTSD using DSM-IV criteria is 6.8% for U.S.
adults. Lifetime prevalence for U.S. adolescents using DSM-IV criteria has ranged from 5.0% to
8.1% and a past 6-month prevalence of 4.9% for adolescents. While definitive, comprehensive
population-based data using DSM-5 are not available, findings are beginning to emerge. In two
U.S. national epidemiological studies, lifetime DSM-5 PTSD prevalence estimates ranged from
6.1% to 8.3%, and the national 12-month DSM-5 prevalence estimate was 4.7% in both studies.
National lifetime DSM-IV PTSD estimates from World Mental Health Surveys in 24 countries
varied substantially among countries, income country groups, and WHO regions but was 3.9%
overall. In conflict-affected populations worldwide, the point prevalence of PTSD with
functional impairment is 11% after adjustment for age differences across studies.
Rates of PTSD are higher among veterans and others whose vocation increases the risk of
traumatic exposure (e.g., police, firefighters, emergency medical personnel). Highest rates
(ranging from one-third to more than one-half of those exposed) are found among survivors of
rape, military combat and captivity, and ethnically or politically motivated internment and
genocide. The prevalence of PTSD may vary across development; children and adolescents,
including preschool children, generally have displayed lower prevalence following exposure to
serious traumatic events; however, this may be because previous criteria were insufficiently
developmentally informed. Racial differences, based on DSM-IV data, show higher rates of
PTSD among U.S. Latinx, African Americans, and American Indians compared with Whites.
Potential reasons for these prevalence variations include differences in predisposing or enabling
factors, such as exposure to past adversity and racism and discrimination, and in availability or
quality of treatment, social support, socioeconomic status, and other social resources that
facilitate recovery and are confounded with ethnic and racialized background.
Development and Course

PTSD can occur at any age, beginning after the first year of life. Symptoms usually begin within
the first 3 months after the trauma, although there may be a delay of months, or even years,
before full criteria for the diagnosis are met. There is abundant evidence for what DSM-IV called
“delayed onset” but is now called “delayed expression,” with the recognition that some
symptoms typically appear immediately and that the delay is in meeting full criteria.
Frequently, an individual’s reaction to a trauma initially meets criteria for acute stress
disorder in the immediate aftermath of the trauma. The symptoms of PTSD and the
relative predominance of different symptoms may vary over time. Duration of the symptoms
also varies, with complete recovery within 3 months occurring in approximately one-half of
adults, while some individuals remain symptomatic for longer than 12 months and sometimes for
more than 50 years. Symptom recurrence and intensification may occur in response to reminders
of the original trauma, ongoing life stressors, or newly experienced traumatic events.
The clinical expression of reexperiencing can vary across development. Developmental
variations in clinical expression inform the use of different criteria in children 6 years and
younger and in individuals who are older. Young children may report new onset of frightening
dreams without content specific to the traumatic event. Children age 6 and younger may develop
PTSD as a result of severe emotional abuse (e.g., threat of abandonment), which can be
perceived as life-threatening. During treatment for life-threatening illness (e.g., cancer, solid
organ transplantation), the experience of young children of the severity and intensity of the
treatment may contribute to risk of developing posttraumatic stress symptoms; the self-appraisal
of threat may also contribute to the risk of developing posttraumatic stress symptoms in
adolescents. Before age 6 years, young children are more likely to express reexperiencing
symptoms through play that refers directly or symbolically to the trauma (see PTSD criteria for
children 6 years and younger). They may not manifest fearful reactions at the time of the
exposure or during reexperiencing. Parents may report a wide range of emotional or behavioral
changes in young children. Children may focus on imagined interventions in their play or
storytelling. In addition to avoidance, children may become preoccupied with reminders.
Because of young children’s limitations in expressing thoughts or labeling emotions, negative
alterations in mood or cognition tend to involve primarily mood changes. Children may
experience co-occurring traumas (e.g., physical abuse, witnessing domestic violence) and in
chronic circumstances may not be able to identify onset of symptomatology. Avoidant behavior
may be associated with restricted play or exploratory behavior in young children; reduced
participation in new activities in school-age children; or reluctance to pursue developmental
opportunities in adolescents (e.g., dating, driving). Older children and adolescents may judge
themselves as cowardly. Adolescents may harbor beliefs of being changed in ways that make
them socially undesirable and estrange them from peers and lose aspirations for the future.
Irritable or aggressive behavior in children and adolescents can interfere with peer relationships
and school behavior. Reckless behavior may lead to accidental injury to self or others, thrillseeking, or high-risk behaviors. In older individuals, the disorder is associated with negative
health perceptions, primary care utilization, and suicidal thoughts. In addition, declining health,
worsening cognitive functioning, and social isolation may exacerbate PTSD symptoms.

Temperamental.
Environmental.
Genetic and physiological.
Environmental.
Temperamental.
Risk and Prognostic Factors
Risk factors for PTSD can operate in many ways, including predisposing individuals to trauma
or to extreme emotional responses when exposed to traumatic events. Risk (and protective)
factors are generally divided into pretraumatic, peritraumatic, and posttraumatic factors.
Pretraumatic Factors
High-risk factors include childhood emotional problems by age 6 years (e.g.,
externalizing or anxiety problems) and prior mental disorders (e.g., panic disorder, depressive
disorder, PTSD, or obsessive-compulsive disorder [OCD]). Individual differences in premorbid
personality may influence the trajectory of response to trauma and treatment outcomes.
Personality traits associated with negative emotional responses such as depressed mood and
anxiousness represent risk factors for the development of PTSD. Such traits might be captured in
measures of negative affectivity (neuroticism) on
standardized personality scales. Premorbid trait impulsivity tends to be associated with
externalizing manifestations of PTSD and comorbidities of the externalizing spectrum, including
substance use disorder or aggressive behavior.
As documented among U.S. civilians and veterans, these risk factors include
lower socioeconomic status; lower education; exposure to prior trauma (especially during
childhood); childhood adversity (e.g., economic deprivation, family dysfunction, parental
separation or death); lower intelligence; ethnic discrimination and racism; and a family
psychiatric history. Social support prior to event exposure is protective.
The risk of developing PTSD following traumatic exposure has been
demonstrated to be modestly heritable in twin studies and molecular studies. Genome-wide
association data from a large multiethnic cohort support the heritability of PTSD and
demonstrate three robust genome-wide significant loci that vary by geographic ancestry.
Susceptibility to PTSD may also be influenced by epigenetic factors. Genome-wide association
data from U.S. veterans identify eight significant regions in Americans of European descent
associated with intrusive reexperiencing symptoms of PTSD; data from the United Kingdom also
support these associations.
Peritraumatic Factors
These include severity (dose) of the trauma, perceived life threat, personal injury,
interpersonal violence (particularly trauma perpetrated by a caregiver or involving a witnessed
threat to a caregiver in children), and, for military personnel, being a perpetrator, witnessing
atrocities, or killing the enemy. Finally, dissociation, fear, panic, and other peritraumatic
responses that occur during the trauma and persist afterward are risk factors.
Posttraumatic Factors
These include negative appraisals, inappropriate coping strategies, and
development of acute stress disorder.

Environmental. These include subsequent exposure to repeated upsetting reminders, subsequent
adverse life events, and financial or other trauma-related losses. Posttraumatic experiences such
as forced migration and high levels of daily stressors may contribute to different conditional risks
of PTSD across cultural contexts. Exposure to racial and ethnic discrimination has been
associated with a more chronic course among African American and Latinx adults. Social
support (including family stability, for children) is a protective factor that moderates outcome
after trauma.
Culture-Related Diagnostic Issues
Different demographic, cultural, and occupational groups have different levels of exposure to
traumatic events, and the relative risk of developing PTSD following a similar level of exposure
(e.g., religious persecution) may also vary across cultural, ethnic, and racialized groups.
Variation in the type of traumatic exposure (e.g., genocide), the impact on disorder severity of
the meaning attributed to the traumatic event (e.g., inability to perform funerary rites after a mass
killing), the ongoing sociocultural context (e.g., residing among unpunished perpetrators in
postconflict settings), exposure to racial and ethnic discrimination, and other cultural factors
(e.g., acculturative stress in migrants) may influence the risk of onset and severity of PTSD
across cultural groups. Some communities are exposed to pervasive and ongoing traumatic
environments, rather than isolated Criterion A events; in these communities, the predictive power
of individual traumatic events for the development of PTSD may diminish. In cultures where
social image (e.g., maintaining a family’s “face”) is emphasized, public defamation or shaming
may magnify the impact of Criterion A events. Some cultures may attribute PTSD syndromes to
negative supernatural experiences.
The clinical expression of the symptoms or symptom clusters of PTSD can vary culturally in
both adults and children. In many non-Western groups, avoidance is less commonly observed,
whereas somatic symptoms (e.g., dizziness, shortness of breath, heat sensations) are more
common; other symptoms that vary cross-culturally are distressing dreams, amnesia not related
to head injury, and reckless but nonsuicidal behavior. Negative moods, especially anger, are
common cross-culturally in individuals with PTSD, as are distressing dreams and sleep paralysis.
Across cultures, somatic symptoms are frequent, occurring in both children and adults, especially
after sexual trauma. Symptoms that vary cross-culturally in relation to PTSD among children
include intrusive thoughts, diminished participation in activities, inability to experience positive
emotions, irritability, aggression, and hypervigilance. Distressing dreams, flashbacks,
psychological distress upon exposure to trauma cues, and efforts to avoid memories and thoughts
are common in children with PTSD across cultures.
In certain cultural contexts, it may be normative to respond to traumatic events with negative
beliefs about oneself or with spiritual attributions that may appear exaggerated to others. For
example, blaming oneself may be consistent with ideas of karma in South and East Asia, destiny
or “spoiled medicine law” in West Africa, and cultural differences in locus of control and
conceptions of self.
In many populations around the world, there are cultural concepts of distress that resemble

Adjustment disorders.
PTSD and are characterized by diverse manifestations of psychological distress attributed to
frightening or traumatic experiences. Thus, cultural concepts of distress influence the expression
of PTSD and the range of its comorbid disorders (see “Culture and Psychiatric Diagnosis” in
Section III).
Sex- and Gender-Related Diagnostic Issues
PTSD is more prevalent among women than among men across the life span. Lifetime
prevalence of PTSD ranges from 8.0% to 11.0% for women and 4.1% to 5.4% for men based on
two large U.S. population-based studies using DSM-5 criteria. Some of the increased risk for
PTSD in women appears to be attributable to a greater likelihood of exposure to childhood
sexual abuse, sexual assault, and other forms of interpersonal violence, which carry the highest
risk for development of PTSD. Women in the general population also experience PTSD for a
longer duration than do men. However, other factors likely contributing to the higher prevalence
in women include gender differences in the emotional and cognitive processing of trauma, as
well as effects of reproductive hormones. When responses of men and women to specific
stressors are compared, gender differences in risk for PTSD persist. On the other hand, PTSD
symptom profiles and factor structures are similar between men and women.
Association With Suicidal Thoughts or Behavior
Traumatic events such as childhood abuse or sexual trauma increase an individual’s suicide risk
in both civilians and veterans. PTSD is associated with suicidal thoughts, suicide attempts, and
death from suicide. The presence of PTSD has been associated with an increased likelihood of
transitioning from suicidal thoughts to a suicide plan or attempt, and this effect of PTSD occurs
independently of the increased risk of mood disorders on the likelihood of suicidal behaviors.
Among adolescents there is also a significant relationship between PTSD and suicidal thoughts
or behavior even after adjustment for the effects of comorbidity.
Functional Consequences of Posttraumatic Stress Disorder
PTSD is associated with high impairment in social, occupational, and physical functioning;
reduced quality of life; and physical health problems. Impaired functioning is exhibited
across social, interpersonal, developmental, educational, physical health, and occupational
domains. In community and veteran samples, PTSD is associated with poor social and family
relationships, absenteeism from work, lower income, and lower educational and occupational
success.
Differential Diagnosis
In adjustment disorders, the stressor can be of any severity or type rather
than a stressor involving exposure to actual or threatened death, serious injury, or sexual violence
as required by PTSD Criterion A. The diagnosis of an adjustment disorder is used when the
response to a stressor that meets PTSD Criterion A does not meet all other PTSD criteria (or

Other posttraumatic disorders and conditions.
Acute stress disorder.
Anxiety disorders and obsessive-compulsive disorder.
Major depressive disorder.
Attention-deficit/hyperactivity disorder.
Personality disorders.
Dissociative disorders.
criteria for another mental disorder). An adjustment disorder is also diagnosed when the
symptom pattern of PTSD occurs in response to a stressor that does not meet PTSD Criterion A
(e.g., spouse leaving, being fired).
Not all psychopathology that occurs in individuals
exposed to an extreme stressor should necessarily be attributed to PTSD. The PTSD diagnosis
requires that trauma exposure precede the onset or exacerbation of pertinent symptoms. If the
symptom response pattern to the extreme stressor meets criteria for another mental disorder,
these diagnoses should be given instead of, or in addition to, PTSD. Other diagnoses and
conditions are excluded if they are better explained by PTSD (e.g., symptoms of panic disorder
that occur only after exposure to traumatic reminders). If severe, symptom response patterns to
the extreme stressor that meet criteria for another mental disorder may warrant a separate
diagnosis (e.g., dissociative amnesia) in addition to PTSD.
Acute stress disorder is distinguished from PTSD because the symptom
pattern in acute stress disorder is restricted to a duration of 3 days to 1 month following exposure
to the traumatic event.
In OCD, there are recurrent intrusive thoughts,
but these meet the definition of an obsession. In addition, the intrusive thoughts are not related to
an experienced traumatic event, compulsions are usually present, and other symptoms of PTSD
or acute stress disorder are typically absent. Neither the arousal and dissociative symptoms of
panic disorder nor the avoidance, irritability, and anxiety of generalized anxiety disorder are
associated with a specific traumatic event. The symptoms of separation anxiety disorder are
clearly related to separation from home or family, rather than to a traumatic event.
Major depression may or may not be preceded by a traumatic event and
should be diagnosed if full criteria have been met. Specifically, major depressive disorder does
not include any PTSD Criterion B or C symptoms. Nor does it include a number of symptoms
from PTSD Criterion D or E. However, if full criteria for PTSD are also met, both diagnoses
may be given.
Both ADHD and PTSD may include problems in attention,
concentration, and learning. In contrast to ADHD, where the problems in attention,
concentration, and learning must have their onset prior to age 12, in PTSD the symptoms have
their onset following exposure to a Criterion A traumatic event. In PTSD, disruptions in the
individual’s attention and concentration can be attributable to alertness to danger and
exaggerated startle responses to reminders of the trauma.
Interpersonal difficulties that had their onset, or were greatly exacerbated,
after exposure to a traumatic event may be an indication of PTSD, rather than a personality
disorder, in which such difficulties would be expected independently of any traumatic exposure.
Dissociative 
amnesia, 
dissociative 
identity 
disorder, 
and
depersonalization-derealization disorder may or may not be preceded by exposure to a traumatic
event or may or may not have co-occurring PTSD symptoms. When full PTSD criteria are also
met, however, the PTSD “with dissociative symptoms” subtype should be considered.

Functional neurological symptom disorder (conversion disorder).
Psychotic disorders.
Traumatic brain injury.
F43.0
New onset of somatic symptoms
within the context of posttraumatic distress might be an indication of PTSD rather than
functional neurological symptom disorder.
Flashbacks in PTSD must be distinguished from illusions, hallucinations,
and other perceptual disturbances that may occur in schizophrenia, brief psychotic disorder, and
other psychotic disorders; depressive and bipolar disorders with psychotic features; delirium;
substance/medication-induced disorders; and psychotic disorders due to another medical
condition. PTSD flashbacks are distinguished from these other perceptual disturbances by being
directly related to the traumatic experience and by occurring in the absence of other psychotic or
substance-induced features.
Some types of traumatic events increase risk of both PTSD and traumatic
brain injury (TBI) because they can produce head injuries (e.g., military combat, bomb blasts,
child physical abuse, intimate partner violence, violent crime, motor vehicle or other accidents).
In such cases, individuals presenting with PTSD may also have TBI, and those presenting with
TBI may also have PTSD. Individuals with PTSD who also have TBI may have persistent
postconcussive symptoms (e.g., headaches, dizziness, sensitivity to light or sound, irritability,
concentration deficits). However, such symptoms may also occur in non-brain-injured
populations, including individuals with PTSD. Because symptoms of PTSD and TBI-related
neurocognitive symptoms can overlap, a differential diagnosis between PTSD and
neurocognitive disorder symptoms attributable to TBI may be possible based on the presence of
symptoms that are distinctive to each presentation. Whereas reexperiencing and avoidance are
characteristic of PTSD and not the effects of TBI, persistent disorientation and confusion are
more specific to TBI (neurocognitive effects) than to PTSD. TBI-related memory problems
concerning the traumatic event are typically attributable to injury-related inability to encode the
information, whereas PTSD-related memory problems typically reflect dissociative amnesia.
Sleep difficulties are common to both disorders.
Comorbidity
Individuals with PTSD are more likely than those without PTSD to have symptoms that meet
diagnostic criteria for at least one other mental disorder, such as depressive, bipolar, anxiety, or
substance use disorders. PTSD is also associated with increased risk of major neurocognitive
disorder. In a U.S.-based study, women were more likely to develop PTSD following a mild TBI.
Although most young children with PTSD also have at least one other diagnosis, the patterns of
comorbidity are different than in adults, with oppositional defiant disorder and separation anxiety
disorder predominating.
Acute Stress Disorder
Diagnostic Criteria
A. Exposure to actual or threatened death, serious injury, or sexual violence in one
(or more) of the following ways:

1. Directly experiencing the traumatic event(s).
2. Witnessing, in person, the event(s) as it occurred to others.
3. Learning that the event(s) occurred to a close family member or close friend.
Note: In cases of actual or threatened death of a family member or friend, the
event(s) must have been violent or accidental.
4. Experiencing repeated or extreme exposure to aversive details of the
traumatic event(s) (e.g., first responders collecting human remains, police
officers repeatedly exposed to details of child abuse).
Note: This does not apply to exposure through electronic media, television,
movies, or pictures, unless this exposure is work related.
B. Presence of nine (or more) of the following symptoms from any of the five
categories of intrusion, negative mood, dissociation, avoidance, and arousal,
beginning or worsening after the traumatic event(s) occurred:
Intrusion Symptoms
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic
event(s). Note: In children, repetitive play may occur in which themes or
aspects of the traumatic event(s) are expressed.
2. Recurrent distressing dreams in which the content and/or affect of the dream
are related to the event(s). Note: In children, there may be frightening dreams
without recognizable content.
3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts
as if the traumatic event(s) were recurring. (Such reactions may occur on a
continuum, with the most extreme expression being a complete loss of
awareness of present surroundings.) Note: In children, trauma-specific
reenactment may occur in play.
4. Intense or prolonged psychological distress or marked physiological reactions
in response to internal or external cues that symbolize or resemble an aspect
of the traumatic event(s).
Negative Mood
5. Persistent inability to experience positive emotions (e.g., inability to
experience happiness, satisfaction, or loving feelings).
Dissociative Symptoms
6. An altered sense of the reality of one’s surroundings or oneself (e.g., seeing
oneself from another’s perspective, being in a daze, time slowing).
7. Inability to remember an important aspect of the traumatic event(s) (typically
due to dissociative amnesia and not to other factors such as head injury,
alcohol, or drugs).
Avoidance Symptoms

8. Efforts to avoid distressing memories, thoughts, or feelings about or closely
associated with the traumatic event(s).
9. Efforts to avoid external reminders (people, places, conversations, activities,
objects, situations) that arouse distressing memories, thoughts, or feelings
about or closely associated with the traumatic event(s).
Arousal Symptoms
10. Sleep disturbance (e.g., difficulty falling or staying asleep, restless sleep).
11. Irritable behavior and angry outbursts (with little or no provocation), typically
expressed as verbal or physical aggression toward people or objects.
12. Hypervigilance.
13. Problems with concentration.
14. Exaggerated startle response.
C. Duration of the disturbance (symptoms in Criterion B) is 3 days to 1 month after
trauma exposure.
Note: Symptoms typically begin immediately after the trauma, but persistence
for at least 3 days and up to a month is needed to meet disorder criteria.
D. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
E. The disturbance is not attributable to the physiological effects of a substance
(e.g., medication or alcohol) or another medical condition (e.g., mild traumatic
brain injury) and is not better explained by brief psychotic disorder.
Diagnostic Features
The essential feature of acute stress disorder is the development of characteristic symptoms
lasting from 3 days to 1 month following exposure to one or more traumatic events (Criterion A),
which are the same type as described in PTSD Criterion A (for more information, see
“Diagnostic Features” for PTSD).
The clinical presentation of acute stress disorder may vary by individual but typically
involves an anxiety response that includes some form of reexperiencing of or reactivity to the
traumatic event. Presentations may include intrusion symptoms, negative mood, dissociative
symptoms, avoidance symptoms, and arousal symptoms (Criterion B1–B14). In some
individuals, a dissociative or detached presentation can predominate, although these individuals
typically will also display strong emotional or physiological reactivity in response to trauma
reminders. In other individuals, there can be a strong anger response in which reactivity is
characterized by irritable or possibly aggressive responses.
Intrusion symptoms (Criterion B1–B4) are the same as described in PTSD Criterion B1–B5
(for discussion of these symptoms, see “Diagnostic Features” for PTSD; note that acute stress
disorder Criterion B4 comprises PTSD Criterion B4 and B5). Individuals with acute stress
disorder may have a persistent inability to feel positive emotions (e.g., happiness, joy,

satisfaction, or emotions associated with intimacy, tenderness, sexuality) but can experience
negative emotions such as fear, sadness, anger, guilt, or shame (Criterion B5). Alterations in
awareness can include depersonalization, a detached sense of oneself (e.g., seeing oneself from
the other side of the room), or derealization, having a distorted view of one’s surroundings (e.g.,
perceiving that things are moving in slow motion, seeing things in a daze, not being aware of
events that one would normally encode) (Criterion B6). Some individuals also report an inability
to remember an important aspect of the traumatic event that was presumably encoded. This
symptom is attributable to dissociative amnesia and is not attributable to head injury, alcohol, or
drugs (Criterion B7). Stimuli associated with the trauma are persistently avoided. The individual
commonly makes deliberate efforts to avoid thoughts, memories, or feelings (e.g., by using
distraction or suppression techniques, including substance use, to avoid internal reminders)
(Criterion B8), and to avoid activities, conversations, objects, situations, or people who arouse
recollections of it (Criterion B9).
It is very common for individuals with acute stress disorder to experience problems with
sleep onset and maintenance, which may be associated with nightmares and safety concerns or
with generalized elevated arousal that interferes with adequate sleep (Criterion B10). Individuals
with acute stress disorder may exhibit irritable behavior and may even engage in aggressive
verbal or physical behavior with little or no provocation (e.g., yelling at people, getting into
fights, destroying objects) (Criterion B11). Acute stress disorder is often characterized by a
heightened vigilance for potential threats, including those that are related to the traumatic
experience (e.g., following a motor vehicle accident, being especially sensitive to the threat
potentially caused by cars or trucks) and those not related to the traumatic event (e.g., being
fearful of suffering a heart attack) (Criterion B12). Concentration difficulties (Criterion B13)
include difficulty remembering familiar facts (e.g.,
forgetting one’s telephone number) or daily events (e.g., having recently read part of a book
or newspaper) or attending to focused tasks (e.g., following a conversation for a sustained period
of time).
Individuals with acute stress disorder may be very reactive to unexpected stimuli, displaying
a heightened startle response or jumpiness to loud noises (e.g., in response to a telephone
ringing) or unexpected movements (Criterion B14). Startle responses are involuntary and
reflexive (automatic, instantaneous), and stimuli that evoke exaggerated startle responses
(Criterion B14) need not be related to the traumatic event.
The full symptom picture must last for at least 3 days after the traumatic event but should not
last longer than 1 month (Criterion C). Symptoms that occur immediately after the event but
resolve in less than 3 days would not meet criteria for acute stress disorder.
Associated Features
Individuals with acute stress disorder commonly engage in catastrophic or extremely negative
thoughts about their role in the traumatic event, their response to the traumatic experience, or the
likelihood of future harm. For example, an individual with acute stress disorder may feel
excessively guilty about not having prevented the traumatic event or about not adapting to the

experience more successfully. Individuals with acute stress disorder may also interpret their
symptoms in a catastrophic manner, such that flashback memories or emotional numbing may be
interpreted as a sign of diminished mental capacity. It is common for individuals with acute
stress disorder to experience panic attacks in the initial month after trauma exposure that may be
triggered by trauma reminders or may apparently occur spontaneously. Additionally, individuals
with acute stress disorder may display chaotic or impulsive behavior. For example, individuals
may drive recklessly, make irrational decisions, or gamble excessively. In children, there may be
significant separation anxiety, possibly manifested by excessive needs for attention from
caregivers. In the case of bereavement following a death that occurred in traumatic
circumstances, the symptoms of acute stress disorder can involve acute grief reactions. In such
cases, reexperiencing, dissociative, and arousal symptoms may involve reactions to the loss, such
as intrusive memories of the circumstances of the individual’s death, disbelief that the individual
has died, and anger about the death. Postconcussive symptoms (e.g., headaches, dizziness,
sensitivity to light or sound, irritability, concentration deficits), which occur frequently following
mild traumatic brain injury (TBI), are also frequently seen in individuals with acute stress
disorder. Postconcussive symptoms are equally common in brain-injured and non-brain-injured
populations, and the frequent occurrence of postconcussive symptoms could be attributable to
acute stress disorder symptoms.
Prevalence
The prevalence of acute stress disorder in recently trauma-exposed populations (i.e., within 1
month of trauma exposure) varies according to the nature of the event and the context in which it
is assessed. In research conducted in Australia, the United Kingdom, and the United States, acute
stress disorder was identified in less than 20% of cases following traumatic events that do not
involve interpersonal assault—for example, motor vehicle accidents, mild TBI, severe burns, and
industrial accidents. Higher rates (i.e., 19%–50%) were usually found following interpersonal
traumatic events (e.g., assault, rape).
Development and Course
By definition, acute stress disorder cannot be diagnosed until 3 days after a traumatic event.
Although acute stress disorder may progress to posttraumatic stress disorder (PTSD) after 1
month, it may also be a transient stress response that remits within 1 month of trauma exposure
and does not result in PTSD. Approximately half of individuals who eventually develop PTSD
initially present with acute stress disorder. Longitudinal analyses indicate
that acute stress symptoms can remit, remain constant, or worsen over time, largely as a result of
ongoing life stressors or further traumatic events.
The forms of reexperiencing can vary across development. Unlike adults or adolescents,
young children may report frightening dreams without content that clearly reflects aspects of the
trauma (e.g., waking in fright in the aftermath of the trauma but being unable to relate the content
of the dream to the traumatic event). Children age 6 years and younger are more likely than older
children to express reexperiencing symptoms through play that refers directly or symbolically to

Temperamental.
Environmental.
Genetic and physiological.
the trauma. For example, a very young child who survived a fire may draw pictures of flames.
Young children also do not necessarily manifest fearful reactions at the time of the exposure or
even during reexperiencing. Parents typically report a range of emotional expressions, such as
anger, shame, or withdrawal, and even excessively bright positive affect, in young children who
are traumatized. Although children may avoid reminders of the trauma, they sometimes become
preoccupied with reminders (e.g., a young child bitten by a dog may talk about dogs constantly
yet avoid going outside because of fear of coming into contact with a dog).
Risk and Prognostic Factors
Risk factors include prior mental disorder, high levels of negative emotional
responses such as depressed mood and anxiousness (also termed negative affectivity or
neuroticism), greater perceived severity of the traumatic event, and an avoidant coping style. A
tendency to make catastrophic appraisals of the traumatic experience, often characterized by
exaggerated appraisals of future harm, guilt, or hopelessness, is strongly predictive of acute
stress disorder.
First and foremost, an individual must be exposed to a traumatic event to be at
risk for acute stress disorder. Risk factors for the disorder include a history of prior trauma.
Elevated reactivity, as reflected by acoustic startle response, prior to
trauma exposure increases the risk for developing acute stress disorder.
Culture-Related Diagnostic Issues
The profile of symptoms of acute stress disorder may vary cross-culturally, particularly with
respect to dissociative symptoms, nightmares, avoidance, and somatic symptoms (e.g., dizziness,
shortness of breath, heat sensations, pain complaints). Acute stress reactions may be shaped by
cultural values and norms regarding the expression of extreme emotions, even in extraordinary
situations. Cultural concepts of distress shape the local symptom profiles of acute stress disorder.
Some cultural groups may display variants of dissociative responses, such as possession or
trancelike behaviors in the initial month after trauma exposure. Panic symptoms may be salient
in acute stress disorder among Cambodians because of the association of traumatic exposure
with panic-like khyâl attacks, and ataque de nervios among Latin Americans may also follow a
traumatic exposure. For more information regarding cultural concepts of distress, refer to the
Section III chapter “Culture and Psychiatric Diagnosis.”
Sex- and Gender-Related Diagnostic Issues
Acute stress disorder is more prevalent among women than among men in studies across
multiple countries. The increased risk for the disorder in women may be attributable to a greater
likelihood of exposure to the types of traumatic events with a high conditional risk for acute
stress disorder, such as rape, other interpersonal violence, and childhood trauma, including
sexual abuse. Other factors likely contributing to the higher prevalence in women include gender
differences in the emotional and cognitive processing of trauma. Sex-linked

Adjustment disorders.
Panic disorder.
Dissociative disorders.
Posttraumatic stress disorder.
Obsessive-compulsive disorder.
Psychotic disorders.
neurobiological differences in stress response as well as sociocultural factors may also contribute
to women’s increased risk for acute stress disorder.
Functional Consequences of Acute Stress Disorder
Impaired functioning in social, interpersonal, or occupational domains has been shown across
survivors of accidents, assault, and rape who develop acute stress disorder. The extreme levels of
anxiety that may be associated with acute stress disorder may interfere with sleep, energy levels,
and capacity to attend to tasks. Avoidance in acute stress disorder can result in generalized
withdrawal from many situations that are perceived as potentially threatening, which can lead to
nonattendance of medical appointments, avoidance of driving to important appointments, and
absenteeism from work.
Differential Diagnosis
In adjustment disorders, the stressor can be of any severity rather than of
the severity and type required by Criterion A of acute stress disorder. The diagnosis of an
adjustment disorder is used when the response to a Criterion A event does not meet the criteria
for acute stress disorder (or another specific mental disorder) and when the symptom pattern of
acute stress disorder occurs in response to a stressor that does not meet Criterion A for exposure
to actual or threatened death, serious injury, or sexual violence (e.g., spouse leaving, being fired).
For example, severe stress reactions to life-threatening illnesses that may include some acute
stress disorder symptoms may be more appropriately described as an adjustment disorder. Some
forms of acute stress response do not include acute stress disorder symptoms and may be
characterized by anger, depression, or guilt. These responses are more appropriately described as
primarily an adjustment disorder. Depressive or anger responses in an adjustment disorder may
involve rumination about the traumatic event, as opposed to involuntary and intrusive distressing
memories in acute stress disorder.
Spontaneous panic attacks are very common in acute stress disorder. However,
panic disorder is diagnosed only if panic attacks are unexpected and there is anxiety about future
attacks or maladaptive changes in behavior associated with fear of dire consequences of the
attacks.
Severe dissociative responses (in the absence of characteristic acute stress
disorder symptoms) may be diagnosed as derealization/depersonalization disorder. If severe
amnesia of the trauma persists in the absence of characteristic acute stress disorder symptoms,
the diagnosis of dissociative amnesia may be indicated.
Acute stress disorder is distinguished from PTSD because the
symptom pattern in acute stress disorder must resolve within 1 month of the traumatic event. If
the symptoms persist for more than 1 month and meet criteria for PTSD, the diagnosis is
changed from acute stress disorder to PTSD.
In obsessive-compulsive disorder, there are recurrent intrusive
thoughts, but these meet the definition of an obsession. In addition, the intrusive thoughts are not
related to an experienced traumatic event, compulsions are usually present, and other symptoms
of acute stress disorder are typically absent.
Flashbacks in acute stress disorder must be distinguished from illusions,

Traumatic brain injury.
hallucinations, and other perceptual disturbances that may occur in schizophrenia, other
psychotic disorders, depressive or bipolar disorder with psychotic features, a delirium,
substance/medication-induced disorders, and psychotic disorders due to another medical
condition. Acute stress disorder flashbacks are distinguished from these other perceptual
disturbances by being directly related to the traumatic experience and by occurring in the
absence of other psychotic or substance-induced features.
When a brain injury occurs in the context of a traumatic event (e.g.,
traumatic accident, bomb blast, acceleration/deceleration trauma), symptoms of acute stress
disorder may appear. An event causing head trauma may also constitute a psychological
traumatic event, and TBI-related neurocognitive symptoms are not mutually exclusive and may
occur concurrently. Symptoms previously termed postconcussive (e.g., headaches, dizziness,
sensitivity to light or sound, irritability, concentration deficits) can occur in brain-injured and
non-brain-injured populations, including individuals with acute stress disorder. Because
symptoms of acute stress disorder and TBI-related neurocognitive symptoms can overlap, a
differential diagnosis between acute stress disorder and neurocognitive disorder symptoms
attributable to TBI may be possible based on the presence of symptoms that are distinctive to
each presentation. Whereas reexperiencing and avoidance are characteristic of acute stress
disorder and not the effects of TBI, persistent disorientation and confusion are more specific to
TBI (neurocognitive effects) than to acute stress disorder. Furthermore, differential is aided by
the fact that symptoms of acute stress disorder persist for up to only 1 month following trauma
exposure.
Adjustment Disorders
Diagnostic Criteria
A. The development of emotional or behavioral symptoms in response to an
identifiable stressor(s) occurring within 3 months of the onset of the stressor(s).
B. These symptoms or behaviors are clinically significant, as evidenced by one or
both of the following:
1. Marked distress that is out of proportion to the severity or intensity of the
stressor, taking into account the external context and the cultural factors that
might influence symptom severity and presentation.
2. Significant impairment in social, occupational, or other important areas of
functioning.
C. The stress-related disturbance does not meet the criteria for another mental
disorder and is not merely an exacerbation of a preexisting mental disorder.
D. The symptoms do not represent normal bereavement and are not better
explained by prolonged grief disorder.

E. Once the stressor or its consequences have terminated, the symptoms do not
persist for more than an additional 6 months.
Specify whether:
F43.21 With depressed mood: Low mood, tearfulness, or feelings of
hopelessness are predominant.
F43.22 With anxiety: Nervousness, worry, jitteriness, or separation anxiety is
predominant.
F43.23 With mixed anxiety and depressed mood: A combination of
depression and anxiety is predominant.
F43.24 With disturbance of conduct: Disturbance of conduct is predominant.
F43.25 With mixed disturbance of emotions and conduct: Both emotional
symptoms (e.g., depression, anxiety) and a disturbance of conduct are
predominant.
F43.20 Unspecified: For maladaptive reactions that are not classifiable as one
of the specific subtypes of adjustment disorder.
Specify if:
Acute: This specifier can be used to indicate persistence of symptoms for less
than 6 months.
Persistent (chronic): This specifier can be used to indicate persistence of
symptoms for 6 months or longer. By definition, symptoms cannot persist for
more than 6 months after the termination of the stressor or its consequences.
The persistent specifier therefore applies when the duration of the disturbance is
longer than 6 months in response to a chronic stressor or to a stressor that has
enduring consequences.
Specifiers
By definition, an adjustment disorder must resolve within 6 months of the termination of the
stressor or its consequences. However, the symptoms may persist for a prolonged period (i.e.,
longer than 6 months) if they occur in response to a persistent stressor (e.g., a chronic disabling
other medical condition) or to a stressor that has enduring consequences (e.g., the financial and
emotional difficulties resulting from a divorce). The duration of the symptoms of an adjustment
disorder can be indicated by using the acute or persistent (chronic) specifiers. The acute specifier
is used to indicate persistence of symptoms for less than 6 months. The persistent (chronic)
specifier is used to indicate persistence of symptoms for 6 months or longer. This latter specifier
therefore applies when the duration of the disturbance is longer than 6 months in response to a
persistent stressor or to a stressor that has enduring consequences.
Diagnostic Features

Environmental.
The presence of emotional or behavioral symptoms in response to an identifiable stressor is the
essential feature of adjustment disorders (Criterion A). The stressor may be a single event (e.g., a
termination of a romantic relationship), or there may be multiple stressors (e.g., marked business
difficulties and marital problems). Stressors may be recurrent (e.g., associated with seasonal
business crises, unfulfilling sexual relationships) or continuous (e.g., a persistent painful illness
with increasing disability, living in a crime-ridden neighborhood). Stressors may affect a single
individual, an entire family, or a larger group or community (e.g., a natural disaster). Some
stressors may accompany specific developmental events (e.g., going to school, leaving a parental
home, reentering a parental home, getting married, becoming a parent, failing to attain
occupational goals, retirement).
Adjustment disorders may be diagnosed following the death of a loved one when the
intensity, quality, or persistence of grief reactions exceeds what normally might be expected,
when cultural, religious, or age-appropriate norms are taken into account and the grief reaction
does not meet criteria for prolonged grief disorder.
Prevalence
Adjustment disorders are common, although prevalence may vary widely as a function of the
population studied and the assessment methods used. The percentage of individuals in outpatient
mental health treatment in the United States with a principal diagnosis of an adjustment disorder
ranges from approximately 5% to 20%. Rates of adjustment disorder may be higher in women,
as noted by research in Denmark. In Australian, Canadian, Israeli, and U.S. hospital psychiatric
consultation settings, an adjustment disorder was often the most common diagnosis in the 1990s,
frequently reaching 50%.
Development and Course
By definition, the disturbance in adjustment disorders begins within 3 months of onset of a
stressor. If the stressor is an acute event (e.g., being fired from a job), the onset of the
disturbance is usually immediate (i.e., within a few days) and the duration is relatively brief
(i.e., no more than a few months). If the stressor or its consequences persist, the adjustment
disorder may also continue to be present and become the persistent form. By definition, if
symptoms persist beyond 6 months after the stressor or its consequences have ceased, the
diagnosis of adjustment disorder would no longer apply.
Risk and Prognostic Factors
Persons from disadvantaged life circumstances experience a high rate of stressors
and may be at increased risk for adjustment disorders.
Culture-Related Diagnostic Issues
Because the nature, meaning, and experience of the stressors and the evaluation of the response
to stressors may vary across cultures, cultural context is key in determining whether the

Major depressive disorder.
Posttraumatic stress disorder and acute stress disorder.
adjustment response is maladaptive. Migrants and refugees may experience stressful major
contextual and cultural changes that can make this assessment challenging. Suffering is assumed
to be an intrinsic aspect of normal life in some cultural contexts, such that distressful reactions to
stressful life events may not be viewed as maladaptive or worthy of treatment. Self-immolation is
also a risk associated with adjustment disorder in some cultural contexts.
Association With Suicidal Thoughts or Behavior
Adjustment disorders are associated with an increased risk of suicide attempts and suicide.
Among migrant populations, including Turkish migrants in Western Europe and South Asian or
South East Asian migrants in Gulf countries, adjustment disorder was found to be among the
most common diagnoses associated with suicide-related behavior.
Functional Consequences of Adjustment Disorders
The subjective distress or impairment in functioning associated with adjustment disorders is
frequently manifested as decreased performance at work or school and temporary changes in
social relationships. An adjustment disorder may complicate the course of illness in individuals
who have another medical condition (e.g., decreased compliance with the recommended medical
regimen; increased length of hospital stay).
Differential Diagnosis
If an individual has symptoms that meet criteria for a major depressive
disorder in response to a stressor, the diagnosis of an adjustment disorder is not applicable. The
symptom profile of major depressive disorder differentiates it from adjustment disorders.
In adjustment disorders, the stressor can be
of any severity rather than of the severity and type required by Criterion A of acute stress
disorder and posttraumatic stress disorder (PTSD). In distinguishing adjustment disorders from
these two posttraumatic diagnoses, there are both timing and symptom profile considerations.
Adjustment disorders can be diagnosed immediately and persist up to 6 months after exposure to
the traumatic event, whereas acute stress disorder can only occur between 3 days and 1 month of
exposure to the stressor, and PTSD cannot be diagnosed until at least 1 month has passed since
the occurrence of the traumatic stressor. The required symptom profiles for PTSD and acute
stress disorder differentiate them from the adjustment disorders. With regard to symptom
profiles, an adjustment disorder may be diagnosed following a traumatic event when an
individual exhibits symptoms of either acute stress disorder or PTSD that do not meet or exceed
the diagnostic threshold for either disorder. Because adjustment disorder cannot persist for more
than 6 months after termination of the stressor or its consequences, cases in which symptoms
occurring in response
to a traumatic event that fall short of the diagnostic threshold for PTSD and that persist for
longer than 6 months should be diagnosed as other specified trauma- and stressor-related
disorder. An adjustment disorder should also be diagnosed for individuals who have not been
exposed to a traumatic event meeting Criterion A for PTSD, but who otherwise exhibit the full

Personality disorders.
Bereavement.
Psychological factors affecting other medical conditions.
Normative stress reactions.
F43.8
symptom profile of either acute stress disorder or PTSD.
With regard to personality disorders, some personality features may be
associated with a vulnerability to situational distress that may resemble an adjustment disorder.
The lifetime history of personality functioning will help inform the interpretation of distressed
behaviors to aid in distinguishing a long-standing personality disorder from an adjustment
disorder. In addition to some personality disorders incurring vulnerability to distress, stressors
may also exacerbate personality disorder symptoms. In the presence of a personality disorder, if
the symptom criteria for an adjustment disorder are met, and the stress-related disturbance
exceeds what may be attributable to maladaptive personality disorder symptoms (i.e., Criterion C
is met), then the diagnosis of an adjustment disorder should be made.
Clinically significant acute bereavement-related distress may sometimes be
diagnosed as an adjustment disorder if the bereavement is judged to be out of proportion to what
would be expected or significantly impairs self-care and interpersonal relations. When such
symptoms persist for more than 12 months after the death, the diagnosis is either prolonged grief
disorder if full criteria are met or else other specified trauma- and stressor-related disorder.
In psychological factors affecting other
medical conditions, specific psychological entities (e.g., psychological symptoms, behaviors,
other factors) exacerbate a medical condition. These psychological factors can precipitate,
exacerbate, or put an individual at risk for medical illness, or they can worsen an existing
condition. In contrast, an adjustment disorder is a reaction to the stressor (e.g., having a medical
illness).
When bad things happen, most people get upset. This is not an
adjustment disorder. The diagnosis should only be made when the magnitude of the distress (e.g.,
alterations in mood, anxiety, or conduct) exceeds what would normally be expected (which may
vary in different cultures) or when the adverse event precipitates functional impairment.
Comorbidity
Adjustment disorders can accompany most mental disorders and any medical condition.
Adjustment disorders can be diagnosed in addition to another mental disorder only if the latter
does not explain the particular symptoms that occur in reaction to the stressor. For example, an
individual may develop an adjustment disorder, with depressed mood, after losing a job and at
the same time have a diagnosis of obsessive-compulsive disorder. Or, an individual may have a
depressive or bipolar disorder and an adjustment disorder as long as the criteria for both are met.
Adjustment disorders are common accompaniments of medical illness and may be the major
psychological response to a medical condition.
Prolonged Grief Disorder
Diagnostic Criteria
A. The death, at least 12 months ago, of a person who was close to the bereaved

individual (for children and adolescents, at least 6 months ago).
B. Since the death, the development of a persistent grief response characterized by
one or both of the following symptoms, which have been present most days to a
clinically significant degree. In addition, the symptom(s) has occurred nearly
every day for at least the last month:
1. Intense yearning/longing for the deceased person.
2. Preoccupation with thoughts or memories of the deceased person (in children
and adolescents, preoccupation may focus on the circumstances of the
death).
C. Since the death, at least three of the following symptoms have been present
most days to a clinically significant degree. In addition, the symptoms have
occurred nearly every day for at least the last month:
1. Identity disruption (e.g., feeling as though part of oneself has died) since the
death.
2. Marked sense of disbelief about the death.
3. Avoidance of reminders that the person is dead (in children and adolescents,
may be characterized by efforts to avoid reminders).
4. Intense emotional pain (e.g., anger, bitterness, sorrow) related to the death.
5. Difficulty reintegrating into one’s relationships and activities after the death
(e.g., problems engaging with friends, pursuing interests, or planning for the
future).
6. Emotional numbness (absence or marked reduction of emotional experience)
as a result of the death.
7. Feeling that life is meaningless as a result of the death.
8. Intense loneliness as a result of the death.
D. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
E. The duration and severity of the bereavement reaction clearly exceed expected
social, cultural, or religious norms for the individual’s culture and context.
F. The symptoms are not better explained by another mental disorder, such as
major depressive disorder or posttraumatic stress disorder, and are not
attributable to the physiological effects of a substance (e.g., medication, alcohol)
or another medical condition.
Diagnostic Features
Prolonged grief disorder represents a prolonged maladaptive grief reaction that can be diagnosed
only after at least 12 months (6 months in children and adolescents) have elapsed since the death
of someone with whom the bereaved had a close relationship (Criterion A). Although in general

this time frame reliably discriminates normal grief from grief that continues to be severe and
impairing, the duration of adaptive grief may vary individually and cross-culturally. The
condition involves the development of a persistent grief response characterized by intense
yearning or longing for the deceased person (often with intense sorrow and frequent crying) or
preoccupation with thoughts or memories of the deceased, although in children and adolescents,
this preoccupation may focus on the circumstances of the death. The intense yearning/longing or
the preoccupation has been present most days to a clinically significant degree and has occurred
nearly every day for at least the last month (Criterion B). Moreover, since the death, at least three
additional symptoms have been present most days to a clinically significant degree and have
occurred nearly every day for at least the past month. These symptoms include identity
disruption since the death (e.g., feeling as though part of oneself has died) (Criterion C1); a
marked sense of disbelief about the death (Criterion C2); avoidance of reminders that the person
is dead, which in children and adolescents may be characterized by efforts to avoid reminders
(Criterion C3); intense emotional pain (e.g., anger, bitterness, guilt) since the death (Criterion
C4); having difficulty reintegrating into personal relationships and activities since the death (e.g.,
problems
engaging with friends, pursuing interests, or planning for the future) (Criterion C5); emotional
numbness (absence or marked reduction of emotional experience) as a result of the death
(Criterion C6); feeling that life is meaningless as a result of the death (Criterion C7); or intense
loneliness as a consequence of the death (Criterion C8).
The symptoms of prolonged grief disorder must result in clinically significant distress or
impairment in social, occupational, or other important areas of functioning in the bereaved
individual (Criterion D). The nature, duration, and severity of the bereavement reaction must
clearly exceed expected social, cultural, or religious norms for the individual’s culture and
context (Criterion E). Although there are variations in how grief can manifest, the symptoms of
prolonged grief disorder occur across genders and in diverse social and cultural groups.
Associated Features
Individuals with symptoms of prolonged grief disorder often experience maladaptive cognitions
about the self, guilt about the death, and diminished future life expectancy and life goals.
Somatic complaints commonly accompany the condition and may be related to comorbid
depression and anxiety, social identity disruption, and increased health care visits; the somatic
symptoms may be associated with those that were experienced by the deceased (e.g., changes in
appetite). Harmful health behaviors related to decreased self-care and concern are also common
in individuals with symptoms of prolonged grief disorder. Hallucinations about the deceased
(e.g., hearing the deceased person’s voice) may occur during normal grief but may be more
common in individuals with symptoms of prolonged grief disorder; hallucinations experienced
by individuals with prolonged grief disorder symptoms may be associated with disruptions of
social identity and purpose related to the death (e.g., confusion about one’s role in life, feeling of
meaninglessness). Other associated features of prolonged grief disorder include bitterness, anger,
or restlessness; blaming others for the death; and decreased sleep quantity and quality.

Prevalence
The prevalence of DSM-5 prolonged grief disorder in adults is unknown. Meta-analysis of
studies across four continents that used a different definition for prolonged grief disorder with at
least a 6-month duration postloss suggests a pooled prevalence of 9.8%; however, there was
substantial methodological heterogeneity across studies (e.g., in symptom definitions, measures,
duration of bereavement), which affected the prevalence findings. Populations with elevated
exposure to trauma may have higher prevalence rates. Mean prevalence of prolonged grief
presentations may be higher in high-income Western countries than in high- and upper-middleincome Asian countries, but recent studies in China have revealed higher rates and substantial
variation. Prevalence of persistent complex bereavement disorder (included in DSM-5 Section
III, “Conditions for Further Study”) among bereaved U.S. youth in the community was estimated
at 18%.
Development and Course
There are limited data on the course of prolonged grief disorder across the life span. Symptoms
usually begin within the initial months after the death, although there may be a delay before the
full syndrome appears. Preliminary evidence suggests that course may be especially prolonged
among parents after the death of a child. The course of prolonged grief disorder may be
complicated by comorbid posttraumatic stress disorder, which is more common in situations of
bereavement following the violent death of a loved one (e.g., murder, suicide) when grief for the
bereaved may be accompanied by personal life threat and/or witnessing of violent and potentially
gruesome death. Older age may be associated with a higher risk of developing the disorder after
the death of a loved one. Older adults with prolonged grief disorder symptoms may be at
elevated risk for progressive cognitive decline.
In children, distress may be expressed in play and behavior, developmental regressions, and
anxious or protest behavior at times of separation and reunion. Young children may experience
symptoms of prolonged grief disorder in specific ways because of their age. The loss of a
primary caregiver may be particularly traumatic for a young child, given the disorganizing
effects of the caregiver’s absence. Young children may protest or become angry when daily care
activities are performed differently than by the deceased (e.g., cooking, discipline, bedtime
rituals). They may express intense insecurity about their future, often manifested as worries
about the health and safety of caregivers and about themselves, with repeated questions about
death. They may engage in searching for the deceased because they do not understand the
permanence of death. Young children tend toward somatic manifestations such as disturbances in
sleep, eating, digestion, and level of energy. They may express yearning in thought and play as a
wish, literally, to physically reunite with the deceased to overcome the painful physical
separation (e.g., to climb a ladder to heaven or lie in the ground next to a parent). Young children
typically do not understand or describe numbing, whereas adolescents may describe “not feeling
anything.”
In children and adolescents, ongoing preoccupation with the circumstances of the death
might involve focusing on distressing aspects of physical deterioration over the course of a fatal

Environmental.
illness and/or the inability of a caregiver to perform vital caregiving functions. Identity
disruption may include feeling profoundly different from others, often in response to loss
reminders (e.g., making Mother’s Day cards at school, watching a friend enjoy a hobby with a
sibling). Children and adolescents may verbally, in their behavior, or through emotional
withdrawal show reluctance to join adults in activities that serve as loss reminders. They may
experience intense emotional pain over feeling deprived (“robbed”) of the deceased’s help with
ongoing developmental tasks (e.g., onset of menses). Separation distress may be predominant in
younger children, and distress over disruptions in social identity (e.g., confusion about purpose
in life) and risk for comorbid depression can increasingly manifest in older children and
adolescents.
Failure to achieve age-appropriate developmental milestones and transitions is a
manifestation of failure to reintegrate into life roles. For older children and adolescents, feeling
that life is meaningless without the person who died may include giving up on developmental
aspirations (“It’s not worth trying if they can’t be here”), not caring about risky behavior (“So
what if I get hurt or die?”), or feeling that their future is “ruined.” Older children and adolescents
may be apprehensive over sharing a similar fate as the deceased, including premature death.
Loneliness may be intensified by keeping grief private, sometimes over not wanting to add to the
distress of a grieving caregiver or to avoid presumed stigma from peers.
Risk and Prognostic Factors
Risk for prolonged grief disorder symptoms is heightened by increased
dependency on the deceased prior to the death, by the death of a child, by violent or unexpected
deaths, and by economic stressors. The disorder has a higher prevalence following the death of a
spouse/partner or child compared with other kinship relationships to the deceased. Disturbances
in caregiver availability and support increase the risk for bereaved children.
Culture-Related Diagnostic Issues
The symptoms of prolonged grief disorder are observed across cultural settings, but grief
responses may manifest in culturally specific ways, including in expected duration, and show
historical variation. For example, across cultures, nightmares about the deceased may be
especially distressing because of their attributed significance; the prevalence of hallucinations of
the deceased or of grief-related somatic symptoms may vary; and indirect expressions of
prolonged grief disorder–related functional impairment (e.g., unhealthy
behaviors like drinking or poor self-care) may be more prevalent than direct expressions of grief.
The inability to carry out funerary rituals in some cultures may worsen symptoms of prolonged
grief disorder, possibly because of interpretation of their impact on the spiritual status of the
deceased. Some studies suggest higher prevalence of the symptoms of prolonged grief disorder
in African Americans relative to non-Hispanic Whites; the cause for these elevations requires
further study in areas such as differential exposure to sudden or violent death. Differences in
mourning practices may contribute to the cultural prescription or prohibition of specific grief
expressions, and cultural norms about the social status of the bereaved may affect grief intensity

Normal grief.
and duration, such as different levels of support or societal sanction toward remarriage
depending on the gender of the bereaved. Diagnosis of the disorder requires that the persistent
and severe responses go beyond cultural norms of grief responses and not be better explained by
culturally specific mourning rituals.
Sex- and Gender-Related Diagnostic Issues
Some studies find higher disorder prevalence or symptom severity among bereaved women, but
other studies conclude the gender disparity is small and/or not statistically significant.
Association With Suicidal Thoughts or Behavior
Individuals with symptoms of prolonged grief disorder are at heightened risk for suicidal
ideation, even after adjustment for the effect of major depression and PTSD. The association of
prolonged grief disorder symptoms and suicidal ideation is consistent across the life span and
cross-nationally. However, the existing literature does not establish whether suicidal ideation
associated with symptoms of prolonged grief disorder is linked to a higher incidence of suicidal
behavior. Stigma, isolation, thwarted belongingness, avoidance, and psychological distress in
bereaved individuals are associated with suicidal ideation. Compared with individuals whose
bereavement is due to nonviolent causes, individuals whose prolonged grief disorder symptoms
are the result of a violent loss (e.g., homicide, suicide, accident) are at greater risk for suicidal
ideation. Similarly, individuals who experience the death of a child, especially if the child is
younger than 25, are more likely to develop prolonged grief disorder symptoms that are
associated with suicidal ideation.
Functional Consequences of Prolonged Grief Disorder
Symptoms of prolonged grief disorder are associated with impairments in work and social
functioning and with harmful health behaviors, such as increased tobacco and alcohol use. They
are also associated with marked increases in risks for serious medical conditions, including
cardiac disease, hypertension, cancer, immunological deficiency, and reduced quality of life.
Long-term developmental consequences among children and adolescents include premature
school withdrawal, diminished educational aspirations, and reduced academic attainment; young
women in particular may be hesitant to marry as they transition to adulthood. Impaired cognitive
functioning may be associated with symptoms of prolonged grief disorder, especially in middleage and older adults.
Differential Diagnosis
Prolonged grief disorder is distinguished from normal grief by the presence of
severe grief reactions that persist at least 12 months (6 months in children or adolescents) after
the death of a person who was close to the bereaved individual. It is only when severe levels of
grief response persist for the specified duration following the death, interfere with the
individual’s capacity to function, and exceed cultural, social, or religious norms that prolonged
grief disorder is diagnosed. In evaluating the requirement for clinically significant symptoms to
be present most days over the past month, it should be noted that marked increases in grief
severity can be seen in normal grieving around calendar

Depressive disorders.
Posttraumatic stress disorder.
Separation anxiety disorder.
Psychotic disorder.
days that are reminders of the loss, such as the anniversary of the death, birthdays, wedding
anniversaries, and holidays; this exacerbation of grief severity does not by itself, in the absence
of persistent grief at other times, constitute evidence of prolonged grief disorder.
Prolonged grief disorder, major depressive disorder, and persistent
depressive disorder share several symptoms, including low mood, crying, and suicidal thinking.
However, in prolonged grief disorder the distress is focused on feelings of loss and separation
from a loved one rather than reflecting generalized low mood. Major depressive disorder may
also be preceded by the death of a loved one, with or without comorbid prolonged grief disorder.
Individuals who experience bereavement as a result of violent or
accidental death may develop both PTSD and prolonged grief disorder. Both conditions can
involve intrusive thoughts and avoidance. Whereas intrusions in PTSD revolve around the
traumatic event (which may have caused the death of a loved one), intrusive memories in
prolonged grief disorder focus on thoughts about many aspects of the relationship with the
deceased, including positive aspects of the relationship and distress over the separation. Unlike
avoidance in PTSD, which is manifested by avoidance of memories, thoughts, or feelings
associated with the traumatic event that led to the death of the loved one (e.g., memories of the
fatal automobile accident that killed the loved one), the avoidance in prolonged grief disorder is
of reminders that the loved one is no longer present (e.g., avoidance of activities carried out
together with the deceased). Moreover, reexperiencing memories in PTSD tend to be more
perceptual, with the individual reporting that the memory feels like it is occurring in the “here
and now,” which tends not to be the case in prolonged grief disorder. In prolonged grief disorder,
there is also a yearning for the deceased, which is absent in PTSD.
Separation anxiety disorder is characterized by anxiety about
separation from current attachment figures, whereas prolonged grief disorder involves distress
about separation from a deceased person.
Hallucinations about the deceased (e.g., seeing the deceased in a favorite
chair) or transient sensations about the presence of the deceased (e.g., by touch, voice, or sight)
are common cross-culturally during normal grief, may be experienced as reassuring, and often
occur while the individual is falling asleep (hypnagogic). To receive a diagnosis of psychotic
disorder, individuals with prolonged grief disorder must also endorse other symptoms of
psychosis, such as delusions, disorganized thinking, or negative symptoms.
Comorbidity
The most common comorbid disorders with symptoms of prolonged grief disorder are major
depressive disorder, PTSD, and substance use disorders. PTSD is more frequently comorbid with
prolonged grief disorder symptoms when the death occurred in violent or accidental
circumstances. Separation anxiety disorder involving major living attachment figures may be
comorbid with symptoms of prolonged grief disorder.
Other Specified Trauma- and Stressor-Related Disorder

F43.8
This category applies to presentations in which symptoms characteristic of a traumaand stressor-related disorder that cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning predominate but do
not meet the
full criteria for any of the disorders in the trauma- and stressor-related disorders
diagnostic class. The other specified trauma- and stressor-related disorder category
is used in situations in which the clinician chooses to communicate the specific
reason that the presentation does not meet the criteria for any specific trauma- and
stressor-related disorder. This is done by recording “other specified trauma- and
stressor-related disorder” followed by the specific reason (e.g., “persistent response
to trauma with PTSD-like symptoms”).
Examples of presentations that can be specified using the “other specified”
designation include the following:
1. Adjustment-like disorders with delayed onset of symptoms that occur more
than 3 months after the stressor.
2. Adjustment-like disorders with prolonged duration of more than 6 months
without prolonged duration of stressor.
3. Persistent response to trauma with PTSD-like symptoms (i.e., symptoms
occurring in response to a traumatic event that fall short of the diagnostic
threshold for PTSD and that persist for longer than 6 months, sometimes referred
to as “subthreshold/partial PTSD”).
4. Ataque de nervios: See “Culture and Psychiatric Diagnosis” in Section III.
5. Other cultural syndromes: See “Culture and Psychiatric Diagnosis” in Section
III.
Unspecified Trauma- and Stressor-Related Disorder
F43.9
This category applies to presentations in which symptoms characteristic of a traumaand stressor-related disorder that cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning predominate but do
not meet the full criteria for any of the disorders in the trauma- and stressor-related
disorders diagnostic class. The unspecified trauma- and stressor-related disorder
category is used in situations in which the clinician chooses not to specify the reason
that the criteria are not met for a specific trauma- and stressor-related disorder and
includes presentations in which there is insufficient information to make a more

specific diagnosis (e.g., in emergency room settings).

# 08 - Dissociative Disorders

# Dissociative Disorders

329

Dissociative Disorders
Dissociative disorders are characterized by a disruption of and/or discontinuity in the
normal integration of consciousness, memory, identity, emotion, perception, body representation,
motor control, and behavior. Dissociative symptoms can potentially disrupt every area of
psychological functioning. This chapter includes dissociative identity disorder, dissociative
amnesia, depersonalization/derealization disorder, other specified dissociative disorder, and
unspecified dissociative disorder.
Dissociative disorders are frequently found in the aftermath of a wide variety of
psychologically traumatic experiences in children, adolescents, and adults. Throughout this
chapter, “traumatic experiences” refers to experiences that result in psychological sequelae, as
opposed to the physical impact that can cause traumatic brain injury. Therefore, in DSM-5, the
dissociative disorders are placed next to, but are not part of, the trauma- and stressor-related
disorders, reflecting the close relationship between these diagnostic classes. Both acute stress
disorder and posttraumatic stress disorder include dissociative symptoms, such as amnesia,
flashbacks, numbing, and depersonalization/derealization.
Dissociative symptoms are experienced as unbidden intrusions into awareness and behavior,
with accompanying losses of continuity in subjective experience (i.e., ‘‘positive’’ dissociative
symptoms such as division of identity, depersonalization, and derealization) and/or inability to
access information or to control mental functions that normally are readily amenable to access or
control (i.e., “negative” dissociative symptoms such as amnesia).
Across cultural contexts, risk factors for dissociative pathology include earlier onset of
trauma; neglect and sexual, physical, and emotional abuse by parents; cumulative early life
trauma and adversities; and repeated sustained trauma or torture associated with captivity (e.g.,
experienced by prisoners of war, victims of trafficking).
Depersonalization/derealization disorder is characterized by clinically significant persistent
or recurrent depersonalization (i.e., experiences of unreality or detachment from one’s mind, self,
or body) and/or derealization (i.e., experiences of unreality or detachment from one’s
surroundings). These alterations of experience are accompanied by intact reality testing. There is
no evidence of any distinction between predominantly depersonalization and predominantly
derealization symptoms. Individuals with this disorder can have depersonalization, derealization,
or both.
Dissociative amnesia is characterized by an inability to recall autobiographical information
that is inconsistent with normal forgetting. The amnesia may be localized (i.e., an event or period
of time), selective (i.e., a specific aspect of an event), or generalized (i.e., identity and life
history). In dissociative amnesia, memory deficits are primarily retrograde and often associated
with traumatic experiences (e.g., lack of recall of third grade when the individual was kidnapped
and held hostage). Although some individuals with amnesia promptly notice that they have gaps
or a sense of fragmentation in their remote memory, most individuals with dissociative disorders

F44.81
are initially unaware of their amnesia or minimize or rationalize the deficits. For them, awareness
of amnesia occurs when they realize that they do not recall their personal identity or when
circumstances make these individuals aware that important autobiographical information is
missing (e.g., when they discover
evidence or are told of past events that they cannot recall). Generalized dissociative amnesia
with loss of a major part or all of the individual’s life history and/or identity is rare.
Dissociative identity disorder is characterized by a) the presence of two or more distinct
personality states or an experience of possession and b) recurrent episodes of dissociative
amnesia. The fragmentation/division of identity may vary across cultural contexts (e.g.,
possession-form presentations) and with circumstance. Thus, individuals may experience
discontinuities in identity and memory that may not be immediately evident to others or are
obscured by attempts to hide dysfunction. Individuals with dissociative identity disorder
experience recurrent, inexplicable intrusions into their conscious functioning and sense of self
(e.g., voices; dissociated actions and speech; intrusive thoughts, emotions, and impulses);
alterations of sense of self (e.g., attitudes, preferences, and feeling like their body or actions are
not their own); odd changes of perception (e.g., depersonalization or derealization, such as
feeling detached, as if watching themself from outside their body); and intermittent functional
neurological symptoms. Stress often produces transient exacerbation of dissociative symptoms
that makes them more evident.
The residual category of other specified dissociative disorder includes presentations in which
symptoms characteristic of a dissociative disorder that cause clinically significant distress or
impairment predominate but do not meet the criteria for any of the specific dissociative
disorders. Examples 
include 
identity disturbances associated with less-than-marked
discontinuities in sense of self and agency, alterations of identity, or episodes of possession in
the absence of a history of episodes of dissociative amnesia; identity disturbance due to
prolonged and intensive coercive persuasion as may occur in sects/cults or terrorist
organizations; acute dissociative reactions to stressful events that last less than 1 month; and
dissociative trance, which is characterized by an acute narrowing or complete loss of awareness
of immediate surroundings that manifests as profound unresponsiveness or insensitivity to
environmental stimuli.
Dissociative Identity Disorder
Diagnostic Criteria
A. Disruption of identity characterized by two or more distinct personality states,
which may be described in some cultures as an experience of possession. The
disruption in identity involves marked discontinuity in sense of self and sense of
agency, accompanied by related alterations in affect, behavior, consciousness,
memory, perception, cognition, and/or sensory-motor functioning. These signs

and symptoms may be observed by others or reported by the individual.
B. Recurrent gaps in the recall of everyday events, important personal information,
and/or traumatic events that are inconsistent with ordinary forgetting.
C. The symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
D. The disturbance is not a normal part of a broadly accepted cultural or religious
practice.
Note: In children, the symptoms are not better explained by imaginary playmates
or other fantasy play.
E. The symptoms are not attributable to the physiological effects of a substance
(e.g., blackouts or chaotic behavior during alcohol intoxication) or another
medical condition (e.g., complex partial seizures).
Diagnostic Features
The defining feature of dissociative identity disorder is the presence of two or more distinct
personality states or an experience of possession (Criterion A). The overtness or covertness of
these personality states varies as a function of psychological motivation, current level of stress,
cultural context, internal conflicts and dynamics, and emotional resilience, among other factors.
Sustained periods of identity confusion/alteration may occur when psychosocial pressures are
severe and/or prolonged. In those cases of dissociative identity disorder that present as the
individual being possessed by external identities (e.g., spirits, demons) (possession-form
dissociative identity disorder), and in a small proportion of non-possession-form cases,
manifestations of alternate identities are readily observable. Most individuals with nonpossession-form dissociative identity disorder do not overtly display, or only subtly display, their
discontinuity of identity, and only a minority present to clinical attention with discernible
alternation of identities. The elaboration of dissociative personality states with different names,
wardrobes, hairstyles, handwritings, accents, and so forth, occurs in only a minority of
individuals with the non-possession-form dissociative identity disorder and is not essential to
diagnosis. In those cases where alternate personality states cannot be directly observed, the
presence of distinct personality states can be identified by sudden alterations or discontinuities in
the individual’s sense of self and sense of agency (Criterion A), and recurrent dissociative
amnesias (Criterion B).
Criterion A symptoms are related to discontinuities of experience that can affect any aspect
of an individual’s functioning. Individuals with dissociative identity disorder may report the
feeling that they have suddenly become depersonalized observers of their own speech and
actions, which they may feel powerless to stop (i.e., impaired sense of self and impaired sense of
agency). These individuals may also report perceptions of voices (e.g., a child’s voice, voices
commenting on the individual’s thoughts or behavior, persecutory voices and command
hallucinations). In some cases, hearing voices is specifically denied, but the individual reports
multiple, perplexing, independent thought streams over which the individual experiences no
control. Individuals with dissociative identity disorder may report hallucinations in all sensory

modalities: auditory, visual, tactile, olfactory, and gustatory.
Strong emotions, impulses, thoughts, and even speech or other actions may suddenly
materialize, without a sense of personal ownership or control (i.e., lack of sense of agency).
Conversely, thoughts and emotions may unexpectedly vanish, and speech and actions are
abruptly inhibited. These experiences are frequently reported as ego-dystonic and puzzling.
Attitudes, outlooks, and personal preferences (e.g., about food, activities, gender identity) may
suddenly shift. Individuals may report that their bodies feel different (e.g., like a small child, the
opposite gender, different ages simultaneously). Alterations in sense of self and agency may be
accompanied by a feeling that attitudes, emotions, and behaviors—even the individual’s own
body—are “not mine” or are “not under my control.” Although most Criterion A symptoms are
subjective, these sudden discontinuities in speech, affect, and behavior may be witnessed by
family, friends, or the clinician.
In most individuals with dissociative identity disorder, switching/shifting of states is subtle
and may occur with only subtle changes in overt presentation. State switching may be more overt
in the possession form of dissociative identity disorder. In general, the individual with
dissociative identity disorder experiences himself or herself as multiple, simultaneously
overlapping and interfering states.
Dissociative amnesia (Criterion B) manifests in several major domains: 1) gaps in any aspect
of autobiographical memory (e.g., important life events like getting married or giving birth, lack
of recall of all school experiences before high school); 2) lapses in memory of recent events or
well-learned skills (e.g., how to do one’s job, use a computer, cook or drive); and 3) discovery of
possessions that the individual has no recollection of ever owning (e.g., clothing, weapons, tools,
writings or drawings that he or she must have created).
Dissociative fugues, with amnesia for travel, are common. Individuals may report suddenly
finding themselves in another city, at work, or even at home: in the closet, under the bed, or
running out of the house. Amnesia in individuals with dissociative identity disorder is not limited
to stressful or traumatic events; it can involve everyday events as well. Individuals may report
major gaps in ongoing memory (e.g., experiencing “time loss,” “blackouts,” or “coming to” in
the midst of doing something). Dissociative amnesia may be apparent to others (e.g., the
individual does not recall something others witnessed that he or she did or said, cannot remember
his or her own name, or may fail to recognize spouse, children, or close friends). Minimization or
rationalization of amnesia is common.
Possession-form identities in dissociative identity disorder typically manifest behaviorally as
if a “spirit,” supernatural being, or outside person has taken control, with the individual speaking
or acting in a distinctly different manner. For example, an individual’s behavior may give the
appearance that her identity has been replaced by the “ghost” of a girl who died by suicide in the
same community years before, speaking and acting as though she were still alive. The identities
that arise during possession-form dissociative identity disorder present recurrently, are unwanted
and involuntary, and cause clinically significant distress or impairment (Criterion C). However,
the majority of possession states that occur around the world are usually part of a broadly
accepted cultural or religious practice and therefore do not meet criteria for dissociative identity
disorder (Criterion D).

Associated Features
Individuals with dissociative identity disorder typically present with comorbid depression,
anxiety, substance abuse, self-injury, or another common symptom. Nonepileptic seizures and
other functional neurological symptoms are prominent in some presentations of dissociative
identity disorder, especially in some non-Western settings. Some individuals, especially in
Western settings, may present with apparently refractory neurological symptoms, such as
headaches, seizures, or symptoms suggestive of multiple sclerosis.
Individuals with dissociative identity disorder often conceal, or are not fully aware of,
disruptions in consciousness, amnesia, or other dissociative symptoms. Many individuals with
dissociative identity disorder report dissociative flashbacks during which they experience a
sensory reliving of a previous event as though it were occurring in the present, often with a
change of identity, a partial or complete loss of contact with or disorientation to current reality
during the flashback, and a subsequent amnesia for the content of the flashback. Individuals with
the disorder typically report multiple types of interpersonal maltreatment during childhood and
adulthood. Other overwhelming early life events, such as multiple long, painful, early-life
medical procedures, also may be reported. Nonsuicidal self-injury is frequent. On standardized
measures, these individuals report higher levels of hypnotizability and dissociative symptoms
compared with other clinical groups and healthy control subjects. Some individuals experience
transient psychotic phenomena or episodes.
Among personality features, avoidant personality features most often rate highest in
individuals with dissociative identity disorder, and some individuals with dissociative identity
disorder are so avoidant that they prefer to be alone. When decompensated, some individuals
with dissociative identity disorder display features of borderline personality disorder (i.e., selfdestructive high-risk behaviors, and mood instability). Many individuals with dissociative
identity disorder display attachment problems but typically do not exhibit frantic activity to
avoid being abandoned. Some have stable long-term relationships, albeit frequently
dysfunctional and/or abusive ones, from which they may have difficulty extricating themselves.
Obsessional personality features are common in dissociative identity disorder, more so than
histrionic personality features. A subgroup of
individuals with dissociative identity disorder have narcissistic and/or antisocial personality
features.
Prevalence
The 12-month prevalence of dissociative identity disorder among adults in a small U.S.
community study was 1.5%. Lifetime prevalence of dissociative identity disorder was 1.1% in a
representative sample of community-based women in mid-eastern Turkey.
Development and Course
The disorder may first manifest at almost any age from early childhood to late life. Children
usually do not present with identity shifting, instead presenting primarily with independently
acting, imaginary companions, or as personified “mood” states (Criterion A phenomena).

Environmental.
Genetic and physiological.
Course modifiers.
Dissociation in children may generate problems with memory, concentration, and attachment,
and may be associated with traumatic play. In adolescents, dissociative identity disorder
commonly comes to clinical attention because of externalizing symptoms, suicidal/selfdestructive behavior, or rapid behavioral shifts often ascribed to other disorders such as
attention-deficit/hyperactivity disorder or childhood bipolar disorder. Some children with
dissociative identity disorder can also be quite aggressive and irritable. Older individuals with
dissociative identity disorder may present with symptoms that appear to be late-life mood
disorders, obsessive-compulsive disorder, paranoia, psychotic mood disorders, or even cognitive
disorders attributable to dissociative amnesia.
Overt identity alteration/confusion may be triggered by many factors, such as later traumatic
experiences (e.g., sexual assault), or even seemingly inconsequential stressors, like a minor
motor vehicle accident. The experience of other major or cumulative life stressors may also
worsen symptoms, including life events such as the individual’s children reaching the same age
at which the individual was significantly abused or traumatized. The death of, or the onset of a
fatal illness in, the individual’s abuser(s) is another example of an event that may worsen
symptoms. Individuals with dissociative identity disorder are at high risk for adult interpersonal
trauma such as rape, intimate partner violence, and sexual exploitation, including ongoing
incestuous abuse into adulthood, as well as adult trafficking.
Risk and Prognostic Factors
In the context of family and attachment pathology, early life trauma (e.g., neglect
and physical, sexual, and emotional abuse, usually before ages 5–6 years) represents a risk factor
for dissociative identity disorder. In studies from diverse geographic regions, about 90% of the
individuals with the disorder report multiple types of early neglect and childhood abuse, often
extending into late adolescence. Some individuals report that maltreatment primarily occurred
outside the family, in school, church, and/or neighborhoods, including being bullied severely.
Other forms of repeated early-life traumatic experiences include multiple, painful childhood
medical and surgical procedures; war; terrorism; or being trafficked beginning in childhood.
Onset has also been described after prolonged and often transgenerational exposure to
dysfunctional family dynamics (e.g., overcontrolling parenting, insecure attachment, emotional
abuse) in the absence of clear neglect or sexual or physical abuse.
Twin studies suggest that genetics account for around 45%–50% of the
interindividual variance in dissociative symptoms, with nonshared, stressful, and traumatic
environmental experiences accounting for most of the additional variance. Several brain regions
have been implicated in the pathophysiology of dissociative identity disorder, including the
orbitofrontal cortex, hippocampus, parahippocampal gyrus, and amygdala.
Ongoing sexual, physical, and emotional trauma often leads to significant
difficulties in later functioning. Poorer outcome in adults is commonly related to severe
psychosocial stressors, revictimization, ongoing sexual or physical abuse or exploitation,
intimate partner violence, refractory substance use, eating disorders, severe medical illness,
enmeshment with the individual’s abusive family of origin, or ongoing involvement in criminal

subgroups. Poorer functioning may also be related to perpetration of child maltreatment or
intimate partner violence by individuals with dissociative identity disorder.
Culture-Related Diagnostic Issues
Many features of dissociative identity disorder can be influenced by the individual’s
sociocultural background. In settings where possession symptoms are common (e.g., rural areas
in low- and middle-income countries, among certain religious groups in the United States and
Europe), all or some of the fragmented identities may take the form of possessing spirits, deities,
demons, animals, or mythical figures. Acculturation or prolonged intercultural contact may shape
the presentation of the other identities (e.g., identities in India may speak English exclusively and
wear Western clothes). Possession-form dissociative identity disorder can be distinguished from
culturally accepted possession states in that the former is involuntary, distressing, and
uncontrollable; involves conflict between the individual and his or her surrounding family,
social, or work milieu; and is manifested at times and in places that violate cultural or religious
norms. Combined dissociative-psychosis episodes may be more common in cultural contexts
with marked communal violence or oppression and limited opportunity for redress.
Sex- and Gender-Related Diagnostic Issues
Women with dissociative identity disorder predominate in adult clinical settings but not in
child/adolescent clinical settings or in general population studies. Few differences in symptom
profiles, clinical history, and childhood trauma history have been found in comparisons between
men and women with dissociative identity disorder, except that women may have higher rates of
somatization.
Association With Suicidal Thoughts or Behavior
Suicidal behavior is frequent. Over 70% of outpatients with dissociative identity disorder have
attempted suicide; multiple attempts are common, and other self-injurious and high-risk
behaviors are highly prevalent. Individuals with dissociative identity disorder have multiple
interacting risk factors for self-destructive and/or suicidal behavior. These include cumulative,
severe early- and later-life trauma; high rates of comorbid posttraumatic stress disorder (PTSD),
depressive disorders, and substance use disorders; and personality disorder features. Dissociation
itself is an independent risk factor for multiple suicide attempts. Greater severity of dissociative
symptom scores is associated with a higher frequency of suicide attempts and nonsuicidal selfinjury among individuals with dissociative disorders.
Functional Consequences of Dissociative Identity Disorder
Some children and adolescents with dissociative identity disorder may function poorly in school
and in relationships. Others do well in school, experiencing it as a respite. In adults impairment
varies widely, from apparently minimal (e.g., in high-functioning professionals) to profound. The
symptoms of higher-functioning individuals may impair their relational, marital, family, and
parenting functions more than their occupational and professional life, although the latter also
may be affected. Many impaired individuals show improvement in occupational and personal
functioning over time, while some individuals with dissociative

Dissociative amnesia.
Depersonalization/derealization disorder.
Major depressive disorder.
Bipolar disorders.
Posttraumatic stress disorder.
identity disorder may be impaired in most activities of living and function at the level of chronic
and persistent mental illness.
Differential Diagnosis
Both dissociative identity disorder and dissociative amnesia are
characterized by gaps in the recall of everyday events, important personal information, or
traumatic events that are inconsistent with ordinary forgetting. Dissociative identity disorder is
distinguished from dissociative amnesia by the additional presence of identity disruption
characterized by two or more distinct personality states.
The essential feature of depersonalization/derealization
disorder is persistent or recurrent episodes of depersonalization, derealization, or both.
Individuals with depersonalization/derealization disorder do not experience the presence of
personality/identity states with alterations of self and agency, nor do they typically report
dissociative amnesia.
Most individuals with dissociative identity disorder endorse a lifelong
negative posttraumatic emotional state, often with childhood onset, and their symptoms may
appear to meet the criteria for a major depressive episode. Moreover, posttraumatic reactivity to
times of year when trauma occurred (anniversary reactions), primarily manifesting with more
despondency, distress, and suicidal ideation, may also appear to be major depressive disorder,
with seasonal pattern. However, individuals with major depressive disorder or persistent
depressive disorder do not experience dissociative fluctuations in self and agency and
dissociative amnesia. It is important to assess if all or most identity states are experiencing the
adverse mood state, since mood disorder symptoms may fluctuate because they are experienced
in some identity states, but not others.
Dissociative identity disorder is commonly misdiagnosed as bipolar disorder,
typically bipolar II disorder, with mixed features. The relatively rapid shifts in behavioral state in
individuals with dissociative identity disorder—usually within minutes or hours—are atypical for
even the most rapid-cycling individuals with bipolar disorders. These state alterations are due to
rapidly shifting dissociative states and/or fluctuating posttraumatic intrusions. Sometimes these
shifts are accompanied by rapid changes in levels of activation, but these usually last minutes to
hours, not days, and are associated with activation of specific identity states. Elevated or
depressed mood may be experienced as loculated in specific identities, through
overlap/interference phenomena. Usually, the individual with dissociative identity disorder does
not have a classic bipolar sleep disturbance (e.g., reduced need for sleep), instead suffering from
chronic, severe nightmares and nocturnal flashbacks that interrupt sleep.
A majority of individuals with dissociative identity disorder will
have symptoms that meet diagnostic criteria for comorbid PTSD. Dissociative symptoms
characteristic of dissociative identity disorder should be differentiated from the dissociative
amnesia, dissociative flashbacks, and depersonalization/derealization characteristic of acute
stress disorder, PTSD, or the dissociative subtype of PTSD. Dissociative amnesia in PTSD
typically manifests only for specific traumatic events or aspects of traumatic events, as opposed

Schizophrenia and other psychotic disorders.
Substance/medication-induced disorders.
Personality disorders.
to the chronic, complex dissociative amnesia characteristic of dissociative identity disorder.
Depersonalization/derealization symptoms in the dissociative subtype of PTSD are related to
specific posttraumatic reminders. Depersonalization/derealization symptoms in dissociative
identity disorder may occur not only in response to posttraumatic reminders, but also in an
ongoing fashion in daily life, including in response to stressful interpersonal interactions and
when there is overlap/interference between states.
Individuals with dissociative identity disorder may
experience symptoms that can superficially appear similar to those of psychotic
disorders. These include auditory hallucinations and symptoms characteristic of intrusions of
personality states into the individual’s awareness; these symptoms can seemingly resemble some
of the Schneiderian first-rank symptoms formerly considered indicative of schizophrenia (e.g.,
thought broadcasting, thought insertion, thought withdrawal, hearing voices keeping up a
running commentary about the individual). For example, hearing different personality states
discussing the individual can resemble auditory hallucinations of voices arguing in
schizophrenia. The individual with dissociative identity disorder may also experience the
thoughts or emotions of an intruding personality state, which can resemble thought insertion in
schizophrenia, as well as experience the sudden disappearance of these thoughts or emotions,
which can resemble thought withdrawal. Such experiences in an individual with schizophrenia
are usually accompanied by delusional beliefs about the cause of those symptoms (i.e., thoughts
being inserted by an outside force), whereas individuals with dissociative identity disorder
typically experience these symptoms as ego-alien and frightening. Individuals with dissociative
identity disorder may also report a range of visual, tactile, olfactory, gustatory, and somatic
hallucinations, which are usually related to autohypnotic, posttraumatic, and dissociative factors,
such as partial flashbacks, in contrast to individuals with schizophrenia, whose hallucinations are
primarily auditory and less commonly visual. Dissociative identity disorder and psychotic
disorders are therefore distinguished by symptoms characteristic of one of these conditions and
not the other (e.g., dissociative amnesia in dissociative identity disorder and not in psychotic
disorders). Finally, individuals with schizophrenia have low hypnotic capacity, whereas
individuals with dissociative identity disorder have the highest hypnotic capacity among all
clinical groups.
Individuals with dissociative identity disorder frequently
have a current or past history of substance use disorders. Symptoms associated with the
physiological effects of a substance (e.g., blackouts) should be distinguished from dissociative
amnesia in dissociative identity disorder if the substance in question is judged to be etiologically
related to the memory loss.
Individuals with dissociative identity disorder often present identities that
appear to encapsulate a variety of severe personality disorder features, suggesting a differential
diagnosis of personality disorder, especially of the borderline type. Importantly, however, the
individual’s longitudinal variability in personality style (attributable to inconsistency among
identities) differs from the pervasive and persistent dysfunction in affect management and
interpersonal relationships typical of those with personality disorders.

Posttraumatic amnesia due to brain injury.
Functional neurological symptom disorder (conversion disorder).
Factitious disorder and malingering.
Both dissociative identity disorder and traumatic brain
injury (TBI) are characterized by gaps in memory. Other characteristics of TBI include loss of
consciousness, disorientation and confusion, or, in more severe cases, neurological signs and
symptoms. A neurocognitive disorder due to TBI manifests either immediately after brain injury
occurs or immediately after the individual recovers consciousness after the injury, and persists
past the acute postinjury period. The cognitive presentation of a neurocognitive disorder
following TBI is variable and includes difficulties in the domains of complex attention, executive
function, and learning and memory, as well as slowed speed of information processing and
disturbances in social cognition. While depersonalization is not uncommon following TBI, the
additional neurocognitive features noted above help distinguish it from dissociative amnesia that
is part of dissociative identity disorder. Moreover, dissociative amnesia occurring in the context
of dissociative identity disorder is accompanied by a marked discontinuity in sense of self and
sense of agency, which are not features of TBI.
Functional neurological symptom
disorder may be distinguished from dissociative identity disorder by the absence of identity
alteration characterized by two or more distinct personality states or an
experience of possession. Dissociative amnesia in functional neurological symptom disorder is
more limited and circumscribed (e.g., amnesia for a nonepileptic seizure).
Individuals who feign dissociative identity disorder usually do
not report the subtle symptoms of intrusion characteristic of the disorder; instead they tend to
overreport media-based symptoms of the disorder, such as dramatic dissociative amnesia and
melodramatic switching behaviors, while underreporting less-publicized comorbid symptoms,
such as depression. Individuals who feign dissociative identity disorder tend to be relatively
undisturbed by or may even seem to enjoy “having” the disorder, or may ask clinicians to “find”
traumatic memories. In contrast, most individuals with genuine dissociative identity disorder are
ashamed of and overwhelmed by their symptoms, deny the diagnosis, underreport their
symptoms, and display minimization and avoidance of their trauma history.
Individuals who feign the symptoms of dissociative identity disorder usually create limited,
stereotyped alternate identities, with feigned amnesia related only to the events for which gain is
sought, with apparent switching behaviors and amnesia only displayed while being observed.
They may present an “all-good” identity and an “all-bad” identity in hopes of gaining
exculpation for a crime.
Comorbidity
Disorders that are comorbid with dissociative identity disorder include PTSD, depressive
disorders, substance-related disorders, feeding and eating disorders, obsessive-compulsive
disorder, antisocial personality disorder, and other specified personality disorder with avoidant,
obsessive-compulsive, or borderline personality traits. The most common forms of functional
neurological symptom disorder include nonepileptic seizures, gait disturbances, and paralyses.
Most commonly, nonepileptic seizures resemble grand mal seizures or complex partial seizures
with temporal lobe foci; others may mimic absence or partial seizures.

F44.0
Dissociative Amnesia
Diagnostic Criteria
A. An inability to recall important autobiographical information, usually of a
traumatic or stressful nature, that is inconsistent with ordinary forgetting.
Note: Dissociative amnesia most often consists of localized or selective amnesia
for a specific event or events; or generalized amnesia for identity and life history.
B. The symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
C. The disturbance is not attributable to the physiological effects of a substance
(e.g., alcohol or other drug of abuse, a medication) or a neurological or other
medical condition (e.g., partial complex seizures, transient global amnesia,
sequelae of a closed head injury/traumatic brain injury, other neurological
condition).
D. The disturbance is not better explained by dissociative identity disorder,
posttraumatic stress disorder, acute stress disorder, somatic symptom disorder,
or major or mild neurocognitive disorder.
Coding note: The code for dissociative amnesia without dissociative fugue is F44.0.
The code for dissociative amnesia with dissociative fugue is F44.1.
Specify if:
F44.1 With dissociative fugue: Apparently purposeful travel or bewildered
wandering that is associated with amnesia for identity or for other important
autobiographical information.
Specifiers
The specifier “with dissociative fugue” applies when dissociative amnesia occurs in the context
of a dissociative fugue, which is characterized by apparently purposeful travel or bewildered
wandering that is associated with amnesia for identity or other important autobiographical
information.
Diagnostic Features
The defining characteristic of dissociative amnesia is an inability to recall important
autobiographical information that 1) should be successfully stored in memory and 2) ordinarily
would be freely recollected (Criterion A). Dissociative amnesia is conceptualized as a potentially
reversible memory retrieval deficit. In this way, among others, it differs from the amnesias
attributable to neurobiological damage or toxicity that impair memory storage or retrieval.
A variety of types of dissociative amnesia may manifest. In general, the memory deficit in

dissociative amnesia is retrograde and, except in rare cases, is not associated with ongoing
amnesia for contemporary life events. Retrospective memory impairments include not only lost
memories of traumatic experiences but also lost memories of everyday life during which no
trauma occurred. Most commonly, individuals with dissociative amnesia report localized
amnesia—a failure to recall events during a circumscribed period of time; and/or selective
amnesia—the individual can recall some, but not all, of the events during a circumscribed period
of time. In systematized amnesia the individual fails to recall a specific category of important
information (e.g., fragmentary recall of home growing up, but continuous memory for school; no
recall of a violent older sibling; lack of recall of a specific room in the individual’s childhood
home). Individuals rarely overtly complain of symptoms of these forms of dissociative amnesia
and attempt to minimize and rationalize the memory loss.
Generalized dissociative amnesia involves a complete loss of memory for most or all of the
individual’s life history. Individuals with generalized amnesia may forget personal identity (e.g.,
a woman loses memory of her entire life history after giving in to repeated pressure from a close
friend to engage in a sexual relationship), lose previous knowledge about the world (e.g., recent
political events, how to use current technology), and less commonly lack access to well-learned
skills (e.g., what contact lenses are and how to put them in). Generalized dissociative amnesia
has an acute onset; the perplexity, disorientation, and purposeless wandering of individuals with
generalized amnesia usually bring them to the attention of the police or psychiatric emergency
services. Dissociative fugue is commonly associated with generalized dissociative amnesia and
can be indicated by using the “with dissociative fugue” specifier. Generalized dissociative
amnesia may be more common among combat veterans, sexual assault victims, and individuals
experiencing extreme emotional stress or conflict. In continuous amnesia (i.e., anterograde
dissociative amnesia), an individual forgets each new event as it occurs.
Individuals with dissociative amnesia are frequently unaware (or only partially aware) of
their memory problems. They may recall some traumatic events, or parts of traumatic events, but
not others of the same type. Many, especially those with localized amnesia, minimize the
importance of their memory loss and may become uncomfortable when prompted to address it.
Associated Features
Many individuals with dissociative amnesia are chronically impaired in their ability to form and
sustain satisfactory relationships. Histories of trauma, especially child abuse, and victimization
are common. Some individuals with dissociative amnesia report dissociative flashbacks (i.e.,
behavioral reexperiencing of traumatic events). Many have a history of
nonsuicidal self-injury, suicide attempts, and other high-risk behaviors. Depressive and
functional neurological symptoms are common, as are depersonalization, auto-hypnotic
symptoms, and high hypnotizability. Sexual dysfunctions are common. Mild traumatic brain
injury (TBI) may precede dissociative amnesia.
Prevalence
The 12-month prevalence for dissociative amnesia among adults in a small U.S. community

Environmental.
study was 1.8%.
Development and Course
Dissociative amnesia has been observed in young children, adolescents, adults, and geriatric
populations. Amnesia in children younger than 12 may be the most difficult to evaluate because
they often have difficulty understanding questions about amnesia, and interviewers may find it
difficult to formulate child-friendly questions about memory and amnesia, especially in younger
children. Observations of apparent dissociative amnesia are often difficult to differentiate from
inattention, absorption, daydreaming, anxiety, oppositional behavior, and learning disorders.
Reports from several different sources (e.g., teacher, therapist, case worker) may be needed to
diagnose amnesia in children. Some traumatized adolescents with dissociative amnesia are less
likely to come to clinical attention because of lower levels of posttraumatic stress disorder
(PTSD) intrusive symptoms and less externalizing behavior. Dissociative fugue behavior in
children and adolescents may be limited by the child’s life space (e.g., a child in a fugue “coming
to” after bicycling to an unfamiliar neighborhood, a teenager finding herself having taken public
transportation to a nearby town).
Onset of generalized amnesia is usually sudden. Individuals may experience multiple
episodes of this type of dissociative amnesia. A single episode may predispose to future
episodes. In between episodes of amnesia, the individual may or may not appear to be acutely
symptomatic. Some episodes of acute generalized amnesia resolve rapidly (e.g., when the
individual is removed from combat or some other stressful situation, and/or is brought to clinical
attention). A substantial subgroup of individuals develop highly impairing, debilitating, chronic
autobiographical memory deficits, such that even “relearning” their life history does not
ameliorate the memory loss.
Removal from the traumatic circumstances generating acute, generalized dissociative
amnesia (e.g., combat) may bring about a rapid return of memory. The memory loss of
individuals with dissociative fugue may be particularly refractory. Later life trauma, life stresses,
or losses may precede breakdown of long-standing autobiographical memory deficits related to
childhood or adult trauma, with the onset of acute PTSD, mood disorders, substance abuse, and
dangerousness to self or others, among other symptoms.
Risk and Prognostic Factors
Severe, acute, or chronic traumatization is the main risk factor for dissociative
amnesia. Cumulative early life trauma and adversities, especially physical and sexual abuse, are
the major risk factors for dissociative amnesia for childhood and adolescence. More severe
sexual abuse, multiple episodes of childhood sexual abuse, and sexual abuse by a relative,
especially with betrayal by a close attachment figure, may increase the extent of childhood
autobiographical memory disturbances. Individuals with dissociative amnesia may deny recall of
specific childhood traumas (e.g., sexual assault), even those documented in medical or social
service reports, although the individual can recall other similar traumatic events, both before and
after the amnestic event. Severe cumulative adult trauma (e.g., repeated combat, trafficking,
prisoner-of-war or concentration camp

Genetic and physiological.
experiences) also may result in extensive localized, selective, and/or systematized dissociative
amnesia. Generalized dissociative amnesia may be more common among individuals who have
recently experienced extreme acute traumas (e.g., brutal military combat, rape, torture, often in
the context of inability to escape) and/or a prior history of major social dislocation, asylumseeking, or refugee status. Others develop generalized amnesia in the context of profound
psychological conflict from which the individual also feels unable to escape. Virtually all
individuals who develop generalized dissociative amnesia in the context of psychological
conflict report past histories of severe early life and/or adult traumatization. Extreme acute
traumatic experiences also may engender major psychological conflicts (e.g., a woman develops
generalized amnesia after experiencing a brutal rape resulting in an unwanted pregnancy and
becomes suicidal; on assessment, she reveals that her religion views abortion as murder and
suicide as a major sin).
Quantitative genetic studies suggest that genetics account for about
50% of the interindividual variance in dissociative symptoms, with nonshared, stressful
environmental experiences accounting for most of the additional variance. Candidate gene
studies suggest a gene x environment interplay with earlier and more chronic childhood
traumatic experiences leading to significant increases in dissociative symptoms later in life.
Culture-Related Diagnostic Issues
In cultural contexts where possession is part of normative religious or spiritual practice,
dissociative amnesia and fugue may be interpreted as resulting from pathological possession. In
contexts or situations where individuals feel highly constrained by social circumstances or
cultural traditions, the precipitants of dissociative amnesia often do not involve frank trauma.
Instead, the amnesia may be preceded by severe psychological stresses or conflicts (e.g., marital
conflict, other family disturbances, attachment problems, or conflicts attributable to restriction or
oppression).
Association With Suicidal Thoughts or Behavior
Suicidal and other self-destructive behaviors are common in individuals with dissociative
amnesia. The psychological forces producing generalized amnesia may be extreme, and suicidal
thoughts, impulses, plans, and behavior are a risk when amnesia decreases. Case reports suggest
that suicidal behavior may be a particular risk when the amnesia remits suddenly and
overwhelms the individual with intolerable memories.
Functional Consequences of Dissociative Amnesia
Impairments in individuals with dissociative amnesia resulting from childhood/adolescent
traumatization range from limited to severe. Some of these individuals may be chronically
impaired in their ability to form and sustain satisfactory attachments. Some may become highly
successful in occupational functioning but often do so by compulsive overwork. Individuals with
acute generalized dissociative amnesia usually have impairment in all aspects of functioning. A
substantial subgroup of individuals with generalized amnesia develop a highly impairing, chronic
autobiographical memory deficit that even relearning their life history does not ameliorate. These
individuals experience a highly debilitated, chronic course with poor overall functioning in most

Dissociative identity disorder.
Posttraumatic stress disorder.
Neurocognitive disorders.
Substance-related disorders.
domains of life.
Differential Diagnosis
Recurrent episodes of dissociative amnesia may be attributable to
dissociative identity disorder. Individuals with dissociative amnesia may report depersonalization
and auto-hypnotic symptoms, as do individuals with dissociative
identity disorder. Individuals with dissociative identity disorder report pervasive discontinuities
in sense of self and agency, accompanied by many other dissociative symptoms. Amnesias in
dissociative identity disorder, in addition to retrospective autobiographical memory deficits,
include ongoing amnesia (“time loss”) for everyday events and interpersonal interactions;
finding unexplained possessions; perplexing major fluctuations in skills and knowledge; and
frequent, brief amnesic gaps during interpersonal interactions.
Some individuals with PTSD cannot recall part or all of a specific
traumatic event (e.g., a rape victim who cannot recall most events for the entire day of the rape).
When that amnesia extends to events beyond the immediate time of the trauma, a comorbid
diagnosis of dissociative amnesia may be warranted. Individuals with the dissociative subtype of
PTSD may also report dissociative amnesia in addition to depersonalization/derealization.
In major neurocognitive disorders, there is typically evidence of neural
tissue damage accompanied by a decline in cognitive function with deficits in attention,
executive function, learning and memory, language, and perceptual-motor and social cognition
that impair capacity for independent everyday activities. Memory loss for personal information is
usually embedded in cognitive, linguistic, affective, attentional, and behavioral disturbances.
Generally, awareness of personal identity is spared until late in the course of the neurocognitive
disorder. In neurocognitive disorders, retrograde amnesia is almost always accompanied by
anterograde amnesia. Anterograde dissociative amnesia can be confused with delirium. However,
medical, laboratory, toxicological, and neurological workups, including imaging studies, are
normal. Careful, repeated evaluations over time will show that as in other forms of dissociative
amnesia, there are no true neurocognitive deficits.
In the context of repeated intoxication with alcohol or other
substances/medications, there may be episodes of “blackouts” or periods for which the individual
has no memory, or partial memory (“grayouts”). To aid in distinguishing these episodes from
dissociative amnesia, a longitudinal history should show that the amnestic episodes occur only in
the context of intoxication. However, the distinction may be difficult when the individual with
dissociative amnesia also misuses alcohol or other substances, particularly in the context of
stressful situations that may also exacerbate dissociative symptoms. This can be a more complex
differential diagnosis when the substance use begins in childhood or adolescence, generally in
the context of intrafamilial abuse, neglect, and substance-related disorders. Sequential
observation of these individuals after detoxification, along with carefully taken history, usually
can distinguish the memory loss attributable to long-standing substance use from dissociative
amnesia. Some individuals with comorbid dissociative amnesia and substance use disorders will
attempt to minimize their dissociative amnesia and attribute memory problems solely to the

Posttraumatic amnesia due to brain injury.
Seizure disorders.
Memory deficits associated with electroconvulsive therapy.
Catatonic stupor.
substance use. Prolonged use of alcohol or other substances may result in a substance-induced
neurocognitive disorder that may be associated with impaired cognitive function. However, in
this context the protracted history of substance use and the persistent deficits associated with the
neurocognitive disorder would serve to distinguish it from dissociative amnesia, where there is
typically no evidence of persistent impairment in intellectual functioning.
Amnesia may occur in the context of a TBI when there
has been an impact to the head or other mechanisms of rapid movement or displacement of the
brain within the skull. Other characteristics of TBI include loss of consciousness, disorientation
and confusion, or, in more severe cases, neurological signs and symptoms (e.g., abnormalities on
neuroimaging, a new onset of seizures or a marked worsening of a preexisting seizure disorder,
visual field cuts, anosmia). A neurocognitive disorder attributable to TBI must present either
immediately after brain injury occurs or immediately after the individual recovers consciousness
after the injury, and persist past the
acute postinjury period. The cognitive presentation of a neurocognitive disorder following TBI is
variable and includes difficulties in the domains of complex attention, executive function,
learning and memory, as well as slowed speed of information processing and disturbances in
social cognition. The patterns of memory deficits are typical of neurocognitive disorders. Mild
TBI may precede acute dissociative amnesia presentations, but the dissociative memory deficits
are out of proportion to the TBI head trauma and typically follow the dissociative, not the
neurocognitive, patterns.
Individuals with seizure disorders may exhibit complex behavior during
seizures or postictally with subsequent amnesia. Some individuals with a seizure disorder engage
in nonpurposive wandering that is limited to the period of seizure activity. Conversely, behavior
during a dissociative fugue is usually purposeful, complex, and goal-directed and may last for
days, weeks, or longer. Occasionally, individuals with a seizure disorder will report that some
autobiographical memories have been “wiped out” as the seizure disorder progresses. Such
memory loss is not associated with psychological trauma or adversities and appears to occur
randomly. In seizure disorders, serial electroencephalograms usually show abnormalities.
Telemetric electroencephalographic monitoring generally shows an association between the
episodes of amnesia and seizure activity. Dissociative and epileptic amnesias may coexist.
Memory deficits after electroconvulsive
therapy (ECT) most commonly occur for the day of ECT administration. More extensive
retrograde and even anterograde amnesia after ECT is usually unrelated to stressful or traumatic
life epochs, and generally remits after the ECT series concludes. ECT in severely depressed
individuals with dissociative disorders does not worsen dissociation, and memory access may
improve as depression remits.
Mutism in catatonic stupor may suggest dissociative amnesia, but failure of
recall is usually absent. Other catatonic symptoms (e.g., rigidity, posturing, negativism) are
usually present. Catatonic symptoms in children can be associated with trauma, abuse, and/or
deprivation. Unlike in dissociative amnesia, the pattern of memory loss in catatonia is only for
the catatonic episode.

Acute dissociative reactions to stressful events (other specified dissociative disorder).
Factitious disorder and malingering.
Memory changes with aging or mild neurocognitive disorder.
The 
acute
dissociative reactions to stressful events example of other specified dissociative disorder is
characterized by a combination of dissociative symptoms that occur together acutely in response
to stressful events and typically last less than 1 month. Amnestic episodes that occur as part of
these reactions are accompanied by other prominent dissociative symptoms, have a short
duration (hours or days), and tend to be circumscribed to limited periods or events in a person’s
life (micro-amnesias).
There is no test, battery of tests, or set of procedures that
invariably distinguishes dissociative amnesia from feigned amnesia. Feigned amnesia is more
common in individuals with 1) acute, florid dissociative amnesia; 2) financial, sexual, or legal
problems; 3) a wish to escape stressful circumstances; 4) a desire to seem to be a more
interesting patient; and/or 5) a plan to engage in litigation for “recovered memories.” However,
dissociative amnesia can be associated with those same circumstances and can coexist with
deliberate feigning. Many individuals who malinger amnesia confess spontaneously or when
confronted.
Memory 
decrements 
in 
mild
neurocognitive disorder differ from those of dissociative amnesia; in mild neurocognitive
disorder, memory changes manifest as difficulty in learning and retaining new information. This
is often measured in tests of verbal learning of word lists or a brief story with evaluation of
immediate and delayed recall. With normal cognitive aging, individuals may also have similar
weaknesses in immediate and delayed recall of new information,
although normal aging may also affect information processing speed and other complex
executive function tasks in addition to memory.
Comorbidity
As is common in individuals with a history of trauma, many comorbidities co-occur with
dissociative amnesia, particularly as dissociative amnesia begins to remit. A wide variety of
affective phenomena may surface, including dysphoria, grief, rage, shame, guilt, and
psychological conflict and turmoil. Individuals may engage in nonsuicidal self-injury and other
high-risk behaviors. These individuals may have symptoms that meet diagnostic criteria for
persistent depressive disorder, major depressive disorder, or subthreshold depression (other
specified depressive disorder). Many individuals with dissociative amnesia develop PTSD at
some point during their life, especially when the traumatic antecedents of their amnesia are
brought into conscious awareness. Many of these individuals may show symptoms of the
dissociative subtype of PTSD. Many individuals with dissociative amnesia have symptoms that
meet diagnostic criteria for a comorbid somatic symptom and related disorder (and vice versa),
particularly functional neurological symptom disorder (conversion disorder). Substance-related
and addictive disorders may be comorbid with dissociative amnesia, as well as feeding and
eating disorders and sexual dysfunctions. The most common comorbid personality disorder is
other specified personality disorder (with mixed personality disorder features), which often
includes avoidant, obsessive-compulsive, dependent, and borderline features.

F48.1
Depersonalization/Derealization Disorder
Diagnostic Criteria
A. The presence of persistent or recurrent experiences of depersonalization,
derealization, or both:
1. Depersonalization: Experiences of unreality, detachment, or being an
outside observer with respect to one’s thoughts, feelings, sensations, body, or
actions (e.g., perceptual alterations, distorted sense of time, unreal or absent
self, emotional and/or physical numbing).
2. Derealization: Experiences of unreality or detachment with respect to
surroundings (e.g., individuals or objects are experienced as unreal,
dreamlike, foggy, lifeless, or visually distorted).
B. During the depersonalization or derealization experiences, reality testing remains
intact.
C. The symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
D. The disturbance is not attributable to the physiological effects of a substance
(e.g., a drug of abuse, medication) or another medical condition (e.g., seizures).
E. The disturbance is not better explained by another mental disorder, such as
schizophrenia, panic disorder, major depressive disorder, acute stress disorder,
posttraumatic stress disorder, or another dissociative disorder.
Diagnostic Features
The essential features of depersonalization/derealization disorder are persistent or recurrent
episodes of depersonalization, derealization, or both. Episodes of depersonalization are
characterized by a feeling of unreality or detachment from, or unfamiliarity with, the individual’s
whole self or from aspects of the self (Criterion A1). The individual may feel detached from his
or her entire being (e.g., “I am no one,” “I have no self”). He or she may
also feel subjectively detached from aspects of the self, including feelings (e.g.,
hypoemotionality: “I know I have feelings, but I don’t feel them”), thoughts (e.g., “My thoughts
don’t feel like my own,” “head filled with cotton”), whole body or body parts, or sensations (e.g.,
touch, proprioception, hunger, thirst, libido). There may also be a diminished sense of agency
(e.g., feeling robotic, like an automaton; lacking control of speech or movements). The
depersonalization experience can sometimes be one of a split self, with one part observing and
one participating, known as an “out-of-body experience” in its most extreme form. The unitary
symptom of “depersonalization” consists of several symptom factors: anomalous body
experiences (i.e., unreality of the self and perceptual alterations); emotional or physical numbing;

and temporal distortions with anomalous subjective recall.
Episodes of derealization are characterized by a feeling of unreality or detachment from, or
unfamiliarity with, the world, be it individuals, inanimate objects, or all surroundings (Criterion
A2). The individual may feel as if he or she were in a fog, dream, or bubble, or as if there were a
veil or a glass wall between the individual and the world around. Surroundings may be
experienced as artificial, colorless, or lifeless. Derealization is commonly accompanied by
subjective visual distortions, such as blurriness, heightened acuity, widened or narrowed visual
field, two-dimensionality or flatness, exaggerated three-dimensionality, or altered distance or
size of objects (i.e., macropsia or micropsia). Auditory distortions can also occur, whereby
voices or sounds are muted or heightened. In addition, Criterion C requires that the symptoms
cause clinically significant distress or impairment in social, occupational, or other important
areas of functioning, and Criteria D and E describe exclusionary diagnoses.
Associated Features
Individuals with depersonalization/derealization disorder may have difficulty describing their
symptoms and may think they are “crazy” or “going crazy.” Another common experience is the
fear of irreversible brain damage. A commonly associated symptom is a subjectively altered
sense of time (i.e., too fast or too slow), as well as a subjective difficulty in vividly recalling past
memories and owning them as personal and emotional. Vague somatic symptoms, such as head
fullness, tingling, or lightheadedness, are not uncommon. Individuals may experience extreme
rumination or obsessional preoccupation (e.g., constantly obsessing about whether they really
exist, or checking their perceptions to determine whether they appear real). Varying degrees of
anxiety and depression are also common associated features. Individuals with the disorder have
been found to have physiological hyporeactivity to emotional stimuli. Neural substrates of
interest include the hypothalamic-pituitary-adrenocortical axis, inferior parietal lobule, and
prefrontal cortical-limbic circuits.
Prevalence
Transient depersonalization/derealization symptoms lasting hours to days are common in the
general population. The 12-month prevalence of depersonalization/derealization disorder is
thought to be markedly less than for transient symptoms, although precise estimates for the
disorder are unavailable. In general, approximately one-half of all adults have experienced at
least one lifetime episode of depersonalization/derealization. However, symptomatology that
meets full criteria for depersonalization/derealization disorder is markedly less common than
transient symptoms. One-month prevalence in the United Kingdom is approximately 1%–2%.
Development and Course
The mean age at onset of depersonalization/derealization disorder is 16 years, although the
disorder can start in early or middle childhood; a minority cannot recall ever not having had the
symptoms. Less than 20% of individuals experience onset after age 20 years and only 5% after
age 25 years. Onset in the fourth decade of life or later is highly unusual.

Temperamental.
Environmental.
Onset can range from extremely sudden to gradual. Duration of depersonalization/derealization
disorder episodes can vary greatly, from brief (hours or days) to prolonged (weeks, months, or
years). Given the rarity of disorder onset after age 40 years, in such cases the individual should
be examined more closely for underlying medical conditions (e.g., brain lesions, seizure
disorders, sleep apnea). The course of the disorder is often persistent. About one-third of cases
involve discrete episodes; another third, continuous symptoms from the start; and still another
third, an initially episodic course that eventually becomes continuous.
While in some individuals the intensity of symptoms can wax and wane considerably, others
report an unwavering level of intensity that in extreme cases can be constantly present for years
or decades. Internal and external factors that affect symptom intensity vary between individuals,
yet some typical patterns are reported. Exacerbations can be triggered by stress, worsening mood
or anxiety symptoms, novel or overstimulating settings, and physical factors such as lighting or
lack of sleep.
Risk and Prognostic Factors
Individuals with depersonalization/derealization disorder are characterized by
harm-avoidant temperament, immature defenses, and both disconnection and overconnection
schemata. Immature defenses such as idealization/devaluation, projection, and acting out result
in denial of reality and poor adaptation. Cognitive disconnection schemata reflect defectiveness
and emotional inhibition and subsume themes of abuse, neglect, and deprivation. Overconnection
schemata involve impaired autonomy with themes of dependency, vulnerability, and
incompetence.
There is a clear association between the disorder and childhood interpersonal
traumas in a substantial portion of individuals, although this association is not as prevalent or as
extreme in the nature of the traumas as in other dissociative disorders, such as dissociative
identity disorder. In particular, emotional abuse and emotional neglect have been most strongly
and consistently associated with the disorder. Other stressors can include physical abuse;
witnessing domestic violence; growing up with a seriously impaired, mentally ill parent; or
unexpected death or suicide of a family member or close friend. Sexual abuse is a much less
common antecedent but can be encountered. The most common proximal precipitants of the
disorder are severe stress (interpersonal, financial, occupational), depression, anxiety
(particularly panic attacks), and illicit drug use. Symptoms may be specifically induced by
substances 
such 
as 
tetrahydrocannabinol, 
hallucinogens, 
ketamine, 
MDMA 
(3,4methylenedioxymethamphetamine; “ecstasy”), and salvia. Marijuana use may precipitate newonset panic attacks and depersonalization/derealization symptoms simultaneously.
Culture-Related Diagnostic Issues
Volitionally induced experiences of depersonalization/derealization can be a part of meditative
practices that are prevalent in many religious, spiritual, and cultural contexts and should not be
diagnosed as a disorder. However, there are individuals who initially induce these states
intentionally but over time lose control over them and may develop a fear and aversion for
related practices. Cultural frameworks may affect the level of distress or perceived severity
associated with uncontrolled depersonalization/derealization experiences by providing
explanations for them (e.g., spiritual/supernatural causes), which may alleviate individuals’ fears

Illness anxiety disorder.
Major depressive disorder.
Obsessive-compulsive disorder.
Other dissociative disorders.
Panic attacks.
that they are “losing their mind.”
Functional Consequences of Depersonalization/Derealization Disorder
Symptoms of depersonalization/derealization disorder are highly distressing and are associated
with major morbidity. The affectively flattened and robotic demeanor that these
individuals often demonstrate may appear incongruent with the extreme emotional pain reported
by those with the disorder. Impairment is often experienced in both interpersonal and
occupational spheres, largely as a result of the hypoemotionality with others, subjective difficulty
in focusing and retaining information, and a general sense of disconnectedness from life.
Differential Diagnosis
Although individuals with depersonalization/derealization disorder can
present with vague somatic complaints as well as fears of permanent brain damage, the diagnosis
of depersonalization/derealization disorder is characterized by the presence of a constellation of
typical depersonalization/derealization symptoms and the absence of other manifestations of
illness anxiety disorder.
Feelings of numbness, deadness, apathy, and being in a dream are not
uncommon in major depressive episodes. However, in depersonalization/derealization disorder,
such 
symptoms 
are 
associated 
with 
further 
symptoms 
of 
the 
disorder. 
If 
the
depersonalization/derealization clearly precedes the onset of a major depressive episode or
clearly continues after its resolution, the diagnosis of depersonalization/derealization disorder
applies.
Some individuals with depersonalization/derealization disorder
can become obsessively preoccupied with their subjective experience or develop rituals checking
on the status of their symptoms. However, other symptoms of obsessive-compulsive disorder
unrelated to depersonalization/derealization are not present.
In order to diagnose depersonalization/derealization disorder, the
symptoms should not occur in the context of another dissociative disorder, such as dissociative
identity disorder. Differentiation from dissociative amnesia and functional neurological symptom
disorder (conversion disorder) is simpler, as the symptoms of these disorders do not overlap with
those of depersonalization/derealization disorder.
Depersonalization/derealization is one of the symptoms of panic attacks,
increasingly 
common 
as 
panic 
attack 
severity 
increases. 
Therefore,
depersonalization/derealization disorder should not be diagnosed when the symptoms occur only
during panic attacks that are part of panic disorder, social anxiety disorder, or specific phobia. In
addition, it is not uncommon for depersonalization/derealization symptoms to first begin in the
context of new-onset panic attacks or as panic disorder progresses and worsens. In such
presentations, the diagnosis of depersonalization/derealization disorder can be made if 1) the
depersonalization/derealization component of the presentation is very prominent from the start,
clearly exceeding in duration and intensity the occurrence of actual panic attacks; or 2) the

Psychotic disorders.
Substance/medication-induced disorders.
Traumatic brain injury.
Dissociative symptoms due to another medical condition.
depersonalization/derealization continues after panic disorder has remitted or has been
successfully treated.
The presence of intact reality testing specifically regarding the
depersonalization/derealization 
symptoms 
is 
essential 
to 
differentiating
depersonalization/derealization disorder from psychotic disorders. Rarely, positive-symptom
schizophrenia can pose a diagnostic challenge when nihilistic delusions are present. For example,
an individual may complain that he or she is dead or the world is not real; this could be either a
subjective experience that the individual knows is not true or a delusional conviction.
Depersonalization/derealization 
associated 
with 
the
physiological effects of substances during acute intoxication or withdrawal is not diagnosed as
depersonalization/derealization disorder. The most common precipitating substances are the
illicit drugs marijuana, hallucinogens, ketamine, ecstasy, and salvia. In
about 15% of all cases of depersonalization/derealization disorder, the symptoms are precipitated
by ingestion of such substances. If the symptoms persist for some time in the absence of any
further substance or medication use, the diagnosis of depersonalization/derealization disorder
applies. This diagnosis is usually easy to establish since the vast majority of individuals with this
presentation become highly phobic and aversive to the triggering substance and do not use it
again.
Depersonalization/derealization symptoms are typical in traumatic brain
injury (TBI) but are distinguished from depersonalization/derealization disorder by onset of
symptoms following TBI and the lack of other symptoms of depersonalization/derealization
disorder.
Features such as onset after age 40 years or
the presence of atypical symptoms and course in any individual suggest the possibility of an
underlying medical condition. In cases with dissociative symptoms, it is essential to conduct a
thorough medical and neurological evaluation, which may include standard laboratory studies,
viral titers, an electroencephalogram, vestibular testing, visual testing, sleep studies, and/or brain
imaging. When the suspicion of an underlying seizure disorder proves difficult to confirm, an
ambulatory electroencephalogram may be indicated; although temporal lobe epilepsy is most
commonly implicated, parietal and frontal lobe epilepsy may also be associated.
Comorbidity
In a convenience sample of adults recruited for a number of depersonalization research studies,
lifetime comorbidities were high for unipolar depressive disorder and for any anxiety disorder,
with a significant proportion of the sample having both disorders. Comorbidity with
posttraumatic stress disorder was low. The three most commonly co-occurring personality
disorders were avoidant, borderline, and obsessive-compulsive.
Other Specified Dissociative Disorder

F44.89
This category applies to presentations in which symptoms characteristic of a
dissociative disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the dissociative disorders diagnostic class.
The other specified dissociative disorder category is used in situations in which the
clinician chooses to communicate the specific reason that the presentation does not
meet the criteria for any specific dissociative disorder. This is done by recording
“other specified dissociative disorder” followed by the specific reason (e.g.,
“dissociative trance”).
Examples of presentations that can be specified using the “other specified”
designation include the following:
1. Chronic and recurrent syndromes of mixed dissociative symptoms: This
category includes identity disturbance associated with less-than-marked
discontinuities in sense of self and agency, or alterations of identity or episodes
of possession in an individual who reports no dissociative amnesia.
2. Identity disturbance due to prolonged and intense coercive persuasion:
Individuals who have been subjected to intense coercive persuasion (e.g.,
brainwashing, thought reform, indoctrination while captive, torture, long-term
political imprisonment, recruitment by sects/cults or by terror organizations) may
present with prolonged changes in, or conscious questioning of, their identity.
3. Acute dissociative reactions to stressful events: This category is for acute,
transient conditions that typically last less than 1 month, and sometimes only a
few hours or days. These conditions are characterized by constriction of
consciousness; depersonalization; derealization; perceptual disturbances (e.g.,
time slowing, macropsia); microamnesias; transient stupor; and/or alterations in
sensory-motor functioning (e.g., analgesia, paralysis).
4. Dissociative trance: This condition is characterized by an acute narrowing or
complete loss of awareness of immediate surroundings that manifests as
profound unresponsiveness or insensitivity to environmental stimuli. The
unresponsiveness may be accompanied by minor stereotyped behaviors (e.g.,
finger movements) of which the individual is unaware and/or that he or she
cannot control, as well as transient paralysis or loss of consciousness. The
dissociative trance is not a normal part of a broadly accepted collective cultural
or religious practice.
Unspecified Dissociative Disorder

F44.9
This category applies to presentations in which symptoms characteristic of a
dissociative disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the dissociative disorders diagnostic class.
The unspecified dissociative disorder category is used in situations in which the
clinician chooses not to specify the reason that the criteria are not met for a specific
dissociative disorder and includes presentations for which there is insufficient
information to make a more specific diagnosis (e.g., in emergency room settings).

# 09 - Somatic Symptom and Related Disorders

# Somatic Symptom and Related Disorders

349

Somatic Symptom and Related Disorders
This chapter includes the diagnoses of somatic symptom disorder, illness anxiety disorder,
functional neurological symptom disorder (conversion disorder), psychological factors affecting
other medical conditions, factitious disorder, other specified somatic symptom and related
disorder, and unspecified somatic symptom and related disorder. All of the disorders in this
chapter share a common feature: the prominence of somatic symptoms and/or illness anxiety
associated with significant distress and impairment. Individuals with disorders with prominent
somatic symptoms or illness anxiety are commonly encountered in primary care and other
medical settings but are less commonly encountered in psychiatric and other mental health
settings. These reconceptualized diagnoses, based on a reorganization of DSM-IV somatoform
disorder diagnoses, are more useful for primary care and other medical (nonpsychiatric)
clinicians.
The major diagnosis in this diagnostic class, somatic symptom disorder, emphasizes
diagnosis made on the basis of the presence of symptoms and signs (distressing somatic
symptoms plus abnormal thoughts, feelings, and behaviors in response to these symptoms) rather
than the absence of a medical explanation for somatic symptoms. A distinctive characteristic of
many individuals with somatic symptom disorder is not the somatic symptoms per se, but instead
the way they present and interpret them. Incorporating affective, cognitive, and behavioral
components into the criteria for somatic symptom disorder provides a more comprehensive and
accurate reflection of the true clinical picture than can be achieved by assessing the somatic
complaints alone.
The principles behind the changes in the somatic symptom and related diagnoses from DSMIV are crucial in understanding the DSM-5 diagnoses. The DSM-IV term somatoform disorders
was confusing and was replaced by somatic symptom and related disorders. In DSM-IV there
was a great deal of overlap across the somatoform disorders and a lack of clarity about the
boundaries of diagnoses. Although individuals with these disorders primarily present in medical
rather than mental health settings, nonpsychiatric physicians found the DSM-IV somatoform
diagnoses difficult to understand and use. The current DSM-5 classification recognizes this
overlap by reducing the total number of disorders as well as their subcategories.
The previous criteria overemphasized the centrality of symptoms being unexplained by
recognized pathophysiological processes. Such symptoms are present to various degrees,
particularly in functional neurological symptom disorder, but somatic symptom disorders can
also accompany recognized medical conditions (i.e., those disorders related to clearly recognized
pathophysiological processes). The reliability of determining that a somatic symptom is
unexplained by a recognized pathophysiological process related to a recognized medical
condition is limited, and grounding a diagnosis on the absence of an explanation is problematic
and reinforces mind-body dualism. It is not appropriate to give an individual a mental disorder
diagnosis solely because a recognized medical condition cannot be demonstrated. Furthermore,

the presence of a recognized medical condition does not exclude the possibility of a comorbid
mental disorder, including a somatic symptom and related disorder. Perhaps because of the
predominant focus on lack of medical explanation in DSM-IV, individuals regarded these
diagnoses as pejorative and demeaning,
implying that their physical symptoms were not “real.” The DSM-5 classification defines the
major diagnosis, somatic symptom disorder, on the basis of positive symptoms (distressing
somatic symptoms plus abnormal thoughts, feelings, and behaviors in response to these
symptoms). In functional neurological symptom disorder and pseudocyesis (other specified
somatic symptom and related disorder), the emphasis is on demonstrating clinical evidence of
incompatibility with recognized pathophysiological processes.
It is important to note that some other mental disorders may initially manifest with primarily
somatic symptoms (e.g., major depressive disorder, panic disorder). Such diagnoses may account
for the somatic symptoms, or they may occur alongside one of the somatic symptom and related
disorders in this chapter. There is also considerable medical comorbidity among individuals with
somatic symptom and related disorders. Although somatic symptoms are frequently associated
with psychological distress and psychopathology, some somatic symptom and related disorders
can arise spontaneously, and their causes can remain obscure. Anxiety disorders and depressive
disorders may accompany somatic symptom and related disorders. The somatic component adds
severity and complexity to depressive and anxiety disorders and results in higher severity,
functional impairment, and even refractoriness to traditional treatments. In rare instances, the
degree of preoccupation may be so severe as to warrant consideration of a delusional disorder
diagnosis.
A number of factors may contribute to somatic symptom and related disorders. These include
genetic and biological vulnerability (e.g., increased sensitivity to pain), early traumatic
experiences (e.g., violence, abuse, deprivation), medical iatrogenesis (e.g., reinforcement of the
sick role, excessive referrals and diagnostic testing), and learning (e.g., lack of reinforcement of
nonsomatic expressions of distress), as well as sociocultural norms that minimize or stigmatize
psychological suffering as compared with physical suffering. Differences in medical care across
cultural contexts affect the presentation, recognition, and management of these somatic
presentations. Variations in symptom presentation are likely the result of the interaction of
multiple factors within cultural contexts that affect how individuals identify and classify bodily
sensations, perceive illness, and seek medical attention for them.
All of these disorders are characterized by the prominent focus on somatic concerns and their
initial presentation mainly in medical rather than mental health care settings. Somatic symptom
disorder and illness anxiety disorder offer more clinically useful methods of characterizing
individuals who may have been considered in the past for a diagnosis of somatization disorder
and hypochondriasis. Furthermore, approximately two-thirds to three-fourths of individuals
previously diagnosed with hypochondriasis are subsumed under the diagnosis of somatic
symptom disorder. However, the remaining one-quarter to one-third of individuals with
previously diagnosed hypochondriasis have high health anxiety in the absence of somatic
symptoms, and many such individuals’ symptoms would not qualify for an anxiety disorder
diagnosis. The DSM-5 diagnosis of illness anxiety disorder is for this latter group of individuals.

F45.1
Illness anxiety disorder can be considered either a somatic symptom and related disorder or an
anxiety disorder. Because of the strong focus on somatic concerns, and because illness anxiety
disorder is most often encountered in medical settings, for utility it is listed with the somatic
symptom and related disorders. In functional neurological symptom disorder, the key to
diagnosis is neurological symptoms that can be demonstrated, on the basis of positive clinical
examination features, to be incompatible with recognized pathophysiology. This is now a “rulein” diagnosis, and not a diagnosis of exclusion, and can be made in the presence of a recognized
neurological disorder. It no longer requires the presence of a recent psychological stressor,
because such stressors are not always present. Psychological factors affecting other medical
conditions is also included in this chapter. Its essential feature is the presence of one or more
clinically significant psychological or behavioral factors that adversely affect a medical condition
by increasing the risk for suffering, death, or disability. Like the other somatic symptom and
related disorders, factitious disorder embodies persistent problems related to illness perception
and identity. In the great majority of reported cases of factitious disorder, both
imposed on self and imposed on another, individuals present with somatic symptoms and
expressed medical disease conviction. Consequently, DSM-5 factitious disorder is included
among the somatic symptom and related disorders. Other specified somatic symptom and related
disorder and unspecified somatic symptom and related disorder include conditions for which
some, but not all, of the criteria for somatic symptom disorder or illness anxiety disorder are met,
as well as pseudocyesis.
Somatic Symptom Disorder
Diagnostic Criteria
A. One or more somatic symptoms that are distressing or result in significant
disruption of daily life.
B. Excessive thoughts, feelings, or behaviors related to the somatic symptoms or
associated health concerns as manifested by at least one of the following:
1. Disproportionate and persistent thoughts about the seriousness of one’s
symptoms.
2. Persistently high level of anxiety about health or symptoms.
3. Excessive time and energy devoted to these symptoms or health concerns.
C. Although any one somatic symptom may not be continuously present, the state
of being symptomatic is persistent (typically more than 6 months).
Specify if:
With predominant pain (previously pain disorder): This specifier is for
individuals whose somatic symptoms predominantly involve pain.

Specify if:
Persistent: A persistent course is characterized by severe symptoms, marked
impairment, and long duration (more than 6 months).
Specify current severity:
Mild: Only one of the symptoms specified in Criterion B is fulfilled.
Moderate: Two or more of the symptoms specified in Criterion B are fulfilled.
Severe: Two or more of the symptoms specified in Criterion B are fulfilled, plus
there are multiple somatic complaints (or one very severe somatic symptom).
Diagnostic Features
Individuals with somatic symptom disorder typically have multiple, current, somatic symptoms
that are distressing or result in significant disruption of daily life (Criterion A), although
sometimes only one severe symptom, most commonly pain, is present. Symptoms may be
specific (e.g., localized pain) or relatively nonspecific (e.g., fatigue). The symptoms sometimes
represent normal bodily sensations or discomfort that does not generally signify serious disease.
Somatic symptoms without an evident medical explanation are not sufficient to make this
diagnosis. The individual’s suffering is authentic, whether or not it is medically explained.
The symptoms may or may not be associated with another medical condition. The diagnoses
of somatic symptom disorder and a concurrent medical illness are not mutually exclusive, and
these frequently occur together. For example, an individual may become seriously disabled by
symptoms of somatic symptom disorder after an uncomplicated myocardial infarction even if the
myocardial infarction itself did not result in any disability. If another medical condition or high
risk for developing one is present (e.g., strong family history), the thoughts, feelings, and
behaviors associated with this condition are excessive (Criterion B).
Individuals with somatic symptom disorder tend to have very high levels of worry about
illness (Criterion B). They appraise their bodily symptoms as unduly threatening, harmful, or
troublesome and often think the worst about their health. Even when there is evidence to the
contrary, some individuals still fear the medical seriousness of their symptoms. In severe somatic
symptom disorder, health concerns may assume a central role in the individual’s life, becoming a
feature of his or her identity and dominating interpersonal relationships.
Individuals typically experience distress that is principally focused on somatic symptoms and
their significance. When asked directly about their distress, some individuals describe it in
relation to other aspects of their lives, while others deny any source of distress other than the
somatic symptoms. Health-related quality of life is often impaired, both physically and mentally.
The diagnosis can further be specified by stating whether complaints predominantly involve pain
and/or if complaints are marked by a persistent course.
Additionally, severity of somatic symptom disorder can be specified by the number of
fulfilled B criteria. Mild forms of somatic symptom disorder (one symptom as specified in
Criterion B is fulfilled) are more prevalent, while moderate (two or more B criteria are present)
and severe cases (two or more symptoms as specified in Criterion B are fulfilled in combination

with multiple somatic complaints or one very severe somatic symptom) are marked by higher
levels of impairment. In severe somatic symptom disorder, the impairment is marked, and when
persistent, the disorder can lead to invalidism.
There is often a high level of medical care utilization, which rarely alleviates the individual’s
concerns. Consequently, the individual may seek care from multiple doctors for the same
symptoms. These individuals often seem unresponsive to medical interventions, and new
interventions may only exacerbate the presenting symptoms. Some individuals with the disorder
seem unusually sensitive to medication side effects. Some feel that their medical assessment and
treatment have been inadequate.
The criteria for somatic symptom disorder appear suitable for use in children and
adolescents, but they have been less studied in youth than among adults.
Associated Features
Cognitive features include attention focused on somatic symptoms, attribution of normal bodily
sensations to physical illness (possibly with catastrophic interpretations), worry about illness, a
self-concept of bodily weakness, and intolerance of bodily complaints. Besides health anxiety,
emotional features may include negative affectivity, desperation, and demoralization related to
somatic symptoms. The relevant associated behavioral features may include repeated bodily
checking for abnormalities, repeated seeking of medical help and reassurance, and avoidance of
physical activity. These behavioral features are most pronounced in severe, persistent somatic
symptom disorder. These features are usually associated with frequent requests for medical help
for different somatic symptoms. This may lead to medical consultations in which individuals are
so focused on their concerns about somatic symptom(s) that they cannot be redirected to other
matters. Any reassurance by the doctor that the symptoms are not indicative of serious physical
illness tends to be short-lived and/or is experienced by the individuals as the doctor not taking
their symptoms with due seriousness. As the focus on somatic symptoms is a primary feature of
the disorder, individuals with somatic symptom disorder typically present to general medical
health services rather than mental health services. The suggestion of referral to a mental health
specialist may be met with surprise or even frank refusal by individuals with somatic symptom
disorder.
Prevalence
The prevalence of somatic symptom disorder is unclear. Estimates about the prevalence of
somatic symptom disorder come from the limited epidemiological literature on
DSM-IV-TR somatoform disorders. However, the prevalence of somatic symptom disorder is
expected to be higher than that of the more restrictive DSM-IV-TR somatization disorder (<1%)
but lower than that of undifferentiated somatoform disorder (approximately 19%). More recent
population-based studies with a questionnaire-based strategy using DSM-5 diagnostic criteria for
somatic symptom disorder in adult and adolescent samples report prevalence rates between 6.7%
and 17.4%. Based on research conducted in Europe and North America, the prevalence of
somatic symptom disorder in the general adult population can be approximated as 4%–6%.

Temperamental.
Environmental.
Somatic symptom disorder has a higher frequency in primary care patients than in the general
population. Based on reviews and meta-analyses of studies from multiple countries that had still
used DSM-IV or ICD-10 criteria, a 12-month prevalence of somatic symptom disorder and
related conditions in primary care patients between 10% and 20% appears plausible. Prevalence
rates are higher in clinical settings that specialize in psychosomatic or functional disorders, with
reported frequencies of somatic symptom disorder between 40% and 60%.
Women tend to report more somatic symptoms than do men, and the prevalence of somatic
symptom disorder is consequently likely to be higher in women.
Development and Course
In a study of Danish children ages 5–7 years, functional somatic symptoms were common health
complaints, which for a significant minority (roughly one-fifth) of those with complaints were
severe enough to cause distress, impairment, school absences, or medical help-seeking. Age at
onset does not seem to affect the duration of untreated illness.
The course of somatic symptom disorder is likely to be chronic and fluctuating and
influenced by the number of symptoms, individual’s age, level of impairment, and any
comorbidity. The course is also influenced by personality traits, with less harm avoidance and
greater cooperativeness associated with a shorter time to remission.
In children, the most common symptoms are recurrent abdominal pain, headache, fatigue,
and nausea. A single prominent symptom is more common in children than in adults. When the
diagnosis is being made in younger individuals, it is important to obtain patient, family, and
other assessments (e.g., school) of symptom presentation. Patient and caregiver engagement
during evaluation and management is fundamental because parents’ interpretation of and
response to symptoms may determine the level of associated distress, the demands for medical
investigations and interventions, and time away from school.
In older individuals, pain localized in several body regions appears to be the most common
symptom. Somatic symptoms and concurrent medical illnesses are common as multimorbidity
increases with age. Prevalence rates of somatic symptom disorder seem to be stable until age 65
years and might decrease thereafter. For making the diagnosis in older individuals, a focus on the
requirement for excessive thoughts, feelings, or behaviors related to the somatic symptoms or
associated health concerns (Criterion B) is crucial. Somatic symptom disorder may be
underdiagnosed in older adults either because certain somatic symptoms (e.g., pain, fatigue) are
considered part of normal aging or because illness worry is considered “understandable” in older
adults who have more general medical illnesses and medications than do younger people.
Risk and Prognostic Factors
The personality trait of negative affectivity (neuroticism) has been identified as
an independent correlate/risk factor of a high number of somatic symptoms. Comorbid anxiety or
depression is common and may exacerbate symptoms and impairment.
Somatic symptom disorder is more frequent in individuals with few years of
education and low socioeconomic status, and in those who have recently experienced stressful or

Course modifiers.
health-related life events. Early lifetime adversity such as childhood sexual abuse is also likely a
risk factor for somatic symptom disorder in adults.
Persistent somatic symptoms are associated with demographic features
(women, older age, fewer years of education, lower socioeconomic status, unemployment), a
reported history of sexual abuse or other childhood adversity, concurrent chronic physical illness
or mental disorder (depression, anxiety, persistent depressive disorder, panic), social stress, and
reinforcing social factors such as illness benefits. Total somatic symptom severity is probably
associated with female gender, anxiety, depression and general medical illness. Cognitive factors
that affect clinical course include sensitization to pain, heightened attention to bodily sensations,
and attribution of bodily symptoms to a possible medical illness rather than recognizing them as
a normal phenomenon or psychological stress.
Culture-Related Diagnostic Issues
High numbers of somatic symptoms are found in population-based and primary care studies
around the world, with a similar pattern of the most commonly reported somatic symptoms,
impairment, and treatment seeking. The relationship between number of somatic symptoms and
illness worry is similar in different cultural contexts, and marked illness worry is associated with
impairment and greater treatment seeking cross-culturally. In many cultural contexts, individuals
with depression commonly present with somatic symptoms.
Despite these similarities, there are differences in somatic symptoms across cultural contexts
and ethnoracial groups. Sociocultural factors, particularly stigma related to mental disorders,
may explain differences in somatic symptom reporting across cultural contexts. The description
of somatic symptoms varies with linguistic and other local cultural factors. These somatic
presentations have been described as “idioms of distress” because somatic symptoms may have
special meanings and shape patient-clinician interactions in the particular cultural contexts. For
example, sensations of heaviness, complaints of “gas,” too much heat in the body, or burning in
the head are common in some cultures or ethnic groups but rare in others. Cultural explanations
also vary, and somatic symptoms may be attributed variously to particular family, work (e.g.,
burnout), or other environmental stresses; general medical illness; the suppression of feelings of
anger and resentment; or certain culturally specific attributions, such as semen loss. Certain
somatic symptoms may be part of specific explanatory models in a given cultural context; for
example, traditional understandings of shenjing shuairuo in China link concepts of “weakness of
nerves” (neurasthenia) and hot-cold imbalance with prominent symptoms such as fatigue and
low energy. There may also be differences in medical treatment seeking and utilization of
nonmedical, traditional, alternative and complementary healing practices among cultural groups,
in addition to differences due to variable access to medical care services. Cultural beliefs,
previous illnesses, insurance status, health literacy, and health care experiences can influence
individuals’ perception of somatic symptoms and health care use. Seeking treatment for multiple
somatic symptoms in general medical clinics is a worldwide phenomenon.
Sex- and Gender-Related Diagnostic Issues
In population-based studies, women report more somatic symptoms than men, and in one study
of primary care patients with chronic pain, women reported more severe somatic symptoms than
men. While exposure to sexual trauma, intimate partner violence, and a childhood trauma history

Other medical conditions.
Psychological factors affecting other medical conditions.
is associated with increased somatic symptom expression in
both women and men, a childhood history of multiple adverse childhood experiences is
especially likely to increase somatic symptom expression in women.
In women, gender is associated with an increased likelihood of developing persistent
symptoms of somatic symptom disorder. There appears to be no evidence that gender is
associated with the duration of untreated illness and response to psychological or
pharmacological treatment.
Association With Suicidal Thoughts or Behavior
Somatic symptom disorder is associated with suicidal thoughts and suicide attempts. It is likely
that suicidal thoughts and behaviors are partly explained by the diagnostic overlap and frequent
comorbidity of somatic symptom disorder and depressive disorders. In addition, dysfunctional
illness perceptions and the severity of somatic symptoms appear to be independently associated
with an increased risk of suicidal ideation.
Functional Consequences of Somatic Symptom Disorder
The disorder is associated with marked impairment of health status and high psychological
distress. Many individuals with severe somatic symptom disorder are likely to have impaired
health status scores more than 2 standard deviations below population norms. Health status is
particularly impaired in the presence of multiple or severe symptoms.
Differential Diagnosis
If the somatic symptoms are consistent with another mental disorder (e.g., panic disorder), and
the diagnostic criteria for that disorder are fulfilled, then that mental disorder should be
considered as an alternative or additional diagnosis. If, as commonly occurs, the criteria for both
somatic symptom disorder and another mental disorder diagnosis are fulfilled, then both should
be diagnosed, as both may require treatment.
The presence of somatic symptoms of unclear etiology is not in itself
sufficient to make the diagnosis of somatic symptom disorder. The symptoms of many
individuals with disorders like irritable bowel syndrome or fibromyalgia would not satisfy the
criterion necessary to diagnose somatic symptom disorder (Criterion B). Conversely, the
presence of somatic symptoms of an established medical condition (e.g., diabetes or heart
disease) does not exclude the diagnosis of somatic symptom disorder if the criteria are otherwise
met. Factors that distinguish individuals with somatic symptom disorder from individuals with
general medical conditions alone include the ineffectiveness of analgesics, a history of mental
disorders, unclear provocative or palliative factors, persistence without cessation, and stress.
The diagnosis of somatic symptom disorder
requires distressing or impairing somatic symptoms that may or may not be associated with
another medical condition but must be accompanied by excessive or disproportionate thoughts,
feelings, or behaviors related to the somatic symptoms or associated health concerns. In contrast,

Panic disorder.
Generalized anxiety disorder.
Depressive disorders.
Illness anxiety disorder.
Functional neurological symptom disorder (conversion disorder).
Delusional disorder.
Body dysmorphic disorder.
Obsessive-compulsive disorder.
Factitious disorder and malingering.
the diagnosis of psychological factors affecting other medical conditions requires the presence of
a medical condition, as well as psychological factors that adversely affect its course or interfere
with its treatment.
In panic disorder, somatic symptoms and anxiety about health tend to occur in
acute episodes, whereas in somatic symptom disorder, anxiety and somatic symptoms are more
persistent.
Individuals with generalized anxiety disorder worry about multiple
events, situations, or activities, only one of which may involve their health. The main focus is not
usually somatic symptoms or fear of illness as it is in somatic symptom disorder.
Depressive disorders are commonly accompanied by somatic symptoms
such as fatigue, headaches, or joint, abdominal, or other pains. However, depressive disorders are
differentiated from somatic symptom disorder by the requirement of the presence of depressed
mood or, in the case of major depressive disorder, either depressed mood or decreased interest or
pleasure in activities. In some cultural contexts, these core symptoms of depression may be
initially denied or deemphasized by individuals whose presentations would otherwise meet
criteria for a depressive disorder. Such individuals might instead emphasize somatic symptoms
that may be idiomatic (e.g., heavy heart) and unfamiliar to clinicians.
If the individual has extensive worries about health but no or minimal
somatic symptoms, it may be more appropriate to consider illness anxiety disorder.
In functional neurological symptom
disorder, the presenting symptom is loss of function (e.g., of a limb), whereas in somatic
symptom disorder, the focus is on the distress that particular symptoms cause. The features listed
under Criterion B of somatic symptom disorder may be helpful in differentiating the two
disorders.
In somatic symptom disorder, the individual’s beliefs that somatic symptoms
might reflect serious underlying physical illness are not held with delusional intensity.
Nonetheless, the individual’s beliefs concerning the somatic symptoms can be firmly held. In
contrast, in delusional disorder, somatic type, the individual’s conviction that the somatic
symptoms are indicative of having a serious underlying illness is stronger than that found in
somatic symptom disorder.
In body dysmorphic disorder, the individual is excessively concerned
about, and preoccupied by, a perceived defect in his or her physical appearance. In contrast, in
somatic symptom disorder, the concern about somatic symptoms reflects fear of underlying
illness, not of a defect in appearance.
In somatic symptom disorder, the recurrent ideas about somatic
symptoms or illness are less intrusive, and individuals with this disorder do not exhibit the
associated repetitive behaviors aimed at reducing anxiety that occur in obsessive-compulsive
disorder.
In factitious disorder and malingering, individuals present
themselves as ill or impaired but have falsified presenting physical signs and symptoms with the

F45.21
intent to deceive. In contrast, the symptoms of somatic symptom disorder are not simulated or
self-induced, and these individuals suffer authentically and seriously from their somatic
complaints.
Comorbidity
Somatic symptom disorder is associated with high rates of comorbidity with other mental
disorders as well as general medical conditions. The most relevant co-occurring mental disorders
are anxiety and depressive disorders, each of which occurs in up to 50% of cases of somatic
symptom disorders and significantly contributes to overall functional impairment and poorer
quality of life. Other mental disorders that have been found to co-occur with somatic symptom
disorder are posttraumatic stress disorder and obsessive-compulsive disorder. Other evidence
indicates an association with sexual dysfunction in men.
Elevated levels of the psychological features (Criterion B) of somatic symptom disorder have
been found in several general medical conditions. When a concurrent general medical condition
is present, the degree of impairment is more marked than would be expected from the physical
illness alone. Moreover, somatization in medical illness has been shown to worsen disease and
treatment outcomes, adherence, and quality of life and to increase health care utilization.
Illness Anxiety Disorder
Diagnostic Criteria
A. Preoccupation with having or acquiring a serious illness.
B. Somatic symptoms are not present or, if present, are only mild in intensity. If
another medical condition is present or there is a high risk for developing a
medical condition (e.g., strong family history is present), the preoccupation is
clearly excessive or disproportionate.
C. There is a high level of anxiety about health, and the individual is easily alarmed
about personal health status.
D. The individual performs excessive health-related behaviors (e.g., repeatedly
checks his or her body for signs of illness) or exhibits maladaptive avoidance
(e.g., avoids doctor appointments and hospitals).
E. Illness preoccupation has been present for at least 6 months, but the specific
illness that is feared may change over that period of time.
F. The illness-related preoccupation is not better explained by another mental
disorder, such as somatic symptom disorder, panic disorder, generalized anxiety
disorder, body dysmorphic disorder, obsessive-compulsive disorder, or
delusional disorder, somatic type.
Specify whether:

Care-seeking type: Medical care, including physician visits or undergoing tests
and procedures, is frequently used.
Care-avoidant type: Medical care is rarely used.
Diagnostic Features
Most individuals who previously would have been diagnosed with hypochondriasis in DSM-IV
(preoccupation with having a serious disease based on the individual’s misinterpretation of
bodily symptoms) are now classified as having somatic symptom disorder; however, in one-third
of cases, the diagnosis of illness anxiety disorder applies instead.
Illness anxiety disorder entails a preoccupation with having or acquiring a serious,
undiagnosed medical illness (Criterion A). Somatic symptoms are not present or, if present, are
only mild in intensity (Criterion B). A thorough evaluation fails to identify a serious medical
condition that accounts for the individual’s concerns. While the concern may be derived from a
nonpathological physical sign or sensation, the individual’s distress emanates not primarily from
the physical complaint itself but rather from his or her anxiety about the meaning, significance,
or cause of the complaint (i.e., the suspected medical diagnosis). If a physical sign or symptom is
present, it is often a normal physiological sensation (e.g., orthostatic dizziness), a benign and
self-limited dysfunction (e.g., transient tinnitus), or a bodily discomfort not generally considered
indicative of disease (e.g., belching). If a diagnosable medical condition is present, the
individual’s anxiety and preoccupation are clearly excessive and disproportionate to the severity
of the condition (Criterion B). Most empirical evidence and existing literature pertain to
previously defined DSM hypochondriasis and health anxiety, and it is unclear to what extent and
how precisely they apply to the description of this new diagnosis.
The preoccupation with the idea that one is sick is accompanied by substantial anxiety about
health and disease (Criterion C). Individuals with illness anxiety disorder are easily alarmed
about illness, such as by hearing about someone else falling ill or reading a health-related news
story. Their concerns about undiagnosed disease do not respond to appropriate medical
reassurance, negative diagnostic tests, or benign course. The physician’s attempts at reassurance
and symptom palliation generally do not alleviate the individual’s
concerns and may heighten them. Illness concerns assume a prominent place in the
individual’s life, affecting daily activities, and may even result in invalidism. Illness becomes a
central feature of the individual’s identity and self-image, a frequent topic of social discourse,
and a characteristic response to stressful life events. Individuals with the disorder often examine
themselves repeatedly (e.g., examining one’s throat in the mirror) (Criterion D). They research
their suspected disease excessively (e.g., on the Internet) and repeatedly seek reassurance from
family, friends, or physicians. This incessant worrying often becomes frustrating for othe rs and
may result in considerable strain within the family. In some cases, the anxiety leads to
maladaptive avoidance of situations (e.g., visiting sick family members) or activities (e.g.,
exercise) that these individuals fear might jeopardize their health.

Environmental.
Associated Features
Because they believe they are medically ill, individuals with illness anxiety disorder are
encountered far more frequently in medical than in mental health settings. The majority of
individuals with illness anxiety disorder have extensive yet unsatisfactory medical care. They
generally have elevated rates of utilization of medical and mental health services compared with
the general population. In a minority of cases of illness anxiety disorder, individuals are too
anxious to seek medical attention and avoid medical health care.
They often consult multiple physicians for the same problem and obtain repeatedly negative
diagnostic test results. At times, medical attention leads to a paradoxical exacerbation of anxiety
or to iatrogenic complications from diagnostic tests and procedures. Individuals with the disorder
are generally dissatisfied with their medical care and find it unhelpful, often feeling they are not
being taken seriously by physicians. At times, these concerns may be justified, since physicians
sometimes are dismissive or respond with frustration or hostility. This response can occasionally
result in a failure to diagnose a medical condition that is present.
Prevalence
Prevalence estimates of illness anxiety disorder are based on estimates of the DSM-III and DSMIV diagnosis hypochondriasis and health anxiety. The 1- to 2-year prevalence of health anxiety
and/or disease conviction in community surveys and population-based samples from highincome countries such as the United States and Germany ranges from 1.3% to 10%. In
ambulatory medical populations, the 6-month/1-year prevalence rates are between 2.2% and 8%
across a range of countries, with weighted mean prevalence rates of 3%. By contrast, in a study
of patients in specialty clinics, about one-fifth of individuals reported illness anxiety. The
prevalence of the disorder is similar in men and women.
Development and Course
The development and course of illness anxiety disorder are unclear. Illness anxiety disorder is
generally thought to be a chronic, episodic, and relapsing condition with an age at onset in early
and middle adulthood. The disorder is thought to be rare in children, although the onset of
health-related anxieties can occur in childhood or adolescence. In some population-based
samples, health-related anxiety increases with age, but in others, health anxiety peaks in middle
age, before declining in older age. The ages of individuals with high health anxiety in medical
settings do not appear to differ from those of other individuals in those settings. In older
individuals, health-related anxiety often focuses on memory loss and sensory loss.
Risk and Prognostic Factors
Illness anxiety disorder may sometimes be precipitated by a major life stress or a
serious but ultimately benign threat to the individual’s health. A history of
childhood abuse or of a serious childhood illness, serious illness in a parent, or death of an ill
parent during childhood may predispose to development of the disorder in adulthood.

Course modifiers.
Other medical conditions.
Adjustment disorders.
Somatic symptom disorder.
Anxiety disorders.
Obsessive-compulsive and related disorders.
Approximately one-third to one-half of individuals with illness anxiety
disorder have a transient form, which is associated with less psychiatric comorbidity, more
medical comorbidity, and less severe illness anxiety disorder.
Culture-Related Diagnostic Issues
The diagnosis should be made with caution in individuals whose ideas about disease are
congruent with widely held cultural beliefs. The prevalence appears to be similar across different
countries, although little is known about the cross-cultural variation in phenomenology.
Functional Consequences of Illness Anxiety Disorder
Illness anxiety disorder causes substantial role impairment and decrements in physical function
and health-related quality of life. Health concerns often interfere with interpersonal relationships,
disrupt family life, and damage occupational performance.
Differential Diagnosis
The first differential diagnostic consideration is an underlying medical
condition, including neurological or endocrine conditions, occult malignancies, and other
diseases that affect multiple body systems. The presence of a medical condition does not rule out
the possibility of coexisting illness anxiety disorder. If a medical condition is present, the healthrelated anxiety and disease concerns are clearly disproportionate to its seriousness. Transient
preoccupations related to a medical condition do not constitute illness anxiety disorder.
Health-related anxiety is a normal response to serious illness and is not a
mental disorder. Such nonpathological health anxiety is clearly related to the medical condition
and is typically time-limited. If the health anxiety is severe enough to cause clinically significant
distress or impairment in one or more important areas of functioning, an adjustment disorder
may be diagnosed. However, if disproportionate health-related anxiety persists for longer than 6
months, a diagnosis of illness anxiety disorder may apply.
Both somatic symptom disorder and illness anxiety disorder may be
characterized by a high level of anxiety about health and excessive health-related behaviors.
They are differentiated by the fact that somatic symptom disorder requires the presence of
somatic symptoms that are distressing or result in significant disruption of daily life, whereas in
illness anxiety disorder, somatic symptoms either are not present or, if present, are only mild in
intensity.
In generalized anxiety disorder, individuals worry about multiple events,
situations, or activities, only one of which may involve health. In panic disorder, the individual
may be concerned that the panic attacks reflect the presence of a medical illness; however,
although these individuals may have health anxiety, their anxiety is typically very acute and
episodic. In illness anxiety disorder, the health anxiety and fears are more persistent and
enduring. Individuals with illness anxiety disorder may experience panic attacks that are
triggered by their illness concerns.
Individuals with illness anxiety disorder may have
intrusive thoughts about having a disease and also may have associated compulsive behaviors

Major depressive disorder.
Psychotic disorders.
(e.g., seeking reassurance). However, in illness anxiety disorder, the preoccupations are usually
focused on having a disease, whereas in obsessive-compulsive disorder (OCD), the thoughts are
intrusive and are usually focused on fears of getting a disease in the future. Most individuals with
OCD have obsessions or compulsions
involving other concerns in addition to fears about contracting disease. In body dysmorphic
disorder, concerns are limited to the individual’s physical appearance, which is viewed as
defective or flawed.
Some individuals with a major depressive episode ruminate about their
health and worry excessively about illness. A separate diagnosis of illness anxiety disorder is not
made if these concerns occur only during major depressive episodes. However, if excessive
illness worry persists after remission of an episode of major depressive disorder, the diagnosis of
illness anxiety disorder should be considered.
Individuals with illness anxiety disorder are not delusional and can
acknowledge the possibility that the feared disease is not present. Their ideas do not attain the
rigidity and intensity seen in the somatic delusions occurring in psychotic disorders (e.g.,
schizophrenia; delusional disorder, somatic type; major depressive disorder, with psychotic
features). True somatic delusions are generally more bizarre (e.g., that an organ is rotting or
dead) than the concerns seen in illness anxiety disorder. The concerns seen in illness anxiety
disorder, though not founded in reality, are plausible.
Comorbidity
Illness anxiety disorder co-occurs with anxiety disorders (in particular, generalized anxiety
disorder and panic disorder), OCD, and depressive disorders. Approximately two-thirds of
individuals with illness anxiety disorder are likely to have at least one other comorbid major
mental disorder. Individuals with illness anxiety disorder may have an elevated risk for
personality disorders.
Functional Neurological Symptom Disorder (Conversion
Disorder)
Diagnostic Criteria
A. One or more symptoms of altered voluntary motor or sensory function.
B. Clinical findings provide evidence of incompatibility between the symptom and
recognized neurological or medical conditions.
C. The symptom or deficit is not better explained by another medical or mental
disorder.
D. The symptom or deficit causes clinically significant distress or impairment in

social, occupational, or other important areas of functioning or warrants medical
evaluation.
Coding note: The ICD-10-CM code depends on the symptom type (see below).
Specify symptom type:
F44.4 With weakness or paralysis
F44.4 With abnormal movement (e.g., tremor, dystonia, myoclonus, gait
disorder)
F44.4 With swallowing symptoms
F44.4 With speech symptom (e.g., dysphonia, slurred speech)
F44.5 With attacks or seizures
F44.6 With anesthesia or sensory loss
F44.6 With special sensory symptom (e.g., visual, olfactory, or hearing
disturbance)
F44.7 With mixed symptoms
Specify if:
Acute episode: Symptoms present for less than 6 months.
Persistent: Symptoms occurring for 6 months or more.
Specify if:
With psychological stressor (specify stressor)
Without psychological stressor
Diagnostic Features
In functional neurological symptom disorder (conversion disorder), there may be one or more
neurological symptoms of various types. Motor symptoms include weakness or paralysis;
abnormal movements, such as tremor, jerks, or dystonic movements; and gait abnormalities.
Sensory symptoms include altered, reduced, or absent skin sensation, vision, or hearing.
Episodes of apparent unresponsiveness with or without limb movements may resemble epileptic
seizures, syncope, or coma (also called dissociative, psychogenic, or nonepileptic seizures or
attacks). Other symptoms include reduced or absent speech volume (dysphonia/aphonia); altered
speech articulation, prosody, or fluency; a sensation of a lump in the throat (globus); and
diplopia. This disorder has been called “conversion disorder” in prior editions of DSM as well as
in much of the psychiatric research literature. The term “conversion” originated in
psychoanalytic theory, which proposes that unconscious psychic conflict is “converted” into
physical symptoms.
The diagnosis rests on clinical findings that show clear evidence of incompatibility with
recognized neurological disease. These should usually be elicited and interpreted in the context
of the whole clinical picture by a health care professional with expertise in the diagnosis of

neurological conditions. The diagnosis is not one of exclusion and can be made in individuals
who also have neurological diseases like epilepsy or multiple sclerosis. The diagnosis should not
be made simply because results from investigations are normal or because the symptom is
“bizarre.” Internal inconsistency during examination is one way to demonstrate incompatibility
(i.e., demonstrating that physical signs elicited through one examination method are no longer
present when tested a different way). There are dozens of examples of such “positive”
examination findings. Examples of examination findings that indicate incompatibility with
recognized neurological disease include the following:
For functional limb weakness or paralysis: Hoover’s sign, in which weakness of hip extension returns to normal strength
with contralateral hip flexion against resistance; the hip abductor sign, in which weakness of thigh abduction returns to
normal with contralateral hip abduction against resistance; or a discrepancy between on-the-bed performance (e.g., weakness
of ankle plantar flexion) compared with another task (e.g., ability to walk on tiptoes).
For functional tremor: the tremor entrainment test, in which a tremor changes when the individual is distracted by copying
the examiner in making a rhythmical movement with the contralateral hand or foot. The test is positive when the tremor
“entrains” the rhythm of the unaffected hand or foot, the tremor is suppressed, or the individual cannot copy simple
rhythmical movements. Other features of functional limb tremor include variability in frequency or direction of the tremor.
For functional dystonia: individuals typically present with fixed inverted position of the ankle, a clenched fist, or unilateral
contraction of platysma, often with sudden onset.
For attacks resembling epileptic seizures or syncope (also called functional or dissociative [nonepileptic] seizures): features
suggestive of functional neurological symptom disorder include persistent eye closure sometimes with resistance to opening,
bilateral motor movements with preserved awareness, or a duration longer than 5 minutes. Clinical features usually need to
be combined and may be supported with a normal simultaneous ictal electroencephalogram (although this alone does not
exclude all forms of epilepsy or syncope.
For functional speech symptoms: internal inconsistencies in speech articulation and phonation.
For functional visual symptoms: a tubular visual field (i.e., tunnel vision) and tests that indicate internal inconsistency in
visual acuity, such as the “fogging test” (i.e., while the individual views the eye chart with both eyes open, the “good” eye is
subtly fogged so that any useful binocular vision must be a result of “bad” eye function).
It is important to note that the diagnosis of functional neurological symptom disorder should
be based on the overall clinical picture and not on a single clinical finding.
Associated Features
Several associated features can support the diagnosis of functional neurological symptom
disorder, although none are specific. There may be a history of other functional somatic
symptoms or disorders, especially involving pain and fatigue. Onset may be associated with
stress or trauma, either psychological or physical in nature. The potential etiological relevance of
this stress or trauma may be suggested by a close temporal relationship. However, while
assessment for stress and trauma is important, it may be absent in up to 50% of individuals, and
the diagnosis should not be withheld if none is found.
Functional neurological symptom disorder is often associated with dissociative symptoms,

Temperamental.
Environmental.
Genetic and physiological.
Course modifiers.
such as depersonalization, derealization, and dissociative amnesia, particularly at symptom onset
or during attacks.
The phenomenon of la belle indifférence (i.e., lack of concern about the nature or
implications of the symptom) has been associated with functional neurological symptom
disorder, but it is not specific and should not be used to make the diagnosis. Similarly, the
concept of secondary gain (i.e., when individuals derive external benefits such as money or
release from responsibilities) is also not specific to functional neurological symptom disorder.
Prevalence
Transient functional neurological symptoms are common, but the precise prevalence of the
disorder is unknown. Based on research in the United States and northern Europe, the incidence
of individual persistent functional neurological symptoms is estimated to be 4–12/100,000 per
year. Prevalence in specialty clinics appears to be higher, although data are limited. For example,
5% of outpatients ages 9–17 in a Japanese psychiatric clinic and 6% of adult and adolescent
admissions to an inpatient psychiatric hospital in Oman received a diagnosis consistent with
functional neurological symptom disorder. In neurology clinics, around 5%–15% of individuals
have a diagnosis of functional neurological symptom disorder in studies from Scotland and
Australia.
Development and Course
Onset has been reported throughout the life course. The mean onset of nonepileptic attacks peaks
at ages 20–29 years, and motor symptoms have their mean onset at ages 30–39 years. The
symptoms can be transient or persistent. The prognosis may be better in younger children than in
adolescents and adults.
Risk and Prognostic Factors
Maladaptive personality traits, especially emotional instability, are commonly
associated with functional neurological symptom disorder.
There may be a history of childhood abuse and neglect. Stressful life events
including physical injury are common but not universal triggering factors.
The presence of neurological disease that causes similar symptoms is a
risk factor (e.g., around one in five individuals with functional [nonepileptic] seizures also have
epilepsy).
Short duration of symptoms and agreement with the diagnosis are positive
prognostic factors. Maladaptive personality traits, the presence of comorbid physical disease, and
the receipt of disability benefits appear to be negative prognostic factors.
Culture-Related Diagnostic Issues
Episodes of unresponsiveness (including seizures) and motor symptoms are the most common
functional neurological symptoms across cultural contexts. High comorbidity between functional

Recognized neurological disease.
Somatic symptom disorder.
Factitious disorder and malingering.
neurological and dissociative symptoms is common cross-culturally, especially in individuals
with nonepileptic seizures. Changes resembling functional neurological (and dissociative)
symptoms are common in certain culturally sanctioned rituals. If the symptoms are fully
explained within the particular cultural context and do not result in clinically significant distress
or disability, then the diagnosis of functional neurological symptom disorder is not made.
Sex- and Gender-Related Diagnostic Issues
Functional neurological symptom disorder is two to three times more common in women for
most symptom presentations. One large clinical study found higher rates of cognitive impairment
and weakness in men and increased past sexual and physical trauma in women.
Association With Suicidal Thoughts or Behavior
Cohort studies of functional neurological symptom disorder mostly show higher rates of suicidal
thoughts and attempts. Individuals with functional symptoms in a neurology clinic have a higher
rate of suicidal thoughts than individuals with recognized neurological disease. A study in
Turkey of 100 consecutive psychiatric outpatients with functional neurological symptom
disorder found that a history of suicide attempt was associated with risky use of alcohol, a
history of childhood maltreatment, and greater severity of dissociative symptoms as compared
with those who did not attempt suicide.
Functional Consequences of Functional Neurological Symptom
Disorder
Individuals with functional neurological symptom disorder may have substantial physical
disability. The severity of disability can be similar to that experienced by individuals with
comparable recognized medical conditions.
Differential Diagnosis
The main differential diagnosis is recognized neurological
disease that might better explain the symptoms. After a thorough neurological assessment, an
unexpected neurological disease cause for the symptoms is rarely found at follow-up. However,
reassessment may be required if the symptoms appear to be progressive. Functional neurological
symptom disorder commonly coexists with recognized neurological disease and may be part of
the prodromal state of some progressive neurological diseases.
Functional neurological symptom disorder may be diagnosed in
addition to somatic symptom disorder. Most of the somatic symptoms
encountered in somatic symptom disorder cannot be demonstrated to be clearly incompatible
with recognized neurological or medical disease, whereas in functional neurological symptom
disorder, such incompatibility is required for the diagnosis.
Functional neurological symptom disorder describes genuinely
experienced symptoms that are not intentionally produced (i.e., not feigned). However, definite

Dissociative disorders.
Body dysmorphic disorder.
Depressive disorders.
Panic disorder.
F54
evidence of feigning (e.g., marked discrepancy between reported and observed activities of daily
living) would suggest malingering if the individual’s apparent aim is to obtain an obvious
external reward, or factitious disorder in the absence of such reward.
Dissociative symptoms are common in individuals with functional
neurological symptom disorder. If both functional neurological symptom disorder and a
dissociative disorder are present, both diagnoses should be made.
Individuals with body dysmorphic disorder are excessively concerned
about a perceived defect in their physical appearance but do not complain of symptoms of
sensory or motor functioning in the affected body part.
In depressive disorders, individuals may report general heaviness of their
limbs, whereas the weakness of functional neurological symptom disorder is more focal and
prominent. Depressive disorders are also differentiated by the presence of core depressive
symptoms.
Episodic neurological symptoms (e.g., tremor and paresthesia) can occur in both
functional neurological symptom disorder and panic attacks. In panic attacks, the neurological
symptoms are typically associated with characteristic cardiorespiratory symptoms and retained
awareness. Loss of awareness with amnesia for the attack occurs in functional seizures but not in
panic attacks.
Comorbidity
Anxiety disorders, especially panic disorder, and depressive disorders commonly co-occur with
functional neurological symptom disorder. Somatic symptom disorder may co-occur as well.
Personality disorders are more common in individuals with functional neurological symptom
disorder than in the general population. Neurological or other medical conditions commonly
coexist with functional neurological symptom disorder as well.
Psychological Factors Affecting Other Medical
Conditions
Diagnostic Criteria
A. A medical symptom or condition (other than a mental disorder) is present.
B. Psychological or behavioral factors adversely affect the medical condition in one
of the following ways:
1. The factors have influenced the course of the medical condition as shown by
a close temporal association between the psychological factors and the
development or exacerbation of, or delayed recovery from, the medical
condition.
2. The factors interfere with the treatment of the medical condition (e.g., poor
adherence).

3. The factors constitute additional well-established health risks for the
individual.
4. The factors influence the underlying pathophysiology, precipitating or
exacerbating symptoms or necessitating medical attention.
C. The psychological and behavioral factors in Criterion B are not better explained
by another mental disorder (e.g., panic disorder, major depressive disorder,
posttraumatic stress disorder).
Specify current severity:
Mild: Increases medical risk (e.g., inconsistent adherence with antihypertension
treatment).
Moderate: Aggravates underlying medical condition (e.g., anxiety aggravating
asthma).
Severe: Results in medical hospitalization or emergency room visit.
Extreme: Results in severe, life-threatening risk (e.g., ignoring heart attack
symptoms).
Diagnostic Features
The essential feature of psychological factors affecting other medical conditions is the presence
of one or more clinically significant psychological or behavioral factors that adversely affect a
medical condition by increasing the risk for suffering, death, or disability (Criterion B). These
factors can adversely affect the medical condition by influencing its course or treatment, by
constituting an additional well-established health risk factor, or by influencing the underlying
pathophysiology to precipitate or exacerbate symptoms or to necessitate medical attention.
Psychological or behavioral factors include psychological distress, patterns of interpersonal
interaction, coping styles, and maladaptive health behaviors, such as denial of symptoms or poor
adherence to medical recommendations. Common clinical examples are anxiety-exacerbating
asthma, denial of need for treatment for acute chest pain, and manipulation of insulin by an
individual with diabetes wishing to lose weight. Many different psychological factors have been
demonstrated to adversely influence medical conditions—for example, symptoms of depression
or anxiety, stressful life events, relationship style, personality traits, and coping styles. The
adverse effects can range from acute, with immediate medical consequences (e.g., Takotsubo
cardiomyopathy), to chronic, occurring over a long period of time (e.g., chronic occupational
stress increasing risk for hypertension). Affected medical conditions can be those with clear
pathophysiology (e.g., diabetes, cancer, coronary disease), functional syndromes (e.g., migraine,
irritable bowel syndrome, fibromyalgia), or idiopathic medical symptoms (e.g., pain, fatigue,
dizziness).
This diagnosis should be reserved for situations in which the effect of the psychological
factor on the medical condition is evident and the psychological factor has clinically significant
effects on the course or outcome of the medical condition. Abnormal psychological or behavioral

Mental disorder due to another medical condition.
symptoms that develop in response to a medical condition are more properly coded as an
adjustment disorder (a clinically significant psychological response to an identifiable stressor).
There must be reasonable evidence to suggest an association between the psychological factors
and the medical condition, although it may often not be possible to demonstrate direct causality
or the mechanisms underlying the relationship.
Prevalence
The prevalence of psychological factors affecting other medical conditions is unclear. In U.S.
private insurance billing data, it was a more common diagnosis than DSM-IV somatic symptom
disorders.
Development and Course
Psychological factors affecting other medical conditions can occur across the lifespan.
Particularly with young children, corroborative history from parents or school can assist the
diagnostic evaluation. Some conditions are characteristic of particular life stages (e.g., in older
individuals, the stress associated with acting as a caregiver for an ill spouse or partner).
Culture-Related Diagnostic Issues
Many differences between cultural contexts may influence psychological factors and their effects
on medical conditions, such as those in language and communication style, idioms of distress,
explanatory models of illness, patterns of seeking health care, service availability and
organization, doctor-patient relationships and other healing practices, family and gender roles,
and attitudes toward pain and death. Psychological factors affecting other medical conditions
must be differentiated from culturally specific coping behaviors such as accessing faith, spiritual,
or traditional healers or other variations in illness management that are acceptable within cultural
contexts and represent an attempt to help heal the medical condition. These local practices may
complement rather than obstruct evidence-based interventions. Use of alternative healing
practices may delay use of medical services and affect outcomes, but when the intent of the
healing practice is to address the problem in a culturally sanctioned way, these practices should
not be pathologized as psychological factors affecting other medical conditions.
Functional Consequences of Psychological Factors Affecting Other
Medical Conditions
Psychological and behavioral factors have been demonstrated to affect the course of many
medical diseases.
Differential Diagnosis
A temporal association between symptoms of a
mental disorder and those of a medical condition is also characteristic of a mental disorder due to
another medical condition, but the presumed causality is in the opposite direction. In a mental

Adjustment disorders.
Somatic symptom disorder.
Illness anxiety disorder.
disorder due to another medical condition, the medical condition is judged to be causing the
mental disorder through a direct physiological mechanism. In psychological factors affecting
other medical conditions, the psychological or behavioral factors are judged to affect the course
of the medical condition.
Abnormal psychological or behavioral symptoms that develop in response
to a medical condition are more properly coded as an adjustment disorder (a clinically significant
psychological response to an identifiable stressor). For example, an individual with angina that is
precipitated whenever he becomes enraged would be diagnosed as having psychological factors
affecting other medical conditions, whereas an individual with angina who developed
maladaptive anticipatory anxiety would be diagnosed as having an adjustment disorder with
anxiety. In clinical practice, however, psychological factors and a medical condition are often
mutually exacerbating (e.g., anxiety as both a precipitant and a consequence of angina), in which
case the distinction is arbitrary. Other mental disorders frequently result in medical
complications, most notably substance use disorders (e.g., alcohol use disorder, tobacco use
disorder). If an individual has a coexisting major mental disorder that adversely affects or causes
another medical condition, diagnoses of the mental disorder and the medical condition are
usually sufficient. Psychological factors affecting other medical conditions is diagnosed when
the psychological traits or behaviors do not meet criteria for a mental diagnosis.
Somatic symptom disorder is characterized by a combination of
distressing somatic symptoms and excessive or maladaptive thoughts, feelings, and behavior in
response to these symptoms or associated health concerns. The individual may or may not have a
diagnosable medical condition. In contrast, in psychological factors
affecting other medical conditions, the psychological factors adversely affect a medical
condition; the individual’s thoughts, feelings, and behavior are not necessarily excessive. The
difference is one of emphasis, rather than a clear-cut distinction. In psychological factors
affecting other medical conditions, the emphasis is on the exacerbation of the medical condition
(e.g., an individual with angina that is precipitated whenever he becomes anxious). In somatic
symptom disorder, the emphasis is on maladaptive thoughts, feelings, and behavior (e.g., an
individual with angina who worries constantly that she will have a heart attack, takes her blood
pressure multiple times per day, and restricts her activities).
Illness anxiety disorder is characterized by high illness anxiety that is
distressing and/or disruptive to daily life with minimal somatic symptoms. The focus of clinical
concern is the individual’s worry about having a disease; in most cases, no serious disease is
present. In psychological factors affecting other medical conditions, anxiety may be a relevant
psychological factor affecting a medical condition, but the clinical concern is the adverse effects
on the medical condition.
Comorbidity
By definition, the diagnosis of psychological factors affecting other medical conditions entails a
relevant psychological or behavioral syndrome or trait and a comorbid medical condition.

F68.10
F68.A
Factitious Disorder
Diagnostic Criteria
Factitious Disorder Imposed on Self
A. Falsification of physical or psychological signs or symptoms, or induction of
injury or disease, associated with identified deception.
B. The individual presents himself or herself to others as ill, impaired, or injured.
C. The deceptive behavior is evident even in the absence of obvious external
rewards.
D. The behavior is not better explained by another mental disorder, such as
delusional disorder or another psychotic disorder.
Specify:
Single episode
Recurrent episodes (two or more events of falsification of illness and/or
induction of injury)
Factitious Disorder Imposed on Another (Previously Factitious
Disorder by Proxy)
A. Falsification of physical or psychological signs or symptoms, or induction of
injury or disease, in another, associated with identified deception.
B. The individual presents another individual (victim) to others as ill, impaired, or
injured.
C. The deceptive behavior is evident even in the absence of obvious external
rewards.
D. The behavior is not better explained by another mental disorder, such as
delusional disorder or another psychotic disorder.
Note: The perpetrator, not the victim, receives this diagnosis.
Specify:
Single episode
Recurrent episodes (two or more events of falsification of illness and/or
induction of injury)
Recording Procedures
When an individual falsifies illness in another (e.g., children, adults, pets), the diagnosis is
factitious disorder imposed on another. The perpetrator, not the victim, is given the diagnosis.

The victim may be given an abuse diagnosis (e.g., T74.12X; see the chapter “Other Conditions
That May Be a Focus of Clinical Attention”). If an individual with factitious disorder imposed on
another has also deceptively represented his or her own illness or injury, both factitious disorder
imposed on self and on another can be diagnosed.
Diagnostic Features
The essential feature of factitious disorder is the falsification of medical or psychological signs
and symptoms in the individual or others that are associated with the identified deception.
Individuals with factitious disorder can also seek treatment for themselves or another following
induction of injury or disease. The diagnosis requires demonstrating that the individual is taking
surreptitious actions to misrepresent, simulate, or cause signs or symptoms of illness or injury
even in the absence of obvious external rewards. The diagnosis of factitious disorder emphasizes
the objective identification of falsification of signs and symptoms of illness and not the
individual motivations of the falsifier. Methods of illness falsification can include exaggeration,
fabrication, simulation, and induction. While a preexisting medical condition may be present, the
deceptive behavior or induction of injury associated with deception causes others to view such
individuals (or, in the case of factitious disorder imposed on another, the victim) as more ill or
impaired, and this can lead to excessive clinical intervention. Individuals with factitious disorder
might, for example, report feelings of depression and suicidal thoughts or behavior following the
death of a spouse despite the death not being true or the individual’s not having a spouse;
deceptively report episodes of neurological symptoms (e.g., seizures, dizziness, or blacking out);
manipulate a laboratory test (e.g., by adding blood to urine) to falsely indicate an abnormality;
falsify medical records to indicate an illness; ingest a substance (e.g., insulin or warfarin) to
induce an abnormal laboratory result or illness; or physically injure themselves or induce illness
in themselves or another (e.g., by injecting fecal material to produce an abscess or to induce
sepsis). Although individuals with factitious disorder most often present to health care
professionals for treatment of their factitious symptoms, some individuals with factitious
disorder choose to mislead community members in person or online about illness or injury
without necessarily engaging health care professionals.
Associated Features
Individuals with factitious disorder imposed on self or factitious disorder imposed on another are
at risk for experiencing great psychological distress or functional impairment by causing harm to
themselves and others. Family, friends, faith leaders, and health care professionals are also often
adversely affected by their behavior (e.g., devoted time, attention, and resources to provide
medical care and emotional support to the falsifier). Individuals with factitious disorder imposed
on another sometimes falsely allege the presence of educational deficits or disabilities in their
children for which they demand special attention, often at considerable inconvenience to
education professionals.
Whereas some aspects of factitious disorders might represent criminal behavior (e.g.,
factitious disorder imposed on another, in which the parent’s actions represent abuse and
maltreatment of a child), such criminal behavior and mental illness are not mutually exclusive.
Moreover, such behaviors, including the induction of injury or disease, are associated with
deception.

Deception to avoid legal liability.
Somatic symptom and related disorders.
Malingering.
Prevalence
The prevalence of factitious disorder is unknown, likely because of the role of deception in this
population. Further complicating efforts at determining prevalence is the fact that health care
professionals infrequently record the diagnosis, even in recognized cases.
Based on a study of general hospital inpatients in the United States referred for psychiatric
consultation, it is estimated that almost 1% have presentations that meet the criteria for factitious
disorder. Factitious disorder imposed on self or another appears to be encountered more
frequently in tertiary care settings than at primary care sites.
Development and Course
The course of factitious disorder is usually one of intermittent episodes. Single episodes and
episodes that are characterized as persistent and unremitting are both less common. Onset is
usually in early adulthood, often after hospitalization for a medical condition or a mental
disorder. When imposed on another, the disorder may begin after hospitalization of the
individual’s child or other dependent. In individuals with recurrent episodes of falsification of
signs and symptoms of illness and/or induction of injury, this pattern of successive deceptive
contact with medical personnel, including hospitalizations, may become lifelong.
Sex- and Gender-Related Diagnostic Issues
While the prevalence is not known, a pooled analysis of all case series and studies finds that twothirds of individuals with factitious disorder are women and one-third are men.
Differential Diagnosis
Caregivers who lie about abuse injuries in dependents solely to
protect themselves from liability are not diagnosed with factitious disorder imposed on another
because protection from liability is an external reward (Criterion C, the deceptive behavior is
evident even in the absence of obvious external rewards). Such caregivers who, upon
observation, analysis of medical records, and/or interviews with others, are found to lie more
extensively than needed for immediate self-protection are diagnosed with factitious disorder
imposed on another.
In somatic symptom disorder and the care-seeking type of
illness anxiety disorder, there may be excessive attention and treatment seeking for perceived
medical concerns, but there is no evidence that the individual is providing false information or
behaving deceptively.
Malingering is differentiated from factitious disorder by the intentional reporting of
symptoms for personal gain (e.g., money, time off work). In contrast, the diagnosis of factitious
disorder requires that the illness falsification is not fully accounted for by external rewards.
Factitious disorder and malingering are not mutually exclusive, however. The motives in any
single case might be multiple and shifting depending on the circumstances and reactions of
others.

Functional neurological symptom disorder (conversion disorder).
Borderline personality disorder.
Medical condition or mental disorder not associated with intentional symptom falsification.
Functional neurological symptom
disorder is characterized by neurological symptoms that are inconsistent with neurological
pathophysiology. Factitious disorder with neurological symptoms is distinguished from
functional neurological symptom disorder by evidence of deceptive falsification of symptoms.
Deliberate physical self-harm in the absence of suicidal intent can
also occur in association with other mental disorders such as borderline personality disorder.
Factitious disorder requires that the induction of injury occur in association with deception.
Presentation
of signs and symptoms of illness that do not conform to an identifiable medical condition or
mental disorder increases the likelihood of the presence of a factitious disorder. However, the
diagnosis of factitious disorder does not exclude the
presence of a true medical condition or mental disorder, as comorbid illness often occurs in the
individual along with factitious disorder. For example, individuals who might manipulate blood
sugar levels to produce symptoms may also have diabetes.
Other Specified Somatic Symptom and Related Disorder
F45.8
This category applies to presentations in which symptoms characteristic of a somatic
symptom and related disorder that cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning predominate but do
not meet the full criteria for any of the disorders in the somatic symptom and related
disorders diagnostic class.
Examples of presentations that can be specified using the “other specified”
designation include the following:
1. Brief somatic symptom disorder: Duration of symptoms is less than 6 months.
2. Brief illness anxiety disorder: Duration of symptoms is less than 6 months.
3. Illness anxiety disorder without excessive health-related behaviors or
maladaptive avoidance: Criterion D for illness anxiety disorder is not met.
4. Pseudocyesis: A false belief of being pregnant that is associated with objective
signs and reported symptoms of pregnancy.
Unspecified Somatic Symptom and Related Disorder
F45.9
This category applies to presentations in which symptoms characteristic of a somatic

symptom and related disorder that cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning predominate but do
not meet the full criteria for any of the disorders in the somatic symptom and related
disorders diagnostic class. The unspecified somatic symptom and related disorder
category should not be used unless there are decidedly unusual situations where
there is insufficient information to make a more specific diagnosis.

# 10 - Feeding and Eating Disorders

# Feeding and Eating Disorders

371

Feeding and Eating Disorders
Feeding and eating disorders are characterized by a persistent disturbance of
eating or eating-related behavior that results in the altered consumption or absorption of food and
that significantly impairs physical health or psychosocial functioning. Diagnostic criteria are
provided for pica, rumination disorder, avoidant/restrictive food intake disorder, anorexia
nervosa, bulimia nervosa, and binge-eating disorder.
The diagnostic criteria for anorexia nervosa, bulimia nervosa, and binge-eating disorder
result in a classification scheme that is mutually exclusive, so that during a single episode, only
one of these diagnoses can be assigned. The rationale for this approach is that, despite a number
of common psychological and behavioral features, the disorders differ substantially in clinical
course, outcome, and treatment needs.
Some individuals with disorders described in this chapter report eating-related symptoms
resembling those typically endorsed by individuals with substance use disorders, such as craving
and patterns of compulsive use. This resemblance may reflect the involvement of the same neural
systems, including those implicated in regulatory self-control and reward, in both groups of
disorders. However, the relative contributions of shared and distinct factors in the development
and perpetuation of eating and substance use disorders remain insufficiently understood.
Finally, obesity is not included in DSM-5 as a mental disorder. Obesity (excess body fat)
results from the long-term excess of energy intake relative to energy expenditure. A range of
genetic, physiological, behavioral, and environmental factors that vary across individuals
contributes to the development of obesity; thus, obesity is not considered a mental disorder.
However, there are robust associations between obesity and a number of mental disorders (e.g.,
binge-eating disorder, depressive and bipolar disorders, schizophrenia). The side effects of some
psychotropic medications contribute importantly to the development of obesity, and obesity may
be a risk factor for the development of some mental disorders (e.g., depressive disorders).
Pica
Diagnostic Criteria
A. Persistent eating of nonnutritive, nonfood substances over a period of at least 1
month.
B. The eating of nonnutritive, nonfood substances is inappropriate to the
developmental level of the individual.
C. The eating behavior is not part of a culturally supported or socially normative
practice.

D. If the eating behavior occurs in the context of another mental disorder (e.g.,
intellectual developmental disorder [intellectual disability], autism spectrum
disorder, schizophrenia) or medical condition (including pregnancy), it is
sufficiently severe to warrant additional clinical attention.
Coding note: The ICD-10-CM codes for pica are F98.3 in children and F50.89 in
adults.
Specify if:
In remission: After full criteria for pica were previously met, the criteria have not
been met for a sustained period of time.
Diagnostic Features
The essential feature of pica is the eating of one or more nonnutritive, nonfood substances on a
persistent basis over a period of at least 1 month (Criterion A) that is severe enough to warrant
clinical attention. Typical substances ingested tend to vary with age and availability and might
include paper, soap, cloth, hair, string, wool, soil, chalk, talcum powder, paint, gum, metal,
pebbles, charcoal or coal, ash, clay, starch, or ice. The term nonfood is included because the
diagnosis of pica does not apply to ingestion of diet products that have minimal nutritional
content. There is typically no aversion to food in general. The eating of nonnutritive, nonfood
substances must be developmentally inappropriate (Criterion B) and not part of a culturally
supported or socially normative practice (Criterion C). A minimum age of 2 years is suggested
for a pica diagnosis to exclude developmentally normal mouthing of objects by infants that
results in ingestion. The eating of nonnutritive, nonfood substances can be an associated feature
of other mental disorders (e.g., intellectual developmental disorder [intellectual disability],
autism spectrum disorder, schizophrenia). If the eating behavior occurs exclusively in the context
of another mental disorder, a separate diagnosis of pica should be made only if the eating
behavior is sufficiently severe to warrant additional clinical attention (Criterion D).
Associated Features
Although deficiencies in vitamins or minerals (e.g., zinc, iron) have been reported, often no
specific biological abnormalities are found. In some cases, pica comes to clinical attention only
following general medical complications (e.g., mechanical bowel problems; intestinal
obstruction, such as that resulting from a bezoar; intestinal perforation; infections such as
toxoplasmosis and toxocariasis as a result of ingesting feces or dirt; poisoning, such as by
ingestion of lead-based paint).
Prevalence
Limited data suggest that the prevalence of pica is approximately 5% among school-age children.
Roughly one-third of pregnant women, especially those with food insecurity (i.e., without
reliable access to affordable and nutritious food), engage in pica. Conditions associated with pica
include lack of available food and vitamin deficiency.

Environmental.
Development and Course
Onset of pica can occur in childhood, adolescence, or adulthood, although childhood onset is
most commonly reported. Pica can occur in otherwise normally developing children, whereas in
adults it appears more likely to occur in the context of intellectual developmental disorder or
other mental disorders. The course of the disorder can be protracted and can result in medical
emergencies (e.g., intestinal obstruction, acute weight loss, poisoning). The disorder can
potentially be fatal depending on substances ingested.
Risk and Prognostic Factors
Neglect, lack of supervision, and developmental delay can increase the risk for
this condition.
Culture-Related Diagnostic Issues
In some populations, the eating of earth or other seemingly nonnutritive substances is believed to
be of spiritual, medicinal, or other social value, or may be a culturally supported
or socially normative practice. Such behavior does not warrant a diagnosis of pica (Criterion C).
Pica behavior may be prevalent in some cultural groups, but it should not be assumed to be
socially normative without further evaluation.
Sex- and Gender-Related Diagnostic Issues
Pica occurs in both genders. The eating of nonnutritive, nonfood substances may manifest in
pregnancy, when specific cravings (e.g., chalk or ice) may occur. The diagnosis of pica during
pregnancy is appropriate only if such cravings lead to the ingestion of nonnutritive, nonfood
substances to the extent that the eating of these substances poses potential medical risks. A
worldwide meta-analysis showed the prevalence rate of pica to be 28% during pregnancy and/or
the postpartum period.
Diagnostic Markers
Abdominal flat plate radiography, ultrasound, and other scanning methods may reveal
obstructions related to pica. Blood tests and other laboratory tests can be used to ascertain levels
of poisoning or the nature of infection.
Functional Consequences of Pica
Pica can significantly impair physical functioning, but it is rarely the sole cause of impairment in
social functioning. Pica often occurs with other disorders associated with impaired social
functioning.
Differential Diagnosis
Eating of nonnutritive, nonfood substances may occur during the course of other mental

Anorexia nervosa.
Factitious disorder.
Nonsuicidal self-injury and nonsuicidal self-injury behaviors in personality disorders.
F98.21
disorders (e.g., autism spectrum disorder, schizophrenia) and in Kleine-Levin syndrome. In any
such instance, an additional diagnosis of pica should be given only if the eating behavior is
sufficiently persistent and severe to warrant additional clinical attention.
Pica can usually be distinguished from the other feeding and eating disorders
by the consumption of nonnutritive, nonfood substances. It is important to note, however, that
some presentations of anorexia nervosa include ingestion of nonnutritive, nonfood substances,
such as paper tissues, as a means of attempting to control appetite. In such cases, when the eating
of nonnutritive, nonfood substances is primarily used as a means of weight control, anorexia
nervosa should be the primary diagnosis.
Some individuals with factitious disorder may intentionally ingest foreign
objects as part of the pattern of falsification of physical symptoms. In such instances, there is an
element of deception that is consistent with deliberate induction of injury or disease.
Some 
individuals
may swallow potentially harmful items (e.g., pins, needles, knives) in the context of maladaptive
behavior patterns associated with personality disorders or nonsuicidal self-injury.
Comorbidity
Disorders most commonly comorbid with pica are autism spectrum disorder and intellectual
developmental disorder (intellectual disability) and, to a lesser degree, schizophrenia and
obsessive-compulsive disorder. Pica can be associated with trichotillomania (hair-pulling
disorder) and excoriation (skin-picking) disorder. In comorbid presentations, the hair or skin is
typically ingested. Pica can also be associated with avoidant/restrictive food intake disorder,
particularly in individuals with a strong sensory component to their presentation. When an
individual is known to have pica, assessment should include consideration of the possibility of
gastrointestinal complications, poisoning, infection, and nutritional deficiency.
Rumination Disorder
Diagnostic Criteria
A. Repeated regurgitation of food over a period of at least 1 month. Regurgitated
food may be re-chewed, re-swallowed, or spit out.
B. The repeated regurgitation is not attributable to an associated gastrointestinal or
other medical condition (e.g., gastroesophageal reflux, pyloric stenosis).
C. The eating disturbance does not occur exclusively during the course of anorexia
nervosa, bulimia nervosa, binge-eating disorder, or avoidant/restrictive food
intake disorder.
D. If the symptoms occur in the context of another mental disorder (e.g., intellectual
developmental disorder [intellectual disability] or another neurodevelopmental

disorder), they are sufficiently severe to warrant additional clinical attention.
Specify if:
In remission: After full criteria for rumination disorder were previously met, the
criteria have not been met for a sustained period of time.
Diagnostic Features
The essential feature of rumination disorder is the repeated regurgitation of food occurring after
feeding or eating over a period of at least 1 month (Criterion A). Previously swallowed food that
may be partially digested is brought up into the mouth without apparent nausea, involuntary
retching, or disgust. The food may be re-chewed and then ejected from the mouth or reswallowed. Regurgitation in rumination disorder should be frequent, occurring at least several
times per week, typically daily. The behavior is not better explained by an associated
gastrointestinal or other medical condition (e.g., gastroesophageal reflux, pyloric stenosis)
(Criterion B) and does not occur exclusively during the course of anorexia nervosa, bulimia
nervosa, binge-eating disorder, or avoidant/restrictive food intake disorder (Criterion C). If the
symptoms occur in the context of another mental disorder (e.g., intellectual developmental
disorder [intellectual disability]), they must be sufficiently severe to warrant additional clinical
attention (Criterion D) and should represent a primary aspect of the individual’s presentation
requiring intervention. The disorder may be diagnosed across the life span, particularly in
individuals who also have intellectual developmental disorder. Many individuals with rumination
disorder can be directly observed engaging in the behavior by the clinician. In other instances
diagnosis can be made on the basis of self-report or corroborative information from parents or
caregivers. Individuals may describe the behavior as habitual or outside of their control.
Associated Features
Infants with rumination disorder display a characteristic position of straining and arching the
back with the head held back, making sucking movements with their tongue. They may give the
impression of gaining satisfaction from the activity. They may be irritable and hungry between
episodes of regurgitation. Weight loss and failure to make expected weight gains are common
features in infants with rumination disorder. Malnutrition may occur despite the infant’s apparent
hunger and the ingestion of relatively large amounts of food, particularly in severe cases, when
regurgitation immediately follows each feeding episode and regurgitated food is expelled.
Malnutrition might also occur in older children and adults, particularly when the regurgitation is
accompanied by restriction of intake. Adolescents and adults may attempt to disguise the
regurgitation behavior by placing a hand over the mouth or coughing. Some will avoid eating
with others because of the acknowledged social undesirability of the
behavior. This may extend to an avoidance of eating prior to social situations, such as work or
school (e.g., avoiding breakfast because it may be followed by regurgitation).
Prevalence

Environmental.
Gastrointestinal conditions.
Anorexia nervosa and bulimia nervosa.
Although rumination disorder was historically described primarily among individuals with
intellectual disability, the limited European data available on prevalence suggest that the disorder
may occur in approximately 1%–2% of grade-school-age children.
Development and Course
Onset of rumination disorder can occur in infancy, childhood, adolescence, or adulthood. The
age at onset in infants is usually between ages 3 and 12 months. In infants, the disorder
frequently remits spontaneously, but its course can be protracted and can result in medical
emergencies (e.g., severe malnutrition). It can potentially be fatal, particularly in infancy.
Rumination disorder can have an episodic course or occur continuously until treated. In infants,
as well as in older individuals with intellectual developmental disorder or other
neurodevelopmental disorders, the regurgitation and rumination behavior appears to have a selfsoothing or self-stimulating function, similar to that of other repetitive motor behaviors such as
head banging.
Risk and Prognostic Factors
Psychosocial problems such as lack of stimulation, neglect, stressful life
situations, and problems in the parent-child relationship may be predisposing factors in infants
and young children.
Functional Consequences of Rumination Disorder
Malnutrition secondary to repeated regurgitation may be associated with growth delay and have
a negative effect on development and learning potential. Some older individuals with rumination
disorder deliberately restrict their food intake because of the social undesirability of
regurgitation. They may therefore present with weight loss or low weight. In older children,
adolescents, and adults, social functioning is more likely to be adversely affected.
Differential Diagnosis
It is important to differentiate regurgitation in rumination disorder
from other conditions characterized by gastroesophageal reflux or vomiting, such as
gastroparesis, pyloric stenosis, hiatal hernia, and Sandifer syndrome in infants. These other
medical conditions can usually be ruled out on the basis of history and clinical observation.
Individuals with anorexia nervosa and bulimia nervosa may
also engage in regurgitation with subsequent spitting out of food as a means of disposing of
ingested calories because of concerns about weight gain.
Comorbidity
Regurgitation with associated rumination can occur in the context of a concurrent medical
condition or another mental disorder (e.g., generalized anxiety disorder). When the regurgitation
occurs in this context, a diagnosis of rumination disorder is appropriate only when the severity of
the disturbance exceeds that routinely associated with such conditions or disorders and warrants
additional clinical attention.

F50.82
Avoidant/Restrictive Food Intake Disorder
Diagnostic Criteria
A. An eating or feeding disturbance (e.g., apparent lack of interest in eating or food;
avoidance based on the sensory characteristics of food; concern about aversive
consequences of eating) associated with one (or more) of the following:
1. Significant weight loss (or failure to achieve expected weight gain or faltering
growth in children).
2. Significant nutritional deficiency.
3. Dependence on enteral feeding or oral nutritional supplements.
4. Marked interference with psychosocial functioning.
B. The disturbance is not better explained by lack of available food or by an
associated culturally sanctioned practice.
C. The eating disturbance does not occur exclusively during the course of anorexia
nervosa or bulimia nervosa, and there is no evidence of a disturbance in the way
in which one’s body weight or shape is experienced.
D. The eating disturbance is not attributable to a concurrent medical condition or
not better explained by another mental disorder. When the eating disturbance
occurs in the context of another condition or disorder, the severity of the eating
disturbance exceeds that routinely associated with the condition or disorder and
warrants additional clinical attention.
Specify if:
In remission: After full criteria for avoidant/restrictive food intake disorder were
previously met, the criteria have not been met for a sustained period of time.
Diagnostic Features
Avoidant/restrictive food intake disorder replaces and extends the DSM-IV diagnosis of feeding
disorder of infancy or early childhood to include older children, adolescents, and adults. The
main diagnostic feature of avoidant/restrictive food intake disorder is avoidance or restriction of
food intake that is associated with one or more of the following consequences: significant weight
loss, significant nutritional deficiency (or related health impact), dependence on enteral feeding
or oral nutritional supplements, or marked interference with psychosocial functioning (Criterion
A).
In some individuals, food avoidance or restriction is based on the sensory characteristics of
qualities of food, such as extreme sensitivity to appearance, color, smell, texture, temperature, or
taste. Such behavior has been described as “restrictive eating,” “selective eating,” “choosy
eating,” “perseverant eating,” “chronic food refusal,” and “food neophobia” and may manifest as

refusal to eat particular brands of foods or to tolerate the smell of food being eaten by others.
Individuals with heightened sensory sensitivities associated with autism may show similar
behaviors.
In other individuals, food avoidance or restriction represents a conditioned negative response
associated with food intake following, or in anticipation of, an aversive experience, such as
choking; a traumatic procedure, usually involving the gastrointestinal tract (e.g.,
esophagoscopy); or repeated vomiting. The terms functional dysphagia and globus hystericus
have also been used for such conditions.
In yet other individuals, food avoidance or restriction manifests as a lack of interest in eating
or food.
The determination of whether weight loss is significant (Criterion A1) is a clinical judgment;
instead of losing weight, children and adolescents who have not completed growth may not
maintain weight or height increases along their developmental trajectory.
Determination of significant nutritional deficiency (Criterion A2) is also based on clinical
assessment (e.g., assessment of dietary intake, physical examination, and laboratory testing), and
related impact on physical health can be of a similar severity to that seen in anorexia nervosa
(e.g., hypothermia, bradycardia, anemia). In severe cases, particularly in infants, malnutrition can
be life-threatening. “Dependence” on enteral feeding or oral nutritional supplements (Criterion
A3) means that supplementary feeding is required to sustain adequate intake. Examples of
individuals requiring supplementary feeding include infants with failure to thrive who require
nasogastric tube feeding, children with neurodevelopmental disorders who are dependent on
nutritionally complete supplements, and individuals who rely on gastrostomy tube feeding or
complete oral nutrition supplements in the absence of an underlying medical condition. Inability
to participate in normal social activities, such as eating with others, attending school or work, or
sustaining relationships as a result of the disturbance would indicate marked interference with
psychosocial functioning (Criterion A4). Substantial disruption of family functioning (e.g.,
marked restriction of foods permitted in the home, inordinate accommodations to provide foods
from specific grocery stores or restaurants) may also satisfy Criterion A4.
Avoidant/restrictive food intake disorder does not include avoidance or restriction of food
intake related to lack of availability of food (e.g., food insecurity) or to cultural practices (e.g.,
religious fasting or normal dieting) (Criterion B). The disturbance is not better explained by
excessive concern about body weight or shape (Criterion C) or by concurrent medical factors or
mental disorders (Criterion D).
Associated Features
Several features may be associated with food avoidance or reduced food intake, and these
features may differ across ages. Very young infants may present with food refusal, gagging, or
vomiting. Infants and young children may not engage with a primary caregiver during feeding or
communicate hunger in favor of other activities. In older children and adolescents, food
avoidance or restriction may be associated with more generalized emotional difficulties that do
not meet diagnostic criteria for an anxiety, depressive, or bipolar disorder, sometimes called

Temperamental.
Environmental.
“food avoidance emotional disorder.”
Prevalence
Little information is available on the prevalence of avoidant/restrictive food intake disorder. A
study in Australia reported a frequency of 0.3% among individuals age 15 years or older.
Development and Course
Food avoidance or restriction associated with insufficient intake or lack of interest in eating most
commonly develops in infancy or early childhood and may persist in adulthood. Likewise,
avoidance based on sensory characteristics of food tends to arise in the first decade of life but
may persist into adulthood. Avoidance related to aversive consequences can arise at any age. The
scant literature regarding long-term outcomes suggests that food avoidance or restriction based
on sensory aspects is relatively stable and long-standing, but when persisting into adulthood,
such avoidance/restriction can be associated with relatively normal functioning. There is
currently insufficient evidence directly linking avoidant/restrictive food intake disorder and
subsequent onset of an eating disorder.
Infants with avoidant/restrictive food intake disorder may be irritable and difficult to console
during feeding, or may appear apathetic and withdrawn. In some instances, caregiver-child
interaction may contribute to the infant’s feeding problem (e.g., presenting food inappropriately,
or interpreting the infant’s behavior as an act of aggression or rejection). Inadequate nutritional
intake may exacerbate the associated features (e.g., irritability, developmental lags) and further
contribute to feeding difficulties. Associated factors
include infant temperament or developmental impairments that reduce an infant’s
responsiveness to feeding. Coexisting parental psychopathology, or child abuse or neglect, is
suggested if feeding and weight improve in response to changing caregivers. In infants, children,
and prepubertal adolescents, avoidant/restrictive food intake disorder may be associated with
growth delay, and the resulting malnutrition negatively affects development and learning
potential. In older children, adolescents, and adults, social functioning tends to be adversely
affected. Regardless of the age, family function may be affected, with heightened stress at
mealtimes and in other feeding or eating contexts involving friends and relatives.
Avoidant/restrictive food intake disorder manifests more commonly in children and
adolescents than in adults, and there may be a long delay between onset and clinical presentation.
Triggers for presentation vary considerably and include physical, social, and emotional
difficulties.
Risk and Prognostic Factors
Anxiety disorders, autism spectrum disorder, obsessive-compulsive disorder, and
attention-deficit/hyperactivity disorder may increase risk for avoidant or restrictive feeding or
eating behavior characteristic of the disorder.
Environmental risk factors for avoidant/restrictive food intake disorder include
familial anxiety. Higher rates of feeding disturbances may occur in children of mothers with

Genetic and physiological.
Other medical conditions (e.g., gastrointestinal disease, food allergies and intolerances, occult
malignancies).
Obsessive-compulsive and related disorder due to pediatric acute-onset neuropsychiatric
eating disorders.
History of gastrointestinal conditions, gastroesophageal reflux disease,
vomiting, and a range of other medical problems has been associated with feeding and eating
behaviors characteristic of avoidant/restrictive food intake disorder.
Culture-Related Diagnostic Issues
Presentations similar to avoidant/restrictive food intake disorder occur in various populations,
including in the United States, Canada, Australia, Europe, Japan, and China. Avoidant/restrictive
food intake disorder should not be diagnosed when avoidance of food intake is solely related to
specific religious or cultural practices.
Sex- and Gender-Related Diagnostic Issues
Avoidant/restrictive food intake disorder appears to be approximately equally common in boys
and girls, but avoidant/restrictive food intake disorder comorbid with autism spectrum disorder
has a male predominance. Food avoidance or restriction related to altered sensory sensitivities
can occur in some physiological conditions, most notably pregnancy, but is not usually extreme
and does not meet full criteria for the disorder.
Functional Consequences of Avoidant/Restrictive Food Intake Disorder
Associated developmental and functional limitations include impairment of physical
development and social difficulties that can have a significant negative impact on family
function.
Differential Diagnosis
Restriction of food intake is a nonspecific symptom that can accompany a number of mental
disorders and medical conditions and that can also be developmentally appropriate.
Avoidant/restrictive food intake disorder can be diagnosed concurrently with the disorders below
if all criteria are met, and the eating disturbance requires specific clinical attention.
Restriction of food intake may occur in other medical conditions, especially those with ongoing
symptoms such as vomiting, loss of appetite, nausea, abdominal pain, or diarrhea. A diagnosis of
avoidant/restrictive food intake disorder requires that the disturbance of intake is beyond that
directly accounted for by physical symptoms consistent with a medical condition; the eating
disturbance may also persist after being triggered by a medical condition and following
resolution of the medical condition.
Underlying medical or comorbid mental conditions may complicate feeding and eating.
Because older individuals, postsurgical patients, and individuals receiving chemotherapy often
lose their appetite, an additional diagnosis of avoidant/restrictive food intake disorder requires
that the eating disturbance is a primary focus for intervention.

syndrome.
Specific neurological/neuromuscular, structural, or congenital disorders and conditions
associated with feeding difficulties.
Reactive attachment disorder.
Autism spectrum disorder.
Specific phobia, social anxiety disorder, and other anxiety disorders.
Anorexia nervosa.
Acute-onset symptoms, late age at onset, or atypical symptoms suggest the need for a thorough
assessment to rule out the diagnosis of obsessive-compulsive and related disorder due to
pediatric acute-onset neuropsychiatric syndrome (PANS). PANS is characterized by abrupt,
dramatic onset of obsessive-compulsive symptoms or severely restricted food intake, together
with a range of additional neuropsychiatric symptoms.
Feeding difficulties are common in a number of congenital and neurological conditions often
related to problems with oral/esophageal/pharyngeal structure and function, such as hypotonia of
musculature, tongue protrusion, and unsafe swallowing. Avoidant/restrictive food intake disorder
can be diagnosed in individuals with such presentations as long as all diagnostic criteria are met.
Some degree of withdrawal from caregivers is characteristic of
reactive attachment disorder and can lead to a disturbance in the caregiver-child relationship that
can affect feeding and the child’s intake. Avoidant/restrictive food intake disorder should be
diagnosed concurrently only if all criteria are met for both disorders and the feeding disturbance
is a primary focus for intervention.
Individuals with autism spectrum disorder often present with rigid
eating behaviors and heightened sensory sensitivities. However, these features do not always
result in the level of impairment that would be required for a diagnosis of avoidant/restrictive
food intake disorder. Avoidant/restrictive food intake disorder should be diagnosed concurrently
only if all criteria are met for both disorders and when the eating disturbance requires specific
treatment.
Specific 
phobia, 
other 
type,
includes as an example “situations that may lead to choking or vomiting” and can represent the
primary trigger for the fear, anxiety, or avoidance required for diagnosis. Distinguishing specific
phobia from avoidant/restrictive food intake disorder can be difficult when a fear of choking or
vomiting has resulted in food avoidance. Although avoidance or restriction of food intake
secondary to a pronounced fear of choking or vomiting can be conceptualized as specific phobia,
in situations when the eating problem becomes the primary focus of clinical attention,
avoidant/restrictive food intake disorder becomes the appropriate diagnosis. In social anxiety
disorder, the individual may present with a fear of being observed by others while eating, which
can also occur in avoidant/restrictive food intake disorder.
Restriction of energy intake relative to requirements leading to significantly
low body weight is a core feature of anorexia nervosa. However, individuals with anorexia
nervosa also display a fear of gaining weight or of becoming fat, or persistent behavior that
interferes with weight gain, as well as specific disturbances in
relation to perception and experience of their own body weight and shape. These features are not
present in avoidant/restrictive food intake disorder, and the two disorders should not be
diagnosed concurrently. Differential diagnosis between avoidant/restrictive food intake disorder
and anorexia nervosa may be difficult, especially in late childhood and early adolescence,
because these disorders may share a number of common symptoms (e.g., food avoidance, low

Obsessive-compulsive disorder.
Major depressive disorder.
Schizophrenia spectrum disorders.
Factitious disorder or factitious disorder imposed on another.
Developmentally normal behavior.
weight). Differential diagnosis is also potentially difficult in individuals with anorexia nervosa
who deny any fear of fatness but nonetheless engage in persistent behaviors that prevent weight
gain and who do not recognize the medical seriousness of their low weight—a presentation
sometimes termed “non–fat phobic anorexia nervosa.” Full consideration of symptoms, course,
and family history is advised, and diagnosis may be best made in the context of a clinical
relationship over time. In some individuals, avoidant/restrictive food intake disorder might
precede the onset of anorexia nervosa.
Individuals with obsessive-compulsive disorder may present with
avoidance or restriction of intake in relation to preoccupations with food or ritualized eating
behavior. Avoidant/restrictive food intake disorder should be diagnosed concurrently only if all
criteria are met for both disorders and when the aberrant eating is a major aspect of the clinical
presentation requiring specific intervention.
In major depressive disorder, appetite might be affected to such an
extent that individuals present with significantly restricted food intake, usually in relation to
overall energy intake and often associated with weight loss. Usually appetite loss and related
reduction of intake abate with resolution of mood problems. Avoidant/restrictive food intake
disorder should only be used concurrently if full criteria are met for both disorders and when the
eating disturbance requires specific treatment.
Individuals with schizophrenia, delusional disorder, or other
psychotic disorders may exhibit odd eating behaviors, avoidance of specific foods because of
delusional beliefs, or other manifestations of avoidant or restrictive intake. In some cases,
delusional beliefs may contribute to a concern about negative consequences of ingesting certain
foods. Avoidant/restrictive food intake disorder should be used concurrently only if all criteria
are met for both disorders and when the eating disturbance requires specific treatment.
Avoidant/restrictive 
food 
intake
disorder should be differentiated from factitious disorder or factitious disorder imposed on
another. In order to assume the sick role, some individuals with factitious disorder may
intentionally describe diets that are much more restrictive than those they are actually able to
consume, as well as complications of such behavior, such as a need for enteral feedings or
nutritional supplements, an inability to tolerate a normal range of foods, and/or an inability to
participate normally in age-appropriate situations involving food. The presentation may be
impressively dramatic and engaging, and the symptoms reported inconsistently. In factitious
disorder 
imposed 
on 
another, 
the 
caregiver 
describes 
symptoms 
consistent 
with
avoidant/restrictive food intake disorder and may induce physical symptoms such as failure to
gain weight. As with any diagnosis of factitious disorder imposed on another, the caregiver
receives the diagnosis rather than the affected individual, and diagnosis should be made only on
the basis of a careful, comprehensive assessment of the affected individual, the caregiver, and
their interaction.
During normal development, some toddlers and children
transiently narrow the variety of foods they are willing to eat. This phenomenon, sometimes
referred to as “picky eating,” usually resolves spontaneously without intervention.
Avoidant/restrictive food intake disorder does not include such developmentally normal
behaviors unless they become sufficiently severe to lead to failure to meet appropriate nutritional

needs or produce significant impairment in functioning (Criterion A).
Comorbidity
The most commonly observed disorders comorbid with avoidant/restrictive food intake disorder
are anxiety disorders, obsessive-compulsive disorder, and neurodevelopmental disorders
(specifically autism spectrum disorder, attention-deficit/hyperactivity disorder, and intellectual
developmental disorder [intellectual disability]).
Anorexia Nervosa
Diagnostic Criteria
A. Restriction of energy intake relative to requirements, leading to a significantly low
body weight in the context of age, sex, developmental trajectory, and physical
health. Significantly low weight is defined as a weight that is less than minimally
normal or, for children and adolescents, less than that minimally expected.
B. Intense fear of gaining weight or of becoming fat, or persistent behavior that
interferes with weight gain, even though at a significantly low weight.
C. Disturbance in the way in which one’s body weight or shape is experienced,
undue influence of body weight or shape on self-evaluation, or persistent lack of
recognition of the seriousness of the current low body weight.
Coding note: The ICD-10-CM code depends on the subtype (see below).
Specify whether:
F50.01 Restricting type: During the last 3 months, the individual has not
engaged in recurrent episodes of binge-eating or purging behavior (i.e., selfinduced vomiting or the misuse of laxatives, diuretics, or enemas). This subtype
describes presentations in which weight loss is accomplished primarily through
dieting, fasting, and/or excessive exercise.
F50.02 Binge-eating/purging type: During the last 3 months, the individual has
engaged in recurrent episodes of binge-eating or purging behavior (i.e., selfinduced vomiting or the misuse of laxatives, diuretics, or enemas).
Specify if:
In partial remission: After full criteria for anorexia nervosa were previously met,
Criterion A (low body weight) has not been met for a sustained period, but either
Criterion B (intense fear of gaining weight or becoming fat or behavior that
interferes with weight gain) or Criterion C (disturbances in self-perception of
weight and shape) is still met.
In full remission: After full criteria for anorexia nervosa were previously met,
none of the criteria have been met for a sustained period of time.

Specify current severity:
The minimum level of severity is based, for adults, on current body mass index (BMI)
(see below) or, for children and adolescents, on BMI percentile. The ranges below
are derived from World Health Organization categories for thinness in adults; for
children and adolescents, corresponding BMI percentiles should be used. The level
of severity may be increased to reflect clinical symptoms, the degree of functional
disability, and the need for supervision.
Mild: BMI ≥ 17 kg/m2.
Moderate: BMI 16–16.99 kg/m2.
Severe: BMI 15–15.99 kg/m2.
Extreme: BMI < 15 kg/m2.
Subtypes
Most individuals with the binge-eating/purging type of anorexia nervosa who binge eat also
purge through self-induced vomiting or the misuse of laxatives, diuretics, or enemas. Some
individuals with this subtype of anorexia nervosa do not binge eat but do regularly purge after
the consumption of small amounts of food.
Crossover between the subtypes over the course of the disorder is not uncommon; therefore,
subtype description should be used to describe current symptoms rather than longitudinal course.
Diagnostic Features
There are three essential features of anorexia nervosa: persistent energy intake restriction; intense
fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain;
and a disturbance in self-perceived weight or shape. The individual maintains a body weight that
is below a minimally normal level for age, sex, developmental trajectory, and physical health
(Criterion A). Individuals’ body weights frequently meet this criterion following a significant
weight loss, but among children and adolescents, there may alternatively be failure to make
expected weight gain or to maintain a normal developmental trajectory (i.e., while growing in
height) instead of weight loss.
Criterion A requires that the individual’s weight be significantly low (i.e., less than
minimally normal or, for children and adolescents, less than that minimally expected). Weight
assessment can be challenging because normal weight range differs among individuals, and
different thresholds have been published defining thinness or underweight status. Body mass
index (BMI; calculated as weight in kilograms/height in meters2) is a useful measure to assess
body weight for height. For adults, a BMI of 18.5 kg/m2 has been employed by the Centers for
Disease Control and Prevention (CDC) and the World Health Organization (WHO) as the lower
limit of normal body weight. Therefore, most adults with a BMI greater than or equal to 18.5
kg/m2 would not be considered to have a significantly low body weight. On the other hand, a
BMI of lower than 17.0 kg/m2 has been considered by the WHO to indicate moderate or severe
thinness; therefore, an individual with a BMI less than 17.0 kg/m2 would likely be considered to

have a significantly low weight. An adult with a BMI between 17.0 and 18.5 kg/m2, or even
slightly above 18.5 kg/m2, might be considered to have a significantly low weight if clinical
history or other physiological information supports this judgment. Adults who are not
underweight by population-based standards—for example, adults with BMIs of 19.0 kg/m2 or
greater—should not be assigned a diagnosis of anorexia nervosa; a diagnosis of other specified
feeding or eating disorder (atypical anorexia nervosa) may be considered for such individuals.
For children and adolescents, determining a BMI-for-age percentile is useful (see, e.g., the
CDC 
BMI 
percentile 
calculator 
for 
children 
and 
teenagers;
https://www.cdc.gov/healthyweight/bmi/calculator.html). As for adults, it is not possible to
provide definitive standards for judging whether a child’s or an adolescent’s weight is
significantly low, and variations in developmental trajectories among youth limit the utility of
simple numerical guidelines. The CDC has used a BMI-for-age below the 5th percentile as
suggesting underweight; children and adolescents with a BMI above this benchmark may be
judged to be significantly underweight in light of failure to maintain their expected growth
trajectory. However, such individuals whose BMI nonetheless remains greater than the median
BMI for age should not be assigned a diagnosis of anorexia nervosa; a diagnosis of other
specified feeding or eating disorder (atypical anorexia nervosa) may be considered for such
individuals.
Individuals with this disorder typically display an intense fear of gaining weight or of
becoming fat (Criterion B). This intense fear of becoming fat is usually not alleviated by weight
loss. In fact, concern about weight gain may increase even as weight falls. Younger individuals
with anorexia nervosa, as well as some adults, may not recognize or
acknowledge a fear of weight gain. In the absence of another explanation for the significantly
low weight, clinician inference drawn from collateral history, observational data, physical and
laboratory findings, or longitudinal course either indicating a fear of weight gain or supporting
persistent behaviors that prevent it may be used to establish Criterion B.
The experience and significance of body weight and shape are distorted in these individuals
(Criterion C). Some individuals feel globally overweight. Others realize that they are thin but are
still concerned that certain body parts, particularly the abdomen, buttocks, and thighs, are “too
fat.” They may employ a variety of techniques to evaluate their body size or weight, including
frequent weighing, obsessive measuring of body parts, and persistent use of a mirror to check for
perceived areas of “fat.” The self-esteem of individuals with anorexia nervosa is highly
dependent on their perceptions of body shape and weight. Weight loss is often viewed as an
impressive achievement and a sign of extraordinary self-discipline, whereas weight gain is
perceived as an unacceptable failure of self-control. Although some individuals with this
disorder may acknowledge being thin, they often do not recognize the serious medical
implications of their malnourished state.
Often, the individual is brought to professional attention by family members after marked
weight loss (or failure to make expected weight gains) has occurred. If individuals seek help on
their own, it is usually because of distress over the somatic and psychological sequelae of
starvation. It is rare for an individual with anorexia nervosa to complain of weight loss per se. In
fact, individuals with anorexia nervosa frequently either lack insight into or deny the problem. It

is therefore often important to obtain information from family members or other sources to
evaluate the history of weight loss and other features of the illness.
Associated Features
The semistarvation of anorexia nervosa, and the purging behaviors sometimes associated with it,
can result in significant and potentially life-threatening medical conditions. The nutritional
compromise associated with this disorder affects most major organ systems and can produce a
variety of disturbances. Physiological disturbances, including amenorrhea and vital sign
abnormalities, are common. While most of the physiological disturbances associated with
malnutrition are reversible with nutritional rehabilitation, some, including loss of bone mineral
density, are often not completely reversible. Behaviors such as self-induced vomiting and misuse
of laxatives, diuretics, and enemas may cause a number of disturbances that lead to abnormal
laboratory findings; however, some individuals with anorexia nervosa exhibit no laboratory
abnormalities.
When seriously underweight, many individuals with anorexia nervosa have depressive signs
and symptoms such as depressed mood, social withdrawal, irritability, insomnia, and diminished
interest in sex. Because these features are also observed in individuals without anorexia nervosa
who are significantly undernourished, many of the depressive features may be secondary to the
physiological sequelae of semistarvation, although they may also be sufficiently severe to
warrant an additional diagnosis of major depressive disorder.
Obsessive-compulsive features, both related and unrelated to food, are often prominent. Most
individuals with anorexia nervosa are preoccupied with thoughts of food. Some collect recipes or
hoard food. Observations of behaviors associated with other forms of starvation suggest that
obsessions and compulsions related to food may be exacerbated by undernutrition. When
individuals with anorexia nervosa exhibit obsessions and compulsions that are not related to
food, body shape, or weight, an additional diagnosis of obsessive-compulsive disorder (OCD)
may be warranted.
Other features sometimes associated with anorexia nervosa include concerns about eating in
public, feelings of ineffectiveness, a strong desire to control one’s environment, inflexible
thinking, limited social spontaneity, and overly restrained emotional expression.
Compared with individuals with anorexia nervosa, restricting type, those with bingeeating/purging type have higher rates of impulsivity and are more likely to abuse alcohol and
other drugs.
Some individuals with anorexia nervosa show excessive levels of physical activity. Increases
in physical activity often precede onset of the disorder, and over the course of the disorder
increased activity accelerates weight loss. During treatment, excessive activity may be difficult
to control, thereby jeopardizing weight recovery.
Individuals with anorexia nervosa may misuse medications, such as by manipulating dosage,
in order to achieve weight loss or avoid weight gain. Individuals with diabetes mellitus may omit
or reduce insulin doses in order to minimize carbohydrate utilization.

Temperamental.
Environmental.
Prevalence
According to two U.S. epidemiological studies conducted in community samples, the 12-month
prevalence of anorexia nervosa ranges from 0.0% to 0.05% with much higher rates in women
than in men (0% to 0.08% in women; 0% to 0.01% in men), and the lifetime prevalence ranges
from 0.60% to 0.80% (0.9% to 1.42% in women; 0.12% to 0.3% in men). By contrast, one study
of adolescents found similar rates in both genders.
Anorexia nervosa appears to be most prevalent in postindustrialized, high-income countries
such as in the United States, many European countries, Australia, New Zealand, and Japan.
Although the prevalence of anorexia nervosa is uncertain in most low- and middle-income
countries, it appears to be increasing in many countries in the Global South, including in Asia
and the Middle East. Anorexia nervosa occurs across U.S. ethnoracial groups; however, its
prevalence seems to be lower among Latinx and non-Latinx Black Americans than among nonLatinx Whites.
Development and Course
Anorexia nervosa commonly begins during adolescence or young adulthood. It rarely begins
before puberty or after age 40, but cases of both early and late onset have been described. The
onset of this disorder is often associated with a stressful life event, such as leaving home for
college. The course and outcome of anorexia nervosa are highly variable. Younger individuals
may manifest atypical features, including denying “fear of fat.” Older individuals more likely
have a longer duration of illness, and their clinical presentation may include more signs and
symptoms of long-standing disorder. Clinicians should not exclude anorexia nervosa from the
differential diagnosis solely on the basis of older age.
Many individuals have a period of changed eating behavior prior to full criteria for the
disorder being met. Some individuals with anorexia nervosa recover fully after a single episode,
with some exhibiting a fluctuating pattern of weight gain followed by relapse, and others
experiencing a chronic course over many years. Hospitalization may be required to restore
weight and to address medical complications. Most individuals with anorexia nervosa experience
remission within 5 years of presentation. Among individuals admitted to hospitals, overall
remission rates may be lower. The crude mortality rate for anorexia nervosa is approximately 5%
per decade. Death most commonly results from medical complications associated with the
disorder itself or from suicide.
Risk and Prognostic Factors
Individuals who develop anxiety disorders or display obsessional traits in
childhood are at increased risk for developing anorexia nervosa.
Historical and cross-cultural variability in the prevalence of anorexia nervosa
supports its association with cultures and settings in which thinness is valued. Occupations and
avocations that encourage thinness, such as modeling and elite athletics, are also associated with
increased risk.

Genetic and physiological.
Hematology.
Serum chemistry.
Endocrine.
Electrocardiography.
Bone mass.
Electroencephalography.
Resting energy expenditure.
There is an increased risk for anorexia nervosa and for other eating and
psychiatric disorders among biological relatives of individuals with anorexia nervosa. Genomewide association studies have begun to identify specific risk loci, including loci associated with
other psychiatric disorders and with metabolic traits such as insulin resistance and lipid profile.
A range of brain abnormalities, many suggesting abnormal processing of reward, has been
described in anorexia nervosa using functional imaging technologies such as functional magnetic
resonance imaging and positron emission tomography. The degree to which these findings reflect
changes associated with malnutrition versus primary abnormalities associated with the disorder
is unclear.
Culture-Related Diagnostic Issues
Anorexia nervosa occurs across culturally and socially diverse populations, although available
evidence suggests cross-cultural variation in its occurrence and presentation. The presentation of
weight concerns among individuals with feeding and eating disorders varies substantially across
cultural contexts. The absence of an expressed intense fear of weight gain, sometimes referred to
as “fat phobia,” appears to be relatively more common in populations in Asia, where the
rationale for dietary restriction is commonly related to a more culturally sanctioned complaint
such as gastrointestinal discomfort. Mental health service utilization in the United States among
individuals with an eating disorder is significantly lower among underserved ethnic and
racialized groups.
Diagnostic Markers
The following laboratory abnormalities may be observed in anorexia nervosa; their presence may
serve to increase diagnostic confidence.
Leukopenia is common, with the loss of all cell types but usually with apparent
lymphocytosis. Mild anemia can occur, as well as thrombocytopenia and, rarely, bleeding
problems.
Dehydration may be reflected by an elevated blood urea nitrogen level.
Hypercholesterolemia is common. Hepatic enzyme levels may be elevated. Hypomagnesemia,
hypozincemia, hypophosphatemia, and hyperamylasemia are occasionally observed. Selfinduced vomiting may lead to metabolic alkalosis (elevated serum bicarbonate), hypochloremia,
and hypokalemia; laxative abuse may cause a mild metabolic acidosis.
Serum thyroxine (T4) levels are usually in the low-normal range; triiodothyronine
(T3) levels are decreased, while reverse T3 levels are elevated. Females have low serum estrogen
levels, whereas males have low levels of serum testosterone.
Sinus bradycardia is common, and, rarely, arrhythmias are noted. Significant
prolongation of the QTc interval is observed in some individuals.
Low bone mineral density, with specific areas of osteopenia or osteoporosis, is often
seen. The risk of fracture is significantly elevated.
Diffuse abnormalities, reflecting a metabolic encephalopathy, may result
from significant fluid and electrolyte disturbances.
There is often a significant reduction in resting energy expenditure.

Physical signs and symptoms.
Medical conditions (e.g., gastrointestinal disease, hyperthyroidism, occult malignancies, and
acquired immunodeficiency syndrome [AIDS]).
Many of the physical signs and symptoms of anorexia nervosa are
attributable to starvation. Amenorrhea is commonly present and appears to be an indicator of
physiological dysfunction. If present, amenorrhea is usually a consequence of the weight loss,
but in a minority of individuals it may actually precede the weight loss. In prepubertal females,
menarche may be delayed. In addition to amenorrhea, there may be complaints of constipation,
abdominal pain, cold intolerance, lethargy, and excess energy.
The most remarkable finding on physical examination is emaciation. Commonly, there is also
significant hypotension, hypothermia, and bradycardia. Some individuals develop lanugo, a fine
downy body hair. Some develop peripheral edema, especially during weight restoration or upon
cessation of laxative and diuretic abuse. Rarely, petechiae or ecchymoses, usually on the
extremities, may indicate a bleeding diathesis. Some individuals evidence a yellowing of the skin
associated with hypercarotenemia. As may be seen in individuals with bulimia nervosa,
individuals with anorexia nervosa who self-induce vomiting may have hypertrophy of the
salivary glands, particularly the parotid glands, as well as dental enamel erosion. Some
individuals may have scars or calluses on the dorsal surface of the hand from repeated contact
with the teeth while inducing vomiting.
Association With Suicidal Thoughts or Behavior
Suicide risk is elevated in anorexia nervosa, with rates reported to be 18 times greater than in an
age- and gender-matched comparison group. A systematic review found that suicide is the
second leading cause of death in anorexia nervosa. Another review found that one-quarter to
one-third of individuals with anorexia nervosa have suicidal ideation, and approximately 9%–
25% of individuals with anorexia nervosa have attempted suicide. Likely contributors to the
increased risk for suicide in those with eating disorders include greater exposure to sexual abuse;
impaired decision-making; high rates of nonsuicidal self-injury, a known risk factor for suicide
attempts; and comorbidity with mood disorders.
Functional Consequences of Anorexia Nervosa
Individuals with anorexia nervosa may exhibit a range of functional limitations associated with
the disorder. While some individuals remain active in social and professional functioning, others
demonstrate significant social isolation and/or failure to fulfill academic or career potential.
Differential Diagnosis
In addition to the general consideration of differential diagnosis for all cases, it is especially
important to consider other possible causes of either significantly low body weight or significant
weight loss when the presenting features are atypical (e.g., onset after age 40 years).
Serious weight loss may occur in medical conditions, but individuals with these disorders usually
do not also manifest a disturbance in the way their body weight or shape is experienced or an
intense fear of weight gain or persist in behaviors that interfere with appropriate weight gain.

Major depressive disorder.
Schizophrenia.
Substance use disorders.
Social anxiety disorder, obsessive-compulsive disorder, and body dysmorphic disorder.
Bulimia nervosa.
Avoidant/restrictive food intake disorder.
Acute weight loss associated with a medical condition can occasionally be followed by the onset
or recurrence of anorexia nervosa, which can initially be masked by the comorbid medical
condition. Rarely, anorexia nervosa develops after bariatric surgery.
In major depressive disorder, severe weight loss may occur, but most
individuals with major depressive disorder do not have either a desire for excessive weight loss
or an intense fear of gaining weight.
Individuals with schizophrenia may exhibit odd eating behavior and occasionally
experience significant weight loss, but they rarely show the fear of gaining weight and the body
image disturbance required for a diagnosis of anorexia nervosa.
Individuals with substance use disorders may experience low weight
because of poor nutritional intake but generally do not fear gaining weight and do not manifest
body image disturbance. Individuals who abuse substances that reduce appetite (e.g., cocaine,
stimulants) and who also endorse fear of weight gain should be carefully evaluated for the
possibility of comorbid anorexia nervosa, given that the substance use may represent a persistent
behavior that interferes with weight gain (Criterion B).
Some 
of 
the
features of anorexia nervosa overlap with the criteria for social anxiety disorder, OCD, and body
dysmorphic disorder. Specifically, individuals may feel humiliated or embarrassed to be seen
eating in public, as in social anxiety disorder; may exhibit obsessions and compulsions related to
food, as in OCD; or may be preoccupied with an imagined defect in bodily appearance, as in
body dysmorphic disorder. If the individual with anorexia nervosa has social fears that are
limited to eating behavior alone, the diagnosis of social anxiety disorder should not be made, but
social fears unrelated to eating behavior (e.g., excessive fear of speaking in public) may warrant
an additional diagnosis of social anxiety disorder. Similarly, an additional diagnosis of OCD
should be considered only if the individual exhibits obsessions and compulsions unrelated to
food (e.g., an excessive fear of contamination), and an additional diagnosis of body dysmorphic
disorder should be considered only if the distortion is unrelated to body shape and size (e.g.,
preoccupation that one’s nose is too big).
Individuals with bulimia nervosa exhibit recurrent episodes of binge eating,
engage in inappropriate behavior to avoid weight gain (e.g., self-induced vomiting), and are
overly concerned with body shape and weight. However, unlike individuals with anorexia
nervosa, binge-eating/purging type, individuals with bulimia nervosa maintain body weight at or
above a minimally normal level.
Individuals with this disorder may exhibit significant
weight loss or significant nutritional deficiency, but they do not have a fear of gaining weight or
of becoming fat, nor do they have a disturbance in the way they experience their body shape and
weight.
Comorbidity
Bipolar, depressive, and anxiety disorders commonly co-occur with anorexia nervosa. Many

F50.2
individuals with anorexia nervosa report the presence of either an anxiety disorder or symptoms
of anxiety prior to onset of their eating disorder. OCD is described in some individuals with
anorexia nervosa, especially those with the restricting type. Alcohol use disorder and other
substance use disorders may also be comorbid with anorexia nervosa, especially among those
with the binge-eating/purging type.
Bulimia Nervosa
Diagnostic Criteria
A. Recurrent episodes of binge eating. An episode of binge eating is characterized
by both of the following:
1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount
of food that is definitely larger than what most individuals would eat in a
similar period of time under similar circumstances.
2. A sense of lack of control over eating during the episode (e.g., a feeling that
one cannot stop eating or control what or how much one is eating).
B. Recurrent inappropriate compensatory behaviors in order to prevent weight gain,
such as self-induced vomiting; misuse of laxatives, diuretics, or other
medications; fasting; or excessive exercise.
C. The binge eating and inappropriate compensatory behaviors both occur, on
average, at least once a week for 3 months.
D. Self-evaluation is unduly influenced by body shape and weight.
E. The disturbance does not occur exclusively during episodes of anorexia nervosa.
Specify if:
In partial remission: After full criteria for bulimia nervosa were previously met,
some, but not all, of the criteria have been met for a sustained period of time.
In full remission: After full criteria for bulimia nervosa were previously met,
none of the criteria have been met for a sustained period of time.
Specify current severity:
The minimum level of severity is based on the frequency of inappropriate
compensatory behaviors (see below). The level of severity may be increased to
reflect other symptoms and the degree of functional disability.
Mild: An average of 1–3 episodes of inappropriate compensatory behaviors per
week.
Moderate: An average of 4–7 episodes of inappropriate compensatory
behaviors per week.

Severe: An average of 8–13 episodes of inappropriate compensatory behaviors
per week.
Extreme: An average of 14 or more episodes of inappropriate compensatory
behaviors per week.
Diagnostic Features
There are three essential features of bulimia nervosa: recurrent episodes of binge eating
(Criterion A), recurrent inappropriate compensatory behaviors to prevent weight gain (Criterion
B), and self-evaluation that is unduly influenced by body shape and weight (Criterion D). To
qualify for the diagnosis, the binge eating and inappropriate compensatory behaviors must occur,
on average, at least once per week for 3 months (Criterion C).
An “episode of binge eating” is defined as eating, in a discrete period of time, an amount of
food that is definitely larger than most individuals would eat in a similar period of time under
similar circumstances (Criterion A1). The context in which the eating occurs may affect the
clinician’s estimation of whether the intake is excessive. For example, a quantity of food that
might be regarded as excessive for a typical meal might be considered normal during a
celebration or holiday meal. A “discrete period of time” refers to a limited period, usually less
than 2 hours. A single episode of binge eating need not be restricted to one setting. For example,
an individual may begin a binge in a restaurant and then continue to eat on returning home.
Continual snacking on small amounts of food throughout the day would not be considered an
eating binge.
An occurrence of excessive food consumption must be accompanied by a sense of lack of
control (Criterion A2) to be considered an episode of binge eating. An indicator of loss of control
is the inability to refrain from eating or to stop eating once started. Some individuals describe a
dissociative quality during, or following, the binge-eating episodes. The impairment in control
associated with binge eating may not be absolute; for example, an individual may continue binge
eating while the telephone is ringing but will cease if a roommate or spouse unexpectedly enters
the room. Some individuals report that their binge-eating episodes are no longer characterized by
an acute feeling of loss of control but rather by a more generalized pattern of uncontrolled eating.
If individuals report that they have abandoned efforts to control their eating, loss of control
should be considered as present. Binge eating can also be planned in some instances.
The type of food consumed during binges varies both across individuals and for a given
individual. Binge eating appears to be characterized more by an abnormality in the amount of
food consumed than by a craving for a specific nutrient. However, during binges, individuals
tend to eat foods they would otherwise avoid.
Individuals with bulimia nervosa are typically ashamed of their eating problems and attempt
to conceal their symptoms. Binge eating usually occurs in secrecy or as inconspicuously as
possible. The binge eating often continues until the individual is uncomfortably, or even
painfully, full. The most common antecedent of binge eating is negative affect.
Other triggers include interpersonal stressors; dietary restraint; negative feelings related to
body weight, body shape, and food; and boredom. Binge eating may minimize or mitigate factors

that precipitated the episode in the short-term, but negative self-evaluation and dysphoria often
are the delayed consequences.
Another essential feature of bulimia nervosa is the recurrent use of inappropriate
compensatory behaviors to prevent weight gain (Criterion B). Many individuals with bulimia
nervosa employ several methods to compensate for binge eating. Self-induced vomiting, a type
of purging behavior, is the most common inappropriate compensatory behavior. The immediate
effects of vomiting include relief from physical discomfort and reduction of fear of gaining
weight. In some cases, vomiting becomes a goal in itself, and the individual will binge eat in
order to vomit or will vomit after eating a small amount of food. Individuals with bulimia
nervosa may use a variety of methods to induce vomiting, including the use of fingers or
instruments to stimulate the gag reflex. Individuals generally become adept at inducing vomiting
and are eventually able to vomit at will. Rarely, individuals consume syrup of ipecac to induce
vomiting. Other purging behaviors include the misuse of laxatives and diuretics and, in rare
cases, the misuse of enemas following episodes of binge eating, although this is seldom the sole
compensatory method employed. A number of compensatory methods other than purging may
also be used in rare cases. Some individuals may take thyroid hormone in an attempt to avoid
weight gain. Individuals with diabetes mellitus and bulimia nervosa may omit or reduce insulin
doses in order to reduce the metabolism of food consumed during eating binges. Individuals with
bulimia nervosa may fast for a day or more or exercise excessively in an attempt to prevent
weight gain. Exercise may be considered excessive when it significantly interferes with
important activities, when it occurs at inappropriate times or in inappropriate settings, or when
the individual continues to exercise despite injury or other medical complications.
Individuals with bulimia nervosa place an excessive emphasis on body shape or weight in
their self-evaluation, and these factors are typically extremely important in determining selfesteem (Criterion D). Individuals with this disorder may closely resemble those with anorexia
nervosa in their fear of gaining weight, in their desire to lose weight, and in the level of
dissatisfaction with their bodies. However, a diagnosis of bulimia nervosa should not be given
when the disturbance occurs only during episodes of anorexia nervosa (Criterion E).
Associated Features
Individuals with bulimia nervosa typically are within the normal weight or overweight range
(body mass index [BMI] ≥ 18.5 and < 30 in adults). The disorder occurs but is uncommon
among obese individuals. Between eating binges, individuals with bulimia nervosa typically
restrict their total caloric consumption and preferentially select low-calorie (“diet”) foods while
avoiding foods that they perceive to be fattening or likely to trigger a binge.
Menstrual irregularity or amenorrhea often occurs among females with bulimia nervosa; it is
uncertain whether such disturbances are related to weight fluctuations, to nutritional deficiencies,
or to emotional distress. The fluid and electrolyte disturbances resulting from the purging
behavior are sometimes sufficiently severe to constitute medically serious problems. Rare but
potentially fatal complications include esophageal tears, gastric rupture, and cardiac arrhythmias.
Serious cardiac and skeletal myopathies have been reported among individuals following
repeated use of syrup of ipecac to induce vomiting. Individuals who chronically abuse laxatives
may become dependent on their use to stimulate bowel movements. Gastrointestinal symptoms
are commonly associated with bulimia nervosa, and rectal prolapse has also been reported among

Temperamental.
individuals with this disorder.
Prevalence
According to two U.S. epidemiological studies conducted in adult community samples, the 12month prevalence of bulimia nervosa ranges from 0.14% to 0.3%, with much higher
rates in women than in men (0.22% to 0.5% in women; 0.05% to 0.1% in men), and the lifetime
prevalence ranges from 0.28% to 1.0% (0.46% to 1.5% in women; 0.05% to 0.08% in men). In
one study of adolescents ages 13–18, lifetime prevalence rates were 1.3% and 0.5% in girls and
boys, respectively.
In the United States, the prevalence of bulimia nervosa is similar across U.S. ethnoracial
groups. The reported prevalence of bulimia nervosa is highest in populations residing in highincome industrialized countries, such as the United States, Canada, Australia, New Zealand, and
many European countries; in most of these countries the prevalence of bulimia nervosa is
roughly comparable.
The prevalence of bulimia nervosa in some regions of Latin America and the Middle East is
similar to the prevalence in most high-income countries. The prevalence of bulimia nervosa
appears to be gradually increasing in many low- and middle-income countries.
Development and Course
Bulimia nervosa commonly begins in adolescence or young adulthood. Onset before puberty or
after age 40 is uncommon. The binge eating frequently begins during or after an episode of
dieting to lose weight. Experiencing multiple stressful life events also can precipitate onset of
bulimia nervosa.
Disturbed eating behavior persists for at least several years in a high percentage of clinical
samples. The course may be chronic or intermittent, with periods of remission alternating with
recurrences of binge eating. However, over longer-term follow-up, the symptoms of many
individuals appear to diminish with or without treatment, although treatment clearly impacts
outcome. Periods of remission longer than 1 year are associated with better long-term outcome.
Significantly elevated risk for mortality (all-cause and suicide) has been reported for
individuals with bulimia nervosa. The crude mortality rate (ratio of the number of deaths during
the year to the average population in that year) for bulimia nervosa is nearly 2% per decade.
Diagnostic crossover from initial bulimia nervosa to anorexia nervosa occurs in a minority of
cases (10%–15%). Individuals who do experience crossover to anorexia nervosa commonly will
revert back to bulimia nervosa or have multiple occurrences of crossovers between these
disorders. A subset of individuals with bulimia nervosa continue to binge eat but no longer
engage in inappropriate compensatory behaviors, and therefore their symptoms meet criteria for
binge-eating disorder or other specified eating disorder. Diagnosis should be based on the current
(i.e., past 3 months) clinical presentation.
Risk and Prognostic Factors
Weight concerns, low self-esteem, depressive symptoms, social anxiety disorder,

Environmental.
Genetic and physiological.
Course modifiers.
and childhood generalized anxiety disorder are associated with increased risk for the
development of bulimia nervosa.
Internalization of a thin body ideal has been found to increase risk for developing
weight concerns, which in turn increases risk for the development of bulimia nervosa.
Individuals who experienced childhood sexual or physical abuse are at increased risk for
developing bulimia nervosa.
Childhood obesity and early pubertal maturation increase risk for
bulimia nervosa. Familial transmission of bulimia nervosa may be present, as well as genetic
vulnerabilities for the disorder.
Severity of psychiatric comorbidity predicts worse long-term outcome of
bulimia nervosa.
Culture-Related Diagnostic Issues
Although data show that community-based prevalence of bulimia nervosa does not differ
significantly across U.S. ethnoracial groups, treatment utilization for bulimia nervosa is lower
among underserved U.S. ethnic and racialized groups than among the non-Latinx White
population.
Sex- and Gender-Related Diagnostic Issues
Bulimia nervosa is much more common in girls and women than in boys and men. Boys and men
are especially underrepresented in treatment-seeking samples, for reasons that have not yet been
systematically examined.
Diagnostic Markers
No specific diagnostic test for bulimia nervosa currently exists. However, several laboratory
abnormalities may occur as a consequence of purging and may increase diagnostic certainty.
These include fluid and electrolyte abnormalities, such as hypokalemia (which can provoke
cardiac arrhythmias), hypochloremia, and hyponatremia. The loss of gastric acid through
vomiting may produce a metabolic alkalosis (elevated serum bicarbonate), and the frequent
induction of diarrhea or dehydration through laxative and diuretic abuse can cause metabolic
acidosis. Some individuals with bulimia nervosa exhibit mildly elevated levels of serum amylase,
probably reflecting an increase in the salivary isoenzyme.
Physical examination usually yields no physical findings. However, inspection of the mouth
may reveal significant and permanent loss of dental enamel, especially from lingual surfaces of
the front teeth because of recurrent vomiting. These teeth may become chipped and appear
ragged and “moth-eaten.” There may also be an increased frequency of dental caries. In some
individuals, the salivary glands, particularly the parotid glands, may become notably enlarged.
Individuals who induce vomiting by manually stimulating the gag reflex may develop calluses or
scars on the dorsal surface of the hand from repeated contact with the teeth. Serious cardiac and
skeletal myopathies have been reported among individuals following repeated use of syrup of
ipecac to induce vomiting.

Anorexia nervosa, binge-eating/purging type.
Binge-eating disorder.
Kleine-Levin syndrome.
Major depressive disorder, with atypical features.
Borderline personality disorder.
Association With Suicidal Thoughts or Behavior
Suicide risk is elevated in bulimia nervosa. A review found that approximately one-quarter to
one-third of individuals with bulimia nervosa have had suicidal ideation, and a similar proportion
have attempted suicide.
Functional Consequences of Bulimia Nervosa
Individuals with bulimia nervosa may exhibit a range of functional limitations associated with
the disorder and have reduced health-related quality of life. A minority of individuals report
severe role impairment, with the social-life domain most likely to be adversely affected by
bulimia nervosa.
Differential Diagnosis
Individuals whose binge-eating behavior occurs only
during episodes of anorexia nervosa are given the diagnosis anorexia nervosa, bingeeating/purging type, and should not be given the additional diagnosis of bulimia nervosa. For
individuals with an initial diagnosis of anorexia nervosa who binge and purge but whose
presentation no longer meets the full criteria for anorexia nervosa, binge-eating/purging type
(e.g., when weight is normal), a diagnosis of bulimia nervosa should be given only when all
criteria for bulimia nervosa have been met for at least 3 months.
Some individuals binge eat but do not engage in regular inappropriate
compensatory behaviors. In these cases, the diagnosis of binge-eating disorder should be
considered.
In certain neurological or other medical conditions, such as Kleine-Levin
syndrome, there is disturbed eating behavior, but the characteristic psychological features of
bulimia nervosa, such as overconcern with body shape and weight, are not present.
Overeating is common in major depressive
disorder, with atypical features, but individuals with this disorder do not engage in inappropriate
compensatory behaviors and do not exhibit the excessive concern with body shape and weight
characteristic of bulimia nervosa. If criteria for both disorders are met, both diagnoses should be
given.
Binge-eating behavior is included in the impulsive behavior
criterion that is part of the definition of borderline personality disorder. If the criteria for both
borderline personality disorder and bulimia nervosa are met, both diagnoses should be given.
Comorbidity
Comorbidity with mental disorders is common in individuals with bulimia nervosa, with most
experiencing at least one other mental disorder and many experiencing multiple comorbidities.
Comorbidity is not limited to any particular subset but rather occurs across a wide range of
mental disorders. There is an increased frequency of depressive symptoms (e.g., low self-esteem)
and bipolar and depressive disorders (particularly depressive disorders) in individuals with

F50.81
bulimia nervosa. In many individuals, the mood disturbance begins at the same time as or
following the development of bulimia nervosa, and individuals often ascribe their mood
disturbances to the bulimia nervosa. However, in some individuals, the mood disturbance clearly
precedes the development of bulimia nervosa. There may also be an increased frequency of
anxiety symptoms (e.g., fear of social situations) or anxiety disorders. These mood and anxiety
disturbances frequently remit following effective treatment of the bulimia nervosa. The lifetime
prevalence of substance use disorder, particularly alcohol use disorder or stimulant use disorder,
is at least 30% among individuals with bulimia nervosa. Stimulant use often begins in an attempt
to control appetite and weight. A substantial percentage of individuals with bulimia nervosa also
have personality features that meet criteria for one or more personality disorders, most frequently
borderline personality disorder.
Binge-Eating Disorder
Diagnostic Criteria
A. Recurrent episodes of binge eating. An episode of binge eating is characterized
by both of the following:
1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount
of food that is definitely larger than what most people would eat in a similar
period of time under similar circumstances.
2. A sense of lack of control over eating during the episode (e.g., a feeling that
one cannot stop eating or control what or how much one is eating).
B. The binge-eating episodes are associated with three (or more) of the following:
1. Eating much more rapidly than normal.
2. Eating until feeling uncomfortably full.
3. Eating large amounts of food when not feeling physically hungry.
4. Eating alone because of feeling embarrassed by how much one is eating.
5. Feeling disgusted with oneself, depressed, or very guilty afterward.
C. Marked distress regarding binge eating is present.
D. The binge eating occurs, on average, at least once a week for 3 months.
E. The binge eating is not associated with the recurrent use of inappropriate
compensatory behavior as in bulimia nervosa and does not occur exclusively
during the course of bulimia nervosa or anorexia nervosa.
Specify if:
In partial remission: After full criteria for binge-eating disorder were previously
met, binge eating occurs at an average frequency of less than one episode per

week for a sustained period of time.
In full remission: After full criteria for binge-eating disorder were previously met,
none of the criteria have been met for a sustained period of time.
Specify current severity:
The minimum level of severity is based on the frequency of episodes of binge eating
(see below). The level of severity may be increased to reflect other symptoms and
the degree of functional disability.
Mild: 1–3 binge-eating episodes per week.
Moderate: 4–7 binge-eating episodes per week.
Severe: 8–13 binge-eating episodes per week.
Extreme: 14 or more binge-eating episodes per week.
Diagnostic Features
The essential feature of binge-eating disorder is recurrent episodes of binge eating that must
occur, on average, at least once per week for 3 months (Criterion D). An “episode of binge
eating” is defined as eating, in a discrete period of time, an amount of food that is definitely
larger than most people would eat in a similar period of time under similar circumstances
(Criterion A1). The context in which the eating occurs may affect the clinician’s estimation of
whether the intake is excessive. For example, a quantity of food that might be regarded as
excessive for a typical meal might be considered normal during a celebration or holiday meal. A
“discrete period of time” refers to a limited period, usually less than 2 hours. A single episode of
binge eating need not be restricted to one setting. For example, an individual may begin a binge
in a restaurant and then continue to eat on returning home. Continual snacking on small amounts
of food throughout the day would not be considered an eating binge.
An occurrence of excessive food consumption must be accompanied by a sense of lack of
control (Criterion A2) to be considered an episode of binge eating. An indicator of loss of control
is the inability to refrain from eating or to stop eating once started. Some individuals describe a
dissociative quality during, or following, the binge-eating episodes. The impairment in control
associated with binge eating may not be absolute; for example, an individual may continue binge
eating while the telephone is ringing but will cease if a roommate or spouse unexpectedly enters
the room. Some individuals report that their binge-eating episodes are no longer characterized by
an acute feeling of loss of control but rather by a more generalized pattern of uncontrolled eating.
If individuals report that they have abandoned efforts to control their eating, loss of control may
still be considered as present. Binge eating can also be planned in some instances.
The type of food consumed during binges varies both across individuals and for a given
individual. Binge eating appears to be characterized more by an abnormality in the amount of
food consumed than by a craving for a specific nutrient.
Binge eating must be characterized by marked distress (Criterion C) and at least three of the
following features: eating much more rapidly than normal; eating until feeling uncomfortably

full; eating large amounts of food when not feeling physically hungry; eating alone because of
feeling embarrassed by how much one is eating; and feeling disgusted with oneself, depressed, or
very guilty afterward (Criterion B).
Individuals with binge-eating disorder are typically ashamed of their eating problems and
attempt to conceal their symptoms. Binge eating usually occurs in secrecy or as inconspicuously
as possible. The most common antecedent of binge eating is negative affect. Other triggers
include interpersonal stressors; dietary restraint; negative feelings related to body weight, body
shape, and food; and boredom. Binge eating may minimize or mitigate factors that precipitated
the episode in the short-term, but negative self-evaluation and dysphoria often are the delayed
consequences.
Associated Features
Binge-eating disorder occurs in normal-weight/overweight and obese individuals. It is reliably
associated with overweight and obesity in treatment-seeking individuals. Nevertheless, bingeeating disorder is distinct from obesity. Most obese individuals do not engage in recurrent binge
eating. In addition, compared with weight-matched obese individuals without binge-eating
disorder, those with the disorder consume more calories in laboratory studies of eating behavior
and have greater functional impairment, lower quality of life, more subjective distress, and
greater psychiatric comorbidity.
Prevalence
According to two U.S. epidemiological studies conducted in community samples, the 12-month
prevalence of binge-eating disorder ranges from 0.44% to 1.2%, with rates two to three times
higher in women than in men (0.6% to 1.6% in women; 0.26% to 0.8% in men), and the lifetime
prevalence ranges from 0.85% to 2.8% (1.25% to 3.5% in women; 0.42% to 2.0% in men).
In the United States, the prevalence of binge-eating disorder appears comparable across
ethnoracial groups.
Binge-eating disorder has a roughly similar prevalence in most high-income industrialized
countries, including the United States, Canada, many European countries, Australia, and New
Zealand, with 12-month prevalence in high-income countries ranging from 0.1% to 1.2%.
Although fewer data are available from populations in low- and middle-income countries, bingeeating disorder prevalence in some regions of Latin America appears to be at least as high as in
the United States and Europe. Mexican Americans in the United States have a higher prevalence
of binge-eating disorder than their counterparts in Mexico.
Development and Course
Little is known about the development of binge-eating disorder. Both binge eating and loss-ofcontrol eating without objectively excessive consumption occur in children and are associated
with increased body fat, weight gain, and increases in psychological symptoms. Binge eating is
common in adolescent and college-age samples. Loss-of-control eating or episodic binge eating
may represent a prodromal phase of eating disorders for some individuals.
Dieting follows the development of binge eating in many individuals with binge-eating
disorder. (This is in contrast to bulimia nervosa, in which dysfunctional dieting usually precedes

Genetic and physiological.
Bulimia nervosa.
the onset of binge eating.) Binge-eating disorder typically begins in adolescence or young
adulthood but can begin in later adulthood. Individuals with binge-eating disorder who seek
treatment usually are older than individuals with either bulimia nervosa or anorexia nervosa who
seek treatment.
Remission rates in both natural course and treatment outcome studies are higher for bingeeating disorder than for bulimia nervosa or anorexia nervosa. The course of binge-eating disorder
is variable and as yet incompletely understood, with at least some affected individuals showing a
relatively persistent, at times relapsing and remitting, symptom trajectory comparable to that of
bulimia nervosa in terms of severity and duration. Crossover from binge-eating disorder to other
eating disorders is uncommon.
Risk and Prognostic Factors
Binge-eating disorder appears to run in families, which may reflect
additive genetic influences.
Culture-Related Diagnostic Issues
Clinical presentations of binge-eating disorder differ across ethnoracial groups in the United
States. Black individuals may report fewer symptoms of distress associated with binge eating and
present for treatment with higher frequency of binge eating compared with White individuals.
Association With Suicidal Thoughts or Behavior
Suicidal ideation has been reported to occur in approximately 25% of individuals with bingeeating disorder.
Functional Consequences of Binge-Eating Disorder
Binge-eating disorder is associated with a range of functional consequences, including social role
adjustment problems, impaired health-related quality of life and life satisfaction, increased
medical morbidity and mortality, and associated increased health care utilization compared with
body mass index (BMI)–matched control subjects. It may also be associated with an increased
risk for weight gain and the development of obesity.
Differential Diagnosis
Binge-eating disorder has recurrent binge eating in common with bulimia
nervosa but differs from the latter disorder in some fundamental respects. In terms of clinical
presentation, the recurrent inappropriate compensatory behavior (e.g., purging, driven exercise)
seen in bulimia nervosa is absent in binge-eating disorder. Unlike individuals with bulimia
nervosa, individuals with binge-eating disorder typically do not show marked or sustained
dietary restriction designed to influence body weight and shape between binge-eating episodes.
They may, however, report frequent attempts at dieting. Binge-eating disorder also differs from
bulimia nervosa in terms of response to treatment. Rates of improvement are consistently higher

Obesity.
Bipolar and depressive disorders.
Borderline personality disorder.
among individuals with binge-eating disorder than among those with bulimia nervosa.
Binge-eating disorder is associated with overweight and obesity but has several key
features that are distinct from obesity. First, levels of overvaluation of body weight and shape are
higher in obese individuals with the disorder than in those without the disorder. Second, rates of
psychiatric comorbidity are significantly higher among obese individuals with the disorder
compared with those without the disorder. Third, the outcome of evidence-based psychological
treatments for binge-eating disorder is more often successful than the treatment of obesity in
individuals with comorbid obesity and binge-eating disorder.
Increases in appetite and weight gain are included in the criteria
for major depressive episode and in the atypical features specifiers for
depressive and bipolar disorders. Increased eating in the context of a major depressive episode
may or may not be associated with loss of control. If the full criteria for both disorders are met,
both diagnoses can be given. Binge eating and other symptoms of disordered eating are seen in
association with bipolar disorder. If the full criteria for both disorders are met, both diagnoses
should be given.
Binge eating is included in the impulsive behavior criterion that is
part of the definition of borderline personality disorder. If the full criteria for both disorders are
met, both diagnoses should be given.
Comorbidity
Binge-eating disorder is associated with significant psychiatric comorbidity that is comparable to
that of bulimia nervosa and anorexia nervosa. The most common comorbid disorders are major
depressive disorder and alcohol use disorder. The psychiatric comorbidity is linked to the
severity of binge eating and not to the degree of obesity.
Other Specified Feeding or Eating Disorder
F50.89
This category applies to presentations in which symptoms characteristic of a feeding
and eating disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the feeding and eating disorders diagnostic
class. The other specified feeding or eating disorder category is used in situations in
which the clinician chooses to communicate the specific reason that the presentation
does not meet the criteria for any specific feeding and eating disorder. This is done
by recording “other specified feeding or eating disorder” followed by the specific
reason (e.g., “bulimia nervosa of low frequency”).
Examples of presentations that can be specified using the “other specified”
designation include the following:

1. Atypical anorexia nervosa: All of the criteria for anorexia nervosa are met,
except that despite significant weight loss, the individual’s weight is within or
above the normal range. Individuals with atypical anorexia nervosa may
experience many of the physiological complications associated with anorexia
nervosa.
2. Bulimia nervosa (of low frequency and/or limited duration): All of the criteria
for bulimia nervosa are met, except that the binge eating and inappropriate
compensatory behaviors occur, on average, less than once a week and/or for
less than 3 months.
3. Binge-eating disorder (of low frequency and/or limited duration): All of the
criteria for binge-eating disorder are met, except that the binge eating occurs, on
average, less than once a week and/or for less than 3 months.
4. Purging disorder: Recurrent purging behavior to influence weight or shape
(e.g., self-induced vomiting; misuse of laxatives, diuretics, or other medications)
in the absence of binge eating.
5. Night eating syndrome: Recurrent episodes of night eating, as manifested by
eating after awakening from sleep or by excessive food consumption after the
evening meal. There is awareness and recall of the eating. The night eating is
not better explained by external influences such as changes in the individual’s
sleep-wake cycle or by local social norms. The night eating causes significant
distress and/or impairment in functioning. The disordered pattern of eating is not
better explained by binge-eating disorder or another mental disorder, including
substance use, and is not attributable to another medical condition or to an effect
of medication.
Unspecified Feeding or Eating Disorder
F50.9
This category applies to presentations in which symptoms characteristic of a feeding
and eating disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the feeding and eating disorders diagnostic
class. The unspecified feeding or eating disorder category is used in situations in
which the clinician chooses not to specify the reason that the criteria are not met for
a specific feeding and eating disorder and includes presentations in which there is
insufficient information to make a more specific diagnosis (e.g., in emergency room
settings).

# 11 - Elimination Disorders

# Elimination Disorders

399

F98.0
Elimination Disorders
Elimination disorders all involve the inappropriate elimination of urine or feces and
are usually first diagnosed in childhood or adolescence. This group of disorders includes
enuresis, the repeated voiding of urine into inappropriate places, and encopresis, the repeated
passage of feces into inappropriate places. Subtypes are provided to differentiate nocturnal from
diurnal (i.e., during waking hours) voiding for enuresis and the presence or absence of
constipation and overflow incontinence for encopresis. Although there are minimum age
requirements for diagnosis of both disorders, these are based on developmental age and not
solely on chronological age. Both disorders may be voluntary or involuntary. Although these
disorders typically occur separately, co-occurrence may also be observed.
Enuresis
Diagnostic Criteria
A. Repeated voiding of urine into bed or clothes, whether involuntary or intentional.
B. The behavior is clinically significant as manifested by either a frequency of at
least twice a week for at least 3 consecutive months or the presence of clinically
significant distress or impairment in social, academic (occupational), or other
important areas of functioning.
C. Chronological age is at least 5 years (or equivalent developmental level).
D. The behavior is not attributable to the physiological effects of a substance (e.g.,
a diuretic, an antipsychotic medication) or another medical condition (e.g.,
diabetes, spina bifida, a seizure disorder).
Specify whether:
Nocturnal only: Passage of urine only during nighttime sleep.
Diurnal only: Passage of urine during waking hours.
Nocturnal and diurnal: A combination of the two subtypes above.
Subtypes
The nocturnal-only subtype of enuresis, sometimes referred to as monosymptomatic enuresis, is
the most common subtype and involves incontinence only during nighttime sleep, typically
during the first one-third of the night. The diurnal-only subtype occurs in the absence of
nocturnal enuresis and may be referred to simply as urinary incontinence. Individuals with this

subtype can be divided into two groups. Individuals with “urge incontinence” have sudden urge
symptoms and detrusor instability, whereas individuals with “voiding postponement”
consciously defer micturition urges until incontinence results. The nocturnal-and-diurnal subtype
is also known as nonmonosymptomatic enuresis.
Diagnostic Features
The essential feature of enuresis is repeated voiding of urine during the day or at night into bed
or clothes (Criterion A). Most often the voiding is involuntary, but occasionally it may be
intentional. To qualify for a diagnosis of enuresis, the voiding of urine must occur at least twice a
week for at least 3 consecutive months or must cause clinically significant distress or impairment
in social, academic (occupational), or other important areas of functioning (Criterion B). The
individual must have reached an age at which continence is expected (i.e., a chronological age of
at least 5 years or, for children with developmental delays, a mental age of at least 5 years)
(Criterion C). The urinary incontinence is not attributable to the physiological effects of a
substance (e.g., a diuretic, an antipsychotic medication) or another medical condition (e.g.,
diabetes, spina bifida, ectopic ureter in a female, posterior urethral valves in a male, tethered
cord, a seizure disorder) (Criterion D).
Associated Features
During nocturnal enuresis, occasionally the voiding takes place during rapid eye movement
(REM) sleep, and the child may recall a dream that involved the act of urinating. During daytime
(diurnal) enuresis, the child defers voiding until incontinence occurs, sometimes because of a
reluctance to use the toilet as a result of social anxiety or a preoccupation with school or play
activity. The enuretic events most commonly occur in the early afternoon on school days or after
returning from school. Children with executive functioning problems and other neurological
problems that may be associated with symptoms of disruptive behavior may be at high risk for
urinary incontinence without sensory awareness. It is not uncommon for children with daytime
urinary incontinence and the nocturnal-and-diurnal subtype of enuresis to have persistence of
incontinence after appropriate treatment of an associated infection.
Prevalence
The prevalence of daytime incontinence ranges from 3.2% to 9.0% in children age 7 years, from
1.1% to 4.2% in youth ages 11–13 years, and from 1.2% to 3.0% in adolescents ages 15–17
years.
The prevalence of nocturnal enuresis in the community decreases with age; in several
geographical settings, including the United States, the Netherlands, and Hong Kong, the range is
around 5%–10% among 5-year-olds, 3%–5% among 10-year-olds, and around 1% among
individuals 15 years or older. Boys and members of socially oppressed groups may have higher
prevalence as found in African American children in the United States and Turkish or Moroccan
children in the Netherlands. The disorder may also have higher prevalence in youth with learning
disabilities or attention-deficit/hyperactivity disorder.

Environmental.
Genetic and physiological.
Development and Course
Enuresis can follow two courses: a “primary” type, in which the individual has never established
urinary continence, and a “secondary” type, in which the disturbance develops after a period of
established urinary continence. There are no differences in prevalence of comorbid mental
disorders between the two types. By definition, primary enuresis begins at age 5 years. The most
common time for the onset of secondary enuresis is between ages 5 and 8 years, but it may occur
at any time. After age 5 years, the rate of spontaneous remission is 5%–10% per year. Most
children with the disorder become continent by adolescence, but in approximately 1% of cases
the disorder continues into adulthood. Diurnal enuresis is uncommon after age 9 years. While
occasional diurnal incontinence is not uncommon in middle childhood, it is substantially more
common in those who also have other co-occurring mental health problems, including cognitive
and behavioral problems. When enuresis persists into late childhood or adolescence, the
incontinence may resolve, but urinary frequency generally persists and incontinence can recur
later in adulthood in women.
Risk and Prognostic Factors
A number of predisposing factors for bladder dysfunction have been suggested, including
developmental delays and neuropsychiatric problems.
Factors recognized to be associated with bladder dysfunction include delayed
toileting and psychosocial stress.
Nocturnal enuresis has been associated with a mismatch between
nocturnal urine production, nocturnal bladder storage capacity, and the ability to arouse from
sleep. Underlying these mechanisms are possibly disorders of central nervous system signal
processing and the default mode network. The increased arousal thresholds do not, however,
mean that these children sleep well; in fact, sleep quality of enuretic children is often poor.
Nocturnal enuresis is a genetically heterogeneous disorder. Heritability has been shown in
family, twin, and segregation analyses. Risk for childhood nocturnal enuresis is approximately
3.6 times higher in offspring of enuretic mothers and 10.1 times higher in the presence of
paternal urinary incontinence. The risk magnitudes for nocturnal enuresis and diurnal
incontinence are similar.
Culture-Related Diagnostic Issues
Enuresis has been reported in a variety of European, African, and Asian countries as well as in
the United States. At a national level, prevalence rates are remarkably similar, and there is great
similarity in the developmental trajectories found in different countries. Local school-based
surveys, however, show wide prevalence variation of nocturnal enuresis across settings in Africa,
South Asia, Europe, and the Caribbean (4%–50%), at least in part due to methodological
variation. The very high rates of enuresis in orphanages and other residential institutions are not
explained by the mode or early timing of toilet training.
Cultural contexts affect both the diagnosis and the perceived etiology of enuresis. For
example, traditional Chinese medicine attributes enuresis to long-term kidney yang (masculine

Neurogenic bladder or another medical condition.
Medication side effects.
energy) deficiency. Heightened impact on parents of children’s enuresis has been reported in
societies with economic limitations in obtaining care for the child or in the context of social
policies that restrict the number of children (e.g., China’s one-child policy), possibly leading to
higher risk of parental emotional disorders.
Sex- and Gender-Related Diagnostic Issues
Nocturnal enuresis is more common in males than in females (almost 2:1). This male
preponderance is particularly true in younger age groups, cases with milder severity, and cases
involving enuresis occurring only at night. Urinary tract infections are frequently associated with
daytime wetting, especially in females. Diurnal incontinence is more common in females than in
males, and the ratio increases with age. The relative risk of having a child who develops enuresis
is greater for previously enuretic fathers than for previously enuretic mothers.
Functional Consequences of Enuresis
The amount of impairment associated with enuresis is a function of the limitation on the child’s
social activities (e.g., ineligibility for sleep-away camp) or its effect on the child’s self-esteem,
the degree of social ostracism by peers, and the anger, punishment, and rejection on the part of
caregivers.
Differential Diagnosis
The diagnosis of enuresis is not made in the
presence of a neurogenic bladder or any other structural condition (such as a posterior urethral
valve or ectopic ureter) or another medical condition that causes polyuria or
urgency (e.g., untreated diabetes mellitus or diabetes insipidus) or during an acute urinary tract
infection. However, a diagnosis is compatible with such medical conditions if urinary
incontinence was regularly present prior to the development of another medical condition or if it
persists after the institution of appropriate treatment of the medical condition.
Enuresis may occur during treatment with antipsychotic medications,
diuretics, or other medications that may induce constipation, polyuria, or alterations in executive
functioning, all of which may lead to incontinence. In this case, the diagnosis should not be made
in isolation but may be noted as a medication side effect. However, a diagnosis of enuresis may
be made if urinary incontinence was regularly present prior to treatment with the medication.
Comorbidity
Although most children with enuresis do not have a comorbid mental disorder, the prevalence of
comorbid behavioral and developmental symptoms is higher in children with both diurnal and
nocturnal enuresis than in children without incontinence. Developmental delays, including
speech, language, learning, and motor skills delays, are also present in a portion of children with
enuresis. Encopresis and constipation are present in both day and night incontinence. Restless
legs syndrome and parasomnias such as non–rapid eye movement sleep arousal disorders

F98.1
(sleepwalking and sleep terror types) are associated with nocturnal enuresis. Additionally, there
is a link between nocturnal enuresis and heavy snoring or sleep apneas. Approximately 50% of
enuretic children with proven sleep-disordered breathing will become dry by undergoing
adenotonsillectomy. Urinary tract infections are more common in children with daytime urinary
incontinence and nonmonosymptomatic nocturnal enuresis, especially the diurnal subtype, than
in those who are continent.
Encopresis
Diagnostic Criteria
A. Repeated passage of feces into inappropriate places (e.g., clothing, floor),
whether involuntary or intentional.
B. At least one such event occurs each month for at least 3 months.
C. Chronological age is at least 4 years (or equivalent developmental level).
D. The behavior is not attributable to the physiological effects of a substance (e.g.,
laxatives) or another medical condition except through a mechanism involving
constipation.
Specify whether:
With constipation and overflow incontinence: There is evidence of
constipation on physical examination or by history.
Without constipation and overflow incontinence: There is no evidence of
constipation on physical examination or by history.
Subtypes
Feces in encopresis, “with constipation and overflow incontinence” subtype, are
characteristically (but not invariably) poorly formed, and leakage can be infrequent to
continuous, occurring throughout the day and at times during sleep. Only part of the feces is
passed during toileting, and the incontinence resolves after treatment of the constipation.
In the “without constipation and overflow incontinence” subtype, feces are likely to be of
normal form and consistency, and soiling is intermittent. Feces may be deposited in a
prominent location. This is usually associated with the presence of oppositional defiant
disorder or conduct disorder or may be the consequence of anal masturbation. Soiling without
constipation is less common than soiling with constipation.
Diagnostic Features
The essential feature of encopresis is repeated passage of feces into inappropriate places (e.g.,
clothing or floor) (Criterion A). Most often the passage is involuntary but occasionally may be

intentional. The event must occur at least once a month for at least 3 months (Criterion B), and
the chronological age of the child must be at least 4 years (or for children with developmental
delays, the mental age must be at least 4 years) (Criterion C). The fecal incontinence must not be
exclusively attributable to the physiological effects of a substance (e.g., laxatives) or another
medical condition except through a mechanism involving constipation (Criterion D).
When the passage of feces is involuntary rather than intentional, it is often related to
constipation, impaction, and retention with subsequent overflow. The constipation may develop
for psychological reasons (e.g., anxiety about defecating in a particular place, a more general
pattern of anxious or oppositional behavior), leading to avoidance of defecation and excessive
volitional stool retention. Physiological predispositions to constipation include ineffectual
straining or paradoxical defecation dynamics, with contraction rather than relaxation of the
external sphincter or pelvic floor during straining for defecation. Dietary habits (such as
insufficient fluid intake), celiac disease, hypothyroidism, or a medication side effect can also
induce constipation. Once constipation has developed, it may be complicated by an anal fissure,
painful defecation, and further fecal retention. The consistency of the stool may vary. In some
individuals the stool may be of normal or near-normal consistency. In other individuals—such as
those with overflow incontinence secondary to fecal retention—it may be liquid.
Associated Features
The child with encopresis often feels ashamed and may wish to avoid situations (e.g., camp,
school) that might lead to embarrassment. The amount of impairment is a function of the effect
on the child's self-esteem, the degree of social ostracism by peers, and the anger, punishment,
and rejection on the part of caregivers. Smearing feces may be deliberate or accidental, resulting
from the child’s attempt to clean or hide feces that were passed involuntarily. When the
incontinence is clearly deliberate, features of oppositional defiant disorder or conduct disorder
may also be present. Many children with encopresis and chronic constipation also have enuresis
symptoms and may have associated urinary reflux in the bladder or ureters that may lead to
chronic urinary infections, the symptoms of which may remit with treatment of the constipation.
Prevalence
It is estimated that the majority of children older than 4 years with encopresis have the subtype
“with constipation and overflow incontinence.” Encopresis affects 1%–4% of children in highincome countries, while in some Asian countries (Iran, South Korea, Sri Lanka) a prevalence of
2%–8% has been reported. Encopresis is more prevalent among children ages 4–6 years (> 4%)
than among children ages 10–12 years (< 2%); prevalence is also higher among children who
experience early abuse or neglect and low-income youth.
Development and Course
Encopresis is not diagnosed until a child has reached a chronological age of at least 4 years (or
for children with developmental delays, a mental age of at least 4 years). Inadequate,
inconsistent toilet training and psychosocial stress (e.g., entering school, the birth of a sibling)

may be predisposing factors. Two types of course have been described: a “primary” type, in
which the individual has never established fecal continence, and a “secondary” type, in which the
disturbance develops after a period of established fecal continence. Encopresis can persist, with
intermittent exacerbations, for years.
Risk and Prognostic Factors
Painful defecation can lead to constipation and a cycle of withholding behaviors that make
encopresis more likely. Male gender and age prior to adolescence are risk factors for encopresis.
A number of factors are thought to contribute to the development of fecal incontinence,
including anxiety, depression, behavioral disorders, psychological stressors (e.g., bullying, poor
school performance), and lower socioeconomic status.
Culture-Related Diagnostic Issues
Differences in food and beverage intake in different cultures, hot climatic conditions in tropical
countries, and psychosocial adversity may influence the incidence of constipation, unexplained
abdominal pain, and fecal retention that lead to encopresis. Parents in some societies may not
seek health services for encopresis because of sociocultural reasons. For example, Turkish and
Moroccan parents in the Netherlands may not report encopresis because of religious concerns
about the impurity of urine and feces.
Sex- and Gender-Related Diagnostic Issues
In children younger than 5 years, the gender ratio appears to be equal, but encopresis tends to be
more common in boys than in girls among older children, with a ratio that varies globally (in
community and hospital-based studies) from 2:1 (in the United States) to 6:1.
Diagnostic Markers
The diagnosis of encopresis is a clinical diagnosis based on history and physical examination and
generally does not require any diagnostic testing. Detection of a rectal fecal impaction by digital
rectal examination would support the diagnosis of encopresis, with constipation and overflow
incontinence. Although not indicated for the diagnosis of encopresis, an abdominal radiograph
demonstrating a fecal impaction would also support the diagnosis of encopresis, with
constipation and overflow incontinence. Colonic transit testing, which typically involves
ingestion of radiopaque markers followed by abdominal imaging to evaluate colonic transit time,
can help differentiate between encopresis with or without constipation and overflow
incontinence. Abdominal imaging demonstrating retention of radiopaque markers would suggest
encopresis, with constipation and overflow incontinence, while prompt evacuation of radiopaque
markers would support the diagnosis of encopresis, without constipation and overflow
incontinence. In certain children, anorectal manometry testing may be helpful for better
understanding physiological factors that may be contributing to encopresis. Anorectal
manometry allows for evaluation of anorectal function and sensation. In the child with refractory
symptoms or signs suggesting the presence of an underlying medical condition leading to fecal
incontinence, further evaluation may be indicated. Such evaluation is designed to exclude other
medical conditions.

Functional Consequences of Encopresis
Encopresis is associated with a significant decrease in health-related quality of life and family
functioning, particularly in older children.
Differential Diagnosis
A diagnosis of encopresis in the presence of another medical condition is appropriate only if the
mechanism involves constipation that cannot be explained by other medical conditions. Fecal
incontinence related to other medical conditions (e.g., chronic diarrhea, spina bifida, anal
stenosis) would not warrant a DSM-5 diagnosis of encopresis.
Comorbidity
Enuresis is often present in children with encopresis, particularly in children with encopresis,
without constipation and overflow incontinence.
Other Specified Elimination Disorder
 
This category applies to presentations in which symptoms characteristic of an
elimination disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the elimination disorders diagnostic class.
The other specified elimination disorder category is used in situations in which the
clinician chooses to communicate the specific reason that the presentation does not
meet the criteria for any specific elimination disorder. This is done by recording
“other specified elimination disorder” followed by the specific reason (e.g., “lowfrequency enuresis”).
Coding note: Code N39.498 for other specified elimination disorder with urinary
symptoms; R15.9 for other specified elimination disorder with fecal symptoms.
Unspecified Elimination Disorder
 
This category applies to presentations in which symptoms characteristic of an
elimination disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the elimination disorders diagnostic class.
The unspecified elimination disorder category is used in situations in which the

clinician chooses not to specify the reason that the criteria are not met for a specific
elimination disorder and includes presentations in which there is insufficient
information to make a more specific diagnosis (e.g., in emergency room settings).
Coding note: Code R32 for unspecified elimination disorder with urinary symptoms;
R15.9 for unspecified elimination disorder with fecal symptoms.

# 12 - Sleep Wake Disorders

# Sleep-Wake Disorders

407

Sleep-Wake Disorders
The DSM-5 classification of sleep-wake disorders is intended for use by mental
health and general medical clinicians (those caring for adult, geriatric, and pediatric individuals).
Sleep-wake disorders encompass 10 disorders or disorder groups: insomnia disorder,
hypersomnolence disorder, narcolepsy, breathing-related sleep disorders, circadian rhythm sleepwake disorders, non–rapid eye movement (NREM) sleep arousal disorders, nightmare disorder,
rapid eye movement (REM) sleep behavior disorder, restless legs syndrome, and
substance/medication-induced sleep disorder. Individuals with these disorders typically present
with sleep-wake complaints of dissatisfaction regarding the quality, timing, and amount of sleep.
Resulting daytime distress and impairment are core features shared by all of these sleep-wake
disorders.
The organization of this chapter is designed to facilitate differential diagnosis of sleep-wake
complaints and to clarify when referral to a sleep specialist is appropriate for further assessment
and treatment planning. The DSM-5 sleep disorders nosology uses a simple, clinically useful
approach, while also reflecting scientific advances in epidemiology, genetics, pathophysiology,
assessment, and interventions research since DSM-IV. The approach taken to the classification
of sleep-wake disorders in DSM-5 can be understood within the context of “lumping versus
splitting.” For example, in some categories (e.g., insomnia disorder), a “lumping” approach has
been adopted (i.e., three categories that were separate in DSM-IV—insomnia with other mental
disorders, insomnia with other medical conditions, and insomnia with other sleep disorders—are
all included in the single insomnia category as specifiers), whereas in other categories (e.g.,
narcolepsy), a “splitting” approach has been taken (i.e., there are four separately coded subtypes
of narcolepsy, such as type 1 with cataplexy or hypocretin deficiency, and type 2 without
cataplexy and either without hypocretin deficiency or hypocretin unmeasured), reflecting the
availability of validators derived from epidemiological, neurobiological, and interventions
research.
Because DSM-5 is intended for use by mental health and general medical clinicians who are
not experts in sleep medicine, DSM-5 presents an effort to simplify sleep-wake disorders
classification and thus aggregates diagnoses under broader, less differentiated labels. In contrast,
the International Classification of Sleep Disorders, 3rd Edition (ICSD-3), elaborates numerous
diagnostic subtypes, reflects the science and opinions of the sleep specialist community, and has
been prepared by and for sleep specialists.
The simpler, less-differentiated approach to the diagnosis of sleep-wake disorders in DSM-5
shows superior interrater reliability, as well as convergent, discriminant, and face validity. The
text accompanying each set of diagnostic criteria provides linkages to the corresponding
disorders included in ICSD-3.
The field of sleep disorders medicine has progressed in this direction since the publication of
DSM-IV. The use of biological validators is now embodied in the DSM-5 classification of sleep-

wake disorders, particularly for disorders of excessive sleepiness, such as narcolepsy, for which
cerebrospinal fluid hypocretin-1 immunoreactivity values can be diagnostic; for breathing-related
sleep disorders, for which formal sleep studies (i.e., polysomnography) are indicated; and for
restless legs syndrome, which can often coexist with periodic limb movements during sleep,
detectable via polysomnography.
Co-Occurring Disorders and Differential Diagnosis
Sleep disorders are often accompanied by depression, anxiety, and cognitive changes that must
be addressed in treatment planning and management. Furthermore, persistent sleep disturbances
(both insomnia and excessive sleepiness) are established risk factors for the subsequent
development of mental illnesses (including substance use and non–substance use disorders) and
other medical conditions. They may also represent a prodromal expression of an episode of
mental illness, allowing the possibility of early intervention to preempt or to attenuate a fullblown episode.
The differential diagnosis of sleep-wake complaints necessitates a multidimensional
approach, with consideration of possibly coexisting clinical conditions, which are the rule and
not the exception. Sleep disturbances furnish a clinically useful indicator of clinical conditions
that often coexist with depression and other common mental disorders. Prominent among these
comorbidities are breathing-related sleep disorders, cardiac and pulmonary conditions (e.g.,
congestive heart failure, chronic obstructive pulmonary disease), neurodegenerative disorders
(e.g., Alzheimer’s disease), and disorders of the musculoskeletal system (e.g., osteoarthritis).
These disorders not only may disturb sleep but also may themselves be worsened during sleep
(e.g., prolonged apneas or electrocardiographic arrhythmias during REM sleep; confusional
arousals in individuals with major neurocognitive disorder; seizures in individuals with complex
partial seizures). REM sleep behavior disorder is often an early indicator of neurodegenerative
disorders (alpha synucleinopathies) like Parkinson’s disease. For all of these reasons—related to
differential diagnosis, clinical comorbidity, and facilitation of treatment planning—sleep
disorders are included in DSM-5.
Key Concepts and Terms
Four distinct sleep stages can be measured by polysomnography: REM sleep and three stages of
NREM sleep (N1, N2, and N3).
REM sleep, during which the majority of typical story-like dreams occur, occupies about 20%–25% of total sleep.
NREM sleep stage 1 (N1) is a transition from wakefulness to sleep and occupies about 5% of time spent asleep in healthy
adults.
NREM sleep stage 2 (N2), which is characterized by specific electroencephalographic waveforms (sleep spindles and K
complexes), occupies about 50% of time spent asleep.
NREM sleep stage 3 (N3) (also known as slow-wave sleep) is the deepest level of sleep and occupies about 20% of sleep
time in healthy, younger adults.

These sleep stages have a characteristic temporal organization across the night. N3 tends to occur
in the first one-third to one-half of the night and increases in duration in response to sleep
deprivation. REM sleep occurs cyclically throughout the night, alternating with NREM sleep
about every 80–100 minutes. REM sleep periods increase in duration toward the morning.
Human sleep also varies characteristically across the life span. After relative stability with
large amounts of slow-wave sleep in childhood and early adolescence, sleep continuity and depth
deteriorate across the adult age range. This deterioration is reflected by increased wakefulness
and N1 sleep and decreased N3 sleep. Because of this, age must be considered in the diagnosis of
a sleep disorder in any individual.
Polysomnography is the monitoring of multiple electrophysiological parameters during sleep.
Most polysomnographic studies are conducted during the individual’s usual sleeping hours—that
is, at night. However, daytime polysomnographic studies also are used to quantify daytime
sleepiness. The most common daytime procedure is the multiple sleep
latency test, in which the individual is instructed to lie down in a dark room and not resist
falling asleep; this protocol is repeated five times during the day. The amount of time required to
fall asleep (sleep latency) is measured on each trial and is used as an index of physiological
sleepiness.
The following standard terminology for polysomnographic measures is used throughout the
text in this chapter, and other terms provide context for the chapter discussion:
Sleep continuity refers to the overall balance of sleep and wakefulness during a night of sleep. “Better” sleep continuity
indicates consolidated sleep with little wakefulness or fragmentation; “worse” sleep continuity indicates disrupted sleep with
more wakefulness and fragmentation.
Specific sleep continuity measures include sleep latency—the amount of time required to
fall asleep (expressed in minutes); wake after sleep onset—the amount of awake time
between initial sleep onset and final awakening (expressed in minutes); the number of
awakenings; and sleep efficiency—the ratio of actual time spent asleep to time spent in bed
(expressed as a percentage, with higher numbers indicating better sleep continuity).
Sleep architecture refers to the amount and distribution of specific sleep stages. Sleep architecture measures include absolute
amounts of REM sleep and each NREM sleep stage (in minutes), relative amount of REM sleep and NREM sleep stages
(expressed as a percentage of total sleep time), and latency between sleep onset and the first REM period (REM latency).
When the latency to onset of REM sleep is < 15 minutes, the terms sleep-onset REM and sleep-onset REM period are
employed.
Association With Suicidal Thoughts or Behavior
A review of multiple studies found that the symptom of insomnia may increase the risk for
suicidal thoughts, suicidal behavior, and death, even after adjustment for depression, and that
nightmares increase risk for suicidal thoughts and behavior. In one study of college students,
31.3% of those with sleep problems had suicidal thoughts, and conversely, nearly all (82.7%)
individuals with suicidal thoughts had sleep problems. A review and consensus statement of the
American Academy of Sleep Medicine concluded that in teenagers, < 8 hours of sleep is

F51.01
associated with increased risk of self-harm, suicidal thoughts, and suicidal behavior.
Insomnia Disorder
Diagnostic Criteria
A. A predominant complaint of dissatisfaction with sleep quantity or quality,
associated with one (or more) of the following symptoms:
1. Difficulty initiating sleep. (In children, this may manifest as difficulty initiating
sleep without caregiver intervention.)
2. Difficulty maintaining sleep, characterized by frequent awakenings or
problems returning to sleep after awakenings. (In children, this may manifest
as difficulty returning to sleep without caregiver intervention.)
3. Early-morning awakening with inability to return to sleep.
B. The sleep disturbance causes clinically significant distress or impairment in
social, occupational, educational, academic, behavioral, or other important areas
of functioning.
C. The sleep difficulty occurs at least 3 nights per week.
D. The sleep difficulty is present for at least 3 months.
E. The sleep difficulty occurs despite adequate opportunity for sleep.
F. The insomnia is not better explained by and does not occur exclusively during
the course of another sleep-wake disorder (e.g., narcolepsy, a breathing-related
sleep disorder, a circadian rhythm sleep-wake disorder, a parasomnia).
G. The insomnia is not attributable to the physiological effects of a substance (e.g.,
a drug of abuse, a medication).
H. Coexisting mental disorders and medical conditions do not adequately explain
the predominant complaint of insomnia.
Specify if:
With mental disorder, including substance use disorders
With medical condition
With another sleep disorder
Coding note: The code F51.01 applies to all three specifiers. Code also the
relevant associated mental disorder, medical condition, or other sleep disorder
immediately after the code for insomnia disorder in order to indicate the
association.
Specify if:
Episodic: Symptoms last at least 1 month but less than 3 months.

Persistent: Symptoms last 3 months or longer.
Recurrent: Two (or more) episodes within the space of 1 year.
Note: Acute and short-term insomnia (i.e., symptoms lasting less than 3 months but
otherwise meeting all criteria with regard to frequency, intensity, distress, and/or
impairment) should be coded as an other specified insomnia disorder.
Note: The diagnosis of insomnia disorder is given whether it occurs as an independent
condition or is comorbid with another mental disorder (e.g., major depressive disorder),
medical condition (e.g., pain), or another sleep disorder (e.g., a breathing-related sleep
disorder). For instance, insomnia may develop its own course with some anxiety and
depressive features without those features meeting criteria for any one mental disorder.
Insomnia may also manifest as a clinical feature of a more predominant mental disorder.
Persistent insomnia is a risk factor for depression, anxiety disorders, and alcohol use
disorder and is a common residual symptom after treatment for these conditions. When
insomnia is comorbid with a mental disorder, treatment may need to target both
conditions. Given these different courses, it is often impossible to establish the precise
nature of the relationship between these clinical entities, and this relationship may
change over time. Therefore, in the presence of insomnia and a comorbid disorder, it is
not necessary to make a causal attribution between the two conditions. Rather, the
diagnosis of insomnia disorder is made with concurrent specification of the comorbid
conditions. A concurrent insomnia diagnosis should only be considered when the
insomnia is sufficiently severe to warrant independent clinical attention; otherwise, no
separate diagnosis is necessary.
Recording Procedures
The specifiers “with mental disorder, including substance use disorders”; “with medical
condition”; and “with another sleep disorder” are available to allow the clinician to note
clinically relevant comorbidities. In such cases, record F51.01 insomnia disorder, with [name of
comorbid condition(s) or disorder(s)] followed by the diagnostic code(s) for the comorbid
conditions or disorders (e.g., F51.01 insomnia disorder, with moderate cocaine use disorder and
trigeminal neuralagia; F14.20 moderate cocaine use disorder; G50.0 trigeminal neuralgia).
Diagnostic Features
The essential feature of insomnia disorder is dissatisfaction with sleep quantity or quality with
complaints of difficulty initiating or maintaining sleep. The sleep complaints are accompanied by
clinically significant distress or impairment in social, occupational, or other important areas of
functioning. The sleep disturbance may occur during the course of another mental disorder or
medical condition, or it may occur independently.
Different manifestations of insomnia can occur at different times of the sleep period. Sleeponset insomnia (or initial insomnia) involves difficulty initiating sleep at bedtime. Sleep
maintenance insomnia (or middle insomnia) involves frequent or prolonged awakenings

throughout the night. Late insomnia involves early-morning awakening with an inability to
return to sleep. Difficulty maintaining sleep is the most common single symptom of insomnia,
affecting about 60% of those with insomnia, followed by early awakening and difficulty falling
asleep, according to a U.S. national sample of health care plan members. A combination of these
symptoms is the most common presentation overall. The specific type of sleep complaint often
varies over time. Individuals who complain of difficulty falling asleep at one time may later
complain of difficulty maintaining sleep, and vice versa. Symptoms of difficulty falling asleep
and difficulty maintaining sleep can be quantified by the individual’s retrospective self-report,
sleep diaries in which information is collected prospectively, or other methods, such as
actigraphy or polysomnography. However, the diagnosis of insomnia disorder is based on the
individual’s subjective perception of sleep or a caretaker’s report. Subjective reports from
individuals with insomnia disorder frequently indicate longer sleep latencies, greater time awake
during the night, and less total sleep time than objective (e.g. polysomnographic) data
demonstrate. The reasons for this discrepancy are not well understood, but disturbances in the
underlying neurophysiology reflective of hyperarousal or cortical activation are believed to play
a role.
Nonrestorative sleep, a complaint of poor sleep quality that does not leave the individual
rested upon awakening despite adequate duration, is a common sleep complaint usually
occurring in association with difficulty initiating or maintaining sleep, or less frequently in
isolation. The precise relationship of isolated nonrestorative sleep to insomnia disorder remains
unclear. The prevalence of isolated nonrestorative sleep has been estimated at about 5% and,
unlike insomnia complaints, is reported more commonly in younger individuals. This complaint
can also be reported in association with another sleep disorder (e.g., breathing-related sleep
disorder). When a complaint of nonrestorative sleep occurs in isolation (i.e., in the absence of
difficulty initiating and/or maintaining sleep or other sleep-wake disorders), a diagnosis of other
specified sleep-wake disorder is made.
Aside from the frequency and duration criteria required to make the diagnosis, additional
guidelines are useful to quantify insomnia severity. These quantitative guidelines, while
arbitrary, are provided for illustrative purpose only. For instance, difficulty initiating sleep is
defined by a subjective sleep latency > 20–30 minutes, and difficulty maintaining sleep is
defined by a subjective time awake after sleep onset > 20–30 minutes. Although there is no
standard definition of early-morning awakening, this symptom involves awakening at least 1
hour before the scheduled time and before total sleep time reaches 6½ hours. It is essential to
take into account not only the final awakening time but also the bedtime on the previous evening.
Awakening at 4:00 A.M. does not have the same clinical significance in those who go to bed at
9:00 P.M. as in those who go to bed at 11:00 P.M. Such a symptom may also reflect an agedependent decrease in the ability to sustain sleep or an age-dependent shift in the timing of the
main sleep period. Although these quantitative criteria are frequently employed in research
designs, they do not in their own right reliably distinguish individuals with insomnia from
normal sleepers. Moreover, individuals whose presentations no longer meet subjective diagnostic
criteria for insomnia disorder may continue to show objective disturbance by these parameters,
as well as daytime impairment.

Insomnia disorder involves daytime impairments as well as nighttime sleep difficulties.
These include fatigue or, less commonly, daytime sleepiness; the latter is more common among
older individuals and when insomnia is comorbid with another medical condition (e.g., chronic
pain) or sleep disorder (e.g., sleep apnea). Impairment in cognitive performance may include
difficulties with attention, concentration and memory, and performing complex manual skills.
Associated mood disturbances are typically described as irritability or mood lability and less
commonly as depressive or anxiety symptoms. Not all individuals with nighttime sleep
disturbances are distressed or have functional impairment. For example, sleep continuity is often
interrupted in healthy older adults who nevertheless identify themselves as good sleepers. A
diagnosis of insomnia disorder should be reserved for those individuals with significant daytime
distress or impairment related to their nighttime sleep difficulties.
Associated Features
Insomnia is often associated with physiological and cognitive arousal and conditioning factors
that interfere with sleep. A preoccupation with sleep and distress attributable to the inability to
sleep may lead to a vicious cycle: the more the individual strives to sleep, the more frustration
builds and further impairs sleep. Thus, excessive attention and efforts to sleep, which override
normal sleep-onset mechanisms, may contribute to the development of insomnia. Individuals
with persistent insomnia may also acquire maladaptive sleep habits (e.g., spending excessive
time in bed; following an erratic sleep schedule; napping) and cognitions (e.g., fear of
sleeplessness; apprehensions of daytime impairments; clock monitoring) during the course of the
disorder. Engaging in such activities in an environment in which the individual has frequently
spent sleepless nights may further compound the conditioned arousal and perpetuate sleep
difficulties. Conversely, the individual may fall asleep more easily when not trying to do so.
Some individuals also report better sleep when away from their own bedrooms and their usual
routines.
Insomnia may be accompanied by a variety of daytime complaints and symptoms, including
fatigue, decreased energy, and mood disturbances. Individuals with insomnia disorder may
appear either fatigued or haggard or, conversely, overaroused and “wired.” There may be an
increased incidence of stress-related psychophysiological symptoms (e.g., tension headache,
muscle tension or pain, gastrointestinal symptoms); however, there are no consistent or
characteristic abnormalities on physical examination. Symptoms of anxiety or depression that do
not meet criteria for a specific mental disorder may be present, as well as an excessive focus on
the perceived effects of sleep loss on daytime functioning.
Individuals with insomnia may have elevated scores on self-report psychological or
personality inventories with profiles indicating mild depression and anxiety, a worrisome
cognitive style, an emotion-focused and internalizing style of conflict resolution, and a somatic
focus. Patterns of neurocognitive impairment among individuals with insomnia disorder are
inconsistent, although there may be impairments in performing tasks of higher complexity and
those requiring frequent changes in performance strategy. Individuals with insomnia often
require more effort to maintain cognitive performance.
Prevalence
Population-based estimates vary, depending on the sample and the criteria employed, but

indicate that, across multiple countries, about one-third of adults report insomnia symptoms,
10%–15% experience associated daytime impairments, and 4%–22% have symptoms that meet
criteria for insomnia disorder, with an average of about 10%. Insomnia disorder is the most
prevalent of all sleep disorders. In primary care settings cross-nationally, approximately 20%–
40% of individuals complain of significant insomnia symptoms. Prevalence rates for medical and
psychiatric populations are significantly higher than those in the general population,
especially among individuals with mood, anxiety, and substance use disorders. Forty to fifty
percent of individuals with an insomnia disorder have a comorbid mental disorder. Insomnia is a
more prevalent complaint among women than among men, with a gender ratio of about 1.3:1 in
multinational samples. The gender ratio rises to 1.7:1 after age 45. The prevalence in Norway
among older adolescents (16–18 years) is nearly double in girls compared with boys. Although
insomnia can be a symptom or an independent disorder, it is most frequently observed as a
comorbid condition with another medical condition or mental disorder.
Development and Course
The onset of insomnia symptoms can occur at any time during life, but the first episode is more
common in young adulthood. Less frequently, insomnia begins in childhood or adolescence. In
women, the incidence of new-onset insomnia increases with menopause and may persist even
after other symptoms (e.g., hot flashes) have resolved. Insomnia may have a late-life onset,
which is often associated with the onset of other health-related conditions.
Insomnia can be situational, persistent, or recurrent. Situational or acute insomnia usually
lasts a few days or a few weeks and is often associated with life events or rapid changes in sleep
schedules or environment. It usually resolves once the initial precipitating event subsides. For
some individuals, perhaps those more vulnerable to sleep disturbances, insomnia may persist
long after the initial triggering event, possibly because of conditioning factors and heightened
arousal. The factors that precipitate insomnia may differ from those that perpetuate it. For
example, an individual who is bedridden with a painful injury and has difficulty sleeping may
then develop negative associations for sleep. Conditioned arousal may then persist and lead to
persistent insomnia. A similar course may develop in the context of an acute psychological stress
or a mental disorder. For instance, insomnia that occurs during an episode of major depressive
disorder can become a focus of attention, with consequent negative conditioning, and persist
even after resolution of the depressive episode in at least 40%–50% of individuals. In some
cases, insomnia may also have an insidious onset without any identifiable precipitating factor.
The course of insomnia may also be episodic, with recurrent episodes of sleep difficulties
associated with the occurrence of stressful events. Chronicity rates range from 45% to 75% for
follow-ups of 1–7 years. Even when the course of the insomnia has become chronic, there is
night-to-night variability in sleep patterns, with an occasional restful night’s sleep interspersed
with several nights of poor sleep. The characteristics of insomnia may also change over time.
Many individuals with insomnia have a history of “light” or easily disturbed sleep prior to onset
of more persistent sleep problems.
Insomnia complaints are more prevalent among middle-age and older adults. The type of

Temperamental.
Environmental.
Genetic and physiological.
insomnia symptom changes as a function of age, with difficulties initiating sleep being more
common among young adults and problems maintaining sleep occurring more frequently among
middle-age and older individuals.
Difficulties initiating and maintaining sleep can also occur in children and adolescents, but
there are more limited data on prevalence, risk factors, and comorbidity during these
developmental phases of the life span. Sleep difficulties in childhood can result from
conditioning factors (e.g., a child who does not learn to fall asleep or return to sleep without the
presence of a parent) or from the absence of consistent sleep schedules and bedtime routines.
Insomnia in adolescence is often triggered or exacerbated by irregular sleep schedules, especially
phase delay. In both children and adolescents, psychological and medical factors can contribute
to insomnia.
The increased prevalence of insomnia in older adults is partly explained by the higher
incidence of physical health problems with aging. Changes in sleep patterns associated with the
normal developmental process must be differentiated from those exceeding age-related changes.
Older individuals may experience significant delays in sleep onset or frequent awakenings that
are not associated with complaints or daytime consequences. Although
polysomnography is of limited value in the routine evaluation of insomnia, it may be more
useful in the differential diagnosis among older adults because comorbid conditions associated
with insomnia (e.g., sleep apnea) are more common in older individuals.
Risk and Prognostic Factors
While the risk and prognostic factors discussed in this section increase vulnerability to insomnia,
sleep disturbances are more likely to occur when predisposed individuals are exposed to
precipitating events, such as major life events (e.g., illness, separation) or less severe but more
chronic daily stress. Most individuals resume normal sleep patterns after the initial triggering
event has disappeared, but others—perhaps those more vulnerable to insomnia—continue
experiencing persistent sleep difficulties. Perpetuating factors such as poor sleep habits, irregular
sleep scheduling, and the fear of not sleeping feed into the insomnia problem and may contribute
to a vicious cycle that may induce persistent insomnia.
Anxiety or worry-prone personality or cognitive styles, increased arousal
predisposition, higher stress reactivity, and tendency to repress emotions can increase
vulnerability to insomnia.
Noise, light, or uncomfortably high or low temperature may increase
vulnerability to insomnia. High altitude may also predispose to insomnia attributable to periodic
breathing difficulties during sleep.
Female sex and advancing age are associated with increased
vulnerability to insomnia. Disrupted sleep and insomnia display a familial disposition. Thirtyfive percent to seventy percent of those with insomnia disorder report one or more first-degree
relatives (most commonly, the mother) with a history of insomnia. Heritability may be highest
for insomnia disorder without comorbidities. The prevalence of insomnia is higher among
monozygotic twins relative to dizygotic twins; it is also higher in first-degree family members

Course modifiers.
compared with the general population. The extent to which this link is inherited through a
genetic predisposition, learned by observations of parental models, or established as a by-product
of another psychopathology remains undetermined, although sleep reactivity to stress appears to
play some role.
Deleterious course modifiers include poor sleep hygiene practices (e.g.,
excessive caffeine use, irregular sleep schedules).
Culture-Related Diagnostic Issues
Insomnia is a universal human experience. Identification of insomnia as a problem, the
explanatory models for the condition, and associated help-seeking choices are affected by
culture. Insomnia may be understood as a normal part of aging or of stress response, leading to
low help-seeking or to coping via social support and traditional activities such as prayer.
Explanatory models of insomnia vary greatly, including attributions to the effect of the
environment (e.g., humidity) and bodily processes (e.g., poor blood circulation, internal heat)
among others, and may be associated with nonbiomedical treatment-seeking.
Sex- and Gender-Related Diagnostic Issues
First onset in females is often associated with the birth of a new child or with menopause.
Despite 
higher 
prevalence 
among 
perimenopausal 
and 
postmenopausal 
females,
polysomnographic studies suggest better preservation of sleep continuity and slow-wave sleep in
older females than in older males.
Diagnostic Markers
Polysomnography usually shows impairments of sleep continuity (e.g., increased sleep latency
and time awake after sleep onset and decreased sleep efficiency [percentage of time
in bed asleep]) and may show increased stage 1 sleep and decreased stage 3 sleep. The severity
of these sleep impairments does not always match the individual’s clinical presentation or
subjective complaint of poor sleep, as individuals with insomnia often underestimate sleep
duration 
and 
overestimate 
wakefulness 
relative 
to 
polysomnography. 
Quantitative
electroencephalographic analyses may indicate that individuals with insomnia have greater highfrequency electroencephalography power relative to good sleepers both around the sleep-onset
period and during non–rapid eye movement sleep, although findings vary according to age and
gender. This feature is consistent with increased cortical arousal. Neuroimaging studies have
suggested altered regional brain function consistent with hyperarousal in insomnia, although
interpretation of these findings is complex. Individuals with insomnia disorder may have a lower
sleep propensity and typically do not show increased daytime sleepiness on objective sleep
laboratory measures compared with individuals without sleep disorders.
Other laboratory measures show evidence, although not consistently, of increased arousal
and a generalized activation of the hypothalamic-pituitary-adrenal axis (e.g., increased cortisol
levels, heart rate variability, reactivity to stress, increased metabolic rate). In general, findings
are consistent with the hypothesis that increased physiological and cognitive arousal plays a

Normal sleep variations.
Situational/acute insomnia.
significant role in insomnia disorder.
Association With Suicidal Thoughts or Behavior
The symptom of insomnia has been identified as an independent risk factor for suicidal thoughts
and behavior.
Functional Consequences of Insomnia Disorder
Interpersonal, social, and occupational problems may develop as a result of insomnia or
excessive concern with sleep, increased daytime irritability, and poor concentration. Decreased
attention and concentration are common and may be related to higher rates of accidents observed
in individuals with insomnia. Persistent insomnia is also associated with long-term
consequences, including twofold or greater increased risk of new-onset major depressive
disorder, anxiety disorders, and substance use disorders. Insomnia symptoms may also be a risk
factor for relapse of major depressive disorder. Insomnia disorder, especially with objectively
demonstrated short-sleep duration (< 6 hours), is a significant risk factor for numerous
cardiovascular diseases, including hypertension, coronary artery disease/myocardial infarction,
congestive heart failure, and cerebrovascular disease. Increased absenteeism and reduced
productivity at work, reduced quality of life, and increased economic burden are also significant
functional consequences of insomnia disorder.
Differential Diagnosis
Normal sleep duration varies considerably across persons. Some
individuals who require little sleep (“short sleepers”) may be concerned about their sleep
duration. Short sleepers differ from individuals with insomnia disorder by the lack of difficulty
falling or staying asleep and by the absence of characteristic daytime symptoms (e.g., fatigue,
concentration problems, irritability). However, some short sleepers may desire or attempt to
sleep for a longer period of time and, by prolonging time in bed, may create an insomnia-like
sleep pattern. Clinical insomnia also should be distinguished from normal, age-related sleep
changes. Insomnia must also be distinguished from sleep deprivation attributable to inadequate
opportunity or circumstance for sleep resulting, for example, from an emergency or from
professional or family obligations forcing the individual to stay awake.
Situational/acute insomnia is a condition lasting a few days to several
weeks, often associated with acute stress due to life events or with changes in
sleep schedules. These acute or short-term insomnia symptoms may also produce significant
distress and interfere with social, personal, and occupational functioning. When such symptoms
are frequent enough and meet all other criteria except for the 3-month duration, a diagnosis of
other specified insomnia disorder or unspecified insomnia disorder is made. While the disorder
often remits with subsidence of the stress or adjustment to the change in sleep schedule, some
individuals will develop maladaptive patterns of thought and behavior that result in the
development of a chronic insomnia disorder.

Delayed sleep phase and shift work types of circadian rhythm sleep-wake disorder.
Restless legs syndrome.
Breathing-related sleep disorders.
Narcolepsy.
Parasomnias.
Substance/medication-induced sleep disorder, insomnia type.
Individuals with the
delayed sleep phase type of circadian rhythm sleep-wake disorder report sleep-onset insomnia
only when they try to sleep at socially normal times, but they do not report difficulty falling
asleep or staying asleep when their bed and rising times are delayed and coincide with their
endogenous circadian rhythm. This pattern is observed particularly among adolescents and
younger adults. Shift work type differs from insomnia disorder by the history of recent shift
work.
Restless legs syndrome often produces difficulties initiating and
maintaining sleep. However, an urge to move the legs and any accompanying unpleasant leg
sensations are features that differentiate this disorder from insomnia disorder.
Most individuals with a breathing-related sleep disorder have a
history of loud snoring, breathing pauses during sleep, and excessive daytime sleepiness.
Nonetheless, as many as 50% of individuals with sleep apnea may also report insomnia
symptoms, a feature that is more common among women and older adults.
Narcolepsy may cause insomnia complaints but is distinguished from insomnia
disorder by the predominance of symptoms of excessive daytime sleepiness, cataplexy, sleep
paralysis, and sleep-related hallucinations.
Parasomnias are characterized by a complaint of unusual behavior or events during
sleep that may lead to intermittent awakenings and difficulty resuming sleep. However, it is these
behavioral events, rather than the insomnia per se, that dominate the clinical picture.
Substance/medication-induced 
sleep
disorder, insomnia type, is distinguished from insomnia disorder by the fact that a substance (i.e.,
a drug of abuse, a medication, or exposure to a toxin) is judged to be etiologically related to the
insomnia (see “Substance/Medication-Induced Sleep Disorder” later in this chapter). For
example, insomnia occurring only in the context of heavy coffee consumption would be
diagnosed as caffeine-induced sleep disorder, insomnia type, with onset during intoxication.
Comorbidity
Insomnia is a common comorbidity of many medical conditions, including but not limited to
cancer, diabetes, coronary heart disease, chronic obstructive pulmonary disease, arthritis,
fibromyalgia, other chronic pain conditions, degenerative brain diseases, and traumatic brain
injury. The risk relationship appears to be bidirectional: insomnia increases the risk of many of
these medical conditions, and medical problems increase the risk of insomnia. The direction of
the relationship is not always clear and may change over time; for this reason, comorbid
insomnia is the preferred terminology when insomnia coexists with another medical condition
(or mental disorder). Insomnia disorder also coexists with numerous other sleep disorders.
Approximately one in seven individuals with insomnia disorder has moderate to severe
obstructive sleep apnea. Rates of insomnia complaints among individuals with narcolepsy are
estimated to be about 50%.
Individuals with insomnia disorder frequently have a comorbid mental disorder, particularly

F51.11
bipolar, depressive, and anxiety disorders. Persistent insomnia represents a risk factor or an early
symptom of subsequent bipolar, depressive, anxiety, and substance use disorders. Individuals
with insomnia may misuse medications or alcohol to help with nighttime sleep, anxiolytics to
combat tension or anxiety, and caffeine or other stimulants to combat excessive daytime fatigue.
In addition to worsening the insomnia, this type of substance use may in some cases progress to a
substance use disorder.
Relationship to International Classification of Sleep Disorders
The International Classification of Sleep Disorders, 3rd Edition (ICSD-3), recognizes three
insomnia diagnoses: chronic insomnia disorder, short-term insomnia disorder, and other
insomnia disorder. DSM-5 insomnia disorder and ICSD-3 chronic insomnia disorder closely
parallel each other with respect to symptom, duration, and frequency criteria; however, unlike
DSM-5, ICSD-3 does not include a separate designation for substance/medication-induced sleep
disorder, insomnia type.
Hypersomnolence Disorder
Diagnostic Criteria
A. Self-reported excessive sleepiness (hypersomnolence) despite a main sleep
period lasting at least 7 hours, with at least one of the following symptoms:
1. Recurrent periods of sleep or lapses into sleep within the same day.
2. A prolonged main sleep episode of more than 9 hours per day that is
nonrestorative (i.e., unrefreshing).
3. Difficulty being fully awake after abrupt awakening.
B. The hypersomnolence occurs at least three times per week, for at least 3
months.
C. The hypersomnolence is accompanied by significant distress or impairment in
cognitive, social, occupational, or other important areas of functioning.
D. The hypersomnolence is not better explained by and does not occur exclusively
during the course of another sleep disorder (e.g., narcolepsy, breathing-related
sleep disorder, circadian rhythm sleep-wake disorder, or a parasomnia).
E. The hypersomnolence is not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication).
F. Coexisting mental and medical disorders do not adequately explain the
predominant complaint of hypersomnolence.
Specify if:
With mental disorder, including substance use disorders
With medical condition
With another sleep disorder

Coding note: The code F51.11 applies to all three specifiers. Code also the
relevant associated mental disorder, medical condition, or other sleep disorder
immediately after the code for hypersomnolence disorder in order to indicate the
association.
Specify if:
Acute: Duration of less than 1 month.
Subacute: Duration of 1–3 months.
Persistent: Duration of more than 3 months.
Specify current severity:
Specify severity based on degree of difficulty maintaining daytime alertness as
manifested by the occurrence of multiple attacks of irresistible sleepiness within any
given day occurring, for example, while sedentary, driving, visiting with friends, or
working.
Mild: Difficulty maintaining daytime alertness 1–2 days/week.
Moderate: Difficulty maintaining daytime alertness 3–4 days/week.
Severe: Difficulty maintaining daytime alertness 5–7 days/week.
Recording Procedures
The specifiers “with mental disorder, including substance use disorders”; “with medical
condition”; and “with another sleep disorder” are available to allow the clinician to note
clinically relevant comorbidities. In such cases, record F51.11 hypersomnolence disorder, with
[name of comorbid condition(s) or disorder(s)] followed by the diagnostic code(s) for the
comorbid conditions or disorders (e.g., F51.11 hypersomnolence disorder, with major depressive
disorder; F33.1 major depressive disorder, recurrent, moderate).
Diagnostic Features
Hypersomnolence disorder includes symptoms of excessive quantity of sleep (e.g., extended
nocturnal sleep or long naps), sleepiness, and sleep inertia (i.e., a period of impaired
performance and reduced vigilance following awakening from the regular sleep episode or from
a nap) (Criterion A). Individuals with this disorder generally fall asleep quickly and have a good
sleep efficiency (> 90%). Individuals typically feel sleepiness developing over a period of time,
rather than experiencing a sudden sleep “attack.” Unintentional sleep episodes typically occur in
sedentary situations (e.g., while attending lectures, reading, watching television, or driving long
distances), but in more severe cases they can manifest in high-attention situations such as at
work, in meetings, or at social gatherings. The persistent need for sleep can lead to automatic
behavior (usually of a very routine, low-complexity type) that the individual carries out with
little or no subsequent recall. For example, individuals may find themselves having driven
several miles from where they thought they were, unaware of the “automatic” driving they did in
the preceding minutes.

About 40% of individuals with hypersomnolence disorder may have sleep inertia (also
referred to as “sleep drunkenness”), and this symptom may help differentiate hypersomnolence
disorder from other causes of sleepiness. They may have difficulty waking up in the morning,
sometimes appearing confused, combative, or ataxic. Individuals may set multiple alarm clocks
or rely on others to help get them out of bed. Sleep inertia can also occur upon awakening from a
daytime nap. During that period, the individual appears awake, but motor coordination is
impaired, behavior may be inappropriate, and memory deficits, disorientation in time and space,
and feelings of grogginess may occur. This period may last some minutes to hours.
For some individuals with hypersomnolence disorder, the major sleep episode (for most
individuals, nocturnal sleep) has a duration of 9 hours or more. In the most extreme cases, sleep
episodes can last up to 20 hours. However, the sleep is often nonrestorative and is followed by
difficulty awakening in the morning. For other individuals with hypersomnolence disorder, the
major sleep episode is of normal nocturnal sleep duration (7–9 hours), and they take relatively
long daytime naps (> 1 hour) that do not improve alertness. Most individuals with
hypersomnolence disorder take daytime naps nearly every day regardless of the nocturnal sleep
duration. While many individuals with hypersomnolence are able to reduce their sleep time
during working days, weekend and holiday sleep is greatly increased (by up to 3 hours).
Associated Features
Approximately 80% of individuals with hypersomnolence disorder report that their sleep is
nonrestorative, but this symptom is nonspecific and can occur with disorders that disrupt sleep,
such as obstructive sleep apnea. Naps are often long (> 1 hour) and unrefreshing. Short naps (i.e.,
duration of < 30 minutes) are often unrefreshing. Individuals with hypersomnolence often appear
sleepy and may even fall asleep in the clinician’s waiting area.
A subset of individuals with hypersomnolence disorder have a family history of
hypersomnolence and also have symptoms of autonomic nervous system dysfunction, including
recurrent vascular-type headaches, reactivity of the peripheral vascular system (Raynaud’s
phenomenon), and fainting.
Prevalence
Approximately 5%–10% of individuals in the United States who consult in sleep disorder clinics
with complaints of daytime sleepiness are diagnosed as having hypersomnolence disorder. It is
estimated that about 1% of the European and U.S. general population has episodes of sleep
inertia. Hypersomnolence occurs with relatively equal frequency in men and women.
Development and Course
Hypersomnolence disorder usually begins in late adolescence or early adulthood, with a mean
age at onset of 17–24 years and a gradual progression over weeks to months. Little is known of
the natural history, but for most individuals, the symptoms are persistent and stable, unless
treatment is initiated. Spontaneous remission occurs in about 11%–25% of individuals after 5–7
years. Individuals with hypersomnolence disorder are diagnosed, on average, 10–15 years after
the appearance of the first symptoms. Pediatric cases are rare. The development of other sleep

Environmental.
Genetic and physiological.
Normative variation in sleep.
disorders (e.g., breathing-related sleep disorder) may worsen the degree of sleepiness.
Risk and Prognostic Factors
Hypersomnolence can be increased temporarily by psychological stress and
alcohol use, but they have not been documented as environmental precipitating factors. Viral
infections have been reported to have preceded or accompanied hypersomnolence in about 10%
of cases. Hypersomnolence is common in the months after traumatic brain injury.
Hypersomnolence may be familial, with an autosomal-dominant mode
of inheritance.
Diagnostic Markers
Nocturnal polysomnography demonstrates a normal to prolonged sleep duration, short sleep
latency, and normal to increased sleep continuity. The nocturnal distribution of rapid eye
movement (REM) sleep is also normal. Sleep efficiency is typically > 90%. The multiple sleep
latency test documents sleep tendency, typically indicated by mean sleep latency values of < 8
minutes. In hypersomnolence disorder, the mean sleep latency is typically < 10 minutes and
frequently 8 minutes or less. Sleep-onset REM periods (i.e., the occurrence of REM sleep within
20 minutes of sleep onset) may be present but occur infrequently. Unfortunately, the multiple
sleep latency test has poor test-retest reliability, and it does not distinguish well between
hypersomnolence disorder and narcolepsy type 2.
A 2-week sleep diary can help document amounts and timing of sleep, and actigraphy
provides more accurate data on habitual sleep patterns. In a 32-hour bed rest protocol in which
subjects were encouraged to sleep ad lib, individuals with hypersomnolence disorder slept > 4
hours more than control subjects.
Functional Consequences of Hypersomnolence Disorder
The low level of alertness that occurs while an individual fights the need for sleep can lead to
reduced efficiency, diminished concentration, and poor memory during daytime activities.
Hypersomnolence can lead to significant distress and dysfunction in work and social
relationships. Prolonged nocturnal sleep and difficulty awakening can result in difficulty in
meeting morning obligations, such as arriving at work on time. Unintentional daytime sleep
episodes can be embarrassing and even dangerous, if, for instance, the individual is driving or
operating machinery when the episode occurs.
Differential Diagnosis
“Normal” sleep duration varies considerably in the general
population. “Long sleepers” (i.e., persons who require a greater than average amount of sleep) do
not have excessive sleepiness, sleep inertia, or automatic behavior when they obtain their
required amount of nocturnal sleep. Sleep is reported to be refreshing. If social or occupational
demands lead to shorter nocturnal sleep, daytime symptoms may appear. In hypersomnolence

Narcolepsy.
Fatigue as a symptom of another mental disorder or medical condition.
Breathing-related sleep disorders.
Circadian rhythm sleep-wake disorders.
Parasomnias.
disorder, by contrast, symptoms of excessive sleepiness occur regardless of nocturnal sleep
duration.
An inadequate amount of nocturnal sleep, or behaviorally induced insufficient sleep
syndrome, can produce symptoms of daytime sleepiness very similar to those of
hypersomnolence disorder. An average sleep duration of fewer than 7 hours per night strongly
suggests inadequate nocturnal sleep, yet in the United States, the average adult obtains only 6.75
hours of sleep on typical weeknights. Individuals with inadequate nocturnal sleep typically
“catch up” with longer sleep durations on days when they are free from social or occupational
demands or on vacations. A diagnosis of hypersomnolence disorder should not be made if there
is a question regarding the adequacy of nocturnal sleep duration. A diagnostic and therapeutic
trial of sleep extension for 10–14 days can often clarify the diagnosis.
As in hypersomnolence disorder, individuals with narcolepsy have chronic
sleepiness, but several clinical and laboratory findings help distinguish the disorders. In contrast
to those with hypersomnolence disorder, individuals with narcolepsy tend to sleep 7–8 hours
each day and generally feel refreshed on waking in the morning. Individuals with narcolepsy
generally feel more alert after a 15- to 20-minute nap, whereas those with hypersomnolence
disorder tend to take longer naps, have trouble waking from naps, and do not feel alert afterward.
Individuals with narcolepsy also have varying amounts of cataplexy, hypnagogic hallucinations,
sleep paralysis, and fragmented nocturnal sleep, whereas cataplexy never occurs in
hypersomnolence disorder and the other symptoms are uncommon. The multiple sleep latency
test typically shows more than two sleep-onset REM periods in narcolepsy.
Hypersomnolence 
disorder
should be distinguished from tiredness related to fatigue that may be a symptom of another
mental disorder (e.g., generalized anxiety disorder) or medical condition (e.g., chronic fatigue
syndrome). Unlike hypersomnolence, tiredness is not necessarily relieved by increased sleep and
is unrelated to sleep quantity or quality.
Chronic sleepiness is common in breathing-related sleep
disorders. Individuals with hypersomnolence and breathing-related sleep disorders may have
similar patterns of excessive sleepiness. Breathing-related sleep disorders are suggested by a
history of loud snoring, pauses in breathing during sleep, and nonrefreshing sleep. Examination
often reveals obesity, a small airway, and large neck diameter. Hypertension is common, and
some individuals may demonstrate signs of heart failure. Polysomnographic studies can confirm
the presence of apneic events in breathing-related sleep disorder (and their absence in
hypersomnolence disorder).
In contrast to individuals with hypersomnolence disorder,
individuals with specific subtypes of circadian rhythm sleep-wake disorder show specific
temporal patterns of symptoms. For example, individuals with delayed sleep phase type often
have sleep inertia and sleepiness in the morning and feel most alert in the evening and night, with
habitually late bedtimes. In contrast, those with advanced sleep phase type become sleepy and go
to bed early in the evening but are alert and wake easily in the early morning.
Parasomnias such as non–REM sleep arousal disorders (sleepwalking/sleep terrors)

Hypersomnolence in other mental disorders and medical conditions.
or REM sleep behavior disorder rarely produce the prolonged, undisturbed nocturnal sleep or
daytime sleepiness characteristic of hypersomnolence disorder. However, parasomnias such as
nightmare disorder, which may result in significant curtailment of total sleep time, may
conceivably manifest with daytime sleepiness.
Hypersomnolence disorder must
be distinguished from hypersomnolence occurring as a symptom of another mental disorder (e.g.,
major depressive episode, especially episodes with atypical features) or medical condition (e.g.,
certain cancers, multiple sclerosis). If the predominant complaint of excessive sleepiness is
adequately explained by another mental disorder or medical condition, then an additional
diagnosis of hypersomnolence disorder is not warranted. However, if the hypersomnolence is not
adequately explained by a comorbid mental disorder or medical condition (e.g., the severity and
nature of the hypersomnolence far exceed what would be expected with the mental disorder or
medical condition), an additional diagnosis of hypersomnolence disorder is warranted.
Comorbidity
Many individuals with hypersomnolence disorder have symptoms of depression that may meet
criteria for a depressive disorder. This presentation may be related to the psychosocial
consequences of persistent increased sleep need. More than half of individuals with
hypersomnolence disorder have attention-deficit/hyperactivity disorder symptoms. Individuals
with hypersomnolence disorder are also at risk for substance-related disorders, particularly
related to self-medication with stimulants. This general lack of specificity may contribute to very
heterogeneous profiles among individuals whose symptoms meet the diagnostic criteria for
hypersomnolence disorder. Neurodegenerative conditions, such as Alzheimer’s disease,
Parkinson’s disease, and multiple system atrophy, may also be associated with hypersomnolence.
Relationship to International Classification of Sleep Disorders
The International Classification of Sleep Disorders, 3rd Edition (ICSD-3), differentiates nine
subtypes of “central disorders of hypersomnolence,” including disorders not covered in DSM
such as Kleine-Levin syndrome (recurrent episodes of hypersomnia), hypersomnolence due to a
medical/neurological condition or substance use, and insufficient sleep syndrome.
Narcolepsy
Diagnostic Criteria
A. Recurrent periods of an irrepressible need to sleep, lapsing into sleep, or
napping occurring within the same day. These must have been occurring at least
three times per week over the past 3 months.
B. The presence of at least one of the following:

1. Episodes of cataplexy, defined as either (a) or (b), occurring at least a few
times per month:
a. In individuals with long-standing disease, brief (seconds to minutes)
episodes of sudden bilateral loss of muscle tone with maintained
consciousness that are precipitated by laughter or joking.
b. In children or in individuals within 6 months of onset, spontaneous
grimaces or jaw-opening episodes with tongue thrusting or a global
hypotonia, without any obvious emotional triggers.
2. Hypocretin deficiency, as measured using cerebrospinal fluid (CSF)
hypocretin-1 immunoreactivity values (less than or equal to one-third of
values obtained in healthy subjects tested using the same assay, or less than
or equal to 110 pg/mL). Low CSF levels of hypocretin-1 must not be observed
in the context of acute brain injury, inflammation, or infection.
3. Nocturnal sleep polysomnography showing rapid eye movement (REM) sleep
latency less than or equal to 15 minutes, or a multiple sleep latency test
showing a mean sleep latency less than or equal to 8 minutes and two or
more sleep-onset REM periods.
Specify whether:
G47.411 Narcolepsy with cataplexy or hypocretin deficiency (type 1):
Criterion B1 (episodes of cataplexy) or Criterion B2 (low CSF hypocretin-1
levels) is met.
G47.419 Narcolepsy without cataplexy and either without hypocretin
deficiency or hypocretin unmeasured (type 2): Criterion B3 (positive
polysomnography/multiple sleep latency test) is met, but Criterion B1 is not met
(i.e., no cataplexy is present) and Criterion B2 is not met (i.e., CSF hypocretin-1
levels are not low or have not been measured).
G47.421 Narcolepsy with cataplexy or hypocretin deficiency due to a
medical condition
G47.429 Narcolepsy without cataplexy and without hypocretin deficiency
due to a medical condition
Coding note: For the subtype narcolepsy with cataplexy or hypocretin deficiency
due to a medical condition and the subtype narcolepsy without cataplexy and without
hypocretin deficiency due to a medical condition, code first the underlying medical
condition (e.g., G71.11 myotonic dystrophy; G47.429 narcolepsy without cataplexy
and without hypocretin deficiency due to myotonic dystrophy).
Specify current severity:
Mild: Need for naps only once or twice per day. Sleep disturbance, if present, is
mild. Cataplexy, when present, is infrequent (occurring less than once per week).
Moderate: Need for multiple naps daily. Sleep may be moderately disturbed.
Cataplexy, when present, occurs daily or every few days.

Severe: Nearly constant sleepiness and, often, highly disturbed nocturnal sleep
(which may include excessive body movement and vivid dreams). Cataplexy,
when present, is drug-resistant, with multiple attacks daily.
Subtypes
A diagnosis of narcolepsy, type 1 (NT1; i.e., with cataplexy or hypocretin deficiency) is most
often based on the presence of recurrent sleepiness and cataplexy (given the limited use of
cerebrospinal fluid [CSF] hypocretin determinations). However, cataplexy can emerge years
following onset of sleepiness. Therefore, some individuals may be initially assigned a diagnosis
of narcolepsy, type 2 (NT2; i.e., without cataplexy and either without hypocretin deficiency or
with hypocretin unmeasured), based on sleepiness and positive multiple sleep latency test
(MSLT) findings, only to be reassigned to a diagnosis of NT1 following emergence of cataplexy.
NT1 established by demonstration of low CSF hypocretin levels may manifest without evidence
of clear cataplexy. Other explanations for excessive daytime sleepiness (e.g., sleep deprivation,
shift work, other sleep disorders) and episodes of sudden loss of muscle tone (e.g., seizures, falls
of other origin, functional neurological symptom disorder [conversion disorder]) should be ruled
out. NT2 is established on the basis of chronic sleepiness and characteristic nocturnal sleep
polysomnography findings (e.g., short REM sleep latency) or MSLT findings showing short
mean sleep latency and two or more sleep-onset REM periods (SOREMPs).
NT1 and NT2 can result from other neurological, infectious, metabolic, and genetic
conditions. Inherited disorders, tumors, and head trauma are the most common causes of
secondary narcolepsy. In other cases, the destruction of hypocretin neurons may be secondary to
trauma or hypothalamic surgery. Head trauma or infections of the central nervous system can,
however, produce transitory decreases in CSF hypocretin-1 levels without hypocretin cell loss,
complicating the diagnosis.
Other etiologies include inflammatory lesions due to multiple sclerosis and acute
disseminated encephalomyelitis, vascular disorders such as stroke, and encephalitis. Autosomal
dominant cerebellar ataxia, deafness, and narcolepsy, or ADCA DN, is a familial degenerative
disorder due to missense mutations of the DNA methyltransferase (DNMT1) gene. Cataplexy
with some degree of sleepiness can be caused by other neurological conditions, including PraderWilli syndrome, Niemann-Pick disease type C, Möbius syndrome, and Norrie disease.
Hypocretin deficiency has been reported in Parkinson’s disease as well. NT2-like physiology has
been reported in myotonic dystrophy and Prader-Willi syndrome.
Diagnostic Features
The essential features of narcolepsy are recurrent daytime naps or lapses into sleep that occur
typically daily but that must occur at a minimum of three times a week for at least 3 months
(Criterion A), and are accompanied by one or more of the following: cataplexy (Criterion B1),
hypocretin deficiency (Criterion B2), or characteristic abnormalities on a nocturnal
polysomnogram or on the MSLT (Criterion B3). In most individuals with NT1, the first
symptom to manifest is sleepiness or increased sleep need, followed by cataplexy. Sleepiness is
worse in sedentary circumstances and typically is relieved by brief (10–20 minutes) naps.
NT1 generally manifests with cataplexy, typically brief episodes (seconds up to 2 minutes) of

sudden, bilateral loss of muscle tone precipitated by emotions. A range of positive emotions can
trigger cataplexy, including those associated with laughter, anticipation, or surprise. Less
commonly, cataplexy can be triggered by negative emotions such as anger and embarrassment.
Muscles affected include those of the neck, jaw, arms, legs, or whole body, resulting in head
bobbing, jaw dropping, or complete falls. Individuals are awake and aware during cataplexy.
Cataplexy should not be confused with “weakness” occurring in
the context of athletic activities (physiological) or exclusively after unusual emotional
triggers such as stress or anxiety (suggesting possible psychopathology).
In children and rarely in adults with acute NT1 symptom onset, cataplexy may manifest as
continuous hypotonia rather than episodic bouts of weakness triggered by strong emotions. This
continuous hypotonia may result in gait instability, ptosis, and slack jaw. Superimposed on this
muscle weakness, some individuals may demonstrate phenomena such as tongue protrusion and
grimacing. This static cataplexy is most common within 6 months of a rapid onset.
NT1 is caused by loss of hypothalamic neurons that produce the hypocretin (orexin)
neuropeptides, and CSF hypocretin levels are typically less than one-third of control values (< 
110 pg/mL in most laboratories). Individuals with cataplexy have been shown to have low CSF
hypocretin levels in 85%–90% of cases. In contrast, most individuals with NT2 have normal or
intermediate levels of CSF hypocretin. Thus, hypocretin deficiency is a sufficient diagnostic test
for NT1 (Criterion B2). If CSF hypocretin is measured and not low, an NT2 diagnosis is based
on clinical symptoms (Criterion A) and sleep study data outlined in Criterion B3.
A nocturnal polysomnogram followed by an MSLT is the conventional method for
confirming the diagnosis of both NT1 (if hypocretin testing is unavailable or not feasible) and
NT2 (Criterion B3). These tests must be performed after the individual has stopped all
psychotropic medications (for a duration based on elimination half-life) and obtained adequate
sleep time on a normal sleep-wake schedule (as documented with sleep diaries or, preferably,
actigraphy), ideally for 2 weeks. Notably, the abrupt discontinuation of antidepressants, αadrenergic agonist medications, or stimulants or use of these medications during testing can alter
REM sleep physiology.
The MSLT result must be positive for a diagnosis of NT2, showing a mean sleep latency of
≤ 8 minutes plus at least two SOREMPs; specifically, REM sleep must occur in at least two of
the five nap opportunities. Alternatively, a nocturnal sleep-onset REM period (nSOREMP; REM
sleep-onset latency ≤ 15 minutes) during polysomnography is sufficient to confirm the diagnosis
and meets Criterion B3. An nSOREMP is highly specific to NT1 (95%–97%) but only
moderately sensitive (54%–57%). False positive findings of SOREMPs can occur with shift
work, circadian rhythm sleep-wake disorders, severe obstructive sleep apnea, medication effects,
and insufficient sleep disorder.
The nocturnal polysomnogram and MSLT are diagnostically limited, especially in NT2.
While reliability of diagnostic MSLT testing is relatively high at 85%–95% for NT1, reliability
for the NT2 diagnosis is poorer. Test-retest reliability may be < 50%. This poor reliability may
be due to day-to-day variability in NT2 physiology and technical aspects of the polysomnogram
and MSLT testing, especially inadequate attention to prior sleep time/schedule and
medication/drug use.

Normal or intermediate CSF hypocretin levels among individuals with cataplexy symptoms
can decline to undetectable levels over time.
Associated Features
When sleepiness is severe, automatic behaviors may occur, with the individual continuing his or
her activities in a semiautomatic, hazelike fashion without memory or consciousness.
Approximately 20%–60% of individuals experience vivid hypnagogic hallucinations before or
upon falling asleep or hypnopompic hallucinations just after awakening. These hallucinations are
typically visual or auditory, and sometimes tactile. They are distinct from the less vivid,
nonhallucinatory dream-like mentation at sleep onset that occurs in persons with normal sleep.
Approximately 20%–60% of affected individuals experience sleep paralysis upon falling
asleep or awakening, leaving them awake but unable to move or speak. However, many normal
sleepers also report occasional sleep paralysis, especially with stress or sleep
deprivation. Individuals with narcolepsy can have a range of nocturnal sleep symptoms,
including disrupted nighttime sleep (frequent, brief awakenings), vivid and realistic dreams,
periodic limb movements of sleep, and REM sleep behavior disorder. Nocturnal eating may
occur. Obesity is common. Individuals may appear sleepy or fall asleep in the waiting area or
during clinical examination. During cataplexy, individuals may slump in a chair and have slurred
speech or drooping eyelids. If the clinician is able to check reflexes during cataplexy (most
attacks are < 10 seconds), reflexes are abolished during whole body cataplexy—an important
finding distinguishing genuine cataplexy from functional neurological symptom disorder
(conversion disorder).
Although IQ testing is generally normal in individuals with narcolepsy, impairments in
working memory and executive functioning have been reported.
Prevalence
Narcolepsy-cataplexy (NT1) affects 0.02%–0.05% of the adult general population worldwide
and has an incidence of 0.74 per 100,000 person-years in the United States. Some prevalence
variation has been reported, including lower rates in Israel and higher rates in Japan than in
Europe and the United States. The true prevalence of NT2 is unknown in part because of
diagnostic variability. Narcolepsy affects both genders fairly equally, but this may vary among
different populations.
Development and Course
Onset occurs most often in childhood and adolescence or young adulthood but rarely in old age.
Peak age at onset is around 15–25 years. Onset can be abrupt or progressive, with cataplexy
developing over years. It has been reported that children presenting with abrupt onset of NT1
symptoms have the highest disease severity but that disease severity in these cases tends to
partially improve in the first few years after onset. Abrupt onset in young, prepubescent children
can be associated with obesity and premature puberty. About 50% of individuals with narcolepsy
diagnosed in adulthood recall symptom onset in childhood or adolescence, highlighting problems

Temperamental.
Environmental.
Genetic and physiological.
of diagnostic delays for this condition. Once the disorder has manifested, the course is persistent
and lifelong.
In 90% of cases, the first symptom to manifest is sleepiness or increased sleep, followed by
cataplexy (within 1 year in 50% of cases, within 3 years in 85%). Sleepiness, hypnagogic
hallucinations, vivid dreaming, and REM sleep behavior disorder (vocalizations or complex
motor behavior during REM sleep) are early symptoms. Excessive sleep rapidly progresses to an
inability to stay awake during the day, and to maintain good sleep at night, without a clear
increase in total 24-hour sleep time. In the first months, cataplexy may be atypical, especially in
children, manifesting with a generalized hypotonia rather than with episodic emotionally
triggered weakness. In general, narcolepsy symptoms remain fairly stable but may fluctuate with
life events such as pregnancy and stressors. Exacerbations of symptoms suggest lack of
compliance with medications or development of a concurrent sleep disorder, notably sleep apnea,
which has been identified in about a quarter of individuals with narcolepsy.
Young children and adolescents with narcolepsy often develop aggression or behavioral
problems secondary to sleepiness and/or nighttime sleep disruption. Workload and social
pressure increase through high school and college, reducing available sleep time at night.
Pregnancy does not seem to modify symptoms consistently. After retirement, individuals
typically have more opportunity for napping, reducing the need for stimulants. Maintaining a
regular schedule benefits individuals at all ages.
Risk and Prognostic Factors
Individuals with narcolepsy commonly report that they need more sleep than
other family members.
Group A streptococcal throat infection, influenza (notably pandemic H1N1
2009), or other winter infections, as well as vaccinations (specifically Pandemrix H1N1
vaccination), may trigger an autoimmune process in some individuals, producing narcolepsy a
few months later. Head trauma and abrupt changes in sleep-wake patterns (e.g., job changes,
stress) may be additional triggers.
Monozygotic twins are 25%–32% concordant for narcolepsy. The
prevalence of narcolepsy is 1%–2% in first-degree relatives (a 10- to 40-fold increase overall).
Narcolepsy is strongly associated with HLA DQB1*06:02 (see “Diagnostic Markers”).
DQB1*03:01 increases, while DQB1*05:01, DQB1*06:01, and DQB1*06:03 reduce risk in the
presence of DQB1*06:02, but the effect is small. Polymorphisms within the T-cell receptor alpha
gene and other immune-modulating genes also modulate risk slightly.
Culture-Related Diagnostic Issues
Narcolepsy has been described in many ethnoracial groups and cultural contexts. One study of
1,097 treatment-seeking individuals suggested that among African Americans, more cases may
manifest without cataplexy or with atypical cataplexy (although CSF hypocretin is low), and
with earlier onset compared with non-Latinx Whites. Diagnosis may be further complicated by
the higher presence of obesity and obstructive sleep apnea in this population, which can be

related to differential exposure to social determinants of health, including food insecurity, food
deserts, and limited access to safe and affordable places for physical activity. Individuals with
narcolepsy often experience sleep paralysis, which may be attributed to supernatural forces (e.g.,
frightening spirit is sitting on the sleeper’s chest) in some cultural contexts, contributing to the
perceived dangerousness of the condition and to help-seeking decisions.
Diagnostic Markers
Nocturnal polysomnography followed by an MSLT is used to confirm the diagnosis of
narcolepsy, especially when the disorder is first being diagnosed and before treatment has begun.
In the presence of clear-cut cataplexy, the polysomnography and MSLT are confirmatory for
NT1. In the absence of cataplexy and hypocretin deficiency (if measured), the MSLT is
diagnostic of NT2. Drug or medication effects (e.g., REM-inhibiting antidepressants or sedating
medications), stimulant withdrawal, prior sleep deprivation, shift work, or severe depression may
result in an inaccurate MSLT result and must be ruled out prior to performance of the MSLT. In
particular, chronically insufficient sleep is common and must be considered.
An nSOREMP is highly specific (approximately 1% positive in control subjects) but
moderately sensitive (approximately 50%) for NT1. In contrast, an nSOREMP was only found in
10%–23% of NT2 persons with normal hypocretin levels, suggesting even lower sensitivity in
this subtype. The MSLT result is considered positive for narcolepsy if it displays an average
sleep latency of ≤ 8 minutes and SOREMPs in two or more naps on a four- or five-nap test. The
MSLT result is positive in 90%–95% of individuals with NT1 versus 2%–4% of control subjects
or individuals with other sleep disorders. As noted, poor test-retest reliability for NT2 precludes
determination of comparable data for NT2. Additional polysomnographic findings among
individuals with narcolepsy often include frequent arousals, decreased sleep efficiency, and
increased stage 1 sleep. Periodic limb movements (found in about 40% of individuals with NT1)
and sleep apnea are often noted.
Hypocretin deficiency is demonstrated by measuring CSF hypocretin-1 levels. The test is
particularly useful in individuals with suspected pseudocataplexy and those without typical
cataplexy, or in treatment-refractory cases. The diagnostic value of the test is not affected by
medications, sleep deprivation, or the time of day or night when it is collected, but the findings
are uninterpretable when the individual is severely ill with a concurrent
infection or head trauma or is comatose. CSF cytology, protein, and glucose are within
normal range even when sampled within weeks of rapid onset of the disorder. When measured in
individuals with typical cataplexy symptoms, CSF hypocretin-1 is often already very diminished
or undetectable.
About 85%–95% of individuals with NT1 are positive for the HLA DQB1*06:02 haplotype.
This gene influences immune system antigen presentation, supporting an underlying autoimmune
pathophysiology of NT1. Outbreaks of NT1 after specific vaccinations and infections further
support an autoimmune etiology. In contrast to NT1, there are no biomarkers of NT2. Only about
40%–50% of individuals with NT2 are positive for DQB1*06:02. As 12%–38% of the general
population is DQB1*06:02 positive, testing for this allele is not very helpful for diagnosing NT2

Other hypersomnias.
Sleep deprivation and insufficient nocturnal sleep.
Sleep apnea syndromes.
Insomnia disorder.
Major depressive disorder.
but can be helpful for screening of NT1.
Functional Consequences of Narcolepsy
School performance, driving, work, or other activities that require sustained attention are
impaired, and individuals with narcolepsy should avoid jobs that place themselves (e.g., working
with machinery) or others (e.g., bus driver, pilot) in danger. Once the narcolepsy is controlled
with therapy, individuals can usually drive, although rarely long distances alone. Untreated
individuals are also at risk for social isolation and accidental injury to themselves or others.
Social relations may suffer as these individuals strive to avert cataplexy by exerting control over
emotions or stimuli that cause emotions.
Differential Diagnosis
Hypersomnolence disorder (also known as idiopathic hypersomnia) and
narcolepsy are similar with respect to the presence of chronic daytime sleepiness, age at onset
(typically adolescence or early adulthood), and stable course over time, but can be distinguished
based on distinctive clinical and laboratory features. Individuals with hypersomnolence disorder
typically have longer and less disrupted nocturnal sleep, greater difficulty awakening, more
persistent daytime sleepiness (as opposed to more discrete “sleep attacks” in narcolepsy), longer
and less refreshing daytime sleep episodes, and little or no dreaming during daytime naps. By
contrast, individuals with NT1 generally have cataplexy. Those with NT1 or NT2 may
demonstrate recurrent intrusions of elements of REM sleep into the transition between sleep and
wakefulness (e.g., sleep-related hallucinations and sleep paralysis). The MSLT typically
demonstrates shorter sleep latencies (i.e., greater physiological sleepiness) as well as the
presence of multiple SOREMPs in individuals with narcolepsy.
Sleep deprivation and insufficient nocturnal sleep
are common in adolescents and shift workers. In adolescents, difficulties falling asleep at night
are common, causing sleep deprivation. The MSLT result may be falsely positive if conducted
while the individual is sleep deprived or while his or her sleep is phase delayed.
Obstructive sleep apnea is common in the general population and can be
present in individuals with narcolepsy due to obesity. Because obstructive sleep apnea is more
frequent than narcolepsy, cataplexy may be overlooked (or absent). Narcolepsy should be
considered in individuals with persistent sleepiness despite treatment of their sleep apnea.
Individuals with narcolepsy may focus on the presence of nocturnal sleep
disruption and incorrectly attribute daytime sleepiness to insomnia disorder. Although
individuals with narcolepsy, like those with insomnia disorder, may experience frequent
awakenings during the night, individuals with narcolepsy typically have no difficulty initiating
sleep or returning to sleep in contrast to those with insomnia disorder.
Moreover, insomnia disorder is not typically associated with the severity of daytime sleepiness
observed in narcolepsy.
Excessive daytime sleepiness is a common complaint of both

Functional neurological symptom disorder (conversion disorder; pseudocataplexy).
Attention-deficit/hyperactivity disorder or other behavioral problems.
Atonic seizures.
Syncope.
Chorea and motor disorders.
Schizophrenia.
individuals with major depression and individuals with narcolepsy. The presence of cataplexy
(which is not a feature of major depressive disorder) along with the severity of excessive daytime
sleepiness indicates a diagnosis of NT1 rather than major depressive disorder. Moreover, in
individuals with major depression, MSLT results are most often normal, and there is dissociation
between subjective and objective sleepiness, as measured by the mean sleep latency during the
MSLT. In a meta-analysis of individuals with psychiatric disorders evaluated for sleepiness,
while 25% had a mean sleep latency of < 8 minutes on the MSLT, only rarely were two or more
SOREMPs noted on the MSLT, highlighting the more specific REM sleep dysfunction of
narcolepsy.
Individuals 
with
functional neurological symptom disorder can present with weakness that may raise questions of
cataplexy. However, in functional neurological symptom disorder, the weakness is often longlasting, has unusual triggers, and can result in frequent falls. Individuals may report sleeping and
dreaming during MSLT naps, yet the MSLT does not show the characteristic SOREMP. Home
video recordings and video during sleep studies can be helpful to distinguish this condition from
true cataplexy. The weakness is usually generalized in pseudocataplexy, without partial attacks.
Full-blown, long-lasting pseudocataplexy may occur during consultation, allowing the
examining physician enough time to verify reflexes, which remain intact.
In 
children 
and 
adolescents,
sleepiness can cause behavioral problems, including aggressiveness and inattention, leading to a
misdiagnosis of attention-deficit/hyperactivity disorder (ADHD).
Atonic seizures, a type of seizure that causes sudden loss of muscle strength,
must be distinguished from cataplexy. Atonic seizures are not commonly triggered by emotions
and tend to manifest as abrupt falls rather than the slower “melting” quality of cataplexy. Atonic
seizures usually occur in individuals with additional seizure types and have distinct signatures on
the electroencephalogram.
Like syncope, cataplexy usually develops over several seconds, but individuals with
cataplexy do not have presyncopal symptoms of dizziness, tunnel vision, and auditory changes.
In young children, cataplexy can be misdiagnosed as chorea or
pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections
(PANDAS), especially in the context of a strep throat infection and high antistreptolysin O
antibody levels. Some children may have an overlapping motor disorder close to onset of the
cataplexy.
In the presence of florid and vivid hypnagogic hallucinations, individuals with
narcolepsy may think these experiences are real—a feature that suggests the presence of a true
hallucination characteristic of schizophrenia. However, clear differences have been described in
the pattern of hallucinatory experiences in narcolepsy compared with schizophrenia. Individuals
with narcolepsy tend to report sleep-related multisensory “holistic” hallucinations (visual,
auditory, tactile) rather than the predominantly verbal-auditory sensory mode of individuals with
schizophrenia. Moreover, high-dose stimulant treatment of individuals with narcolepsy may
result in the development of persecutory delusions. If cataplexy is present with hallucinations or
delusions, the first clinical supposition would be that these symptoms are secondary to
narcolepsy before consideration of a co-occurring diagnosis of schizophrenia.

G47.33
Comorbidity
Medical and psychiatric comorbidities are common among individuals with narcolepsy and
include obesity, bruxism, enuresis, precocious puberty (among individuals with pediatric-onset
narcolepsy), mood disorders, and ADHD. Rapid weight gain is common in young children with a
sudden disease onset. Parasomnias (e.g., sleepwalking, REM sleep behavior disorder),
obstructive sleep apnea, restless legs syndrome, and periodic limb movements are common in
individuals who develop narcolepsy. Comorbid sleep apnea should be considered if there is a
sudden aggravation of preexisting narcolepsy.
Relationship to International Classification of Sleep Disorders
The International Classification of Sleep Disorders, 3rd Edition (ICSD-3), differentiates two
subtypes of narcolepsy: NT1 (narcolepsy with cataplexy or hypocretin deficiency) and NT2
(narcolepsy without cataplexy or hypocretin deficiency). NT1 secondary to another medical
condition (G47.421) and NT2 secondary to another medical condition (G47.429) are reported in
ICSD-3 as secondary narcolepsy subtypes.
Breathing-Related Sleep Disorders
The breathing-related sleep disorders category encompasses three relatively distinct disorders:
obstructive sleep apnea hypopnea, central sleep apnea, and sleep-related hypoventilation.
Obstructive Sleep Apnea Hypopnea
Diagnostic Criteria
A. Either (1) or (2):
1. Evidence by polysomnography of at least five obstructive apneas or
hypopneas per hour of sleep and either of the following sleep symptoms:
a. Nocturnal breathing disturbances: snoring, snorting/gasping, or breathing
pauses during sleep.
b. Daytime sleepiness, fatigue, or unrefreshing sleep despite sufficient
opportunities to sleep that is not better explained by another mental
disorder (including a sleep disorder) and is not attributable to another
medical condition.
2. Evidence by polysomnography of 15 or more obstructive apneas and/or
hypopneas per hour of sleep regardless of accompanying symptoms.
Specify current severity:
Mild: Apnea hypopnea index is less than 15.

Moderate: Apnea hypopnea index is 15–30.
Severe: Apnea hypopnea index is greater than 30.
Specifiers
Disease severity is measured by a count of the number of apneas plus hypopneas per hour of
sleep (apnea hypopnea index) using polysomnography or other overnight monitoring.
Apnea refers to the total absence of airflow, and hypopnea refers to a reduction in airflow.
Overall severity is also informed by levels of nocturnal desaturation and sleep fragmentation
(measured by brain cortical arousal frequency and sleep stages) and degree of associated
symptoms and daytime impairment. However, the exact number and thresholds may vary
according to the specific measurement techniques used, and these numbers may change over
time. Regardless of the apnea hypopnea index (count) per se, the disorder is considered to be
more severe when apneas and hypopneas are accompanied by significant oxygen hemoglobin
desaturation (e.g., when more than 10% of the sleep time is spent at desaturation levels of < 
90%) or when sleep is severely fragmented as shown by an elevated arousal index (arousals per
hour of sleep > 30) or reduced time in deep sleep (e.g., percentage stage N3 [slow-wave sleep] < 
5%).
Diagnostic Features
Obstructive sleep apnea hypopnea is the most common breathing-related sleep disorder. It is
characterized by repeated episodes of upper (pharyngeal) airway obstruction (apneas and
hypopneas) during sleep. Each apnea or hypopnea represents a reduction in breathing of at least
10 seconds in duration in adults or two missed breaths in children and is typically associated with
drops in oxygen saturation of ≥ 3% and/or an electroencephalographic arousal. Both sleeprelated (nocturnal) and wake-time symptoms are common. The cardinal symptoms of obstructive
sleep apnea hypopnea are snoring and daytime sleepiness.
Obstructive sleep apnea hypopnea in adults is diagnosed on the basis of findings from a
polysomnogram (or sleep testing performed outside of the sleep center, referred to as out of
center sleep testing [OCST]) and symptoms. The diagnosis is based on symptoms of 1) nocturnal
breathing disturbances (i.e., snoring, snorting/gasping, breathing pauses during sleep), or 2)
daytime sleepiness, fatigue, or unrefreshing sleep despite sufficient opportunities to sleep that are
not better explained by another mental disorder and not attributable to another medical condition,
along with 3) evidence by polysomnography (or OCST) of five or more obstructive apneas or
hypopneas per hour of sleep (Criterion A1). Diagnosis can be made in the absence of these
symptoms if there is evidence by polysomnography (or limited OCST) of 15 or more obstructive
apneas and/or hypopneas per hour of sleep (Criterion A2).
Criteria for a diagnosis of obstructive sleep apnea hypopnea in children differ from those for
a diagnosis in adults. An obstructive apnea hypopnea index of one or more events per hour or
evidence of obstructive hypoventilation in association with snoring or polysomnographic
evidence of airflow obstruction is used to define thresholds of abnormality in children.

Polysomnographic findings in children may differ from those in adults in that children may
demonstrate labored breathing; partial obstructive hypoventilation (sustained reductions of tidal
volume due to upper airway flow limitations) with cyclical oxygen desaturations; hypercapnia;
and paradoxical breathing.
Most cases of obstructive sleep apnea remain undiagnosed. Therefore, specific attention to
symptoms of disturbed sleep occurring in association with snoring or breathing pauses and
physical findings that increase risk of obstructive sleep apnea hypopnea (e.g., central obesity,
crowded pharyngeal airway, elevated blood pressure) is important to reduce the chance of failure
to diagnose this treatable condition.
Associated Features
Because of the frequency of nocturnal awakenings that occur with obstructive sleep apnea
hypopnea, individuals may report symptoms of insomnia. Other common, though nonspecific,
symptoms of obstructive sleep apnea hypopnea are heartburn, nocturia, morning headaches, dry
mouth, erectile dysfunction, and reduced libido. Individuals may complain of difficulty breathing
while lying supine or sleeping. Hypertension may occur in more than 60% of individuals with
obstructive sleep apnea hypopnea.
Arterial blood gas measurements while the individual is awake are usually normal, but some
individuals may demonstrate waking hypoxemia or hypercapnia. This pattern should alert the
clinician to the possibility of coexisting lung disease or hypoventilation. Imaging procedures
may reveal narrowing of the upper airway. Cardiac testing may show evidence of impaired
ventricular function. Arrhythmias such as sinus pauses, frequent atrial and ventricular ectopic
beats, or atrial fibrillation may be present during sleep. Individuals with severe nocturnal oxygen
desaturation may also have elevated hemoglobin or hematocrit values.
Prevalence
Obstructive sleep apnea hypopnea is a very common disorder. Prevalence may be particularly
high among men as compared with women, ranging from 2:1 to 4:1; older adults; and certain
racial and ethnic groups. Prevalence varies cross-nationally, partly because of differences in
assessment methods. Because the disorder is strongly associated with obesity, the rise in obesity
rates has resulted in an increased prevalence of this disorder.
In the United States, 13% of men and 6% of women have polysomnographic evidence of 15
or more obstructive apneas or hypopneas per hour of sleep, and 14% of men and 5% of women
have more than 5 obstructive apneas or hypopneas per hour of sleep, plus symptoms of daytime
sleepiness. Gender differences decline in older age, possibly because of increased prevalence in
females after menopause; postmenopausal females are 2.6–3.5 times more likely to have
obstructive sleep apnea compared with premenopausal females.
In the general community, prevalence rates in the United States of undiagnosed obstructive
sleep apnea hypopnea may be very high in elderly individuals. Obstructive sleep apnea also
occurs in children, with an estimated prevalence of 1%–4%; there is no gender difference among
prepubertal children. Children who are obese have higher rates.

Prevalence of obstructive sleep apnea appears to be higher among African Americans than
among U.S. non-Latinx Whites. An increased prevalence among African Americans, American
Indians, and Hispanics may be related to higher rates of obesity, which can be associated with
differential exposure to social determinants of health, including food insecurity, food deserts, and
limited access to safe and affordable places for physical activity.
Development and Course
The age distribution of obstructive sleep apnea hypopnea has several peaks. The first occurs in
children ages 3–8 years when the nasopharynx may be compromised by a relatively large mass
of tonsillar tissue compared with the size of the upper airway. With growth of the airway and
regression of lymphoid tissue during later childhood, there is reduction in prevalence. However,
with the increase of obesity in adolescents, a second peak in prevalence occurs in that age group.
Finally, as obesity prevalence continues to increase in midlife and women enter menopause, rates
of obstructive sleep apnea hypopnea further increase. The course in older age is unclear;
prevalence of the disorder may plateau after age 65 years, but in some individuals, severity may
worsen with aging. Polysomnographic results must be interpreted in light of other clinical data.
Significant clinical symptoms of insomnia or hypersomnia should be investigated regardless of
the individual’s age.
Obstructive sleep apnea hypopnea usually has an insidious onset, gradual progression, and
persistent course. Typically, the loud snoring has been present for many years, often since
childhood, but an increase in its severity may lead the individual to seek evaluation. Weight gain
may precipitate an increase in symptoms. Although obstructive sleep apnea hypopnea can occur
at any age, it most commonly manifests among individuals ages 40–60 years. Over 4–5 years,
the average apnea hypopnea index increases in adults and older individuals by approximately
two apneas or hypopneas per hour. The apnea hypopnea index is increased and incident
obstructive sleep apnea hypopnea is greater among
individuals who are older, who are male, or who have a higher baseline body mass index
(BMI) or increase their BMI over time. Spontaneous resolution of obstructive sleep apnea
hypopnea has been reported with weight loss, particularly after bariatric surgery. In children,
seasonal variation in obstructive sleep apnea hypopnea has been observed, as has improvement
with overall growth.
In young children, the signs and symptoms of obstructive sleep apnea hypopnea may be more
subtle than in adults, making diagnosis more difficult to establish. Polysomnography is useful in
confirming diagnosis. Evidence of fragmentation of sleep on the polysomnogram may not be as
apparent as in studies of older individuals, possibly because of the high homeostatic drive in
young individuals. Symptoms such as snoring are usually parent-reported and thus have reduced
sensitivity. Agitated arousals and unusual sleep postures, such as sleeping on the hands and
knees, may occur. Nocturnal enuresis also may occur and should raise the suspicion of
obstructive sleep apnea hypopnea if it recurs in a child who was previously dry at night. Children
may also manifest excessive daytime sleepiness, although this is not as common or pronounced
as in adults. Daytime mouth breathing, difficulty in swallowing, and poor speech articulation are

Genetic and physiological.
also common features in children. Children younger than 5 years more often present with
nighttime symptoms, such as observed apneas or labored breathing, than with behavioral
symptoms (i.e., the nighttime symptoms are more noticeable and more often bring the child to
clinical attention). In children older than 5 years, daytime symptoms such as sleepiness and
behavioral problems (e.g., impulsivity and hyperactivity), attention-deficit/hyperactivity
disorder, learning difficulties, and morning headaches are more often the focus of concern.
Children with obstructive sleep apnea hypopnea also may present with delayed growth, failure to
thrive, and developmental delays. Although obesity is a less important risk factor in young
children, it nevertheless contributes to the occurrence of obstructive sleep apnea.
Risk and Prognostic Factors
The major risk factors for obstructive sleep apnea hypopnea are obesity
and male sex. Others include maxillary-mandibular retrognathia or micrognathia, positive family
history of sleep apnea, genetic syndromes that reduce upper airway patency (e.g., Down
syndrome, Treacher Collins syndrome), adenotonsillar hypertrophy (especially in young
children), menopause (in females), and various endocrine syndromes (e.g., acromegaly).
Compared with premenopausal females, males are at increased risk for obstructive sleep apnea
hypopnea, possibly reflecting the influences of sex hormones on ventilatory control and body fat
distribution, as well as gender differences in airway structure. Medications for mental disorders
and medical conditions that tend to induce somnolence may worsen the course of apnea
symptoms if these medications are not managed carefully.
Obstructive sleep apnea hypopnea has a strong genetic basis, as evidenced by the significant
familial aggregation of the apnea hypopnea index. The prevalence of obstructive sleep apnea
hypopnea is approximately twice as high among the first-degree relatives of probands with
obstructive sleep apnea hypopnea as compared with members of control families. One-third of
the variance in the apnea hypopnea index is explained by shared familial factors. Although
genetic markers with diagnostic or prognostic value are not yet available for use, eliciting a
family history of obstructive sleep apnea hypopnea should increase the clinical suspicion for the
disorder.
Culture-Related Diagnostic Issues
There is a potential for sleepiness and fatigue to be reported differently across cultures. In some
groups, snoring may be considered a sign of normal health and thus may not trigger concerns,
leading to underdiagnosis.
Sex- and Gender-Related Diagnostic Issues
Menopause, pregnancy, and polycystic ovarian syndrome increase the risk of obstructive sleep
apnea in females. The transition from premenopause to postmenopause is associated with
increased severity of obstructive sleep apnea. Women may more commonly report fatigue, lack
of energy, or insomnia rather than sleepiness and may underreport snoring.
Diagnostic Markers

Primary snoring and other sleep disorders.
Central sleep apnea.
Polysomnography provides quantitative data on frequency of sleep-related respiratory
disturbances and associated changes in oxygen saturation and sleep continuity. Validated sleep
measures (e.g., multiple sleep latency test, maintenance of wakefulness test) may identify
sleepiness.
Functional Consequences of Obstructive Sleep Apnea Hypopnea
More than 50% of individuals with moderate to severe obstructive sleep apnea hypopnea report
symptoms of daytime sleepiness. A twofold increased risk of occupational accidents has been
reported in association with symptoms of snoring and sleepiness. Motor vehicle crashes also
have been reported to be as much as sevenfold higher among individuals with elevated apnea
hypopnea index values. Clinicians should be cognizant of state government requirements for
reporting this disorder, especially in relationship to commercial drivers. Reduced scores on
measures of health-related quality of life are common in individuals with obstructive sleep apnea
hypopnea. Although the greatest functional impact is observed in the “vitality” domain, severe
obstructive sleep apnea negatively affects general health and physical and social functioning as
well.
Differential Diagnosis
Individuals with obstructive sleep apnea hypopnea must
be differentiated from individuals with primary snoring (i.e., otherwise asymptomatic individuals
who snore and do not have abnormalities on overnight polysomnography). Individuals with
obstructive sleep apnea hypopnea may additionally report nocturnal gasping and choking, which
can be confused with the presence of asthma or gastroesophageal reflux. The presence of
sleepiness or other daytime symptoms not explained by other etiologies suggests the diagnosis of
obstructive sleep apnea hypopnea, but this differentiation requires polysomnography. Definitive
differential diagnosis between hypersomnolence disorder, central sleep apnea, sleep-related
hypoventilation, and obstructive sleep apnea hypopnea also requires polysomnographic studies.
Obstructive sleep apnea hypopnea must be differentiated from other causes of sleepiness,
such as narcolepsy, hypersomnolence disorder, insufficient sleep, and circadian rhythm sleep
disorders. Obstructive sleep apnea hypopnea can be differentiated from narcolepsy by the
absence of cataplexy, sleep-related hallucinations, and sleep paralysis and by the presence of
loud snoring, gasping during sleep, or observed apneas in sleep. Daytime sleep episodes in
narcolepsy are characteristically shorter, more refreshing, and more often associated with
dreaming. Obstructive sleep apnea hypopnea shows characteristic apneas and hypopneas and
oxygen desaturation during nocturnal polysomnographic studies. Narcolepsy results in multiple
sleep-onset rapid eye movement (REM) periods during the MSLT. Narcolepsy, like obstructive
sleep apnea hypopnea, may be associated with obesity, and some individuals have concurrent
narcolepsy and obstructive sleep apnea hypopnea. A diagnosis of narcolepsy does not exclude
the diagnosis of obstructive sleep apnea hypopnea, as the two conditions may co-occur.
Central sleep apnea can be distinguished from obstructive sleep apnea by the
presence of repetitive apneas or hypopneas due to reduction or absence of respiratory effort on

Insomnia disorder.
Panic attacks.
Nocturnal asthma.
Attention-deficit/hyperactivity disorder.
Substance/medication-induced insomnia or hypersomnia.
polysomnogram recording. Snoring may be present, although it may be less prominent than
observed in obstructive sleep apnea hypopnea or absent altogether. Individuals with central sleep
apnea often exhibit fragmented sleep and may also complain of daytime sleepiness. Central sleep
apnea is seen most commonly in individuals with congestive heart failure (Cheyne-Stokes
breathing) or neurological disease, or those using opioid medications.
For individuals complaining of difficulty initiating or maintaining sleep or
early-morning awakenings, insomnia disorder can be differentiated from obstructive sleep apnea
hypopnea by the absence of snoring and the absence of the history, signs, and symptoms
characteristic of the latter disorder. However, insomnia and obstructive sleep apnea hypopnea
may coexist, and if so, both disorders may need to be addressed concurrently to improve sleep.
Nocturnal panic attacks may include symptoms of gasping or choking during sleep
that may be difficult to distinguish clinically from obstructive sleep apnea hypopnea. However,
the lower frequency of episodes, intense autonomic arousal, and lack of excessive sleepiness
differentiate nocturnal panic attacks from obstructive sleep apnea hypopnea. Polysomnography
(or OCST) in individuals with nocturnal panic attacks does not reveal the typical pattern of
apneas or oxygen desaturation characteristic of obstructive sleep apnea hypopnea. Individuals
with obstructive sleep apnea hypopnea do not provide a history of daytime panic attacks.
Nocturnal asthma can often cause sudden awakening from sleep with
symptoms of gasping or choking that are indistinguishable from dyspneic episodes resulting
from obstructive sleep apnea. However, a history of asthma is generally present and
polysomnography (or OCST) does not find evidence of apneas, hypopneas, or oxygen
desaturation indicative of obstructive apnea. Nevertheless, nocturnal asthma and obstructive
sleep apnea can coexist, and this can make it difficult to determine the relative contributions of
each condition.
Attention-deficit/hyperactivity disorder in children may
include symptoms of inattention, academic impairment, hyperactivity, and internalizing
behaviors, all of which may also be symptoms of childhood obstructive sleep apnea hypopnea.
The presence of other symptoms and signs of childhood obstructive sleep apnea hypopnea (e.g.,
labored breathing or snoring during sleep and adenotonsillar hypertrophy) would suggest the
presence of obstructive sleep apnea hypopnea. Obstructive sleep apnea hypopnea and attentiondeficit/hyperactivity disorder may commonly co-occur, and there may be causal links between
them; therefore, risk factors such as enlarged tonsils, obesity, or a family history of sleep apnea
may help alert the clinician to their co-occurrence.
Substance use and substance withdrawal
(including medications) can produce insomnia or hypersomnia. A careful history is usually
sufficient to identify the relevant substance/medication, and follow-up shows improvement of the
sleep disturbance after discontinuation of the substance/medication. In other cases, the use of a
substance/medication (e.g., alcohol, barbiturates, benzodiazepines, opiates) has been shown to
exacerbate obstructive sleep apnea hypopnea. An individual with symptoms and signs consistent
with obstructive sleep apnea hypopnea should receive that diagnosis, even in the presence of
concurrent substance use that is exacerbating the condition.
Comorbidity

Systemic hypertension, coronary artery disease, heart failure, stroke, diabetes, and increased
mortality are consistently associated with obstructive sleep apnea hypopnea. Risk
estimates vary from 30% to as much as 300% for moderate to severe obstructive sleep apnea
hypopnea. Obstructive sleep apnea and cardiovascular disease are strongly related, and treatment
of obstructive sleep apnea reduces morbidity and mortality of cardiovascular disease. Ethnic and
racialized groups that have not received adequate health care may be at higher risk for undetected
cardiovascular risk factors associated with obstructive sleep apnea. Evidence of pulmonary
hypertension and right heart failure (e.g., cor pulmonale, ankle edema, hepatic congestion) is rare
in obstructive sleep apnea hypopnea and when present indicates either very severe disease or
associated hypoventilation or cardiopulmonary comorbidities. Obstructive sleep apnea hypopnea
also may occur with increased frequency in association with a number of medical or neurological
conditions (e.g., cerebrovascular disease, Parkinson’s disease). Physical findings reflect the cooccurrence of these conditions.
As many as one-third of individuals referred for evaluation of obstructive sleep apnea
hypopnea report symptoms of depression, with as many of 10% having depression scores
consistent with moderate to severe depression. Severity of obstructive sleep apnea hypopnea, as
measured by the apnea hypopnea index, has been found to be correlated with severity of
symptoms of depression. This association may be stronger in men than in women.
Relationship to International Classification of Sleep Disorders
The International Classification of Sleep Disorders, 3rd Edition (ICSD-3), differentiates 11
subtypes of “sleep-related breathing disorders,” including central sleep apneas (CSAs) (e.g.,
primary CSA, CSA due to a medical/neurological condition, CSA due to a substance or
medication), obstructive sleep apnea (adult and pediatric), and sleep-related hypoventilation
disorders.
Central Sleep Apnea
Diagnostic Criteria
A. Evidence by polysomnography of five or more central apneas per hour of sleep.
B. The disorder is not better explained by another current sleep disorder.
Specify whether:
G47.31 Idiopathic central sleep apnea: Characterized by repeated episodes of
apneas and hypopneas during sleep caused by variability in respiratory effort but
without evidence of airway obstruction.
R06.3 Cheyne-Stokes breathing: A pattern of periodic crescendo-decrescendo
variation in tidal volume that results in central apneas and hypopneas at a
frequency of at least five events per hour, accompanied by frequent arousal.

G47.37 Central sleep apnea comorbid with opioid use: The pathogenesis of
this subtype is attributed to the effects of opioids on the respiratory rhythm
generators in the medulla as well as the differential effects on hypoxic versus
hypercapnic respiratory drive.
Coding note (for G47.37 code only): When an opioid use disorder is present, first
code the opioid use disorder: F11.10 mild opioid use disorder or F11.20 moderate
or severe opioid use disorder; then code G47.37 central sleep apnea comorbid with
opioid use. When an opioid use disorder is not present (e.g., after a one-time heavy
use of the substance), code only G47.37 central sleep apnea comorbid with opioid
use.
Specify current severity:
Severity of central sleep apnea is graded according to the frequency of the
breathing disturbances as well as the extent of associated oxygen desaturation
and sleep fragmentation that occur as a consequence of repetitive respiratory
disturbances.
Subtypes
There are several subtypes of central sleep apnea. Idiopathic central sleep apnea (alternatively
termed primary central sleep apnea) and central sleep apnea with Cheyne-Stokes breathing are
characterized by increased gain of the ventilatory control system, also referred to as high loop
gain, which leads to instability in ventilation and PaCO2 levels. This instability is termed
periodic breathing and can be recognized by hyperventilation alternating with hypoventilation.
Individuals with these disorders typically have pCO2 levels while awake that are slightly
hypocapnic or normocapnic. Central sleep apnea may also manifest during initiation of treatment
of obstructive sleep apnea hypopnea (termed treatment-emergent central sleep apnea) or may
occur in association with obstructive sleep apnea hypopnea syndrome. The occurrence of central
sleep apnea in association with obstructive sleep apnea is also considered to be due to high loop
gain. In contrast, the pathogenesis of central sleep apnea comorbid with opioid use has been
attributed to the effects of opioids on the respiratory rhythm generators in the medulla as well as
to its differential effects on hypoxic versus hypercapnic respiratory drive. These individuals may
have elevated pCO2 levels while awake. Individuals receiving chronic methadone maintenance
therapy have been noted to have increased somnolence and depression, although the role of
opioid-induced breathing disorders in causing these problems has not been studied. Similarly,
central apnea due to a medical disorder without Cheyne-Stokes breathing is a result of a
pathological process that affects brain-stem ventilatory control centers.
Specifiers
An increase in the central apnea index (i.e., number of central apneas per hour of sleep) reflects
an increase in severity of central sleep apnea. Sleep continuity and quality may be markedly
impaired with reductions in restorative stages of non–rapid eye movement (NREM) sleep (i.e.,

decreased slow-wave sleep [stage N3]). In individuals with severe Cheyne-Stokes breathing, the
pattern can also be observed during resting wakefulness, a finding that is thought to be a
prognostic marker for increased mortality.
Diagnostic Features
Central sleep apnea disorders are characterized by repeated episodes of apneas and hypopneas
during sleep caused by variability in respiratory effort. These are disorders of ventilatory control
in which respiratory events occur in a periodic or intermittent pattern. Idiopathic central sleep
apnea is characterized by sleepiness, insomnia, and awakenings due to dyspnea in association
with five or more central apneas per hour of sleep. Individuals with heart failure, stroke, or renal
failure who have central sleep apnea typically have a breathing pattern called Cheyne-Stokes
breathing, which is characterized by a pattern of periodic crescendo-decrescendo variation in
tidal volume that results in central apneas and hypopneas occurring at a frequency of at least five
events per hour. Events are often associated with arousal, but arousals are not required for the
diagnosis. Central sleep apnea observed at high altitude occurs after ascent to high altitude,
generally at least 2,500 meters above sea level. Central and obstructive sleep apneas may coexist;
a diagnosis of central sleep apnea hypopnea requires that central events be > 50% of the total
number of respiratory events.
Alterations in neuromuscular control of breathing can occur in association with medications
or substances, which can cause or exacerbate impairments of respiratory rhythm and ventilation.
Individuals taking medications with these effects may have a sleep-related breathing disorder
that could contribute to sleep disturbances and symptoms such
as sleepiness, confusion, and depression. Specifically, chronic use of long-acting opioid
medications is often associated with impairment of respiratory control leading to central sleep
apnea.
Associated Features
Individuals with central sleep apnea hypopneas may present with sleepiness or insomnia. They
may have complaints of sleep fragmentation, including awakening with dyspnea. Some
individuals are asymptomatic. Obstructive sleep apnea hypopnea can coexist with CheyneStokes breathing, and thus snoring and abruptly terminated obstructive events may be observed
during sleep.
Physical findings seen in individuals with a Cheyne-Stokes breathing pattern relate to its risk
factors. Findings consistent with heart failure, such as jugular venous distension, S3 heart sound,
lung crackles, and lower-extremity edema, may be present.
Prevalence
The prevalence of idiopathic central sleep apnea is unknown but thought to be rare. The
prevalence of Cheyne-Stokes breathing is high in individuals with depressed cardiac ventricular
ejection fraction. In individuals with an ejection fraction of < 45%, the prevalence has been
reported to range from 15% to 44%. The gender ratio for prevalence in North America, Europe,

Genetic and physiological.
and Australia is even more highly skewed toward men than for obstructive sleep apnea
hypopnea. Prevalence increases with age, and most individuals with the disorder are older than
60 years. Cheyne-Stokes breathing occurs in approximately 20% of individuals with acute stroke
as assessed in Barcelona and Toronto. Central sleep apnea comorbid with opioid use occurs in
approximately 24% of individuals taking opioids chronically for nonmalignant pain and similarly
in individuals receiving methadone maintenance therapy as seen in several high-income
countries. Higher opioid doses are associated with greater severity, especially at morphineequivalent daily dosages > 200 mg. In children assessed in France and Canada, the prevalence
ranges from 4% to 6%.
Development and Course
Polysomnography parameters for diagnosing central sleep apnea are different for children than
for adults and comprise any of the following: 1) cessation of airflow and respiratory effort for
more than 20 seconds, two breath cycles that are associated with an arousal from sleep, or > 3%
oxygen desaturation; or 2) two breath cycles that are associated with bradycardia.
The onset of Cheyne-Stokes breathing appears tied to the development of heart failure. The
Cheyne-Stokes breathing pattern is associated with oscillations in heart rate, blood pressure, and
oxygen desaturation, and elevated sympathetic nervous system activity that can promote
progression of heart failure. The clinical significance of Cheyne-Stokes breathing in the setting
of stroke is not known, but Cheyne-Stokes breathing may be a transient finding that resolves
with time after acute stroke. Central sleep apnea comorbid with opioid use has been documented
with chronic use (i.e., several months).
Risk and Prognostic Factors
Cheyne-Stokes breathing is frequently present in individuals with heart
failure. The coexistence of atrial fibrillation further increases risk, as do older age and male sex.
Cheyne-Stokes breathing is also seen in association with acute stroke and possibly renal failure.
The underlying ventilatory instability in the setting of heart failure has been attributed to
increased ventilatory chemosensitivity and hyperventilation due to pulmonary vascular
congestion and circulatory delay. Central sleep apnea is seen in individuals taking long-acting
opioids. In children, central sleep apnea can be found in
individuals with congenital abnormalities, particularly Arnold-Chiari malformation, or comorbid
medical conditions such as gastroesophageal reflux. Rarely, central sleep apnea resulting from a
congenital condition may not manifest until adulthood (e.g., Arnold-Chiari malformation and
congenital central hypoventilation).
Diagnostic Markers
Polysomnography is used to characterize the breathing characteristics of each breathing-related
sleep disorder subtype. Central sleep apneas are recorded when periods of breathing cessation for
longer than 10 seconds occur. Cheyne-Stokes breathing is characterized by a pattern of periodic
crescendo-decrescendo variation in tidal volume that results in central apneas and hypopneas

Other breathing-related sleep disorders and sleep disorders.
occurring at a frequency of at least five events per hour with the number of central apneas and
hypopneas > 50% of the total number of apneas and hypopneas. The cycle length of CheyneStokes breathing (or time from end of one central apnea to the end of the next apnea) is about 60
seconds.
Functional Consequences of Central Sleep Apnea
Idiopathic central sleep apnea has been reported to cause symptoms of disrupted sleep, including
insomnia and sleepiness. Cheyne-Stokes breathing with comorbid heart failure has been
associated with excessive sleepiness, fatigue, and insomnia, although many individuals may be
asymptomatic. Coexistence of heart failure and Cheyne-Stokes breathing may be associated with
increased cardiac arrhythmias and increased mortality or cardiac transplantation. Individuals with
central sleep apnea comorbid with opioid use may present with symptoms of sleepiness or
insomnia.
Differential Diagnosis
Idiopathic central sleep apnea must be distinguished from other breathing-related sleep disorders,
other sleep disorders, and medical conditions and mental disorders that cause sleep
fragmentation, sleepiness, and fatigue. This is achieved using polysomnography.
Central sleep apnea can be distinguished
from obstructive sleep apnea hypopnea by the presence of at least five central apneas per hour of
sleep. These conditions may co-occur, but central sleep apnea is considered to predominate when
central respiratory events are > 50% of the total number of respiratory events.
Cheyne-Stokes breathing can be distinguished from other mental disorders, including other
sleep disorders, and other medical conditions that cause sleep fragmentation, sleepiness, and
fatigue based on the presence of a predisposing condition (e.g., heart failure or stroke) and signs
and polysomnographic evidence of the characteristic breathing pattern. Polysomnographic
respiratory findings can help distinguish Cheyne-Stokes breathing from insomnia due to other
medical conditions. For example, central sleep apnea due to high-altitude periodic breathing has
a pattern that resembles Cheyne-Stokes breathing but has a shorter cycle time, occurs only at
high altitude, and is not associated with heart failure.
Central sleep apnea comorbid with opioid use can be differentiated from other types of
breathing-related sleep disorders based on the use of long-acting opioid medications in
conjunction with polysomnographic evidence of central apneas and periodic or ataxic breathing.
It can be distinguished from insomnia due to drug or substance use based on polysomnographic
evidence of central sleep apnea.
Comorbidity
Central sleep apnea disorders are frequently present in users of long-acting opioids, such as
methadone. Individuals taking these medications have a breathing-related sleep disorder that
could contribute to sleep disturbances and symptoms such as sleepiness,
confusion, and depression. While the individual is asleep, breathing patterns such as central

apneas, periodic apneas, and ataxic breathing may be observed. Obstructive sleep apnea
hypopnea may coexist with central sleep apnea, and features consistent with this condition can
also be present (see “Obstructive Sleep Apnea Hypopnea” earlier in this chapter). Cheyne-Stokes
breathing is more commonly observed in association with conditions that include heart failure,
stroke, and renal failure and is seen more frequently in individuals with atrial fibrillation.
Individuals with Cheyne-Stokes breathing are more likely to be older, to be male, and to have
lower weight than individuals with obstructive sleep apnea hypopnea.
Relationship to International Classification of Sleep Disorders
The International Classification of Sleep Disorders, 3rd Edition (ICSD-3), includes eight
subtypes of central sleep apnea (central sleep apnea with Cheyne-Stokes breathing, central apnea
due to a medical disorder without Cheyne-Stokes breathing, central sleep apnea due to highaltitude periodic breathing, central sleep apnea due to a medication or substance, primary central
sleep apnea, primary central sleep apnea of infancy, primary central sleep apnea of prematurity,
and treatment-emergent central sleep apnea). As in DSM-5, most of these diagnoses require a
frequency of 5 or more central events per hour of sleep. In addition, ICSD-3 criteria also require
the presence of signs or symptoms (e.g., complaints of insomnia or daytime sleepiness). Central
events must constitute at least 50% of the total number of apneas and hypopneas. Primary central
sleep apnea of infancy and primary central sleep apnea of prematurity have their own distinct
criteria sets that differ from adult forms of central sleep apnea.
Sleep-Related Hypoventilation
Diagnostic Criteria
A. Polysomnograpy demonstrates episodes of decreased respiration associated
with elevated CO2 levels. (Note: In the absence of objective measurement of
CO2, persistent low levels of hemoglobin oxygen saturation unassociated with
apneic/hypopneic events may indicate hypoventilation.)
B. The disturbance is not better explained by another current sleep disorder.
Specify whether:
G47.34 Idiopathic hypoventilation: This subtype is not attributable to any
readily identified condition.
G47.35 Congenital central alveolar hypoventilation: This subtype is a rare
congenital disorder in which the individual typically presents in the perinatal
period with shallow breathing, or cyanosis and apnea during sleep.
G47.36 Comorbid sleep-related hypoventilation: This subtype occurs as a
consequence of a medical condition, such as a pulmonary disorder (e.g.,
interstitial lung disease, chronic obstructive pulmonary disease) or a
neuromuscular or chest wall disorder (e.g., muscular dystrophies, postpolio
syndrome, cervical spinal cord injury, kyphoscoliosis), or medications (e.g.,

benzodiazepines, opiates). It also occurs with obesity (obesity hypoventilation
disorder), where it reflects a combination of increased work of breathing due to
reduced chest wall compliance and ventilation-perfusion mismatch and variably
reduced ventilatory drive. Such individuals usually are characterized by body
mass index of greater than 30 and hypercapnia during wakefulness (with a pCO2
of greater than 45), without other evidence of hypoventilation.
Specify current severity:
Severity is graded according to the degree of hypoxemia and hypercarbia
present during sleep and evidence of end organ impairment due to these
abnormalities (e.g., right-sided heart failure). The presence of blood gas
abnormalities during wakefulness is an indicator of greater severity.
Subtypes
Subtypes of sleep-related hypoventilation include the following:
Idiopathic hypoventilation, also referred to as idiopathic central alveolar hypoventilation, is characterized by reduction of
tidal volume and elevated CO2 during sleep, in the absence of any identifiable comorbidity that would account for the
hypoventilation.
Congenital central alveolar hypoventilation is a rare disorder associated with mutation of the gene PHOX2B. It typically
manifests at birth.
Comorbid sleep-related hypoventilation is due to one of numerous potential comorbidities, including pulmonary disease
(e.g., chronic obstructive pulmonary disease [COPD]), chest wall abnormalities (e.g., kyphoscoliosis), neuromuscular
disease (e.g., amyotrophic lateral sclerosis), and obesity (referred to as obesity hypoventilation), as well as use of
medications or substances, especially opioids.
Diagnostic Features
Sleep-related hypoventilation can occur independently or, more frequently, comorbid with
medical or neurological disorders, medication use, or substance use disorder. Although
symptoms are not mandatory to make this diagnosis, individuals often report excessive daytime
sleepiness, frequent arousals and awakenings during sleep, morning headaches, and insomnia
complaints.
Associated Features
Individuals with sleep-related hypoventilation can present with sleep-related complaints of
insomnia or sleepiness. Episodes of orthopnea can occur in individuals with diaphragm
weakness. Headaches upon awakening may be present. During sleep, episodes of shallow
breathing may be observed, and obstructive sleep apnea hypopnea or central sleep apnea may
coexist. Consequences of ventilatory insufficiency, including pulmonary hypertension, cor
pulmonale (right heart failure), polycythemia, and neurocognitive dysfunction, can be present.

Environmental.
Genetic and physiological.
With progression of ventilatory insufficiency, blood gas abnormalities extend into wakefulness.
Features of a medical condition causing sleep-related hypoventilation can also be present.
Episodes of hypoventilation may be associated with frequent arousals or bradytachycardia.
Individuals may complain of excessive sleepiness and insomnia or morning headaches or may
present with findings of neurocognitive dysfunction or depression. Hypoventilation may not be
present during wakefulness.
Prevalence
Idiopathic sleep-related hypoventilation in adults is very uncommon. The prevalence of
congenital central alveolar hypoventilation is unknown, but the disorder is rare. Comorbid sleeprelated hypoventilation (i.e., hypoventilation comorbid with other conditions, such as COPD,
neuromuscular disorders, or obesity) is more common.
The prevalence of comorbid sleep-related hypoventilation due to obesity in the general
population is estimated to be approximately 0.14%–0.6% based on national obesity rates and
prevalence of obstructive sleep apnea across several countries. Increasing rates of obesity are
associated with increasing prevalence of comorbid sleep-related hypoventilation
due to obesity. In individuals referred to a sleep clinic who have a body mass index > 35
kg/m2, prevalence may be as high as 42%.
Development and Course
Idiopathic sleep-related hypoventilation is thought to be a slowly progressive disorder of
respiratory impairment. When sleep-related hypoventilation disorder occurs comorbidly with
other disorders (e.g., COPD, neuromuscular disorders, obesity), disease severity reflects the
severity of the underlying condition, and the disorder progresses as the condition worsens.
Complications such as pulmonary hypertension, cor pulmonale, cardiac dysrhythmias,
polycythemia, neurocognitive dysfunction, and worsening respiratory failure can develop with
increasing severity of blood gas abnormalities.
Congenital central alveolar hypoventilation usually manifests at birth with shallow, erratic, or
absent breathing. This disorder can also manifest during infancy, childhood, and adulthood
because of variable penetrance of the PHOX2B mutation.
Risk and Prognostic Factors
Ventilatory drive can be reduced in individuals who are using central nervous
system depressants, including benzodiazepines, opiates, and alcohol.
Idiopathic sleep-related hypoventilation is associated with reduced
ventilatory drive due to a blunted chemoresponsiveness to CO2 (reduced respiratory drive; i.e.,
“won’t breathe”), reflecting underlying neurological deficits in centers governing the control of
ventilation. More commonly, sleep-related hypoventilation is comorbid with another medical
condition, such as a pulmonary disorder, a neuromuscular or chest wall disorder, or
hypothyroidism, or with use of medications (e.g., benzodiazepines, opiates). In these conditions,

the hypoventilation may be a consequence of increased work of breathing and/or impairment of
respiratory muscle function (i.e., “can’t breathe”) or reduced respiratory drive.
Neuromuscular disorders influence breathing through impairment of respiratory motor
innervation or respiratory muscle function. They include conditions such as amyotrophic lateral
sclerosis, spinal cord injury, diaphragmatic paralysis, myasthenia gravis, Lambert-Eaton
syndrome, toxic or metabolic myopathies, postpolio syndrome, and Charcot-Marie-Tooth
syndrome.
Congenital central alveolar hypoventilation is a genetic disorder attributable to mutations of
PHOX2B, a gene that is crucial for the development of the embryonic autonomic nervous system
and neural crest derivatives. Children with congenital central alveolar hypoventilation show
blunted ventilatory responses to hypercapnia, especially in non–rapid eye movement sleep.
Sex- and Gender-Related Diagnostic Issues
Gender distributions for sleep-related hypoventilation occurring in association with comorbid
conditions reflect the gender distributions of the comorbid conditions. For example, COPD is
more frequently present in men and with increasing age. Contrary to previous data, obesity
hypoventilation is now thought to occur equally between genders, and in some studies there may
be even a slightly greater prevalence in women.
Diagnostic Markers
Sleep-related hypoventilation is diagnosed using polysomnography, which demonstrates sleeprelated hypoxemia and hypercapnia that is not better explained by another breathing-related sleep
disorder. The documentation of 1) increased arterial pCO2 levels to > 55 mmHg during sleep or
2) a ≥ 10-mmHg increase in pCO2 levels (to a level that also exceeds
50 mmHg) during sleep in comparison to awake supine values, in each case exceeding 10
minutes’ duration, is the gold standard for diagnosis. However, obtaining arterial blood gas
determinations during sleep is impractical, and non-invasive measures of pCO2 have not been
adequately validated during sleep and are not widely used during polysomnography in adults.
Prolonged and sustained decreases in oxygen saturation (oxygen saturation of < 90% for more
than 5 minutes with a nadir of at least 85%, or oxygen saturation of < 90% for at least 30% of
sleep time) in the absence of evidence of upper airway obstruction are often used as an indication
of sleep-related hypoventilation; however, this finding is not specific, as there are other potential
causes of hypoxemia, such as that due to lung disease.
Children with congenital central alveolar hypoventilation are more likely to have disorders of
the autonomic nervous system, Hirschsprung’s disease, neural crest tumors, and characteristic
box-shaped face (i.e., the face is short relative to its width).
Functional Consequences of Sleep-Related Hypoventilation
The consequences of sleep-related hypoventilation are related to the effects of chronic exposure
to hypercapnia and hypoxemia. These blood gas derangements cause vasoconstriction of the

Other medical conditions affecting ventilation.
Other breathing-related sleep disorders.
pulmonary vasculature leading to pulmonary hypertension, which, if severe, can result in rightsided heart failure (cor pulmonale). Hypoxemia can lead to dysfunction of organs such as the
brain, blood, and heart, leading to outcomes such as cognitive dysfunction, polycythemia, and
cardiac arrhythmias. Hypercapnia can depress ventilatory drive, leading to progressive
respiratory failure.
Differential Diagnosis
In adults, the idiopathic variety of sleep-related
hypoventilation is very uncommon and is determined by excluding the presence of lung diseases,
skeletal malformations, neuromuscular disorders, and other medical and neurological disorders
or medications that affect ventilation. Sleep-related hypoventilation must be distinguished from
other causes of sleep-related hypoxemia, such as that due to lung disease.
Sleep-related hypoventilation can be distinguished from
obstructive sleep apnea hypopnea and central sleep apnea based on clinical features and findings
on polysomnography. Sleep-related hypoventilation typically shows more sustained periods of
oxygen desaturation rather than the periodic episodes seen in obstructive sleep apnea hypopnea
and central sleep apnea. Obstructive sleep apnea hypopnea and central sleep apnea also show a
pattern of discrete episodes of repeated airflow reductions that can be absent in sleep-related
hypoventilation. However, both obstructive and central apneas and hypopneas can occur in
association with sleep-related hypoventilation. In obesity hypoventilation, most individuals will
have comorbid obstructive sleep apnea.
Comorbidity
Sleep-related hypoventilation often occurs in association with a pulmonary disorder (e.g.,
interstitial lung disease, COPD), with a neuromuscular or chest wall disorder (e.g., muscular
dystrophies, post-polio syndrome, cervical spinal cord injury, kyphoscoliosis), with obesity, or,
most relevant to the clinician, with medication use (e.g., benzodiazepines, opiates). Congenital
central alveolar hypoventilation often occurs in association with autonomic dysfunction and may
occur in association with Hirschsprung’s disease. COPD, a disorder of lower airway obstruction
usually associated with cigarette smoking, can result in sleep-related hypoventilation and
hypoxemia. The presence of coexisting obstructive sleep apnea
hypopnea is thought to exacerbate hypoxemia and hypercapnia during sleep and wakefulness.
The relationship between congenital central alveolar hypoventilation and idiopathic sleep-related
hypoventilation is unclear; in some individuals, idiopathic sleep-related hypoventilation may
represent cases of late-onset congenital central alveolar hypoventilation.
Relationship to International Classification of Sleep Disorders
The International Classification of Sleep Disorders, 3rd Edition (ICSD-3), recognizes six
subtypes of sleep hypoventilation disorders. Congenital central alveolar hypoventilation
syndrome and idiopathic hypoventilation (idiopathic central alveolar hypoventilation in the
ICSD-3) are identically classified in DSM-5 and ICSD-3. However, the ICSD-3 subtypes obesity

hypoventilation syndrome, sleep-related hypoventilation due to a medication or substance, and
sleep-related hypoventilation due to a medical disorder are subsumed under comorbid sleeprelated hypoventilation in DSM-5. The subtype late-onset central hypoventilation with
hypothalamic dysfunction is not in DSM-5. The DSM-5 approach to classification reflects the
frequent co-occurrence of disorders that lead to hypoventilation and hypoxemia. In contrast, the
classification used in ICSD-3 reflects evidence that there are distinct sleep-related pathogenetic
processes leading to hypoventilation.
Circadian Rhythm Sleep-Wake Disorders
Diagnostic Criteria
A. A persistent or recurrent pattern of sleep disruption that is primarily due to an
alteration of the circadian system or to a misalignment between the endogenous
circadian rhythm and the sleep-wake schedule required by an individual’s
physical environment or social or professional schedule.
B. The sleep disruption leads to excessive sleepiness or insomnia, or both.
C. The sleep disturbance causes clinically significant distress or impairment in
social, occupational, and other important areas of functioning.
Specify whether:
G47.21 Delayed sleep phase type: A pattern of delayed sleep onset and
awakening times, with an inability to fall asleep and awaken at a desired or
conventionally acceptable earlier time.
Specify if:
Familial: A family history of delayed sleep phase is present.
Specify if:
Overlapping with non-24-hour sleep-wake type: Delayed sleep
phase type may overlap with another circadian rhythm sleep-wake
disorder, non-24-hour sleep-wake type.
G47.22 Advanced sleep phase type: A pattern of advanced sleep onset and
awakening times, with an inability to remain awake or asleep until the desired or
conventionally acceptable later sleep or wake times.
Specify if:
Familial: A family history of advanced sleep phase is present.
G47.23 Irregular sleep-wake type: A temporally disorganized sleep-wake
pattern, such that the timing of sleep and wake periods is variable throughout the
24-hour period.

444
G47.24 Non-24-hour sleep-wake type: A pattern of sleep-wake cycles that is
not synchronized to the 24-hour environment, with a consistent daily drift (usually
to later and later times) of sleep onset and wake times.
G47.26 Shift work type: Insomnia during the major sleep period and/or
excessive sleepiness (including inadvertent sleep) during the major awake
period associated with a shift work schedule (i.e., requiring unconventional work
hours).
G47.20 Unspecified type
Specify if:
Episodic: Symptoms last at least 1 month but less than 3 months.
Persistent: Symptoms last 3 months or longer.
Recurrent: Two or more episodes occur within the space of 1 year.
Delayed Sleep Phase Type
Diagnostic Features
The delayed sleep phase type is based primarily on a history of a delay in the timing of the major
sleep period (usually more than 2 hours) in relation to the desired sleep and wake-up time,
resulting in symptoms of insomnia and excessive sleepiness. When allowed to set their own
schedule, individuals with delayed sleep phase type exhibit normal sleep quality and duration for
age. Symptoms of sleep-onset insomnia, difficulty waking in the morning, and excessive
sleepiness early in the day are prominent.
Associated Features
Common associated features of delayed sleep phase type include a history of mental disorders or
a concurrent mental disorder. Extreme and prolonged difficulty awakening with morning
confusion is also common. Insomnia disorder may develop as a result of maladaptive behaviors
that impair sleep and increase arousal because of repeated attempts to fall asleep at an earlier
time.
Prevalence
The prevalence of delayed sleep phase type is highest in adolescents and young adults, with rates
estimated between 3.3% and 4.6% in Norway and Sweden. Studies of adult prevalence yield
significantly lower rates, estimated to be 0.2%–1.7% in Norway and New Zealand. Although the
prevalence of familial delayed sleep phase type has not been established, a family history of
delayed sleep phase is often present in individuals with delayed sleep phase type.
Development and Course
Course is persistent, with intermittent exacerbations throughout adulthood in some individuals.

Genetic and physiological.
Although age at onset is variable, symptoms begin typically in adolescence and early adulthood
and persist for several months to years before diagnosis is established. Severity may decrease
with age. Relapse of symptoms is common.
Clinical expression may vary across the life span depending on social, school, and work
obligations. Exacerbation is usually triggered by a change in work or school schedule that
requires an early rise time. Individuals who can alter their work schedules to accommodate the
delayed circadian sleep and wake timing can experience remission of symptoms.
Increased prevalence in adolescence may be a consequence of both physiological and
behavioral factors. Hormonal changes may be involved specifically, as delayed sleep phase is
associated with the onset of puberty. Thus, delayed sleep phase type in adolescents should be
differentiated from the common delay in the timing of circadian rhythms in this age group. In the
familial form, the course is persistent and may not improve significantly with age.
Risk and Prognostic Factors
Predisposing factors may include a longer than average circadian
period, changes in light sensitivity, and impaired homeostatic sleep drive. Some individuals with
delayed sleep phase type may be hypersensitive to evening light, which can serve as a delay
signal to the circadian clock, or they may be hyposensitive to morning light such that its phaseadvancing effects are reduced. Genetic factors may play a role in the pathogenesis of familial and
sporadic forms of delayed sleep phase type. A study of unrelated families showing strong
heritability of the disorder described a mutation in the clock gene, CRY1, occurring in about
0.6% of the population, which results in increased inhibition of transcription of the activator
clock genes, CLOCK and BMAL1.
Diagnostic Markers
Confirmation of the diagnosis includes a complete history and use of a sleep diary or actigraph
(i.e., a wrist-worn motion detector that monitors motor activity for prolonged periods; if
measured for at least 7 days, motor activity can be used as a proxy for sleep-wake patterns). The
period covered should include weekends, when social and occupational obligations are less strict,
to ensure that the individual exhibits a consistently delayed sleep-wake pattern. The most
commonly available laboratory-derived phase marker is salivary dim light melatonin onset
(DLMO) time. However, not all individuals with diagnosed delayed sleep phase exhibit delayed
DLMO. An investigation of rigorously diagnosed individuals found that only 57% exhibited
physiological phase delays (as gauged by a DLMO time occurring subsequent to the desired
bedtime), whereas the remaining 43% had DLMO times that occurred before the desired
bedtimes. As noted above, behavior, rather than circadian physiological alteration, may play a
more predominant role in the latter (earlier DLMO) group. Given this, phase markers may
ultimately demonstrate more value for optimization of treatment timing and/or as a measure of
treatment response.
Functional Consequences of Delayed Sleep Phase Type
Excessive early day sleepiness is prominent. Extreme and prolonged difficulty awakening with

Normative variations in sleep.
Other sleep disorders.
morning confusion (i.e., sleep inertia) is also common. The severity of insomnia and excessive
sleepiness symptoms varies substantially among individuals and largely depends on the
occupational and social demands on the individual.
Differential Diagnosis
Delayed sleep phase type must be distinguished from “normal” sleep
patterns in which a person has a late schedule that does not cause personal, social, or
occupational distress (most commonly seen in adolescents and young adults).
Insomnia disorder and other circadian rhythm sleep-wake disorders should
be included in the differential. Excessive sleepiness may also be caused by other sleep
disturbances, such as breathing-related sleep disorders, insomnias, restless legs syndrome, and
medical, neurological, and mental disorders. Overnight polysomnography may help in evaluating
for other comorbid sleep disorders, such as sleep apnea. The circadian nature of delayed sleep
phase type, however, should differentiate it from other disorders with similar complaints.
Comorbidity
Delayed sleep phase type is associated with depressive disorders, personality disorders, somatic
symptom disorder or illness anxiety disorder, obsessive-compulsive disorder, attentiondeficit/hyperactivity disorder, and autism spectrum disorder. In addition, comorbid sleep
disorders, such as insomnia disorder, restless legs syndrome, and sleep apnea, as
well as depressive and bipolar disorders and anxiety disorders, can exacerbate symptoms of
insomnia and excessive sleepiness. Delayed sleep phase type may overlap with another circadian
rhythm sleep-wake disorder, non-24-hour sleep-wake type. Sighted individuals with non-24-hour
sleep-wake type disorder commonly also have a history of delayed circadian sleep phase.
Advanced Sleep Phase Type
Specifiers
The presence of a family history of advanced sleep phase type may be indicated with the
specifier “familial.” In the familial form, specific mutations demonstrate an autosomal dominant
mode of inheritance, the course is persistent, and the severity of symptoms may increase with
age. The prevalence of familial advanced sleep phase type has not been established.
Diagnostic Features
Advanced sleep phase type is characterized by sleep-wake times that are several hours earlier
than desired or conventional times. Diagnosis is based primarily on a history of an advance in the
timing of the major sleep period (usually more than 2 hours) in relation to the desired sleep and
wake-up time, with symptoms of early-morning insomnia and excessive daytime sleepiness.
When allowed to set their schedule, individuals with advanced sleep phase type will exhibit
normal sleep quality and duration for age.

Environmental.
Genetic and physiological.
Associated Features
Individuals with advanced sleep phase type are “morning types,” having earlier sleep-wake
times, with the timing of circadian biomarkers such as melatonin and core body temperature
rhythms occurring 2–4 hours earlier than normal. When required to keep a conventional schedule
requiring a delay of bedtime, these individuals will continue to have an early rise time, leading to
persistent sleep deprivation and daytime sleepiness. Use of hypnotics or alcohol to combat sleepmaintenance insomnia and stimulants to reduce daytime sleepiness may lead to substance abuse
in these individuals.
Prevalence
The estimated prevalence of advanced sleep phase type is approximately 1% in middle-age
adults in the United States. Sleep-wake times and circadian phase advance in older individuals
probably account for the higher prevalence in this population.
Development and Course
Onset is usually in late adulthood, although in the familial form, onset can be earlier (during
childhood or early adulthood). The course is typically persistent, lasting more than 3 months, but
the severity may increase depending on work and social schedules. The advanced sleep phase
type is more common in older adults.
Clinical expression may vary across the life span depending on social, school, and work
obligations. Individuals who can alter their work schedules to accommodate the advanced
circadian sleep and wake timing can experience remission of symptoms. Increasing age tends to
advance the sleep phase. However, it is unclear whether the common age-associated advanced
sleep phase type is attributable solely to a change in circadian timing (as seen in the familial
form) or also to age-related changes in the homeostatic regulation of sleep, resulting in earlier
awakening. Severity, remission, and relapse of symptoms are dependent on adherence to
behavioral and environmental treatments designed to control sleep and wake structure and light
exposure.
Risk and Prognostic Factors
Decreased late afternoon/early evening exposure to light and/or increased
exposure to early-morning light because of early-morning awakening can increase the risk of
advanced sleep phase type by advancing circadian rhythms. By going to bed early, these
individuals are not exposed to light in the phase delay region of the curve, resulting in
perpetuation of advanced phase. In familial advanced sleep phase type, a shortening of the
endogenous circadian period can result in an advanced sleep phase, although circadian period
does not appear to systematically decrease with age.
Advanced sleep phase type has demonstrated an autosomal dominant
mode of inheritance, including a PER2 gene mutation causing hypophosphorylation of the PER2
protein and a missense mutation in CKI.

Normal variations in sleep.
Other disorders that cause early-morning awakening.
Diagnostic Markers
A sleep diary and actigraphy are used as diagnostic markers, as described earlier for delayed
sleep phase type.
Functional Consequences of Advanced Sleep Phase Type
Excessive sleepiness associated with advanced sleep phase can have a negative effect on
cognitive performance, social interaction, and safety. Use of wake-promoting agents to combat
sleepiness later in the day or sedatives to inhibit early-morning awakening may increase potential
for substance abuse.
Differential Diagnosis
Behavioral factors such as irregular sleep schedules, voluntary early
awakening, and exposure to light in the early morning should be considered, particularly in older
adults.
Careful attention should be taken to rule out
other sleep-wake disorders (e.g., insomnia disorder), other mental disorders (e.g., depressive
disorders, bipolar disorders), and medical conditions that can cause early-morning awakening.
Comorbidity
Repetitive attempts to resume sleep and the development of maladaptive cognitions and sleeprelated behaviors may result in the development of a comorbid insomnia disorder that requires
clinical attention.
Irregular Sleep-Wake Type
Diagnostic Features
Irregular sleep-wake type is characterized by a lack of discernible sleep-wake circadian rhythm.
The diagnosis of irregular sleep-wake type is based primarily on a history of symptoms of
insomnia at night (during the usual sleep period) and excessive sleepiness (napping) during the
day. There is no major sleep period, and sleep and wake periods across 24 hours are fragmented,
with sleep fragmented into at least three periods during the 24-hour day. The longest sleep period
tends to occur between 2:00 A.M. and 6:00 A.M. and is usually < 4 hours.
Associated Features
A history of isolation or reclusion may occur in association with the disorder and contribute to
the symptoms via a lack of external stimuli to help entrain a normal pattern.
Individuals or their caregivers report frequent naps throughout the day. Irregular sleep-wake type
is most commonly associated with neurodegenerative disorders, such as major neurocognitive
disorder, and many neurodevelopmental disorders in children.

Environmental.
Genetic and physiological.
Normative variations in sleep.
Other medical conditions and mental disorders.
Prevalence
Prevalence of irregular sleep-wake type in the general population is unknown.
Development and Course
The course of irregular sleep-wake type is persistent. Age at onset is variable, but the disorder is
more common in older adults.
Risk and Prognostic Factors
Decreased exposure to environmental light and structured daytime activity can be
associated with a low-amplitude circadian rhythm. Hospitalized individuals are especially prone
to such weak external entraining stimuli, and even outside the hospital setting, individuals with
major neurocognitive disorder are exposed to significantly less bright light.
Neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s
disease, and Huntington’s disease, and neurodevelopmental disorders in children increase the
risk for irregular sleep-wake type.
Diagnostic Markers
A detailed sleep history and a sleep diary (by a caregiver) or actigraphy help confirm the
irregular sleep-wake pattern.
Functional Consequences of Irregular Sleep-Wake Type
Lack of a clearly discernible major sleep and wake period in irregular sleep-wake type results in
insomnia or excessive sleepiness at irregular times of the day. Disruption of the caregiver’s sleep
also often occurs and is an important consideration.
Differential Diagnosis
Irregular sleep-wake type should be distinguished from a voluntary
irregular sleep-wake schedule and poor sleep hygiene, which can result in insomnia and
excessive sleepiness.
Other causes of insomnia and daytime sleepiness,
including comorbid medical conditions and mental disorders or medication, should be
considered.
Comorbidity
Irregular sleep-wake type is often comorbid with neurodegenerative and neurodevelopmental
disorders, such as major neurocognitive disorder, intellectual developmental disorder
(intellectual disability), and traumatic brain injury. It is also comorbid with other medical
conditions and mental disorders in which there is social isolation and/or lack of light and
structured activities.
Non-24-Hour Sleep-Wake Type

Environmental.
Diagnostic Features
The diagnosis of non-24-hour sleep-wake type is based primarily on a history of symptoms of
insomnia or excessive sleepiness related to abnormal synchronization between the 24-hour lightdark cycle and the endogenous circadian rhythm. Individuals typically present with periods of
insomnia, excessive sleepiness, or both, which alternate with short
asymptomatic periods. Starting with the asymptomatic period, when the individual’s sleep phase
is aligned to the external environment, sleep latency will gradually increase and the individual
will complain of sleep-onset insomnia. As the sleep phase continues to drift so that sleep time is
now in the daytime, the individual will have trouble staying awake during the day and will
complain of sleepiness. Because the circadian period is not aligned to the external 24-hour
environment, symptoms will depend on when an individual tries to sleep in relation to the
circadian rhythm of sleep propensity.
Associated Features
Non-24-hour sleep-wake type is most common among blind or visually impaired individuals
who have decreased light perception. In sighted individuals, there is often a history of delayed
sleep phase and of decreased exposure to light and structured social and physical activity.
Sighted individuals with non-24-hour sleep-wake type also demonstrate increased sleep duration.
Prevalence
Prevalence of non-24-hour sleep-wake type in the general population is unclear, but the disorder
appears rare in sighted individuals. The prevalence in blind individuals in the United States is
estimated to be 50%.
Development and Course
Course of non-24-hour sleep-wake type is persistent, with intermittent remission and
exacerbations as a result of changes in work and social schedules throughout the life span. Age at
onset is variable, depending on the onset of visual impairment. In sighted individuals, because of
the overlap with delayed sleep phase type, non-24-hour sleep-wake type may develop in
adolescence or early adulthood. Remission and relapse of symptoms in blind and sighted
individuals largely depend on adherence to treatments designed to control sleep and wake
structure and light exposure.
Clinical expression may vary across the life span depending on social, school, and work
obligations. In adolescents and adults, irregular sleep-wake schedules and exposure to light or
lack of light at critical times of the day can exacerbate the effects of sleep loss and disrupt
circadian entrainment. Consequently, symptoms of insomnia, daytime sleepiness, and school,
occupational, and interpersonal functioning may worsen.
Risk and Prognostic Factors
In sighted individuals, decreased exposure or sensitivity to light and social and

Genetic and physiological.
Other circadian rhythm sleep-wake disorders.
Depressive disorders.
physical activity cues may contribute to a free-running circadian rhythm. With the high
frequency of mental disorders involving social isolation and cases of non-24-hour sleep-wake
type developing after a change in sleep habits (e.g., night shift work, job loss), behavioral factors
in combination with physiological tendency may precipitate and perpetuate this disorder in
sighted individuals. Hospitalized individuals with neurological and psychiatric disorders can
become insensitive to social cues, predisposing them to the development of non-24-hour sleepwake type.
Blindness is a risk factor for non-24-hour sleep-wake type. Non-24hour sleep-wake type has been associated with traumatic brain injury.
Diagnostic Markers
Diagnosis is confirmed by history and sleep diary or actigraphy for an extended period.
Sequential measurement of phase markers (e.g., melatonin) can help determine circadian phase
in both sighted and blind individuals.
Functional Consequences of Non-24-Hour Sleep-Wake Type
Complaints of insomnia (sleep onset and sleep maintenance), excessive sleepiness, or both are
prominent. The unpredictability of sleep and wake times (typically a daily delay drift) results in
difficulty attending school or maintaining a steady job and may increase potential for social
isolation.
Differential Diagnosis
In sighted individuals, non-24-hour sleep-wake type
should be differentiated from delayed sleep phase type, as individuals with delayed sleep phase
type may display a similar progressive delay in sleep period for several days.
Depressive disorders may result in similar circadian dysregulation and
symptoms.
Comorbidity
Blindness is often comorbid with non-24-hour sleep-wake type, as are depressive and bipolar
disorders with social isolation.
Shift Work Type
Diagnostic Features
Diagnosis is primarily based on a history of the individual working outside of the normal 8:00
A.M. to 6:00 P.M. daytime window (particularly at night) on a regularly scheduled (i.e., nonovertime) basis. Symptoms of excessive sleepiness at work, and impaired sleep at home, on a
persistent basis are prominent. Presence of both sets of symptoms are usually required for a
diagnosis of shift work type. Typically, when the individual reverts to a day-work routine,

Temperamental.
Environmental.
Genetic and physiological.
Normative variations in sleep with shift work.
Other sleep disorders.
symptoms resolve.
Prevalence
The prevalence of shift work type is unclear, but the disorder is estimated to affect 5%–10% of
the night worker population in the United States (16%–20% of the workforce). Prevalence rises
with advancement into middle age and beyond.
Development and Course
Shift work type can appear in individuals of any age but is more prevalent in individuals older
than 50 years and typically worsens with the passage of time if the disruptive work schedule
persists. Although older adults may show similar rates of circadian phase adjustment to a change
in routine as do younger adults, they appear to experience significantly more sleep disruption as
a consequence of the circadian phase shift.
Risk and Prognostic Factors
Predisposing factors include a morning-type disposition and a need for long (i.e.,
more than 8 hours) sleep durations in order to feel well rested.
Trying to balance strong competing social and domestic needs (e.g., in parents of
young children) can lead to the development of the shift work type. Persons who are able to
commit to a nocturnal lifestyle, with few competing day-oriented demands, appear at lower risk
for shift work type.
Because shift workers are more likely than day workers to be obese,
obstructive sleep apnea may be present and may exacerbate the symptoms.
Diagnostic Markers
A history and sleep diary or actigraphy may be useful in diagnosis, as discussed earlier for
delayed sleep phase type.
Functional Consequences of Shift Work Type
Individuals with shift work type not only may perform poorly at work but also appear to be at
risk for accidents both at work and on the drive home. Individuals with a history of bipolar
disorder are particularly vulnerable to shift work type–related episodes of mania resulting from
missed nights of sleep. Shift work type often results in interpersonal problems.
Differential Diagnosis
The diagnosis of shift work type, as opposed to the
“normal” difficulties of shift work, depends to some extent on the severity of symptoms and/or
level of distress experienced by the individual.
The presence of shift work type symptoms even when the individual is able

Jet lag.
to live on a day-oriented routine for several weeks at a time may suggest the presence of other
sleep disorders, such as sleep apnea, insomnia, and narcolepsy, which should be ruled out.
Individuals who travel across many time zones on a very frequent basis may experience
effects similar to those experienced by individuals with shift work type who work rotating shifts.
The distinction should be clear, based on the travel history.
Comorbidity
Shift work type has been associated with increased alcohol use disorder, other substance use
disorders, and depression. A variety of physical health disorders (e.g., gastrointestinal disorders,
cardiovascular disease, diabetes, cancer) have been found to be associated with prolonged
exposure to shift work.
Relationship to International Classification of Sleep Disorders
The International Classification of Sleep Disorders, 3rd Edition, circadian rhythm sleep-wake
disorders closely parallel DSM-5 but also include jet lag type.
Parasomnias
Parasomnias are disorders characterized by abnormal behavioral, experiential, or physiological
events occurring in association with sleep, specific sleep stages, or sleep-wake transitions. The
most common parasomnias are non–rapid eye movement (NREM) sleep arousal disorders and
rapid eye movement (REM) sleep behavior disorder. These conditions each have distinct
pathophysiology, clinical characteristics, and prognostic and therapeutic considerations discussed
in the following sections specific to each disorder.
Non–Rapid Eye Movement Sleep Arousal Disorders
Diagnostic Criteria
A. Recurrent episodes of incomplete awakening from sleep, usually occurring
during the first third of the major sleep episode, accompanied by either one of
the following:
1. Sleepwalking: Repeated episodes of rising from bed during sleep and
walking about. While sleepwalking, the individual has a blank, staring face; is
relatively unresponsive to the efforts of others to communicate with him or
her; and can be awakened only with great difficulty.
2. Sleep terrors: Recurrent episodes of abrupt terror arousals from sleep,

usually beginning with a panicky scream. There is intense fear and signs of
autonomic arousal, such as mydriasis, tachycardia, rapid breathing, and
sweating, during each episode. There is relative unresponsiveness to efforts
of others to comfort the individual during the episodes.
B. No or little (e.g., only a single visual scene) dream imagery is recalled.
C. Amnesia for the episodes is present.
D. The episodes cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
E. The disturbance is not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication).
F. Coexisting mental disorders and medical conditions do not explain the episodes
of sleepwalking or sleep terrors.
Specify whether:
F51.3 Sleepwalking type
Specify if:
With sleep-related eating
With sleep-related sexual behavior (sexsomnia)
F51.4 Sleep terror type
Diagnostic Features
The essential feature of non–rapid eye movement (NREM) sleep arousal disorders is the repeated
occurrence of incomplete arousals, usually beginning during the first third of the major sleep
episode (Criterion A), that typically are brief, lasting 1–10 minutes, but may be protracted,
lasting up to 1 hour. The maximum duration of an event is unknown. The eyes are typically open
during these events. Many individuals exhibit both subtypes of arousal (i.e., sleepwalking type
and sleep terror type) on different occasions, which underscores the unitary underlying
pathophysiology. The subtypes reflect varying degrees of simultaneous occurrence of
wakefulness and NREM sleep, resulting in complex behaviors arising from sleep with varying
degrees of conscious awareness, motor activity, and autonomic activation.
The essential feature of sleepwalking is repeated episodes of complex motor behavior
initiated during sleep, including rising from bed and walking about (Criterion A1). Sleepwalking
episodes begin during any stage of NREM sleep, most commonly during slow-wave sleep and
therefore most often occurring during the first third of the night. During episodes, the individual
has reduced alertness and responsiveness, a blank stare, and relative unresponsiveness to
communication with others or efforts by others to awaken the individual. If awakened during the
episode (or on awakening the following morning), the
individual has limited recall for the episode. After the episode, there may initially be a brief
period of confusion or difficulty orienting, followed by full recovery of cognitive function and
appropriate behavior.

The essential feature of sleep terrors is the repeated occurrence of precipitous awakenings
from sleep, usually beginning with a panicky scream or cry (Criterion A2). Sleep terrors usually
begin during the first third of the major sleep episode and last 1–10 minutes, but they may last
considerably longer, particularly in children. The episodes are accompanied by impressive
autonomic arousal and behavioral manifestations of intense fear. During an episode, the
individual is difficult to awaken or comfort. If the individual awakens after the sleep terror, little
or none of the dream, or only fragmentary, single images, are recalled. During a typical episode
of sleep terrors, the individual abruptly sits up in bed screaming or crying, with a frightened
expression and autonomic signs of intense anxiety (e.g., tachycardia, rapid breathing, sweating,
dilation of the pupils). The individual may be inconsolable and is usually unresponsive to the
efforts of others to awaken or comfort him or her. Sleep terrors are also called “night terrors” or
“pavor nocturnus.”
For both subtypes of NREM sleep arousal disorders, the determination of “disorder” depends
on a number of factors, which may vary on an individual basis and will depend on the frequency
of events, potential for violence or injurious behaviors, embarrassment, or disruption/distress of
other household members. Severity determination is best made based on the nature or
consequence of the behaviors rather than simply on frequency.
Associated Features
Sleepwalking episodes can include a wide variety of behaviors. Episodes may begin with
confusion: the individual may simply sit up in bed, look about, or pick at the blanket or sheet.
This behavior then becomes progressively complex. The individual may actually leave the bed
and walk into closets, out of the room, and even out of buildings. Individuals may use the
bathroom, eat, talk, or engage in more complex behaviors. Running and frantic attempts to
escape some apparent threat can also occur. Most behaviors during sleepwalking episodes are
routine and of low complexity. However, cases of unlocking doors and even operating
machinery (driving an automobile) have been reported. Sleepwalking can also include
inappropriate behavior (e.g., commonly, urinating in a closet or wastebasket). Most episodes last
for several minutes to a half hour but may be more protracted. Inasmuch as sleep is a state of
relative analgesia, painful injuries sustained during sleepwalking may not be appreciated until
awakening after the fact.
There are two “specialized” forms of sleepwalking: sleep-related eating behavior and sleeprelated sexual behavior (sexsomnia or sleep sex). Individuals with sleep-related eating
experience unwanted recurrent episodes of eating with varying degrees of amnesia, ranging from
no awareness to full awareness without the ability to avoid or stop eating. During these episodes,
inappropriate foods or even nonfood items (i.e., candy wrappers, small food boxes, or even small
toys) may be ingested. Individuals with sleep-related eating disorder may find evidence of their
eating only the next morning. In sexsomnia, varying degrees of sexual activity (e.g.,
masturbation, fondling, groping, sexual intercourse) occur as complex behaviors arising from
sleep without conscious awareness. This condition is more common in males and may result in
serious interpersonal relationship problems or medicolegal consequences.
During a typical episode of sleep terrors, there is often a sense of overwhelming dread, with a
compulsion to escape. Although fragmentary vivid dream images may occur, a storylike dream
sequence (as in nightmares) is not reported. Most commonly, the individual does not awaken

Environmental.
Genetic and physiological.
fully, but returns to sleep and has amnesia for the episode on awakening the next morning.
Usually only one episode will occur on any one night. Occasionally, several episodes may occur
at intervals throughout the night. These events rarely arise during daytime naps.
Prevalence
Isolated or infrequent NREM sleep arousal behaviors are very common in the general population
worldwide. From 10% to 30% of children have had at least one episode of sleepwalking, and the
cross-national 12-month prevalence rate for sleepwalking in children is approximately 5%. The
prevalence of sleepwalking episodes (not sleepwalking disorder) is estimated to be 12%–14.5%
of children in Canada and 1.0%–7.0% among adults in the United Kingdom, with weekly to
monthly episodes occurring in just 0.5%–0.7% of adults. Estimates for the lifetime prevalence of
sleepwalking overall range from approximately 6.9% to 29.2% around the world, with a pastyear prevalence of sleepwalking of 1.5%–3.6% in adults.
The prevalence of sleep terror disorder in the general population is unknown. The prevalence
of sleep terror episodes (as opposed to sleep terror disorder, in which there is recurrence and
distress or impairment) is approximately 34.4%–36.9% at 18 months of age and 19.7% at 30
months of age in Canadian toddlers, and 2.2% in Canadian and British adults.
Development and Course
NREM sleep arousal disorders occur most commonly in childhood and diminish in frequency
with increasing age. Sleepwalking and sleep terrors are frequently outgrown following infancy
and childhood and become less frequent by adolescence, with remission rates between 50% and
65%; for individuals ages 10–18 years, frequency is reported at 1.1% for sleepwalking and 0.6%
for sleep terrors.
Violent or sexual activity during sleepwalking episodes is more likely to occur in adults. The
onset of sleepwalking in adults with no history of sleepwalking as children should prompt a
search for specific etiologies, such as obstructive sleep apnea, nocturnal seizures, or effect of
medication.
Older children and adults may provide a more detailed recollection of fearful images
associated with sleep terrors than do younger children, who are more likely to have complete
amnesia or report only a vague sense of fear.
Risk and Prognostic Factors
Sedative use, sleep deprivation, sleep-wake schedule disruptions, fatigue, and
physical or emotional stress increase the likelihood of episodes. Fever and sleep deprivation can
produce an increased frequency of NREM sleep arousal disorders.
A family history of sleepwalking or sleep terrors may occur in up to
80% of individuals who sleepwalk. The risk for sleepwalking is further increased (to as much as
60% of offspring) when both parents have a history of the disorder. Familial aggregation of sleep
terrors and sleepwalking has been described, as parental sleepwalking history predicts incident
and persistent sleep terrors in their offspring. Individuals with sleep terrors frequently have a

positive family history of either sleep terrors or sleepwalking, with as high as a 10-fold increase
in the prevalence of the disorder among first-degree biological relatives. Sleep terrors are much
more common in monozygotic twins as compared with dizygotic twins. The exact mode of
inheritance is unknown.
Sex- and Gender-Related Diagnostic Issues
Eating during sleepwalking episodes is more commonly seen in women. Sleepwalking occurs
more often in girls during childhood but more often in men during adulthood.
Among children, sleep terrors are more common in boys than in girls. Among adults, they are
equally common in men and women.
Diagnostic Markers
NREM sleep arousal disorders arise from any stage of NREM sleep but most commonly from
deep NREM sleep (slow-wave sleep). They are most likely to appear in the first third of the night
and do not commonly occur during daytime naps. During the episode, the polysomnogram may
be obscured with movement artifact. In the absence of such artifact, the electroencephalogram
(EEG) may show a variety of patterns, including continuation of rhythmic delta activity into
awakening, indicating partial or incomplete arousal; or alternatively, theta, alpha, or mixed
frequency EEG activity may be seen during the episode, with frequent mixed slow/mixed
frequency EEG arousals during slow-wave sleep being more common in individuals with NREM
sleep arousal disorders than in control subjects. In distinction to an epileptic seizure, NREM
sleep parasomnia disorders of arousal do not show features of spatiotemporal evolution of EEG
rhythms during the episode.
Polysomnography in conjunction with audiovisual monitoring can be used to document
episodes of sleepwalking. In the absence of actually capturing an event during a
polysomnographic recording, there are no reliable polysomnographic features that can serve as a
marker for sleepwalking. Sleep deprivation may increase the likelihood of capturing an event. As
a group, individuals who sleepwalk show instability of deep NREM sleep, but the overlap in
findings with persons who do not sleepwalk is great enough to preclude use of this indicator in
establishing a diagnosis. Unlike arousals from REM sleep associated with nightmares, in which
there is an increase in heart rate and respiration prior to the arousal, the NREM sleep arousals of
sleep terrors begin precipitously from sleep, without anticipatory autonomic changes. The
arousals are associated with impressive autonomic activity, with doubling or tripling of the heart
rate. The pathophysiology is poorly understood, but there appears to be instability in the deeper
stages of NREM sleep. Aside from capturing an event during a formal sleep study, there are no
reliable polysomnographic indicators of the tendency to experience sleep terrors.
Functional Consequences of Non–Rapid Eye Movement Sleep Arousal
Disorders
For the diagnosis of an NREM sleep arousal disorder to be made, the individual or household
members must experience clinically significant distress or impairment, although such symptoms
may occur occasionally in nonclinical populations and would be subthreshold for the diagnosis.

Nightmare disorder.
Breathing-related sleep disorders.
REM sleep behavior disorder.
Parasomnia overlap syndrome.
Sleep-related seizures.
Alcohol-induced blackouts.
Embarrassment concerning the episodes can impair social relationships. Social isolation or
occupational difficulties can result. Uncommonly, NREM sleep arousal disorders may result in
serious injury to the individual or to someone trying to console the individual. Injuries to others
are confined to those in close proximity; individuals are not “sought out.” For individuals with
sleep-related eating behaviors, unknowingly preparing or eating food during the sleep period
may create problems such as poor diabetes control, weight gain, injury (cuts and burns), or
consequences of eating dangerous or toxic inedibles. NREM sleep arousal disorders may rarely
result in violent or injurious behaviors with forensic implications.
Differential Diagnosis
In contrast to individuals with NREM sleep arousal disorders, individuals
with nightmare disorder typically awaken easily and completely, report vivid storylike dreams
accompanying the episodes, and tend to have episodes later in the night. NREM sleep arousal
disorders occur during NREM sleep, whereas nightmares usually occur during REM sleep.
Parents of children with NREM sleep arousal disorders may misinterpret reports of fragmentary
imagery as nightmares.
Breathing disorders during sleep can also produce confusional
arousals with subsequent amnesia. However, breathing-related sleep disorders are also
characterized by symptoms of snoring, breathing pauses, and daytime sleepiness. In some
individuals, a breathing-related sleep disorder may precipitate episodes of sleepwalking.
REM sleep behavior disorder may be difficult to distinguish from
NREM sleep arousal disorders. REM sleep behavior disorder is characterized by episodes of
prominent, complex movements, often involving personal injury arising from sleep. In contrast
to NREM sleep arousal disorders, REM sleep behavior disorder occurs during REM sleep.
Individuals with REM sleep behavior disorder may be awakened easily during an episode and
report more detailed and vivid dream content than do individuals with NREM sleep arousal
disorders. These individuals and/or their bed partners often report that they “act out dreams.”
Parasomnia 
overlap 
syndrome 
consists 
of 
clinical 
and
polysomnographic features of both sleepwalking and REM sleep behavior disorder.
Some types of seizures can produce episodes of very unusual behaviors
that occur predominantly or exclusively during sleep. Nocturnal seizures may closely mimic
NREM sleep arousal disorders but tend to be more stereotypic in nature, occur multiple times
nightly, and be more likely to occur from daytime naps. In addition, seizures may arise from
wakefulness, which does not occur with NREM sleep arousal disorders. The presence of sleeprelated seizures does not preclude the presence of NREM sleep arousal disorders. When
recurrent, sleep-related seizures are considered to be a form of epilepsy.
Alcohol-induced blackouts may be associated with extremely complex
behaviors in the absence of other suggestions of intoxication. They do not involve the loss of
consciousness but rather reflect an isolated disruption of memory for events during a drinking
episode. By history, these behaviors may be indistinguishable from those seen in NREM sleep

Dissociative amnesia, with dissociative fugue.
Malingering or other voluntary behavior.
Panic disorder.
Medication-induced complex behaviors.
Night eating syndrome.
F51.5
arousal disorders.
Dissociative fugue may be extremely difficult to
distinguish from sleepwalking. Unlike all other parasomnias, nocturnal dissociative fugue arises
from a period of wakefulness during sleep, rather than precipitously from sleep without
intervening wakefulness. A history of recurrent childhood physical or sexual abuse is usually
present (but may be difficult to obtain).
As with dissociative fugue, malingering or other voluntary
behavior occurs during wakefulness.
Panic attacks may also cause abrupt awakenings from deep NREM sleep
accompanied by fearfulness, but these episodes produce rapid and complete awakening without
the confusion, amnesia, or motor activity typical of NREM sleep arousal disorders.
Behaviors similar to those in NREM sleep arousal disorders
can be induced by use of, or withdrawal from, substances or medications (e.g., benzodiazepines,
nonbenzodiazepine sedative-hypnotics, opiates, cocaine, nicotine, antipsychotics or other
dopamine receptor–blocking agents, tricyclic antidepressants, chloral hydrate). Such behaviors
may arise from the sleep period and may be extremely complex. The underlying pathophysiology
appears to be a relatively isolated amnesia. In such cases, substance/medication-induced sleep
disorder, parasomnia type, should be diagnosed (see “Substance/Medication-Induced Sleep
Disorder” later in this chapter).
In contrast to the sleep-related eating form of sleepwalking, which is
characterized by recurrent episodes of eating during incomplete arousals from sleep, night eating
syndrome is considered to be an abnormality in the circadian rhythm of meal timing, with a
normal circadian timing of sleep onset in which the individual wakes up in the middle of the
night and overeats.
Comorbidity
Typically, sleepwalking in both children and adults is not associated with significant mental
disorders. However, in adults, there is an association between sleepwalking and major depressive
episodes and obsessive-compulsive disorder. Children or adults with sleep terrors may have
elevated scores for depression and anxiety on personality inventories.
Relationship to International Classification of Sleep Disorders
The International Classification of Sleep Disorders, 3rd Edition, includes “confusional arousal,
sleep terrors, and sleepwalking” as NREM sleep arousal disorders.
Nightmare Disorder
Diagnostic Criteria

A. Repeated occurrences of extended, extremely dysphoric, and well-remembered
dreams that usually involve efforts to avoid threats to survival, security, or
physical integrity and that generally occur during the second half of the major
sleep episode.
B. On awakening from the dysphoric dreams, the individual rapidly becomes
oriented and alert.
C. The sleep disturbance causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
D. The nightmare symptoms are not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication).
E. Coexisting mental disorders and medical conditions do not adequately explain
the predominant complaint of dysphoric dreams.
Specify if:
During sleep onset
Specify if:
With mental disorder, including substance use disorders
With medical condition
With another sleep disorder
Coding note: The code F51.5 applies to all three specifiers. Code also the
relevant associated mental disorder, medical condition, or other sleep disorder
immediately after the code for nightmare disorder in order to indicate the
association.
Specify if:
Acute: Duration of period of nightmares is 1 month or less.
Subacute: Duration of period of nightmares is greater than 1 month but less
than 6 months.
Persistent: Duration of period of nightmares is 6 months or greater.
Specify current severity:
Severity can be rated by the frequency with which the nightmares occur:
Mild: Less than one episode per week on average.
Moderate: One or more episodes per week but less than nightly.
Severe: Episodes nightly.
Recording Procedures
The specifiers “with mental disorder, including substance use disorders”; “with medical
condition”; and “with another sleep disorder” are available to allow the clinician to note
clinically relevant comorbidities. In such cases, record F51.5 nightmare disorder with [name of

comorbid condition(s) or disorder(s)] followed by the diagnostic code(s) for the comorbid
conditions or disorders (e.g., F51.5 nightmare disorder with moderate alcohol use disorder and
rapid eye movement sleep behavior disorder; F10.20 moderate alcohol use disorder; G47.52
REM sleep behavior disorder).
Diagnostic Features
Nightmares are typically lengthy, elaborate, story-like sequences of dream imagery that seem
real and that incite anxiety, fear, or other dysphoric emotions. Nightmare content typically
focuses on attempts to avoid or cope with imminent danger but may involve themes that evoke
other negative emotions. Nightmares occurring after traumatic experiences may replicate the
threatening situation (“replicative nightmares”), but most do not. On awakening, nightmares are
well remembered and can be described in detail. They arise almost exclusively during REM
sleep and can thus occur throughout sleep but are more likely in the second half of the major
sleep episode when dreaming is longer and more intense. Factors that increase early-night REM
intensity, such as sleep fragmentation or deprivation, jet lag, and medications that affect REM
sleep, might facilitate nightmares earlier in the night, including at sleep onset.
Nightmares usually terminate with awakening and rapid return of full alertness. However, the
dysphoric emotions may persist into wakefulness and contribute to difficulty returning to sleep
and lasting daytime distress. Some nightmares, known as “bad dreams,” may not induce
awakening and are recalled only later. If nightmares occur during sleep-onset REM periods
(hypnagogic), the dysphoric emotion is frequently accompanied by an awakening and being
unable to move voluntarily (sleep paralysis), which may also occur in isolation without a
preceding dream or nightmare.
Associated Features
Mild autonomic arousal, including sweating, tachycardia, and tachypnea, may characterize
nightmares. Body movements and vocalizations are not characteristic because of REM sleep–
related loss of skeletal muscle tone. When talking or emoting occurs in nightmare disorder, the
vocal or motor behaviors are typically brief events terminating the nightmare. Distinct from such
motor or vocal activity, true dream enactment behavior may occur when there is a loss of normal
REM atonia (REM sleep behavior disorder).
Prevalence
Prevalence of nightmares during childhood is approximately 1%–5%. From 1.3% to 3.9% of
parents report that their preschool children have nightmares “often” or “always.” Prevalence
increases to 5.2% in children ages 5–15 years. Family history of nightmares, parasomnia
symptoms, and daytime consequences of temper outbursts/mood disturbance and poor academic
performance are associated with frequent nightmares during childhood and adolescence, with
comorbid insomnia seen in approximately 20% of children with frequent nightmares. Among
adults, prevalence of nightmares at least monthly is 6%. Among adults in several countries,
prevalence of weekly nightmares is 2%–6%, whereas prevalence of frequent nightmares is 1%–
5%. Estimates often combine idiopathic and posttraumatic nightmares indiscriminately.

Environmental.
Genetic and physiological.
Course modifiers.
Development and Course
Nightmares often begin between ages 3 and 6 years but reach a peak prevalence and severity in
late adolescence or early adulthood. Nightmares most likely appear in children
exposed to acute or chronic psychosocial stressors and thus may not resolve spontaneously. In a
minority, frequent nightmares persist into adulthood, becoming virtually a lifelong disturbance.
Although specific nightmare content may reflect the individual’s age, the essential features of the
disorder are the same across age groups.
Risk and Prognostic Factors
Frequent nightmares in middle-age adults in the general community population have been shown
in two studies in Hong Kong and Finland to be associated with low income, mood disturbance,
insomnia or sleep-disordered breathing, and use of antidepressants or frequent heavy alcohol use.
Sleep deprivation or fragmentation, and irregular sleep-wake schedules that alter
the timing, intensity, or quantity of REM sleep can put individuals at risk for nightmares.
Individuals who experience nightmares report more frequent past adverse events, but not
necessarily trauma.
Twin studies have identified genetic effects on the disposition to
nightmares and their co-occurrence with other nocturnal behaviors (e.g., sleeptalking).
Adaptive parental bedside behaviors, such as soothing the child following
nightmares, may protect against developing chronic nightmares.
Culture-Related Diagnostic Issues
The significance attributed to nightmares may vary by culture, and sensitivity to such beliefs
may facilitate disclosure. In several cultural contexts, nightmares may be viewed as important
indicators of the individual’s spiritual status or the condition of those who have died (e.g., among
Indonesian civil war survivors, American Indian veterans, and Cambodian refugees). Frequent
nightmares among Cambodian refugees are strongly associated with the presence of
posttraumatic stress disorder (PTSD); assessment of the temporal sequence and severity of
nightmares relative to other symptoms is needed to determine whether a separate diagnosis of
nightmare disorder is warranted. Among Hmong immigrants to the United States, frequent
nightmares are more common than among non-Latinx Whites in the same region and are
associated with traumatic experiences and other sleep disorders, such as sleep paralysis and
restless sleep.
Sex- and Gender-Related Diagnostic Issues
Adult women report having nightmares more frequently than adult men, but this gender
difference was not found in children and the elderly. Nightmare content differs by gender, with
women tending to report themes of sexual harassment or of loved ones disappearing/dying, and
men tending to report themes of physical aggression or war/terror.

Sleep terror disorder.
REM sleep behavior disorder.
Bereavement.
Diagnostic Markers
Polysomnographic studies demonstrate abrupt awakenings from REM sleep, usually during the
second half of the night, prior to report of a nightmare. Heart, respiratory, and eye movement
rates may quicken or increase in variability before awakening. Nightmares following traumatic
events may also arise during light non-REM (NREM) sleep, particularly stage 2 sleep (now
called N2 sleep). The typical sleep of individuals with nightmares is mildly impaired (e.g.,
reduced efficiency, less slow-wave sleep, more awakenings), with more frequent periodic leg
movements in sleep and relative sympathetic nervous system activation after REM sleep
deprivation.
Association With Suicidal Thoughts or Behavior
Individuals with frequent nightmares are at substantially greater risk for suicidal thoughts or
behavior, even when gender and mental illness are taken into account.
Functional Consequences of Nightmare Disorder
Nightmares cause more significant subjective distress than demonstrable social or occupational
impairment. However, if awakenings are frequent or result in sleep avoidance, individuals may
experience excessive daytime sleepiness, poor concentration, depression, anxiety, or irritability.
Frequent childhood nightmares (e.g., several per week) may cause significant distress to parents
and children.
Differential Diagnosis
Both nightmare disorder and sleep terror disorder include awakenings or
partial awakenings with fearfulness and autonomic activation, but the two disorders can be
readily differentiated. Nightmares typically occur later in the night, during REM sleep, and
produce vivid, story-like, and clearly recalled dreams; mild autonomic arousal; and complete
awakenings. Sleep terrors typically arise in the first third of the night during deep NREM sleep
(especially during stage 3 sleep, now called N3 sleep) and produce either no dream recall or
images without an elaborate story-like quality. Sleep terrors are thought to be caused by partial
awakenings intermixed with persisting sleep, with clinical manifestations of confusion,
disorientation, and only partial responsiveness, and often with substantial autonomic arousal.
There is usually amnesia for the event in the morning.
The presence of complex vocal and motor activity during frightening
dreams should prompt further evaluation for REM sleep behavior disorder, which occurs more
typically among late middle- and older-age men but may also affect women. Although
nightmares are typically characteristic of REM sleep behavior disorder, unlike nightmare
disorder, REM sleep behavior disorder is associated with dream enactment that may cause
nocturnal injuries. If the nightmares precede REM sleep behavior disorder and warrant
independent clinical attention, an additional diagnosis of nightmare disorder may be given.
Dysphoric dreams may occur during bereavement but typically involve loss and
sadness and are followed by self-reflection and insight, rather than distress, on awakening.

PTSD or acute stress disorder.
Narcolepsy.
Sleep-related seizures.
Breathing-related sleep disorders.
Panic disorder.
Sleep-related dissociative disorders.
Substance or medication use.
Nightmares in which the content or affect of the dream is related to
a traumatic event may be a component of PTSD or acute stress disorder. An additional diagnosis
of nightmare disorder may be warranted if the severity or frequency of the nightmares
necessitates independent clinical attention.
Nightmares are a frequent complaint in narcolepsy, but the presence of excessive
sleepiness, with or without cataplexy, differentiates this condition from nightmare disorder.
Nocturnal seizures usually involve stereotyped motor activity. Associated
nightmares, if recalled, are often also repetitively stereotyped in nature or reflect epileptogenic
features such as the content of diurnal auras, phosphenes (visual sensations in the absence of
light input), or ictal imagery.
Breathing-related sleep disorders can lead to awakenings with
autonomic arousal, but these are not usually accompanied by recall of nightmares.
Panic attacks arising during sleep can produce abrupt awakenings with autonomic
arousal and fearfulness, but nightmares are typically not reported and symptoms are similar to
panic attacks arising during wakefulness.
Individuals may recall actual physical or emotional trauma as
a “dream” during electroencephalography-documented awakenings.
Numerous substances/medications can precipitate nightmares,
including dopaminergic drugs; β-adrenergic antagonists and other antihypertensives;
amphetamine-type substances, cocaine, and other stimulants; antidepressants; smoking cessation
aids; and melatonin. Withdrawal of REM sleep–suppressant medications
(e.g., antidepressants) and alcohol can produce REM sleep rebound accompanied by nightmares.
If nightmares are sufficiently severe to warrant independent clinical attention, a diagnosis of
substance/medication-induced sleep disorder should be considered.
Comorbidity
Nightmares may be comorbid with several medical conditions, including coronary heart disease,
cancer, parkinsonism, and pain, and can accompany medical treatments, such as hemodialysis, or
withdrawal from medications or substances of abuse. Nightmares frequently co-occur with other
mental disorders, including PTSD, acute stress disorder, insomnia disorder, REM sleep behavior
disorder, and psychotic, mood, anxiety, adjustment, and personality disorders, as well as with
grief during bereavement. A concurrent nightmare disorder diagnosis should only be considered
when independent clinical attention is warranted. These conditions should be listed with the
appropriate comorbid category specifier (e.g., “with REM sleep behavior disorder”); see also
“Recording Procedures.”
Relationship to International Classification of Sleep Disorders
The International Classification of Sleep Disorders, 3rd Edition, presents similar diagnostic
criteria for nightmare disorder.

G47.52
Rapid Eye Movement Sleep Behavior Disorder
Diagnostic Criteria
A. Repeated episodes of arousal during sleep associated with vocalization and/or
complex motor behaviors.
B. These behaviors arise during rapid eye movement (REM) sleep and therefore
usually occur more than 90 minutes after sleep onset, are more frequent during
the later portions of the sleep period, and uncommonly occur during daytime
naps.
C. Upon awakening from these episodes, the individual is completely awake, alert,
and not confused or disoriented.
D. Either of the following:
1. REM sleep without atonia on polysomnographic recording.
2. A history suggestive of REM sleep behavior disorder and an established
synucleinopathy diagnosis (e.g., Parkinson’s disease, multiple system
atrophy).
E. The behaviors cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning (which may include injury to
self or the bed partner).
F. The disturbance is not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication) or another medical condition.
G. Coexisting mental disorders and medical conditions do not explain the episodes.
Diagnostic Features
The essential feature of rapid eye movement (REM) sleep behavior disorder is repeated episodes
of vocalizations and/or complex motor behaviors arising from REM sleep (Criterion A). These
behaviors often reflect motor responses to the content of action-filled or violent dreams of being
attacked or trying to escape from a threatening situation, which may be termed dream enacting
behaviors. The vocalizations are often loud, emotion-filled, and profane. These behaviors may be
very bothersome to the individual and the bed partner and
may result in significant injury (e.g., falling, jumping, or flying out of bed; running, punching,
thrusting, hitting, or kicking). However, individuals with REM sleep behavior disorder may also
present with relatively subtle vocal or motor behaviors during REM sleep, which are typically
not the primary presenting sleep complaint but manifest during history taking or
polysomnography in sleep, neurological, and psychiatric clinical visits. Upon awakening, the
individual is usually immediately awake, alert, and oriented (Criterion C) and is often able to
recall dream mentation, which closely correlates with the observed behavior. The eyes typically

remain closed during these events. The presence of REM sleep without atonia during a
polysomnogram is typically required for the diagnosis of REM sleep behavior disorder.
Alternatively, if polysomnography has not been performed, a provisional diagnosis of probable
REM sleep behavior disorder may be given if there is an established synucleinopathy diagnosis
(e.g., Parkinson's disease, multiple system atrophy) and the history is suggestive of REM sleep
behavior disorder (Criterion D). The diagnosis of REM sleep behavior disorder requires
clinically significant distress or impairment (Criterion E); this determination will depend on a
number of factors, including the frequency of events, the potential for violence or injurious
behaviors, embarrassment, and distress in other household members.
Severity determination is best made based on the nature or consequence of the behavior
rather than simply on frequency. Although the behaviors are typically prominent and violent,
lesser behaviors may also occur.
Prevalence
The prevalence of REM sleep behavior disorder was approximately 1% in a middle- to older-age
general population sample in Switzerland and approximately 2% in an elderly general population
sample in South Korea. One prevalence study found an equal prevalence between men and
women in individuals younger than 50 years, while another study reported a prevalence of just
over 1% with no difference between men and women in a population with a mean age of 59
years. Prevalence in individuals with psychiatric disorders may be greater, possibly related to
medications prescribed for the psychiatric disorder.
Development and Course
The onset of REM sleep behavior disorder may be gradual or rapid. Because of the very high
association with the later appearance of an underlying neurodegenerative disorder, the
neurological status of individuals with REM sleep behavior disorder should be closely
monitored. In individuals with idiopathic REM sleep behavior disorder, the risk of developing a
defined neurodegenerative disease, most often a synucleinopathy (i.e., Parkinson’s disease,
major or mild neurocognitive disorder with Lewy bodies, or multiple system atrophy), is
approximately 75% within 10–15 years following diagnosis, with an annualized risk of
approximately 6%–7% per year.
Symptoms in young individuals, particularly young women, should raise the possibility of
narcolepsy; substance/medication-induced sleep disorder, parasomnia type; a brainstem lesion;
or an autoimmune encephalopathy.
Culture-Related Diagnostic Issues
Chinese individuals diagnosed with REM sleep behavior disorder by a neurology service in
Taiwan had similar clinical and laboratory characteristics as non-Latinx White individuals in the
United States; however, they differed in having a higher rate of nocturnal wandering out of the
bedroom and a lower rate of sleep-related injuries, possibly as a result of earlier detection by the
family.
Sex- and Gender-Related Diagnostic Issues

Other parasomnias.
REM sleep behavior disorder is more common in men older than 50 years, but increasingly this
disorder is being identified in women and in younger individuals. Women are younger than men
in age at onset and age at diagnosis.
Diagnostic Markers
Associated laboratory findings from polysomnography indicate increased tonic and/or phasic
electromyographic activity during REM sleep, which is normally associated with muscle atonia.
The increased muscle activity variably affects different muscle groups; more extensive
electromyographic monitoring with arm electromyography (e.g., biceps brachii) should be
considered because this measure is more specific for a REM sleep behavior disorder diagnosis. It
is suggested that electromyographic monitoring also include the submentalis, bilateral flexor
digitorum superficialis, and bilateral anterior tibialis muscle groups. Continuous video
monitoring should accompany the polysomnography. Other polysomnographic findings may
include very frequent periodic and aperiodic extremity electromyography activity during nonREM (NREM) sleep. REM sleep without atonia is present in virtually all cases of REM sleep
behavior disorder but may also be an asymptomatic polysomnographic finding. It is not known
whether isolated REM sleep without atonia is a precursor to REM sleep behavior disorder,
although a pilot study suggested that isolated REM sleep without atonia may also be associated
with neurodegenerative markers (i.e., hyposmia, orthostatic hypotension, color vision loss) and
that 7%–14% of individuals with isolated REM sleep without atonia later develop clinical REM
sleep behavior disorder. Thresholds for normative REM sleep without atonia levels have also
been published that may serve to distinguish borderline cases and those whose neurological
status should be further monitored.
Functional Consequences of Rapid Eye Movement Sleep Behavior
Disorder
The most serious consequences of REM sleep behavior disorder are the short-term risks for
injury to the individual or bed partner related to attacks of dream enactment, and the long-term
risk of developing a defined neurodegenerative disease. According to surveys of individuals and
their bed partners, approximately 55% of individuals with REM sleep behavior disorder may
experience injury as a consequence of their attacks, with 12% of injuries being serious (including
long bone or rib fractures or subdural hematomas) and requiring medical attention.
Differential Diagnosis
Confusional arousals, sleepwalking, and sleep terrors can easily be confused
with REM sleep behavior disorder. In general, these disorders occur in individuals younger than
50 years. Unlike REM sleep behavior disorder, they arise from NREM sleep and therefore tend
to occur in the early portion of the sleep period. Awakening from a confusional arousal is
associated with confusion, disorientation, and incomplete recall of dream mentation
accompanying the behavior. Polysomnographic monitoring in the disorders of arousal generally
reveals normal REM sleep atonia unless there is a comorbid parasomnia.

Medication-induced sleep disorder, parasomnia type.
Asymptomatic REM sleep without atonia.
Nocturnal seizures.
Obstructive sleep apnea.
Other specified dissociative disorder (sleep-related psychogenic dissociative disorder).
Malingering.
Many widely prescribed medications, including
tricyclic antidepressants, selective serotonin reuptake inhibitors, and serotonin-norepinephrine
reuptake inhibitors, may result in polysomnographic evidence of REM sleep without atonia and
in frank REM sleep behavior disorder, which is diagnosed as a medication-induced sleep
disorder, parasomnia type. It is not known whether the medications per se result in REM sleep
without atonia and/or REM sleep behavior disorder, or whether they unmask an underlying
predisposition.
Clinical dream-enacting behaviors coupled with the
polysomnographic finding of REM sleep without atonia is necessary for the diagnosis of REM
sleep behavior disorder. REM sleep without atonia without a clinical history of dream-enacting
behaviors is simply an asymptomatic polysomnographic observation with an as yet unknown
clinical significance.
Nocturnal seizures may mimic REM sleep behavior disorder, but the
behaviors characteristic of nocturnal seizures are generally stereotyped. Polysomnographic
monitoring employing a full electroencephalographic seizure montage may differentiate the two.
REM sleep without atonia is generally not present on polysomnographic monitoring in
individuals with epilepsy.
Obstructive sleep apnea may result in vocalizations and motor behaviors
that very closely resemble REM sleep behavior disorder, such as talking, shouting, gesturing,
and punching, along with unpleasant dreams. Polysomnographic monitoring is necessary to
differentiate between these two disorders. In REM sleep behavior disorder, the parasomnia
symptoms occur during periods of REM sleep without atonia. In obstructive sleep apnea, the
parasomnia symptoms only occur during arousals at the end of the obstructive sleep apneic
events and resolve following effective treatment of the obstructive sleep apnea (continuous
positive airway pressure). REM sleep without atonia is not typically observed in obstructive
sleep apnea.
Unlike virtually
all other parasomnias, which arise precipitously from NREM or REM sleep, psychogenic
dissociative behaviors arise from a period of well-defined wakefulness during the sleep period.
Unlike REM sleep behavior disorder, this condition is more prevalent in young women.
Many cases of malingering in which the individual reports problematic sleep
movements mimic the clinical features of REM sleep behavior disorder, and polysomnographic
documentation is mandatory.
Comorbidity
REM sleep behavior disorder is present concurrently in approximately 30% of patients with
narcolepsy. When it occurs in narcolepsy, the demographics reflect the younger age range of
narcolepsy, with equal frequency in men and women. Based on findings from individuals
presenting to sleep clinics, most individuals (>70%) with initially “idiopathic” REM sleep
behavior disorder will eventually develop a neurodegenerative disease—most notably, one of the

G25.81
synucleinopathies (Parkinson’s disease, multiple system atrophy, or major or mild
neurocognitive disorder with Lewy bodies). REM sleep behavior disorder often predates any
other sign of these disorders by many years (often more than a decade).
Relationship to International Classification of Sleep Disorders
REM sleep behavior disorder is virtually identical to REM sleep behavior disorder in the
International Classification of Sleep Disorders, 3rd Edition.
Restless Legs Syndrome
Diagnostic Criteria
A. An urge to move the legs, usually accompanied by or in response to
uncomfortable and unpleasant sensations in the legs, characterized by all of the
following:
1. The urge to move the legs begins or worsens during periods of rest or
inactivity.
2. The urge to move the legs is partially or totally relieved by movement.
3. The urge to move the legs is worse in the evening or at night than during the
day, or occurs only in the evening or at night.
B. The symptoms in Criterion A occur at least three times per week and have
persisted for at least 3 months.
C. The symptoms in Criterion A are accompanied by significant distress or
impairment in social, occupational, educational, academic, behavioral, or other
important areas of functioning.
D. The symptoms in Criterion A are not attributable to another mental disorder or
medical condition (e.g., arthritis, leg edema, peripheral ischemia, leg cramps)
and are not better explained by a behavioral condition (e.g., positional
discomfort, habitual foot tapping).
E. The symptoms are not attributable to the physiological effects of a drug of abuse
or medication (e.g., akathisia).
Diagnostic Features
Restless legs syndrome (RLS) is a sensorimotor, neurological sleep disorder characterized by a
desire to move the legs or arms, usually associated with uncomfortable sensations typically
described as creeping, crawling, tingling, burning, or itching (Criterion A). Frequent movements

of the legs occur in an effort to relieve the uncomfortable sensations. Although symptoms can
occur during the daytime, they commonly occur in the late afternoon or evening hours, and in
some individuals, symptoms occur only in the evening or night. Symptoms are often most severe
at night when the individual is at rest, such as sitting or lying in bed. Evening worsening occurs
independently of any differences in activity. The diagnosis of RLS is based primarily on
individual self-report and history. It is important to differentiate RLS from other conditions that
cause leg discomfort, such as positional discomfort and leg cramps (Criterion D).
The symptoms of RLS can delay sleep onset and awaken the individual from sleep and are
associated with significant sleep fragmentation. The relief obtained from moving the legs may no
longer be apparent in severe cases. RLS is associated with daytime sleepiness and is frequently
accompanied by significant clinical distress or functional impairment.
Associated Features
Periodic leg movements in sleep (PLMS) can serve as corroborating evidence for RLS, with up
to 90% of individuals diagnosed with RLS demonstrating PLMS when recordings are taken over
multiple nights. Periodic leg movements during wakefulness are also supportive of an RLS
diagnosis. Reports of difficulty initiating and maintaining sleep and of excessive daytime
sleepiness substantiate a diagnosis of RLS. Additional supportive features include a family
history of RLS among first-degree relatives and a reduction in symptoms, at least initially, with
dopaminergic treatment.
Prevalence
Prevalence rates of RLS vary widely when broad criteria are utilized. When frequency of
symptoms is at least three times per week with moderate or severe distress, the prevalence rate in
the United States and Europe has been estimated as 1.6%. RLS that is severe enough to
significantly impair functioning or is associated with mental disorders, including depression and
anxiety, occurs in approximately 2%–3% of the population, as assessed in Western Europe, the
United States, and South Korea. RLS is about twice as common in women as men and increases
in prevalence with age. Reports of RLS vary across geographic regions, with lower prevalence in
several Asian populations (e.g., Japan, South Korea).
Development and Course
The onset of RLS typically occurs in the second or third decade. Approximately 40% of
individuals diagnosed with RLS during adulthood report having experienced symptoms before
age 20 years, and 20% report having experienced symptoms before age 10 years. Prevalence
rates of RLS increase steadily with age until about age 60 years, with symptoms remaining stable
or decreasing slightly in older age groups. Compared with nonfamilial cases, familial RLS
usually has a younger age at onset and a slower progressive course. The clinical course of RLS
differs by age at onset. When onset occurs before age 45, there is often a slow progression of
symptoms. In late-onset RLS, rapid progression is typical, and aggravating factors are common.
The RLS phenotype appears similar across the life span.
Diagnosis of RLS in children can be difficult because of the centrality of self-report in

Genetic and physiological.
establishing the diagnosis. While Criterion A for adults assumes that the description of “urge to
move” is by the individual, pediatric diagnosis also requires a description in the child’s own
words rather than by a parent or caretaker. Typically children age 6 years or older are able to
provide detailed, adequate descriptors of RLS. However, children rarely use or understand the
word “urge,” reporting instead that their legs “have to” or “got to” move. Also, potentially
related to prolonged periods of sitting during class, two-thirds of children and adolescents with
RLS report daytime leg sensations. Thus, for diagnostic Criterion A3, it is important to compare
equal duration of sitting or lying down in the day to sitting or lying down in the evening or night.
Nocturnal worsening tends to persist even in pediatric RLS. As with RLS in adults, there is a
significant negative impact on sleep, mood, cognition, and function. Impairment in children and
adolescents is manifested more often in behavioral and educational domains.
Risk and Prognostic Factors
Predisposing factors include female sex, advancing age, genetic risk
variants, and family history of RLS. Precipitating factors such as iron deficiency are often timelimited, with most individuals resuming normal sleep patterns after the triggering event has
disappeared. Genetic risk variants also play a role in RLS secondary to disorders such as uremia,
suggesting that individuals with a genetic susceptibility develop RLS in the presence of
additional risk factors.
Genome-wide association studies have found that RLS is significantly associated with
multiple genetic variants in intronic or intergenic regions. The variant in MEIS1 has the strongest
association with RLS of these genes, with nearly double the risk of RLS in the 7% of the
population with this polymorphism among European-ancestry samples studied.
Pathophysiological mechanisms in RLS also include disturbances in the central dopaminergic
and opioidergic systems and disturbances in iron metabolism. Treatment efficacy of
dopaminergic drugs, opioids, and iron provides further support that these systems play a role in
the pathophysiology of RLS. RLS may predispose to depression, and the effective treatment of
RLS may significantly reduce depressive symptoms. However, serotonergic antidepressants can
induce or aggravate RLS in some individuals.
Culture-Related Diagnostic Issues
Among indigenous-descent Latin American adult populations in the United States, including
Mexican Americans with low acculturation to U.S. society, the reported prevalence of RLS
appears to be lower when compared with Mexican Americans with higher acculturation. Among
participants who reported RLS in a large population-based survey, risk factors associated with
RLS were different in Mexican Americans (higher among women and persons who smoke)
compared with non-Latinx Whites (older age, defined as ≥ 48 years).
Sex- and Gender-Related Diagnostic Issues
Although RLS is more prevalent in women than in men, there are no diagnostic differences
according to gender. The prevalence of RLS during pregnancy is two to three times greater

than in the general population. RLS associated with pregnancy peaks during the third trimester
and improves or resolves in most cases soon after delivery. The sex difference in prevalence of
RLS is explained at least in part by parity, with nulliparous females being at the same risk for
RLS as age-matched males.
Diagnostic Markers
Polysomnography demonstrates significant abnormalities in RLS, including increased latency to
sleep and higher arousal index. Periodic limb movements are the motor sign of RLS and are
usually present on overnight polysomnography, as well as during waking immobilization tests
and during quiet resting, both of which can provoke RLS symptoms.
Functional Consequences of Restless Legs Syndrome
Although the impact of milder symptoms is less well characterized, individuals with RLS
complain of disruption in at least one activity of daily living, with up to 50% reporting a negative
impact on mood and a lack of energy. A common consequence of RLS is sleep disturbance,
including difficulty falling asleep and sleep fragmentation, with associated reduction in total
sleep time. RLS is also associated with quality-of-life impairments. RLS can result in daytime
sleepiness or fatigue and is frequently accompanied by significant distress or impairment in
affective, social, occupational, educational, academic, behavioral, or cognitive functioning.
Differential Diagnosis
The most important conditions in the differential diagnosis of RLS are leg cramps, positional
discomfort, arthralgias/arthritis, myalgias, positional ischemia (numbness), leg edema, peripheral
neuropathy, radiculopathy, and habitual foot tapping. Muscle cramps, relief with a single
postural shift, limitation to joints, soreness to palpation (myalgias), and other abnormalities on
physical examination are not characteristic of RLS. Unlike RLS, nocturnal leg cramps do not
typically manifest with the desire to move the limbs nor are there frequent limb movements. Less
common conditions to be differentiated from RLS include neuroleptic-induced akathisia,
myelopathy, symptomatic venous insufficiency, peripheral artery disease, eczema, other
orthopedic problems, and anxiety-induced restlessness. Worsening at night and periodic limb
movements are more common in RLS than in medication-induced akathisia or peripheral
neuropathy.
While it is important that RLS symptoms not be solely accounted for by another medical or
behavioral condition, it should also be appreciated that any of these similar conditions can occur
in an individual with RLS. This necessitates a separate focus on each possible condition in the
diagnostic process and when assessing impact. For cases in which the diagnosis of RLS is not
certain, evaluation for the supportive features of RLS, particularly PLMS or a family history of
RLS, may be helpful. Clinical features, such as response to a dopaminergic agent and positive
family history for RLS, can help with the differential diagnosis.
Comorbidity
RLS is associated with higher rates of depression, generalized anxiety disorder, panic disorder,
and posttraumatic stress disorder. The main medical condition comorbid with RLS is

cardiovascular disease. There may be an association with numerous other medical conditions,
including hypertension, migraine, Parkinson’s disease, multiple sclerosis, peripheral neuropathy,
diabetes mellitus, fibromyalgia, osteoporosis, obesity, thyroid disease, and cancer, as well as
other sleep disorders including narcolepsy and obstructive sleep apnea. RLS is common in those
with iron deficiency, pregnancy, and chronic renal failure and can dramatically improve once
these conditions resolve.
Relationship to International Classification of Sleep Disorders
The International Classification of Sleep Disorders, 3rd Edition, presents similar diagnostic
criteria for RLS but does not contain a criterion specifying frequency or duration of symptoms.
Substance/Medication-Induced Sleep Disorder
Diagnostic Criteria
A. A prominent and severe disturbance in sleep.
B. There is evidence from the history, physical examination, or laboratory findings
of both (1) and (2):
1. The symptoms in Criterion A developed during or soon after substance
intoxication or withdrawal or after exposure to or withdrawal from a
medication.
2. The involved substance/medication is capable of producing the symptoms in
Criterion A.
C. The disturbance is not better explained by a sleep disorder that is not
substance/medication-induced. Such evidence of an independent sleep disorder
could include the following:
The symptoms precede the onset of the substance/medication use; the
symptoms persist for a substantial period of time (e.g., about 1 month) after
the cessation of acute withdrawal or severe intoxication; or there is other
evidence 
suggesting 
the 
existence 
of 
an 
independent 
nonsubstance/medication-induced sleep disorder (e.g., a history of recurrent nonsubstance/medication-related episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Note: This diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the symptoms in Criterion A
predominate in the clinical picture and when they are sufficiently severe to warrant
clinical attention.

Coding note: The ICD-10-CM codes for the [specific substance/medication]-induced
sleep disorders are indicated in the table below. Note that the ICD-10-CM code
depends on whether or not there is a comorbid substance use disorder present for
the same class of substance. In any case, an additional separate diagnosis of a
substance use disorder is not given. If a mild substance use disorder is comorbid
with the substance-induced sleep disorder, the 4th position character is “1,” and the
clinician should record “mild [substance] use disorder” before the substance-induced
sleep disorder (e.g., “mild cocaine use disorder with cocaine-induced sleep
disorder”). If a moderate or severe substance use disorder is comorbid with the
substance-induced sleep disorder, the 4th position character is “2,” and the clinician
should record “moderate [substance] use disorder” or “severe [substance] use
disorder,” depending on the severity of the comorbid substance use disorder. If there
is no comorbid substance use disorder (e.g., after a one-time heavy use of the
substance), then the 4th position character is “9,” and the clinician should record
only the substance-induced sleep disorder.
There are two exceptions to this coding convention as it applies to caffeine- and
tobacco-induced sleep disorders. Because caffeine use disorder is not an official
DSM-5 category,
there is only a single ICD-10-CM code for caffeine-induced sleep disorder: F15.982.
Moreover, because ICD-10-CM assumes that tobacco-induced sleep disorder can
only occur in the context of moderate or severe tobacco use disorder, the ICD-10CM code for tobacco-induced sleep disorder is F17.208.
ICD-10-CM
With mild use
disorder
With moderate or
severe use disorder
Without use
disorder
Alcohol
F10.182
F10.282
F10.982
Caffeine
NA
NA
F15.982
Cannabis
F12.188
F12.288
F12.988
Opioid
F11.182
F11.282
F11.982
Sedative, hypnotic, or anxiolytic
F13.182
F13.282
F13.982
Amphetamine-type substance (or other
stimulant)
F15.182
F15.282
F15.982
Cocaine
F14.182
F14.282
F14.982
Tobacco
NA
F17.208
NA
Other (or unknown) substance
F19.182
F19.282
F19.982
Specify whether:
Insomnia type: Characterized by difficulty falling asleep or maintaining sleep,
frequent nocturnal awakenings, or nonrestorative sleep.
Daytime sleepiness type: Characterized by predominant complaint of

excessive sleepiness/fatigue during waking hours or, less commonly, a long
sleep period.
Parasomnia type: Characterized by abnormal behavioral events during sleep.
Mixed type: Characterized by a substance/medication-induced sleep problem
characterized by multiple types of sleep symptoms, but no symptom clearly
predominates.
Specify (see Table 1 in the chapter “Substance-Related and Addictive Disorders,”
which indicates whether “with onset during intoxication” and/or “with onset during
withdrawal” applies to a given substance class; or specify “with onset after
medication use”):
With onset during intoxication: If criteria are met for intoxication with the
substance and the symptoms develop during the intoxication.
With onset during withdrawal: If criteria are met for withdrawal from the
substance and the symptoms develop during, or shortly after, withdrawal.
With onset after medication use: If symptoms developed at initiation of
medication, with a change in use of medication, or during withdrawal of
medication.
Recording Procedures
The name of the substance/medication-induced sleep disorder begins with the specific substance
(e.g., alcohol) that is presumed to be causing the sleep disturbance. The ICD-10-CM code that
corresponds to the applicable drug class is selected from the table included in the criteria set. For
substances that do not fit into any of the classes (e.g., fluoxetine), the ICD-10-CM code for the
other (or unknown) substance class should be used and the name
of the specific substance recorded (e.g., F19.982 fluoxetine-induced sleep disorder, insomnia
type). In cases in which a substance is judged to be an etiological factor but the specific
substance is unknown, the ICD-10-CM code for the other (or unknown) substance class is used
and the fact that the substance is unknown is recorded (e.g., F19.982 unknown substanceinduced sleep disorder, hypersomnia type).
To record the name of the disorder, the comorbid substance use disorder (if any) is listed
first, followed by “with substance/medication-induced sleep disorder” (incorporating the name of
the specific etiological substance/medication), followed by the specification of onset (i.e., with
onset during intoxication, with onset during withdrawal, with onset after medication use),
followed by the subtype designation (i.e., insomnia type, daytime sleepiness type, parasomnia
type, mixed type). For example, in the case of insomnia occurring during withdrawal in a man
with a severe lorazepam use disorder, the diagnosis is F13.282 severe lorazepam use disorder
with lorazepam-induced sleep disorder, with onset during withdrawal, insomnia type. A separate
diagnosis of the comorbid severe lorazepam use disorder is not given. If the substance-induced
sleep disorder occurs without a comorbid substance use disorder (e.g., with medication use as

prescribed), no accompanying substance use disorder is noted (e.g., F19.982 bupropion-induced
sleep disorder, with onset during medication use, insomnia type). When more than one substance
is judged to play a significant role in the development of the sleep disturbance, each should be
listed separately (e.g., F10.282 severe alcohol use disorder with alcohol-induced sleep disorder,
with onset during intoxication, insomnia type; F14.282 severe cocaine use disorder with cocaineinduced sleep disorder, with onset during intoxication, insomnia type).
Specifiers
Depending on the substance involved, one of four types of sleep disturbances is indicated.
Insomnia type and daytime sleepiness type are most common, whereas parasomnia type is seen
less often. The mixed type is noted when more than one type of sleep disturbance–related
symptom is present and none predominates.
Diagnostic Features
The essential feature of substance/medication-induced sleep disorder is a prominent sleep
disturbance that is sufficiently severe to warrant independent clinical attention (Criterion A). The
sleep disturbance may be characterized by insomnia, daytime sleepiness, a parasomnia, or some
combination of these. The sleep disturbance is judged to be primarily associated with the
pharmacological effects of a substance (i.e., a drug of abuse, a medication, toxin exposure)
(Criterion B). The disturbance must not be better explained by another sleep disorder that is not
substance/medication-induced (Criterion C). A substance/medication-induced sleep disorder is
distinguished from insomnia disorder or a disorder associated with excessive daytime sleepiness
by considering onset and course. For drugs of abuse, there must be evidence of intoxication or
withdrawal 
from 
the 
history, 
physical 
examination, 
or 
laboratory 
findings.
Substance/medication-induced sleep disorder arises only in association with intoxication or
discontinuation/withdrawal states, whereas other sleep disorders may precede the onset of
substance use or occur during times of sustained abstinence. As discontinuation/withdrawal
states for some substances can be protracted, onset of the sleep disturbance can occur 4 weeks
after cessation of substance use, and the disturbance may have features atypical of other sleep
disorders (e.g., atypical age at onset or course). The diagnosis is not made if the sleep
disturbance occurs only during a delirium (Criterion D). The symptoms must cause clinically
significant distress or impairment in social, occupational, or other important areas of functioning
(Criterion E). This diagnosis should be made instead of a diagnosis of substance intoxication or
substance withdrawal only when the symptoms in Criterion A predominate in the clinical picture
and when the symptoms warrant independent clinical attention.
Associated Features
During periods of substance/medication use, intoxication, or withdrawal, individuals frequently
complain of dysphoric mood, including depression and anxiety, irritability, cognitive
impairment, inability to concentrate, and fatigue.
Prominent and severe sleep disturbances can occur in association with intoxication with the
following classes of substances: alcohol; caffeine; cannabis; opioids; sedatives, hypnotics, or

Alcohol.
Caffeine.
Cannabis.
Opioids.
anxiolytics; stimulants (including cocaine); and other (or unknown) substances. Prominent and
severe sleep disturbances can occur in association with withdrawal from the following classes of
substances: alcohol; caffeine; cannabis; opioids; sedatives, hypnotics, or anxiolytics; stimulants
(including cocaine); tobacco; and other (or unknown) substances. Medications that invoke sleep
disturbances include adrenergic agonists and antagonists, dopamine agonists and antagonists,
cholinergic agonists and antagonists, serotonergic agonists and antagonists, antihistamines, and
corticosteroids.
Alcohol-induced sleep disorder typically occurs as insomnia type. During acute
intoxication with doses > 1 g/kg, alcohol produces an immediate sedative effect depending on
dose, accompanied by a reduction in sleep latency, increased non–rapid eye movement (NREM)
sleep stages 2 and 3 (N2 and N3), and reduced rapid eye movement (REM) sleep. Following
these initial effects, there may be increased wakefulness, restless sleep, and vivid and anxietyladen dreams for the remaining sleep period. In parallel, N2 and N3 are reduced, and
wakefulness and REM sleep are increased during the latter portion of the night. With habitual
use, alcohol continues to show a short-lived sedative effect in the first half of the night, followed
by sleep continuity disruption in the second half. During acute alcohol withdrawal, there is
extremely disrupted sleep continuity, and an increased amount and intensity of REM sleep,
associated frequently with vivid dreaming, which in extreme form constitutes part of alcohol
withdrawal delirium. After acute withdrawal, chronic alcohol users may continue to complain of
light, fragmented sleep for months to years associated with a persistent prolongation of sleep
latency and deficit in slow-wave sleep. Alcohol also aggravates breathing-related sleep disorder,
including obstructive sleep apnea and sleep-related hypoventilation.
Caffeine consumed in low to moderate doses during the morning hours typically
produces no significant effect on nighttime sleep in normal sleepers or those with insomnia.
Caffeine may produce insomnia in a dose- and timing–dependent manner, particularly when
larger doses are consumed later in the day or during evening hours. Prolongation of sleep
latency, reduction of slow-wave sleep, increased nocturnal awakening, and reduced sleep
duration are reported. Some individuals, particularly high consumers, may present with daytime
sleepiness and performance impairments related to withdrawal.
Acute administration of cannabis may shorten sleep latency, though arousing effects
with increments in sleep latency also occur. Cannabis enhances slow-wave sleep and suppresses
REM sleep after acute administration. In chronic users, tolerance to the sleep-inducing and slowwave sleep–enhancing effects develops. Upon withdrawal, sleep difficulties and unpleasant
dreams have been reported lasting for several weeks. Polysomnographic studies demonstrate
reduced slow-wave sleep and increased REM sleep during this phase.
Opioids may produce an increase in sleepiness and in subjective depth of sleep, and
reduced REM and slow-wave sleep, during acute short-term use. With continued administration,
tolerance to the sedative effects of opioids develops and there are complaints of insomnia.
Polysomnographic studies demonstrate reduced sleep efficiency and total sleep time, with
reduction of slow-wave sleep and possibly REM sleep. Consistent with their respiratory
depressant effects, opioids exacerbate obstructive sleep apnea. Emergence of central sleep apnea
is also observed, especially with chronic use of longer-acting opioids.

Sedative, hypnotic, or anxiolytic substances.
Amphetamine-type substances, other stimulants, and MDMA.
Tobacco.
Other or unknown substances/medications.
Sedatives, 
hypnotics, 
and 
anxiolytics 
(e.g.,
barbiturates, benzodiazepine receptor agonists, meprobamate, glutethimide, methyprylon) have
similar effects as opioids on sleep. During acute intoxication, sedative-hypnotic drugs produce
the expected increase in sleepiness and decrease in wakefulness. Daytime sleepiness may occur,
primarily with longer-acting agents. Chronic benzodiazepine use may be associated with
development of tolerance, rebound insomnia, and potentially serious withdrawal effects. Newer
benzodiazepine receptor agonists such as zolpidem and eszopiclone have been shown to maintain
efficacy over periods of 6 months to 2 years, without evidence of dosage escalation or major
withdrawal effects. Newer hypnotic agents such as ramelteon, low-dose doxepin, and suvorexant
do not appear to have significant abuse potential, respiratory depression, or major withdrawal
syndromes. Sedative, hypnotic, or anxiolytic drugs with short durations of action are most likely
to produce complaints of rebound insomnia. Some sedative-hypnotic drugs may increase the
frequency and severity of obstructive sleep apnea events, although neither benzodiazepines nor
benzodiazepine receptor agonists have been found to definitively worsen obstructive sleep apnea.
Hypoventilation may worsen in susceptible individuals. Parasomnias (sleepwalking and sleeprelated eating) have been associated with use of benzodiazepine receptor agonists, especially
when these medications are taken at higher doses and when they are combined with other
sedative drugs.
Sleep 
disorders 
induced 
by
amphetamine-type substances and other stimulants are characterized by insomnia during
intoxication and excessive sleepiness during withdrawal. During acute intoxication, stimulants
reduce the total amount of sleep, increase sleep latency and sleep continuity disturbances, and
decrease REM sleep. Slow-wave sleep tends to be reduced. During withdrawal from chronic
stimulant use, there is both prolonged nocturnal sleep duration and excessive daytime sleepiness.
Multiple sleep latency tests may show increased daytime sleepiness during the withdrawal phase.
Drugs like 3,4-methylenedioxymethamphetamine (MDMA; “ecstasy”) and related substances
lead to restless and disturbed sleep within 48 hours of intake; frequent use of these compounds is
associated with persisting symptoms of anxiety, depression, and sleep disturbances, even during
longer-term abstinence. There is also evidence that suggests an increased frequency of
obstructive sleep apnea in young MDMA users, even after a period of abstention from the drug.
Chronic tobacco use is associated primarily with symptoms of insomnia, decreased
slow-wave sleep with a reduction of sleep efficiency, and increased daytime sleepiness.
Withdrawal from tobacco can lead to impaired sleep. Individuals who smoke heavily may
experience regular nocturnal awakenings caused by tobacco craving.
Other substances/medications may produce sleep
disturbances, particularly medications that affect the central or autonomic nervous systems (e.g.,
adrenergic agonists and antagonists, dopamine agonists and antagonists, cholinergic agonists and
antagonists, serotonergic agonists and antagonists, antihistamines, corticosteroids).
Development and Course
Insomnia in children can be identified by either a parent or the child. Often the child has a clear
sleep disturbance associated with initiation of a medication but may not report symptoms,
although parents observe the sleep disturbances. The use of some recreational substances (e.g.,

Temperamental.
cannabis, ecstasy) is prevalent in adolescence and early adulthood. Insomnia or any other sleep
disturbance encountered in this age group should prompt careful consideration of whether the
sleep disturbance is attributable to consumption of these substances. Help-seeking behavior for
the sleep disturbance in these age groups is limited, and
thus corroborative report may be elicited from a parent, caregiver, or teacher. Older individuals
take more medications and are at increased risk for developing a substance/medication-induced
sleep disorder. They may interpret sleep disturbance as part of normal aging and fail to report
symptoms. Individuals with major neurocognitive disorder (e.g., dementia) are at risk for
substance/medication-induced sleep disorders but may not report symptoms, making
corroborative report from caregiver(s) particularly important.
Risk and Prognostic Factors
Risk and prognostic factors involved in substance or medication use are normative for certain
age groups. They are relevant for, and likely applicable to, the type of sleep disturbance
encountered (see the chapter “Substance-Related and Addictive Disorders” for descriptions of
respective substance use disorders).
Substance use generally precipitates or accompanies insomnia in vulnerable
individuals. Thus, presence of insomnia in response to stress or change in sleep environment or
timing can represent a risk for developing substance/medication-induced sleep disorder. A
similar risk may be present for individuals with other sleep disorders (e.g., individuals with
hypersomnia who use stimulants).
Sex- and Gender-Related Diagnostic Issues
The same amount and duration of consumption of a given substance may lead to highly different
sleep-related outcomes in males and females based on, for example, sex-specific differences in
hepatic functioning.
Diagnostic Markers
Each of the substance/medication-induced sleep disorders produces electroencephalographic
sleep patterns that are associated with, but cannot be considered diagnostic of, other disorders.
The electroencephalographic sleep profile for each substance is related to the stage of use and
whether it is in the context of intake/intoxication, chronic use, or withdrawal following
discontinuation of the substance. All-night polysomnography can help define the severity of
insomnia complaints, while the multiple sleep latency test provides information about the
severity of daytime sleepiness. Monitoring of nocturnal respiration and periodic limb movements
with polysomnography may verify a substance’s impact on nocturnal breathing and motor
behavior. Sleep diaries for 2 weeks and actigraphy are considered helpful in confirming the
presence of substance/medication-induced sleep disorder, especially in the case of suspected
insomnia type. Drug screening can be of use when the individual is not aware or unwilling to
relate information about substance intake.

Substance intoxication and substance withdrawal.
Delirium.
Other sleep disorders.
Sleep disorder associated with medical condition.
Functional Consequences of Substance/Medication-Induced Sleep
Disorder
While there are many functional consequences associated with sleep disorders, the only unique
consequence for substance/medication-induced sleep disorder is increased risk for relapse. For
example, the degree of sleep disturbance during alcohol withdrawal (e.g., REM sleep rebound)
predicts risk of relapse of drinking. Monitoring of sleep quality and daytime sleepiness during
and after withdrawal may provide clinically meaningful information on whether an individual is
at increased risk for relapse.
Differential Diagnosis
Sleep disturbances are commonly encountered in
the context of substance intoxication and substance withdrawal. A diagnosis of
substance/medication-induced sleep disorder should be made instead of a
diagnosis of substance intoxication or substance withdrawal only when the sleep disturbance is
predominant in the clinical picture and is sufficiently severe to warrant independent clinical
attention.
If the substance/medication-induced sleep disturbance occurs exclusively during the
course of a delirium, it is not diagnosed separately.
A substance/medication-induced sleep disorder is distinguished from
another sleep disorder if a substance/medication is judged to be etiologically related to the
symptoms. A substance/medication-induced sleep disorder attributed to a prescribed medication
for a mental disorder or medical condition must have its onset while the individual is receiving
the medication or during discontinuation, if there is a discontinuation/withdrawal syndrome
associated with the medication. Once treatment is discontinued, the sleep disturbance will
usually remit within days to several weeks. If symptoms persist beyond 4 weeks, other causes for
the sleep disturbance–related symptoms should be considered. Not infrequently, individuals with
another sleep disorder use medications or drugs of abuse to self-medicate their symptoms (e.g.,
alcohol for management of insomnia). If the substance/medication is judged to play a significant
role in the exacerbation of the sleep disturbance, an additional diagnosis of a
substance/medication-induced sleep disorder may be warranted.
Substance/medication-induced sleep disorder and
sleep disorders with a medical condition (i.e., insomnia disorder, hypersomnolence disorder, and
nightmare disorder) may produce similar symptoms of insomnia, daytime sleepiness, or
nightmares, respectively. Many medical conditions that cause sleep disturbance are treated with
medications that may also cause sleep disturbances. The chronology of symptoms is the most
important factor in distinguishing between these two sources of sleep symptoms. Difficulties
with sleep in an individual with a comorbid medical condition that clearly preceded the use of
any medication for treatment of that medical condition would suggest a diagnosis of insomnia
disorder, hypersomnolence disorder, or nightmare disorder with the specifier “with [specific
medical condition]” applicable to the diagnosis. Conversely, sleep symptoms that appear only

after the initiation of a particular substance/medication suggest a substance/medication-induced
sleep disorder. If the sleep disturbance is comorbid with another medical condition and is also
exacerbated by substance use, both diagnoses are given (i.e., insomnia disorder,
hypersomnolence disorder, or nightmare disorder, “with [specific medical condition]”
respectively; and [specific substance/medication]-induced sleep disorder). When there is
insufficient evidence to determine whether the sleep disturbance is attributable to a
substance/medication or a medical condition, or independent (i.e., not attributable to either a
substance/medication or a medical condition), a diagnosis of unspecified sleep-wake disorder is
indicated.
Comorbidity
See the “Comorbidity” sections for other sleep disorders in this chapter, including insomnia
disorder, hypersomnolence disorder, central sleep apnea, sleep-related hypoventilation, and
circadian rhythm sleep-wake disorders, shift work type.
Relationship to International Classification of Sleep Disorders
The International Classification of Sleep Disorders, 3rd Edition (ICSD-3), lists sleep disorders
“due to a medication or substance” under their respective phenotypes (e.g., hypersomnia,
movement disorder, parasomnia). ICSD-3 does not identify a separate diagnosis for “insomnia
due to a medication or substance” based on evidence that the reliability of distinguishing
specific, single etiological factors for chronic insomnia is poor.
Other Specified Insomnia Disorder
G47.09
This category applies to presentations in which symptoms characteristic of insomnia
disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for insomnia disorder or any of the disorders in the sleep-wake
disorders diagnostic class. The other specified insomnia disorder category is used in
situations in which the clinician chooses to communicate the specific reason that the
presentation does not meet the criteria for insomnia disorder or any specific sleepwake disorder. This is done by recording “other specified insomnia disorder” followed
by the specific reason (e.g., “short-term insomnia disorder”).
Examples of presentations that can be specified using the “other specified”
designation include the following:
1. Short-term insomnia disorder: Duration is less than 3 months.
2. Restricted to nonrestorative sleep: Predominant complaint is nonrestorative
sleep unaccompanied by other sleep symptoms such as difficulty falling asleep
or remaining asleep.

Unspecified Insomnia Disorder
G47.00
This category applies to presentations in which symptoms characteristic of insomnia
disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for insomnia disorder or any of the disorders in the sleep-wake
disorders diagnostic class. The unspecified insomnia disorder category is used in
situations in which the clinician chooses not to specify the reason that the criteria are
not met for insomnia disorder or a specific sleep-wake disorder, and includes
presentations in which there is insufficient information to make a more specific
diagnosis.
Other Specified Hypersomnolence Disorder
G47.19
This category applies to presentations in which symptoms characteristic of
hypersomnolence disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for hypersomnolence disorder or any of the disorders in the
sleep-wake disorders diagnostic class. The other specified hypersomnolence
disorder category is used in situations in which the clinician chooses to communicate
the specific reason that the presentation does not meet the criteria for
hypersomnolence disorder or any specific sleep-wake disorder. This is done by
recording “other specified hypersomnolence disorder” followed by the specific
reason (e.g., “brief-duration hypersomnolence,” as in Kleine-Levin syndrome).
Unspecified Hypersomnolence Disorder
G47.10
This category applies to presentations in which symptoms characteristic of
hypersomnolence disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for hypersomnolence disorder or any of the disorders in the

sleep-wake disorders diagnostic class. The unspecified hypersomnolence disorder
category is used in situations in which the clinician chooses not to specify the reason
that the criteria are not met for hypersomnolence disorder or a specific sleep-wake
disorder, and includes presentations in which there is insufficient information to
make a more specific diagnosis.
Other Specified Sleep-Wake Disorder
G47.8
This category applies to presentations in which symptoms characteristic of a sleepwake disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the sleep-wake disorders diagnostic class
and do not qualify for a diagnosis of other specified insomnia disorder or other
specified hypersomnolence disorder. The other specified sleep-wake disorder
category is used in situations in which the clinician chooses to communicate the
specific reason that the presentation does not meet the criteria for any specific
sleep-wake disorder. This is done by recording “other specified sleep-wake disorder”
followed by the specific reason (e.g., “repeated arousals during rapid eye movement
sleep without polysomnography or history of Parkinson’s disease or other
synucleinopathy”).
Unspecified Sleep-Wake Disorder
G47.9
This category applies to presentations in which symptoms characteristic of a sleepwake disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the sleep-wake disorders diagnostic class
and do not qualify for a diagnosis of unspecified insomnia disorder or unspecified
hypersomnolence disorder. The unspecified sleep-wake disorder category is used in
situations in which the clinician chooses not to specify the reason that the criteria are
not met for a specific sleep-wake disorder, and includes presentations in which there
is insufficient information to make a more specific diagnosis.

# 13 - Sexual Dysfunctions

# Sexual Dysfunctions

477

Sexual Dysfunctions
Sexual dysfunctions include delayed ejaculation, erectile disorder, female orgasmic
disorder, female sexual interest/arousal disorder, genito-pelvic pain/penetration disorder, male
hypoactive sexual desire disorder, premature (early) ejaculation, substance/medication-induced
sexual dysfunction, other specified sexual dysfunction, and unspecified sexual dysfunction.
Sexual dysfunctions are a heterogeneous group of disorders that are typically characterized by a
clinically significant disturbance in a person’s ability to respond sexually or to experience sexual
pleasure. An individual may have several sexual dysfunctions at the same time. In such cases, all
of the dysfunctions should be diagnosed.
Clinical judgment should be used to determine if the sexual difficulties are the result of
inadequate sexual stimulation; in these cases, there may still be a need for care, but a diagnosis
of a sexual dysfunction would not be made. These cases may include, but are not limited to,
conditions in which lack of knowledge about effective stimulation prevents the experience of
arousal or orgasm.
Subtypes are used to designate the onset of the difficulty. In many individuals with sexual
dysfunctions, the time of onset may indicate different etiologies and interventions. Lifelong
refers to a sexual problem that has been present from first sexual experiences, and acquired
applies to sexual dysfunctions that develop after a period of relatively normal sexual function.
Generalized refers to sexual difficulties that are not limited to certain types of stimulation,
situations, or partners, and situational refers to sexual difficulties that only occur with certain
types of stimulation, situations, or partners.
In addition to the lifelong/acquired and generalized/situational subtypes, a number of factors
must be considered during the assessment of sexual dysfunction, given that they may be relevant
to etiology or treatment and may contribute, to varying degrees, across individuals: 1) partner
factors (e.g., partner’s sexual problems; partner’s health status); 2) relationship factors (e.g., poor
communication; discrepancies in desire for sexual activity); 3) individual vulnerability factors
(e.g., poor body image; history of sexual or emotional abuse), psychiatric comorbidity (e.g.,
depression, anxiety), or stressors (e.g., job loss, bereavement); 4) cultural or religious factors
(e.g., inhibitions related to prohibitions against sexual activity or pleasure; attitudes toward
sexuality); and 5) medical factors relevant to prognosis, course, or treatment.
Clinical judgment about the diagnosis of sexual dysfunction should take into consideration
cultural factors that may influence expectations or engender prohibitions about the experience of
sexual pleasure. Aging and relationship duration may be associated with a normative decrease in
sexual response.
Sexual response has a requisite biological underpinning, yet is usually experienced in an
intrapersonal, interpersonal, and cultural context. Thus, sexual function involves a complex
interaction among biological, sociocultural, and psychological factors. In many clinical contexts,
a precise understanding of the etiology of a sexual problem is unknown. Nonetheless, a sexual

F52.32
dysfunction diagnosis requires ruling out problems that are better explained by a nonsexual
mental disorder, by the effects of a substance (e.g., drug or
medication), by a medical condition (e.g., due to pelvic nerve damage), or by severe
relationship distress, partner violence, or other stressors.
The population of gender-diverse persons, including transgender, nonbinary, and agender,
may not identify with or appear to fit into the existing sex- and gender-based diagnostic
categories described in this chapter. Despite the names given to male hypoactive sexual desire
disorder and female sexual interest arousal disorder, the diagnostic criteria describe symptoms
and experiences that are not dependent on the individual’s specific sex or gender. As such, either
diagnosis can be applied to gender-diverse individuals based on clinical judgment. For diagnoses
linked to reproductive anatomy (e.g., erectile dysfunction, premature [early] ejaculation, delayed
ejaculation, and genito-pelvic pain/penetration disorder), diagnoses should be based on the
individual’s current anatomy and not on the individual’s sex assigned at birth. Much more
research is needed to understand experiences of sexual dysfunction among gender-diverse
persons. In the meantime, as with all categories in DSM, clinicians should use their best
judgment.
If the sexual dysfunction is mostly explainable by another nonsexual mental disorder (e.g.,
depressive or bipolar disorder, anxiety disorder, posttraumatic stress disorder, psychotic
disorder), then only the other mental disorder diagnosis should be made. If the problem is
thought to be better explained by the use/misuse or discontinuation of a drug or substance, it
should be diagnosed accordingly as a substance/medication-induced sexual dysfunction. If the
sexual dysfunction is attributable to another medical condition (e.g., peripheral neuropathy), the
person would not receive a psychiatric diagnosis. If severe relationship distress, partner violence,
or significant stressors better explain the sexual difficulties, then a sexual dysfunction diagnosis
is not made, but an appropriate Z code for the relationship problem or stressor may be listed
(e.g., Z63.0 Relationship distress with spouse or intimate partner); see the chapter “Other
Conditions That May Be a Focus of Clinical Attention.” In many cases, a precise etiological
relationship between another condition (e.g., a medical condition) and a sexual dysfunction
cannot be established. It is possible to have a diagnosis of a sexual dysfunction and a coexisting
medical condition, nonsexual mental disorder, or use/misuse or discontinuation of a drug or
substance; and it is possible to have one or more diagnoses of sexual dysfunction.
Delayed Ejaculation
Diagnostic Criteria
A. Either of the following symptoms must be experienced on almost all or all
occasions (approximately 75%–100%) of partnered sexual activity (in identified
situational contexts or, if generalized, in all contexts), and without the individual
desiring delay:

1. Marked delay in ejaculation.
2. Marked infrequency or absence of ejaculation.
B. The symptoms in Criterion A have persisted for a minimum duration of
approximately 6 months.
C. The symptoms in Criterion A cause clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexual mental disorder or
as a consequence of severe relationship distress or other significant stressors
and is not attributable to the effects of a substance/medication or another
medical condition.
Specify whether:
Lifelong: The disturbance has been present since the individual became
sexually active.
Acquired: The disturbance began after a period of relatively normal sexual
function.
Specify whether:
Generalized: Not limited to certain types of stimulation, situations, or partners.
Situational: Only occurs with certain types of stimulation, situations, or partners.
Specify current severity:
Mild: Evidence of mild distress over the symptoms in Criterion A.
Moderate: Evidence of moderate distress over the symptoms in Criterion A.
Severe: Evidence of severe or extreme distress over the symptoms in Criterion
A.
Diagnostic Features
The essential feature of delayed ejaculation is a marked delay in or inability to achieve
ejaculation or marked infrequency of ejaculation on all or almost all occasions of partnered
sexual activity, despite the presence of adequate sexual stimulation and the desire to ejaculate
(Criterion A). In order to qualify for a DSM-5 diagnosis of delayed ejaculation, the symptoms
must have persisted for a minimum duration of approximately 6 months (Criterion B) and must
cause clinically significant distress in the individual (Criterion C). The partnered sexual activity
may include manual, oral, coital, or anal stimulation. In most cases, the diagnosis will be made
by self-report, although for men in heterosexual partnered relationships, it is frequently the
female partner’s distress that motivates treatment seeking. It is common for men who present
with delayed ejaculation to be able to ejaculate with self-stimulation, but not during partnered
sexual activity.
The definition of “delay” does not have precise boundaries, as there is no consensus as to
what constitutes a reasonable time to reach orgasm or what is unacceptably long for most men
and their sexual partners. Although the definitions of delayed ejaculation apply equally well to

both heterosexual and homosexual orientation, the vast majority of the research focus has been
based on the concept of intravaginal latency, and therefore male-female intercourse. The findings
from those studies document that the majority of men’s intravaginal ejaculatory latency time
(IELT) range is approximately 4–10 minutes. There is also no clear diagnostic delineation
between delayed ejaculation as a sexual dysfunction and delay that is a consequence of normal
aging. Therefore, the diagnosis of delayed ejaculation is based on clinical judgment, taking into
consideration the individual’s psychosexual and medical history, age, relationship context, and
sexual stimulation patterns and behaviors. The diagnosis of delayed ejaculation should not be
given if the clinician judges that the individual’s dissatisfaction is entirely attributable to
unrealistic expectations.
Associated Features
The man and his partner may report prolonged thrusting to achieve orgasm to the point of
exhaustion or genital discomfort and sometimes even injury to himself and/or his partner before
finally ceasing. Some males may report avoiding sexual activity because of a repetitive pattern of
difficulty ejaculating.
Delayed ejaculation is associated with highly frequent masturbation, use of masturbation
techniques not easily duplicated by a partner, and marked disparities between sexual fantasies
during masturbation and the reality of sex with a partner.
Males with delayed ejaculation typically report less coital activity, higher levels of
relationship distress, sexual dissatisfaction, lower subjective arousal, anxiety about their sexual
performance, and general health issues than sexually functional men.
In addition to considerations of applicable subtypes (i.e., whether the ejaculatory delay has
been present since the individual became sexually active or began after a period of relatively
normal sexual function, and whether the ejaculatory delay is generalized or occurs only with
certain types of stimulation, situations, or partners), the following factors are important to
consider in the assessment of delayed ejaculation: 1) partner factors (e.g., partner’s sexual
problems or health); 2) relationship factors (e.g., poor communication, discrepancies
in desire for sexual activity); 3) individual vulnerability factors (e.g., hypoactive sexual
desire), psychiatric comorbidity (e.g., depression, anxiety), or stressors such as job loss or stress;
4) cultural/religious factors (e.g., inhibitions related to prohibitions against sexual activity;
attitudes toward sexuality); 5) medical factors, particularly hypogonadism or neurological
disorders (e.g., multiple sclerosis, diabetic neuropathy); and 6) use of substances or medications
that might inhibit ejaculation (e.g., use of serotonergic drugs).
Prevalence
The prevalence of delayed ejaculation in the United States is estimated at 1%–5% but has ranged
as high as 11% in international studies. However, variation in syndrome definitions across
studies may have contributed to differences in the prevalence of the DSM-5 disorder.
Development and Course

Genetic and physiological.
Another medical condition or injury and/or its treatment.
Lifelong delayed ejaculation begins with early sexual experiences and continues throughout the
course of an individual’s life. Acquired delayed ejaculation begins after a period of normal
sexual function. A number of biomedical, psychosocial, and cultural factors can contribute to the
predisposition to or maintenance of lifelong or acquired delayed ejaculation (see the section
“Risk and Prognostic Factors”), and either subtype can be generalized or situational in nature.
The prevalence of delayed ejaculation increases with age. As males age, they are more likely
to have progressively more of the following changes in ejaculatory function, including, but not
limited to, reduced ejaculatory volume, force, and sensation, and increased “refractory time.”
Refractory latency increases for males secondary to surgical, medical, and pharmaceutical
complications, as well as aging.
Risk and Prognostic Factors
Ejaculatory latency is an end point consequence that is determined by a range of factors. A large
number of psychosocial factors increase the probability of an individual experiencing delayed
ejaculation, with depression and relationship dissatisfaction being predominant contributors.
Numerous medical conditions may lead to delayed ejaculation,
including procedures that disrupt sympathetic or somatic innervation to the genital region such as
radical prostatectomy for cancer treatment. Neurological and endocrine disorders, including
spinal cord injury, stroke, multiple sclerosis, pelvic-region surgery, severe diabetes, epilepsy,
hormonal abnormalities, and sleep apnea, as well as alcohol abuse, bowel dysfunction, cannabis
use, and environmental factors, may be associated with delayed ejaculation.
Additionally, medications that inhibit α-adrenergic innervation of the ejaculatory system
(e.g., tamsulosin) are associated with delayed ejaculation, as well as antihypertensive agents,
antidepressants (e.g., selective serotonin reuptake inhibitors), and antipsychotic drugs.
Age-related loss of the fast-conducting peripheral sensory nerves and age-related decreased
sex steroid secretion may be associated with an increase in delayed ejaculation in males as they
age. Reduced androgen levels with age may also be associated with delayed ejaculation.
Sex- and Gender-Related Diagnostic Issues
By definition, the diagnosis of delayed ejaculation is only given to males. Distressing difficulties
with orgasm in women would be considered under female orgasmic disorder.
Functional Consequences of Delayed Ejaculation
Delayed ejaculation is often associated with considerable psychological distress in one or both
partners.
Difficulty with ejaculation may contribute to difficulties in conception and lead to significant
fertility assessment, as the lack of ejaculation is not often spontaneously discussed by individuals
unless there is direct inquiry from their physician.
Differential Diagnosis
A 
major 
diagnostic 
challenge 
is

Substance/medication use.
Dysfunction with orgasm.
F52.21
differentiating between a delayed ejaculation that is fully explained by another medical condition
or injury (or its treatment) and a delayed ejaculation attributable to a variety of proportionally
different biomedical-psychosocial and cultural factors that determine the symptom(s). A number
of medical conditions or injuries, along with their treatments, may produce delays in ejaculation
independent of psychosocial and cultural issues.
Delayed ejaculation must be differentiated from a number of urological conditions
(especially other ejaculatory disorders), including retrograde ejaculation or anejaculation, which
is typically the result of etiologies ranging from hormonal to neurological and/or anatomical
abnormalities, including ejaculatory duct obstruction and other urological disorders.
A number of pharmacological agents, such as antidepressants,
antipsychotics, α sympathetic drugs, alcohol, and opioid drugs, can cause ejaculatory problems.
In such cases, the diagnosis is substance/medication-induced sexual dysfunction instead of
delayed ejaculation.
It is important in the history to ascertain whether the complaint concerns
delayed ejaculation or the sensation of orgasm, or both. Ejaculation occurs in the genitals,
whereas the experience of orgasm is believed to be primarily subjective. Ejaculation and orgasm
usually occur together but not always. For example, a male with a normal ejaculatory pattern
may complain of decreased pleasure (i.e., anhedonic ejaculation). Such a complaint would not be
coded as delayed ejaculation but could be coded as other specified sexual dysfunction or
unspecified sexual dysfunction.
Comorbidity
There is some evidence to suggest that delayed ejaculation may be more common in severe
forms of major depressive disorder.
Erectile Disorder
Diagnostic Criteria
A. At least one of the three following symptoms must be experienced on almost all
or all (approximately 75%–100%) occasions of sexual activity (in identified
situational contexts or, if generalized, in all contexts):
1. Marked difficulty in obtaining an erection during sexual activity.
2. Marked difficulty in maintaining an erection until the completion of sexual
activity.
3. Marked decrease in erectile rigidity.
B. The symptoms in Criterion A have persisted for a minimum duration of
approximately 6 months.
C. The symptoms in Criterion A cause clinically significant distress in the individual.

D. The sexual dysfunction is not better explained by a nonsexual mental disorder or
as a consequence of severe relationship distress or other significant stressors
and is not attributable to the effects of a substance/medication or another
medical condition.
Specify whether:
Lifelong: The disturbance has been present since the individual became
sexually active.
Acquired: The disturbance began after a period of relatively normal sexual
function.
Specify whether:
Generalized: Not limited to certain types of stimulation, situations, or partners.
Situational: Only occurs with certain types of stimulation, situations, or partners.
Specify current severity:
Mild: Evidence of mild distress over the symptoms in Criterion A.
Moderate: Evidence of moderate distress over the symptoms in Criterion A.
Severe: Evidence of severe or extreme distress over the symptoms in Criterion
A.
Diagnostic Features
The essential feature of erectile disorder is a marked difficulty in obtaining or maintaining an
erection or a marked decrease in erectile rigidity in all or almost all occasions of sexual activity
(Criterion A) that has persisted for at least 6 months (Criterion B) and that causes clinically
significant distress in the individual (Criterion C). A careful sexual history is necessary to
ascertain that the problem has been present for a significant duration of time (i.e., at least
approximately 6 months) and occurs on the majority of sexual occasions (i.e., at least 75% of the
time). Symptoms may occur only in specific situations involving certain types of stimulation or
partners, or they may occur in a generalized manner in all types of situations, stimulation, or
partners.
This chapter uses the terms erectile disorder and erectile dysfunction, which are not
synonymous. Erectile dysfunction is a widely used descriptive term (including in ICD-10) that
refers to difficulty getting and maintaining an erection. Erectile disorder is the more specific
DSM-5 diagnostic category in which erectile dysfunction persists for at least 6 months and
causes distress in the individual.
Associated Features
Many males with erectile disorder may have low self-esteem, low self-confidence, and a
decreased sense of masculinity, and may experience depressed mood. Erectile dysfunction is also
strongly associated with feelings of guilt, self-blame, sense of failure, anger, and concern about
disappointing one’s partner. Fear and/or avoidance of future sexual encounters may occur.
Decreased sexual satisfaction and reduced sexual desire in the individual’s partner are common.
In addition to considerations of applicable subtypes (i.e., whether the erectile dysfunction has

been present since the individual became sexually active or began after a period of relatively
normal sexual function, and whether the erectile dysfunction is generalized or occurs only with
certain types of stimulation, situations, or partners), the following factors are important to
consider in the assessment of erectile disorder: 1) partner factors (e.g., partner’s sexual problems
or health); 2) relationship factors (e.g., poor communication, discrepancies in desire for sexual
activity); 3) individual vulnerability factors (e.g., hypoactive sexual desire), psychiatric
comorbidity (e.g., depression, anxiety), or stressors such as job loss or stress; 4) cultural/religious
factors (e.g., inhibitions related to prohibitions against sexual activity; attitudes toward
sexuality); 5) medical factors, particularly surgery (e.g., transurethral resection of the prostate),
hypogonadism, or neurological conditions
(e.g., multiple sclerosis, diabetic neuropathy); and 6) use of substances or medications that
might inhibit ejaculation (e.g., use of serotonergic drugs).
Prevalence
The prevalence of lifelong versus acquired erectile disorder is unknown. There is a strong agerelated increase in both prevalence and incidence of problems with erection, particularly after
age 50 years. Internationally, the prevalence of erectile disorder in the general population is
approximately 13%–21% of males ages 40–80 years. Rates appear to be lower than 10% in
males younger than 40 years, about 20%–40% in males in their 60s, and 50%–75% in males
older than 70 years. In a longitudinal study in Australia, 80% of males age 70 and older
experienced erectile disorder. In a review of studies largely from Western countries, about 20%
of males feared erectile problems on their first sexual experience, whereas approximately 8%
experienced erectile problems that hindered penetration during their first sexual experience.
Among U.S.-based respondents to an online survey, there was no statistically significant
difference in the prevalence of erectile disorder by ethnoracial background. Nationally
representative U.S. data show that the prevalence of erectile difficulties is similar in older males
who have sex with males or with both males and females.
Development and Course
Erectile failure on first sexual attempt has been found to be related to having sex with a
previously unknown partner, concomitant use of drugs or alcohol, not wanting to have sex, and
peer pressure. There is minimal evidence regarding the persistence of such problems after the
first attempt. It is assumed that most of these problems spontaneously remit without professional
intervention, but some males may continue to have episodic problems. In contrast, acquired
erectile disorder is often associated with biological factors such as diabetes and cardiovascular
disease. Acquired erectile disorder is likely to be persistent in most men.
The natural history of lifelong erectile disorder is unknown. Clinical observation supports the
association of lifelong erectile disorder with psychological factors that are self-limiting or
responsive to psychological interventions, whereas, as noted above, acquired erectile disorder is
more likely to be related to biological factors and to be persistent. The incidence of erectile
disorder increases with age. A minority of males diagnosed as having moderate erectile failure

Course modifiers.
may experience spontaneous remission of symptoms without medical intervention. Distress
associated with erectile disorder is lower in older males as compared with younger males.
Risk and Prognostic Factors
Risk factors for acquired erectile dysfunction and, as a consequence, erectile
disorder include age, smoking tobacco, lack of physical exercise, diabetes, and decreased desire.
Culture-Related Diagnostic Issues
Prevalence of erectile disorder varies across countries. It is unclear to what extent these
variations represent differences in cultural expectations as opposed to genuine differences in the
frequency of erectile failure. Differential endorsement may be related to cultural concerns about
appearing weak or less masculine or to diverse cultural norms about changes in erectile function
during healthy aging. Cultural expectations concerning marital relationships, sexual
performance, fertility, and gender roles can influence anxieties that may contribute to erectile
disorder. Based on responses to an online survey, erectile disorder may be associated with
concern about genital size in the United States and the Middle East and with fears of male
infertility more frequently in the Middle East.
Sex- and Gender-Related Diagnostic Issues
By definition, the diagnosis of erectile dysfunction is only given to males. Distressing difficulties
with sexual arousal in women would be considered under female sexual interest/arousal disorder.
Diagnostic Markers
Nocturnal penile tumescence testing and measured erectile turgidity during sleep can be
employed to help differentiate organic from psychogenic erectile problems on the assumption
that adequate erections during rapid eye movement sleep indicate a psychological etiology to the
problem. A number of other diagnostic procedures may be employed depending on the
clinician’s assessment of their relevance given the individual’s age, comorbid medical problems,
and clinical presentation. Doppler ultrasonography and intravascular injection of vasoactive
drugs, as well as invasive diagnostic procedures such as dynamic infusion cavernosography, can
be used to assess vascular integrity. Pudendal nerve conduction studies, including somatosensory
evoked potentials, can be employed when a peripheral neuropathy is suspected. Testing for low
levels of serum bioavailable or free testosterone is appropriate especially when diabetes is
present, for men who also experience hypoactive desire, and for those who do not respond to
phosphodiesterase type 5 inhibitors. Thyroid function may also be assessed. Determination of
fasting serum glucose is useful to screen for the presence of diabetes mellitus. The assessment of
serum lipids is important, as erectile disorder in males 40 years and older is predictive of the
future risk for coronary artery disease.
Association With Suicidal Thoughts or Behavior
Among males receiving treatment for erectile disorder with comorbid depression, elevated rates

Nonsexual mental disorders.
Normal erectile function.
Substance/medication use.
Another medical condition.
of suicidal thoughts or behavior have been observed; while the affected males attributed the
suicidal symptoms to their erectile disorder, the presence of depression was also a likely
contributing factor. Elevated suicide rates among males with prostate cancer may in part be
related to treatment-associated erectile dysfunction and consequent depressive symptoms.
Functional Consequences of Erectile Disorder
Erectile disorder can interfere with fertility and produce both individual and interpersonal
distress. Fear and/or avoidance of sexual encounters may interfere with the ability to develop
intimate relationships. Significant psychological distress may occur among males presenting
with erectile disorder.
Differential Diagnosis
Major depressive disorder and erectile disorder are closely associated,
and erectile disorder accompanying severe depressive disorder may occur. If the erectile
difficulties are better explained by another mental disorder, such as major depression, then a
diagnosis of erectile disorder would not be made.
The differential should include consideration of normal erectile function
in males with excessive expectations.
An onset of erectile dysfunction that coincides with the beginning of
substance/medication use and that dissipates with discontinuation of the substance/medication or
dose reduction is suggestive of a substance/medication-induced sexual dysfunction, which
should be diagnosed instead of erectile disorder.
The most difficult aspect of the differential diagnosis of erectile
disorder is ruling out erectile problems that are fully explained by medical factors. Such cases
would not receive a diagnosis of a mental disorder. The distinction between erectile disorder as a
mental disorder and erectile dysfunction as the result of another medical condition is usually
unclear, and many cases will have complex, interactive biological and psychiatric etiologies. If
the individual is older than 40–50 years and/or has concomitant medical problems, the
differential diagnosis should include medical etiologies, especially vascular disease. The
presence of an organic disease known to cause erectile problems does not confirm a causal
relationship. For example, a male with diabetes mellitus can develop erectile disorder in response
to psychological stress. In general, erectile dysfunction due to organic factors is generalized and
gradual in onset. An exception would be erectile problems after traumatic injury to the nervous
innervation of the genital organs (e.g., spinal cord injury). Erectile problems that are situational
and inconsistent and that have an acute onset after a stressful life event are most often
attributable to psychological events. An age younger than 40 years is also suggestive of a
psychological etiology to the difficulty.
Comorbidity
Erectile disorder can be comorbid with other sexual diagnoses, such as premature (early)

F52.31
ejaculation and male hypoactive sexual desire disorder, as well as with anxiety and depressive
disorders. The risk of depression is significantly higher in males with erectile disorder, with a
markedly higher risk of depression in the first year after onset. In males diagnosed with
posttraumatic stress disorder, erectile problems are common. Erectile disorder is common in
males with lower urinary tract symptoms related to prostatic hypertrophy. Erectile disorder may
be comorbid with dyslipidemia, cardiovascular disease, hypogonadism, multiple sclerosis,
diabetes mellitus, and other diseases that interfere with the vascular, neurological, or endocrine
function necessary for normal erectile function.
Female Orgasmic Disorder
Diagnostic Criteria
A. Presence of either of the following symptoms and experienced on almost all or
all (approximately 75%–100%) occasions of sexual activity (in identified
situational contexts or, if generalized, in all contexts):
1. Marked delay in, marked infrequency of, or absence of orgasm.
2. Markedly reduced intensity of orgasmic sensations.
B. The symptoms in Criterion A have persisted for a minimum duration of
approximately 6 months.
C. The symptoms in Criterion A cause clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexual mental disorder or
as a consequence of severe relationship distress (e.g., partner violence) or other
significant 
stressors 
and 
is 
not 
attributable 
to 
the 
effects 
of 
a
substance/medication or another medical condition.
Specify whether:
Lifelong: The disturbance has been present since the individual became
sexually active.
Acquired: The disturbance began after a period of relatively normal sexual
function.
Specify whether:
Generalized: Not limited to certain types of stimulation, situations, or partners.
Situational: Only occurs with certain types of stimulation, situations, or partners.
Specify if:
Never experienced an orgasm under any situation.
Specify current severity:
Mild: Evidence of mild distress over the symptoms in Criterion A.

Moderate: Evidence of moderate distress over the symptoms in Criterion A.
Severe: Evidence of severe or extreme distress over the symptoms in Criterion
A.
Diagnostic Features
Female orgasmic disorder is characterized by difficulty experiencing orgasm and/or markedly
reduced intensity of orgasmic sensations (Criterion A). Women show wide variability in the type
or intensity of stimulation that elicits orgasm. Similarly, subjective descriptions of orgasm are
extremely varied, suggesting that it is experienced in very different ways, both across women
and on different occasions by the same woman. For a diagnosis of female orgasmic disorder,
symptoms must be experienced on almost all or all (approximately 75%–100%) occasions of
sexual activity (in identified situational contexts or, if generalized, in all contexts) and have a
minimum duration of approximately 6 months. The use of the minimum severity and duration
criteria is intended to distinguish transient orgasm difficulties from more persistent orgasmic
dysfunction. The inclusion of “approximately” in Criterion B allows for clinician judgment in
cases in which symptom duration does not meet the recommended 6-month threshold.
For a woman to have a diagnosis of female orgasmic disorder, clinically significant distress
must accompany the symptoms (Criterion C). In many cases of orgasm problems, the causes are
multifactorial or cannot be determined. If female orgasmic disorder is deemed to be better
explained by another mental disorder, the effects of a substance/medication, or a medical
condition, then a diagnosis of female orgasmic disorder would not be made. Finally, if
interpersonal or significant contextual factors, such as severe relationship distress, intimate
partner violence, or other significant stressors, are present, then a diagnosis of female orgasmic
disorder would not be made.
Many women require clitoral stimulation to reach orgasm, and a relatively small proportion
of women report that they always experience orgasm during penile-vaginal intercourse. Thus, a
woman’s experiencing orgasm through clitoral stimulation but not during intercourse does not
meet criteria for a clinical diagnosis of female orgasmic disorder. It is also important to consider
whether orgasm difficulties are the result of inadequate sexual stimulation; in these cases, there
may still be a need for care, but a diagnosis of female orgasmic disorder would not be made.
Associated Features
Associations between specific patterns of personality traits or psychopathology and orgasmic
dysfunction have generally not been supported. Compared with women without the disorder,
some women with female orgasmic disorder may have greater difficulty communicating about
sexual issues. Overall sexual satisfaction, however, is not strongly correlated with orgasmic
experience. Many women report high levels of sexual satisfaction despite rarely or never
experiencing orgasm. Orgasm difficulties in women often co-occur with problems related to
sexual interest and arousal.
In addition to the subtypes “lifelong/acquired” and “generalized/situational,” the following
five factors must be considered during assessment and diagnosis of female orgasmic disorder
given that they may be relevant to etiology or treatment: 1) partner factors (e.g., partner’s sexual
problems, partner’s health status); 2) relationship factors (e.g., poor

Temperamental.
Environmental.
Genetic and physiological.
communication, discrepancies in desire for sexual activity); 3) individual vulnerability
factors (e.g., poor body image, history of sexual or emotional abuse), psychiatric comorbidity
(e.g., depression, anxiety), or stressors (e.g., job loss, bereavement); 4) cultural/religious factors
(e.g., inhibitions related to prohibitions against sexual activity; attitudes toward sexuality); and 5)
medical factors relevant to prognosis, course, or treatment. Each of these factors may contribute
differently to the presenting symptoms of different women with this disorder.
Prevalence
Reported prevalence rates for orgasm problems in premenopausal women vary widely, from 8%
to 72%, depending on multiple factors (e.g., age, cultural background and context, duration,
severity of symptoms); however, these estimates do not take into account the presence of
distress. Only a proportion of women experiencing orgasm difficulties also report associated
distress. Variation in how symptoms are assessed (e.g., the duration of symptoms and the recall
period) also influence prevalence rates. Internationally, approximately 10% of women do not
experience orgasm throughout their lifetime.
Development and Course
By definition, lifelong female orgasmic disorder indicates that the orgasm difficulties have
always been present, whereas the acquired subtype would be assigned if the woman’s orgasm
difficulties developed after a period of normal orgasmic functioning.
A woman’s first experience of orgasm can occur any time from the prepubertal period to well
into adulthood. Women show a more variable pattern in age at first orgasm than do men, and
women’s reports of having experienced orgasm increase with age. Many women learn to
experience orgasm as they experience a wide variety of stimulation and acquire more knowledge
about their bodies. Women’s rates of orgasmic consistency (defined as “usually or always”
experiencing orgasm) are higher during masturbation than during sexual activity with a partner.
Risk and Prognostic Factors
A wide range of psychological factors, such as anxiety and concerns about
pregnancy, can potentially interfere with a woman’s ability to experience orgasm.
There is a strong association between relationship problems, physical health, and
mental health and orgasm difficulties in women. Sociocultural factors (e.g., gender role
expectations and religious norms) are also important influences on the experience of orgasm
difficulties.
Many physiological factors may influence a woman’s experience of
orgasm, including medical conditions and medications. Conditions such as multiple sclerosis,
pelvic nerve damage from radical hysterectomy, and spinal cord injury can all influence
orgasmic functioning in women. Selective serotonin reuptake inhibitors are known to delay or
inhibit orgasm in women. Women with vulvovaginal atrophy (characterized by symptoms such
as vaginal dryness, itching, and pain) are significantly more likely to report orgasm difficulties
than are women without this condition. Menopausal status is not consistently associated with the

Nonsexual mental disorders.
likelihood of orgasm difficulties. There may be a significant genetic contribution to variation in
female orgasmic function. However, psychological, sociocultural, and physiological factors
likely interact in complex ways to influence women’s experience of orgasm and of orgasm
difficulties.
Culture-Related Diagnostic Issues
The degree to which lack of orgasm in women is regarded as a problem that requires treatment
may vary depending on cultural context. Cultural views that undervalue women’s
sexual satisfaction or that perceive marital sex as a duty for women rather than a pleasurable
activity are associated with lower help-seeking. In addition, women differ in how important
orgasm is to their sexual satisfaction. There may be marked sociocultural and generational
differences in women’s orgasmic ability. For example, reports of the prevalence of inability to
reach orgasm vary over a twofold range across world regions.
Sex- and Gender-Related Diagnostic Issues
By definition, the diagnosis of female orgasmic disorder is given only to women. Distressing
difficulties with orgasm in men would be considered under delayed ejaculation.
Diagnostic Markers
Although measurable physiological changes occur during female orgasm, including changes in
hormones, pelvic floor musculature, and brain activation, there is significant variability in these
indicators of orgasm across women. In clinical situations, the diagnosis of female orgasmic
disorder is based on a woman’s self-report.
Association With Suicidal Thoughts or Behavior
Dysfunctions of sexual arousal and satisfaction have been associated with suicidal thoughts
among female veterans and military service members even after adjustment for probable
posttraumatic stress disorder, probable depression, history of deployment, married status, age,
service in the army, and race.
Functional Consequences of Female Orgasmic Disorder
The functional consequences of female orgasmic disorder are unclear. Although there is a strong
association between relationship problems and orgasm difficulties in women, it is unclear
whether relationship factors are risk factors for orgasm difficulties or are consequences of those
difficulties.
Differential Diagnosis
If the orgasm difficulties are better explained by another mental
disorder, such as major depression, then a diagnosis of female orgasmic disorder would not be
made.

Substance/medication-induced sexual dysfunction.
Another medical condition.
Interpersonal factors.
Other sexual dysfunctions.
F52.22
An onset of orgasmic dysfunction that coincides
with the beginning of substance/medication use and that dissipates with discontinuation of the
substance/medication or dose reduction is suggestive of a substance/medication-induced sexual
dysfunction, which should be diagnosed instead of female orgasmic disorder.
If the disorder is attributable to another medical condition (e.g.,
multiple sclerosis, spinal cord injury), then a diagnosis of female orgasmic disorder would not be
made.
If interpersonal or significant contextual factors, such as severe relationship
distress, intimate partner violence, or other significant stressors, are associated with the orgasm
difficulties, then a diagnosis of female orgasmic disorder would not be made.
Female orgasmic disorder may occur in association with other sexual
dysfunctions (e.g., female sexual interest/arousal disorder). The presence of another sexual
dysfunction does not rule out a diagnosis of female orgasmic disorder. Occasional orgasm
difficulties that are short-term or infrequent and are not accompanied by clinically significant
distress or impairment are not diagnosed as female orgasmic disorder. A diagnosis is also not
appropriate if the problems are the result of inadequate sexual stimulation.
Comorbidity
Women with female orgasmic disorder may have co-occurring sexual interest/arousal
difficulties. Women with diagnoses of other nonsexual mental disorders, such as major
depressive disorder, may experience lower sexual interest/arousal, and this may indirectly
increase the likelihood of orgasm difficulties.
Female Sexual Interest/Arousal Disorder
Diagnostic Criteria
A. Lack of, or significantly reduced, sexual interest/arousal, as manifested by at
least three of the following:
1. Absent/reduced interest in sexual activity.
2. Absent/reduced sexual/erotic thoughts or fantasies.
3. No/reduced initiation of sexual activity, and typically unreceptive to a partner’s
attempts to initiate.
4. Absent/reduced sexual excitement/pleasure during sexual activity in almost
all or all (approximately 75%–100%) sexual encounters (in identified
situational contexts or, if generalized, in all contexts).
5. Absent/reduced sexual interest/arousal in response to any internal or external
sexual/erotic cues (e.g., written, verbal, visual).
6. Absent/reduced genital or nongenital sensations during sexual activity in

almost all or all (approximately 75%–100%) sexual encounters (in identified
situational contexts or, if generalized, in all contexts).
B. The symptoms in Criterion A have persisted for a minimum duration of
approximately 6 months.
C. The symptoms in Criterion A cause clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexual mental disorder or
as a consequence of severe relationship distress (e.g., partner violence) or other
significant 
stressors 
and 
is 
not 
attributable 
to 
the 
effects 
of 
a
substance/medication or another medical condition.
Specify whether:
Lifelong: The disturbance has been present since the individual became
sexually active.
Acquired: The disturbance began after a period of relatively normal sexual
function.
Specify whether:
Generalized: Not limited to certain types of stimulation, situations, or partners.
Situational: Only occurs with certain types of stimulation, situations, or partners.
Specify current severity:
Mild: Evidence of mild distress over the symptoms in Criterion A.
Moderate: Evidence of moderate distress over the symptoms in Criterion A.
Severe: Evidence of severe or extreme distress over the symptoms in Criterion
A.
Diagnostic Features
In assessing female sexual interest/arousal disorder, interpersonal context must be taken into
account. A “desire discrepancy,” in which a woman has lower desire for sexual activity than her
partner, is not sufficient to diagnose female sexual interest/arousal disorder. For the criteria for
the disorder to be met, there must be absence or reduced frequency or
intensity of at least three of six indicators (Criterion A) for a minimum duration of approximately
6 months (Criterion B). There may be different symptom profiles across women, as well as
variability in how sexual interest and arousal are expressed. For example, in one woman, sexual
interest/arousal disorder may be expressed as a lack of interest in sexual activity, an absence of
erotic or sexual thoughts, and reluctance to initiate sexual activity and respond to a partner’s
sexual invitations. In another woman, an inability to become sexually excited, an inability to
respond to sexual stimuli with sexual desire, and a corresponding lack of signs of physical sexual
arousal may be the primary features. Difficulties in desire and sexual arousal may also occur
simultaneously, as women with loss of sexual desire may be nine times more likely to also have
lost sexual excitement or arousal. Short-term changes in sexual interest or arousal are common

and may be adaptive responses to events in a woman’s life and do not represent a sexual
dysfunction. Diagnosis of female sexual interest/arousal disorder requires a minimum duration of
symptoms of approximately 6 months as a reflection that the symptoms must be a persistent
problem. The estimation of persistence may be determined by clinical judgment when a duration
of 6 months cannot be ascertained precisely.
There may be absent or reduced frequency or intensity of interest in sexual activity (Criterion
A1), which was previously the single criterion for hypoactive sexual desire disorder; this
condition is now represented by female sexual interest/arousal disorder. The frequency or
intensity of sexual and erotic thoughts or fantasies may be absent or reduced (Criterion A2). The
expression of fantasies varies widely across women and may include memories of past sexual
experiences. The normative decline in sexual thoughts with age should be taken into account
when this criterion is being assessed. Absence or reduced frequency of initiating sexual activity
and of receptivity to a partner’s sexual invitations (Criterion A3) is a behaviorally focused
criterion. A couple’s beliefs and preferences for sexual initiation patterns are highly relevant to
the assessment of this criterion. There may be absent or reduced sexual excitement or pleasure
during sexual activity in almost all or all (approximately 75%–100%) sexual encounters
(Criterion A4). Lack of pleasure is a common presenting clinical complaint in women with low
desire. Among women who report low sexual desire, there are fewer sexual or erotic cues that
elicit sexual interest or arousal (i.e., there is a lack of “responsive desire”). Evidence suggests
that there may be at least two types of female sexual interest/arousal disorder: one based on low
sensitivity to sexual cues and a second based on overactivation of sexual inhibition. Assessment
of the adequacy of sexual stimuli will assist in determining if there is a difficulty with responsive
sexual desire (Criterion A5). Frequency or intensity of genital or nongenital sensations during
sexual activity may be reduced or absent (Criterion A6). This may include reduced vaginal
lubrication/vasocongestion, but because physiological measures of genital sexual response do not
differentiate women who report sexual arousal concerns from those who do not, the self-report of
reduced or absent genital or nongenital sensations is sufficient.
For a diagnosis of female sexual interest/arousal disorder to be made, clinically significant
distress must accompany the symptoms in Criterion A. Distress may be experienced as a result of
the lack of sexual interest/arousal or as a result of significant interference in a woman’s life and
well-being. If a lifelong lack of sexual desire is better explained by one’s self-identification as
“asexual,” then a diagnosis of female sexual interest/arousal disorder would not be made.
Associated Features
Female sexual interest/arousal disorder is frequently associated with problems in experiencing
orgasm, pain experienced during sexual activity, infrequent sexual activity, and couple-level
discrepancies in desire. Relationship difficulties, chronic stress, and mood disorders are also
frequently associated features of female sexual interest/arousal disorder. Unrealistic expectations
and norms regarding the “appropriate” level of sexual
interest or arousal, along with poor sexual techniques and lack of information about sexuality,
may also be evident in women diagnosed with female sexual interest/arousal disorder. The latter,

Temperamental.
as well as normative beliefs about gender roles, are important factors to consider.
In addition to the subtypes “lifelong/acquired” and “generalized/situational,” the following
five factors must be considered during assessment and diagnosis of female sexual interest/arousal
disorder given that they may be relevant to etiology and/or treatment: 1) partner factors (e.g.,
partner’s sexual problems, partner’s health status, partner-related distress); 2) relationship factors
(e.g., poor communication, discrepancies in desire for sexual activity; relationship duration); 3)
individual vulnerability factors (e.g., poor body image, history of sexual or emotional abuse),
psychiatric comorbidity (e.g., depression, anxiety), or stressors (e.g., job loss, bereavement); 4)
cultural/religious factors (e.g., inhibitions related to prohibitions against sexual activity; attitudes
toward sexuality); and 5) medical factors relevant to prognosis, course, or treatment. Note that
each of these factors may contribute differently to the presenting symptoms of different women
with this disorder.
Prevalence
Approximately 30% of women experience chronic low desire, with approximately half of these
experiencing significant partner-related distress and a quarter experiencing personal distress. The
prevalence of low sexual desire and of problems with sexual arousal (with and without
associated distress) may vary markedly in relation to age, cultural context, duration of symptoms,
and presence of distress. Regarding duration of symptoms, there are striking differences in
prevalence estimates between short-term and persistent problems related to lack of sexual
interest. When distress about sexual functioning is required, prevalence estimates are markedly
lower. Though there is a strong relationship between low desire and age, the prevalence of sexrelated distress associated with low desire decreases as women age.
Development and Course
By definition, lifelong female sexual interest/arousal disorder suggests that the lack of sexual
interest or arousal has been present for the woman’s entire sexual life. For Criteria A3, A4, and
A6, which assess functioning during sexual activity, a subtype of lifelong would mean presence
of symptoms since the individual’s first sexual experiences. The acquired subtype would be
assigned if the difficulties with sexual interest or arousal developed after a period of
nonproblematic sexual functioning. Adaptive and normative changes in sexual functioning may
result from partner-related, interpersonal, or personal events and may be transient in nature.
However, persistence of symptoms for approximately 6 months or more would constitute a
sexual dysfunction.
There are normative changes in sexual interest and arousal across the life span. Furthermore,
women in relationships of longer duration are more likely to report engaging in sex despite no
obvious feelings of sexual desire at the outset of a sexual encounter compared with women in
shorter-duration relationships. Vaginal dryness in older women is related to age and menopausal
status.
Risk and Prognostic Factors
Temperamental factors include negative cognitions and attitudes about sexuality
and past history of mental disorders. Differences in propensity for sexual excitation and sexual

Environmental.
Genetic and physiological.
Nonsexual mental disorders.
inhibition may also predict the likelihood of developing sexual problems.
Environmental 
factors 
include 
relationship 
difficulties, 
partner 
sexual
functioning, and developmental history, such as early relationships with caregivers and
childhood stressors.
Some medical conditions (e.g., diabetes mellitus, thyroid dysfunction)
can be risk factors for female sexual interest/arousal disorder. There appears to be a strong
influence of genetic factors on vulnerability to sexual problems in women. Psychophysiological
research using vaginal photoplethysmography has not found differences between women with
and without perceived lack of genital arousal.
Culture-Related Diagnostic Issues
There is marked variability in reported prevalence rates of low desire across world regions,
ranging from 26% to 43%. Low levels of sexual desire have been reported by some ethnoracial
and migrant groups. Although lower levels of reported sexual desire and arousal may reflect less
interest in sex, such group differences may be an artifact of the measures used to quantify desire
and of cultural factors affecting response, such as the desirability of reporting sexual activity by
nonmarried, menopausal, or widowed women. A judgment about whether low sexual desire
reported by a woman from a certain ethnocultural background meets criteria for female sexual
interest/arousal disorder must take into account the fact that different cultural groups may vary in
norms and expectations for sexual behavior.
Sex- and Gender-Related Diagnostic Issues
By definition, the diagnosis of female sexual interest/arousal disorder is only given to women.
Distressing difficulties with sexual desire in men would be considered under male hypoactive
sexual desire disorder. There are no data showing that rates or expressions of female sexual
interest/arousal disorder differ between heterosexual and lesbian women.
Association With Suicidal Thoughts or Behavior
Dysfunctions of sexual arousal and satisfaction have been associated with suicidal thoughts
among female veterans and military service members even after adjustment for probable PTSD,
probable depression, history of deployment, married status, age, service in the army, and race.
Functional Consequences of Female Sexual Interest/Arousal Disorder
Difficulties in sexual interest/arousal are often associated with decreased relationship
satisfaction.
Differential Diagnosis
Nonsexual mental disorders, such as major depressive disorder, in
which there is “markedly diminished interest or pleasure in all, or almost all, activities most of
the day, nearly every day,” may explain the lack of sexual interest/arousal. If the lack of interest

Substance/medication use.
Another medical condition.
Interpersonal factors.
Other sexual dysfunctions.
Inadequate or absent sexual stimuli.
F52.6
or arousal is completely attributable to another mental disorder, then a diagnosis of female sexual
interest/arousal disorder would not be made.
An onset of difficulties in desire or arousal that coincides with the
beginning of substance/medication use and that dissipates with discontinuation of the
substance/medication or dose reduction is suggestive of a substance/medication-induced sexual
dysfunction, which should be diagnosed instead of female sexual interest/arousal disorder.
If the sexual symptoms are considered to be almost exclusively
associated with the effects of another medical condition (e.g., diabetes mellitus,
endothelial disease, thyroid dysfunction, central nervous system disease), then a diagnosis of
female sexual interest/arousal disorder would not be made.
If interpersonal or significant contextual factors, such as severe relationship
distress, intimate partner violence, or other significant stressors, explain the sexual
interest/arousal symptoms, then a diagnosis of female sexual interest/arousal disorder would not
be made.
The presence of another sexual dysfunction does not rule out a
diagnosis of female sexual interest/arousal disorder. It is common for women to experience more
than one sexual dysfunction. For example, the presence of chronic genital pain may lead to a lack
of desire for the (painful) sexual activity. Lack of interest and arousal during sexual activity may
impair orgasmic ability. For some women, all aspects of the sexual response may be unsatisfying
and distressing.
When differential diagnoses are being considered, it is
important to assess the adequacy of sexual stimuli within the woman’s sexual experience. In
cases where inadequate or absent sexual stimuli are contributing to the clinical picture, there may
be evidence for clinical care, but a sexual dysfunction diagnosis would not be made. Similarly,
transient and adaptive alterations in sexual functioning that are secondary to a significant life or
personal event must be considered in the differential diagnosis.
Comorbidity
Comorbidity between sexual interest/arousal problems and other sexual difficulties is extremely
common. Sexual distress and dissatisfaction with sex life are also highly correlated in women
with low sexual desire. Distressing low desire is associated with depression, thyroid problems,
anxiety, urinary incontinence, and other medical factors. Arthritis and inflammatory or irritable
bowel disease are also associated with sexual arousal problems. Low desire appears to be
comorbid with depression, sexual and physical abuse in adulthood, and use of alcohol.
Genito-Pelvic Pain/Penetration Disorder
Diagnostic Criteria

A. Persistent or recurrent difficulties with one (or more) of the following:
1. Vaginal penetration during intercourse.
2. Marked vulvovaginal or pelvic pain during vaginal intercourse or penetration
attempts.
3. Marked fear or anxiety about vulvovaginal or pelvic pain in anticipation of,
during, or as a result of vaginal penetration.
4. Marked tensing or tightening of the pelvic floor muscles during attempted
vaginal penetration.
B. The symptoms in Criterion A have persisted for a minimum duration of
approximately 6 months.
C. The symptoms in Criterion A cause clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexual mental disorder or
as a consequence of a severe relationship distress (e.g., partner violence) or
other significant stressors and is not attributable to the effects of a
substance/medication or another medical condition.
Specify whether:
Lifelong: The disturbance has been present since the individual became
sexually active.
Acquired: The disturbance began after a period of relatively normal sexual
function.
Specify current severity:
Mild: Evidence of mild distress over the symptoms in Criterion A.
Moderate: Evidence of moderate distress over the symptoms in Criterion A.
Severe: Evidence of severe or extreme distress over the symptoms in Criterion
A.
Diagnostic Features
Genito-pelvic pain/penetration disorder refers to four commonly comorbid symptom dimensions:
1) difficulty having intercourse, 2) genito-pelvic pain, 3) fear of pain or vaginal penetration, and
4) tension of the pelvic floor muscles (Criterion A). Because major difficulty in any one of these
symptom dimensions is often sufficient to cause clinically significant distress, a diagnosis can be
made on the basis of marked difficulty in only one symptom dimension. However, all four
symptom dimensions should be assessed even if a diagnosis can be made on the basis of only
one symptom dimension.
Marked difficulty having vaginal intercourse/penetration (Criterion A1) can vary from a total
inability to experience vaginal penetration in any situation (e.g., intercourse, gynecological
examinations, tampon insertion) to the ability to easily experience penetration in one situation
but not in another. Although the most common clinical situation is when a female is unable to

experience intercourse or penetration with a partner, difficulties in undergoing required
gynecological examinations may also be present. Marked vulvovaginal or pelvic pain during
vaginal intercourse or penetration attempts (Criterion A2) refers to pain occurring in different
locations in the genito-pelvic area. Location of pain as well as intensity should be assessed.
Typically, pain can be characterized as superficial (vulvovaginal or occurring during penetration)
or deep (pelvic; i.e., not felt until deeper penetration). The intensity of the pain is often not
linearly related to distress or interference with vaginal penetration or other sexual activities.
Some genito-pelvic pain only occurs when provoked (i.e., by intercourse or mechanical
stimulation); other genito-pelvic pain may be spontaneous as well as provoked. Genito-pelvic
pain can also be usefully characterized qualitatively (e.g., “burning,” “cutting,” “shooting,”
“throbbing”). The pain may persist for a period after intercourse is completed and may also occur
during urination. Typically, the pain experienced during vaginal intercourse can be reproduced
during a gynecological examination.
Marked fear or anxiety about vulvovaginal or pelvic pain either in anticipation of, or during,
or as a result of vaginal penetration (Criterion A3) is commonly reported by females who have
regularly experienced pain during vaginal penetration. This “normal” reaction may lead to
avoidance of sexual/intimate situations. In other cases, this marked fear does not appear to be
closely related to the experience of pain but nonetheless leads to avoidance of intercourse and
vaginal penetration situations. Some have described this as similar to a phobic reaction except
that the phobic object may be vaginal penetration or the fear of pain.
Marked tensing or tightening of the pelvic floor muscles during attempted vaginal
penetration (Criterion A4) can vary from reflexive-like spasm of the pelvic floor in response to
attempted vaginal entry to “normal/voluntary” muscle guarding in response to the anticipated or
the repeated experience of pain or to fear or anxiety. In the case of “normal/guarding” reactions,
penetration may be possible under circumstances of relaxation. The characterization and
assessment of pelvic floor dysfunction is often best undertaken by a specialist gynecologist or by
a pelvic floor physical therapist.
Symptoms of genito-pelvic pain/penetration disorder may be characterized by previous
terms, including dyspareunia (pain during sexual intercourse) and vaginismus (defined by
involuntary contraction of muscles making penetration painful or impossible). Specific
medical disorders, such as vulvodynia (chronic idiopathic vulvar pain lasting at least 3 months)
and provoked vestibulodynia (contact-induced vulvodynia localized to the vulvar vestibule), may
be a primary cause of genito-pelvic pain/penetration disorder and may be a focus in studies of the
disorder. Females diagnosed with these other conditions report significant distress, and their
symptoms are likely to meet criteria for genito-pelvic pain/penetration disorder.
Associated Features
Genito-pelvic pain/penetration disorder is frequently associated with other sexual dysfunctions,
particularly reduced sexual desire and interest (female sexual interest/arousal disorder).
Sometimes desire and interest are preserved in sexual situations that are not painful or do not
require penetration. Even when individuals with genito-pelvic pain/penetration disorder report

sexual interest/motivation, there is often behavioral avoidance of sexual situations and
opportunities. Avoidance of gynecological examinations despite medical recommendations is
also frequent. The pattern of avoidance is similar to that seen in phobic disorders. It is common
for females who have not succeeded in having vaginal penetration to come for treatment only
when they wish to conceive. Many females with genito-pelvic pain/penetration disorder will
experience associated relationship/marital problems; they also often report that the symptoms
significantly diminish their feelings of femininity.
In addition to the subtype “lifelong/acquired,” five factors should be considered during
assessment and diagnosis of genito-pelvic pain/penetration disorder because they may be
relevant to etiology or treatment: 1) partner factors (e.g., partner’s sexual problems, partner’s
health status); 2) relationship factors (e.g., partner responses to the pain, including solicitous,
negative, and facilitative responses; discrepancies in desire for sexual activity); 3) individual
vulnerability factors (e.g., poor body image, history of sexual or emotional abuse), psychiatric
comorbidity (e.g., depression, anxiety), or stressors (e.g., job loss, bereavement); 4)
cultural/religious factors (e.g., inhibitions related to prohibitions against sexual activity; attitudes
toward sexuality); and 5) medical factors relevant to prognosis, course, or treatment. Each of
these factors may contribute differently to the presenting symptoms of different females with this
disorder.
Prevalence
The prevalence of genito-pelvic pain/penetration disorder is unknown. However, approximately
10%–28% of females of reproductive age in the United States report recurrent pain during
intercourse. Difficulties having intercourse appear to be a frequent referral to sexual dysfunction
clinics and to specialist clinicians. Internationally, prevalence of genito-pelvic pain upon
intercourse ranges from 8% to 28% among females of reproductive age and varies by country.
Prevalence of genito-pelvic pain during sexual activities involving vaginal penetration among
lesbian women relative to heterosexual women remains uncertain but may be similar or lower.
Prevalence rates among other sexual minorities, including transgender women, are unknown.
Development and Course
The development and course of genito-pelvic pain/penetration disorder is unclear. Because
women generally do not seek treatment until they experience problems in sexual functioning, it
can, in general, be difficult to characterize genito-pelvic pain/penetration disorder as lifelong
(primary) or acquired (secondary). Although women typically come to clinical attention after the
initiation of sexual activity, there are often earlier clinical signs. For example, difficulty with or
the avoidance of use of tampons is an important predictor of later
problems. Difficulties with vaginal penetration (inability or fear or pain) may not be obvious
until intercourse is attempted during sexual activity. Even once intercourse is attempted, the
frequency of attempts may not be significant or regular. In cases where it is difficult to establish
whether symptomatology is lifelong or acquired, it is useful to determine the presence of any
consistent period of successful pain-, fear-, and tension-free intercourse. If the experience of such

Temperamental.
Environmental.
Genetic and physiological.
a period can be established, then genito-pelvic pain/penetration disorder can be characterized as
acquired. Once symptomatology is present for a period of approximately 6 months, the
probability of spontaneous and significant symptomatic remission appears to diminish.
Complaints related to genito-pelvic pain peak during early adulthood and in the peri- and
postmenopausal period. There may also be an increase in genito-pelvic pain–related symptoms in
the postpartum period.
Risk and Prognostic Factors
Females with antecedent mood and anxiety disorders are four times more likely
to develop symptoms of genito-pelvic pain/penetration disorder compared with those without
these antecedent disorders. Psychosocial factors (e.g., pain catastrophizing, pain self-efficacy,
avoidance of pain, negative mood) and interpersonal factors (e.g., insecure attachment, negative
partner responses to the pain, sexual motives that focus on avoiding negative relationship
outcomes) may exacerbate and maintain symptoms.
Females with genito-pelvic pain/penetration disorder are more likely to report a
history of sexual and/or physical abuse, and fear of abuse than females without this disorder,
although not all women with presenting symptoms have this history.
Females experiencing superficial pain during vaginal penetration often
report the onset of the pain after a history of vaginal infections. Even after the infections have
resolved and there are no known residual physical findings, the pain persists. Pain during tampon
insertion or the inability to insert tampons before any sexual contact has been attempted is an
important risk factor for genito-pelvic pain/penetration disorder.
Additional biomedical risk factors include early puberty, inflammation, early use of oral
contraceptives, vulvar pain receptor proliferation (i.e., increase in the number of receptors) and
sensitization (i.e., touch may become perceived as pain), and lower touch and pain thresholds.
Abnormalities of the pelvic floor muscles while at rest, including hypertonicity, poor muscle
control, hypersensitivity, and altered contractility, may close the vaginal hiatus and interfere with
penetration.
Culture-Related Diagnostic Issues
Cultural contexts can affect the experience and reporting of genito-pelvic pain related to
intercourse. Affected females experience negative implications related to social narratives of
womanhood, sexuality, and femininity, including pressures to prioritize men’s sexual desire and
penetrative sex, and depictions of sex as easy and natural. Cultural views that devalue female
sexual experience may affect the way women interpret the experience of pain during sex, their
help-seeking choices, and how they discuss their symptoms with their caregivers. For example,
some females may not report genito-pelvic pain specifically but rather refer to being unhappy in
their marriages.
In the United States, Hispanic females endorse significantly higher rates of genito-pelvic pain
and are more likely to report pain with first intercourse (i.e., primary genito-pelvic
pain/penetration disorder) compared with non-Hispanic women. In a Minneapolis, Minnesota
survey, only about half of females with genito-pelvic pain sought treatment, and those who did
frequently reported feeling stigmatized. Such experiences may be heightened for

Another medical condition.
sexual minorities and underserved ethnic and racialized groups, especially given evidence of
inequities in pain treatment for females and African Americans.
Sex- and Gender-Related Diagnostic Issues
Gendered social constructions relating to womanhood and femininity are implicated in the
experience of genito-pelvic pain/penetration disorder, including the prioritization of both
penetrative sex and men’s sexual desires above women’s own needs and desires. The disorder is
associated with feelings of shame and inadequacy as a female, contributing further to enhanced
psychological distress.
By definition, the diagnosis of genito-pelvic pain/penetration disorder is only given to
females. There is relatively new research concerning urological chronic pelvic pain syndrome in
males, suggesting that males may experience some similar problems. The prevalence of male
genito-pelvic pain is estimated to be 2.2%–9.7% worldwide. The research and clinical experience
are not sufficiently developed yet to justify the application of this diagnosis to males. Other
specified sexual dysfunction or unspecified sexual dysfunction may be diagnosed in males
appearing to fit this pattern.
Diagnostic Markers
Validated physiological measures of Criterion A2 symptoms (Marked vulvovaginal or pelvic
pain during vaginal intercourse or penetration attempts) can be assessed in real time (e.g., the
cotton-swab test, vulvalgesiometer, tampon test). Although these measures are well validated for
pain intensity during penetration attempts, none approximate the sexual context in which the pain
is experienced, which can only be assessed via self-report. Criterion A4 symptoms (Marked
tensing or tightening of the pelvic floor muscles during attempted vaginal penetration) can also
be measured (e.g., via electromyographic amplitude, dynamometer, 4D ultrasound by a qualified
physical therapist). There are no validated physiological measures of component symptoms for
Criterion A1 or A3. Validated psychometric inventories may be used to formally assess the pain
and anxiety components related to genito-pelvic pain/penetration disorder.
Functional Consequences of Genito-Pelvic Pain/Penetration Disorder
Functional difficulties in genito-pelvic pain/penetration disorder are often associated with
interference in various aspects of the romantic relationship—including the initiation of such
relationships—and sometimes with the ability to conceive via penile/vaginal intercourse.
Differential Diagnosis
In many instances, females with genito-pelvic pain/penetration
disorder will also be diagnosed with another medical condition (e.g., lichen sclerosus,
endometriosis, pelvic inflammatory disease, genitourinary syndrome of menopause). In some
cases, treating the medical condition may alleviate the genito-pelvic pain/penetration disorder.
Much of the time, this is not the case. There are no reliable tools or diagnostic methods to allow
clinicians to know whether the medical condition or genito-pelvic pain/penetration disorder is

Somatic symptom and related disorders.
Inadequate sexual stimuli.
F52.0
primary. Often, the associated medical conditions are difficult to diagnose and treat. For
example, the increased incidence of postmenopausal pain during intercourse may sometimes be
attributable to vaginal dryness or irritation associated with declining estrogen levels. The
relationship, however, between genital symptoms, estrogen, and pain is not well understood.
Some females with genito-pelvic pain/penetration disorder
may also be diagnosable with somatic symptom disorder. Since both genito-pelvic
pain/penetration disorder and the somatic symptom and related disorders are new diagnoses in
DSM-5, it is not yet clear whether they can be reliably differentiated. Some females diagnosed
with genito-pelvic pain/penetration disorder will also be diagnosed with a specific phobia.
It is important that the clinician, in considering differential diagnoses,
assess the adequacy of sexual stimuli within the female’s sexual experience. Sexual situations in
which there is inadequate foreplay or arousal may lead to difficulties in penetration, pain, or
avoidance. Erectile dysfunction or premature (early) ejaculation in the male partner may result in
difficulties with penetration. These conditions should be carefully assessed. In some situations, a
diagnosis of genito-pelvic pain/penetration disorder may not be appropriate.
Comorbidity
Comorbidity between genito-pelvic pain/penetration disorder and other sexual difficulties
appears to be common. Comorbidity with relationship distress is also common and typically
related to the lack of sexual intimacy rather than (solely) the pain itself. This is not surprising,
because the inability to have (pain-free) intercourse with a desired partner and the avoidance of
sexual opportunities may be either a contributing factor to or the result of other sexual or
relationship problems. Because pelvic floor symptoms are implicated in the diagnosis of genitopelvic pain/penetration disorder, there is likely to be a higher prevalence of other disorders
related to the pelvic floor or reproductive organs (e.g., interstitial cystitis, constipation, vaginal
infection, endometriosis, irritable bowel syndrome). Females with genito-pelvic pain/penetration
disorder frequently experience comorbid chronic pain conditions (e.g., fibromyalgia, chronic
headaches), and the prevalence of these comorbidities increases with the severity of vulvar pain
symptoms.
Lesbian women also report genito-pelvic pain and penetration difficulties during sexual
activities; the frequency of genito-pelvic pain/penetration symptoms among nonheterosexual
women has been shown to be less than or the same as among heterosexual women.
Male Hypoactive Sexual Desire Disorder
Diagnostic Criteria
A. Persistently or recurrently deficient (or absent) sexual/erotic thoughts or
fantasies and desire for sexual activity. The judgment of deficiency is made by

the clinician, taking into account factors that affect sexual functioning, such as
age and general and sociocultural contexts of the individual’s life.
B. The symptoms in Criterion A have persisted for a minimum duration of
approximately 6 months.
C. The symptoms in Criterion A cause clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexual mental disorder or
as a consequence of severe relationship distress or other significant stressors
and is not attributable to the effects of a substance/medication or another
medical condition.
Specify whether:
Lifelong: The disturbance has been present since the individual became
sexually active.
Acquired: The disturbance began after a period of relatively normal sexual
function.
Specify whether:
Generalized: Not limited to certain types of stimulation, situations, or partners.
Situational: Only occurs with certain types of stimulation, situations, or partners.
Specify current severity:
Mild: Evidence of mild distress over the symptoms in Criterion A.
Moderate: Evidence of moderate distress over the symptoms in Criterion A.
Severe: Evidence of severe or extreme distress over the symptoms in Criterion
A.
Diagnostic Features
When an assessment for male hypoactive sexual desire disorder is being made, interpersonal
context must be taken into account. A “desire discrepancy,” in which a man has lower desire for
sexual activity than his partner, is not sufficient to diagnose male hypoactive sexual desire
disorder. Both low/absent desire for sex and deficient/absent sexual thoughts or fantasies
(Criterion A) are required for a diagnosis of the disorder. There may be variation across men in
how sexual desire is expressed.
The lack of desire for sex and deficient/absent erotic thoughts or fantasies must be persistent
or recurrent and must occur for a minimum duration of approximately 6 months. The inclusion of
this duration criterion is meant to safeguard against making a diagnosis in cases in which a man’s
low sexual desire may represent a reactive but temporary response to adverse life conditions. For
example, the man’s low sexual desire may be related to an acute stressor or loss of self-esteem
(e.g., being fired from a job or experiencing financial difficulty such as business failure). If these
stressors persist beyond 6 months along with low sexual desire, then clinician judgment
determines the appropriateness of the male hypoactive sexual desire disorder diagnosis.

Associated Features
Male hypoactive sexual desire disorder is sometimes associated with erectile and/or ejaculatory
concerns. For example, persistent difficulties obtaining an erection may lead a man to lose
interest in sexual activity. Men with hypoactive sexual desire disorder often report that they no
longer initiate sexual activity and that they are minimally receptive to a partner’s attempt to
initiate. Sexual activities (e.g., masturbation or partnered sexual activity) may sometimes occur
even in the presence of low sexual desire. Relationship-specific preferences regarding patterns of
sexual initiation must be taken into account when making a diagnosis of male hypoactive sexual
desire disorder. Although men are more likely to initiate sexual activity, and thus low desire may
be characterized by a pattern of noninitiation, many men may prefer to have their partner initiate
sexual activity. In such situations, the man’s lack of receptivity to a partner’s initiation should be
considered when evaluating low desire.
In addition to the subtypes “lifelong/acquired” and “generalized/situational,” the following
five factors must be considered during assessment and diagnosis of male hypoactive sexual
desire disorder given that they may be relevant to etiology and/or treatment: 1) partner factors
(e.g., partner’s sexual problems, partner’s health status); 2) relationship factors (e.g., poor
communication, discrepancies in desire for sexual activity); 3) individual vulnerability factors
(e.g., poor body image, history of sexual or emotional abuse), psychiatric comorbidity (e.g.,
depression, anxiety), or stressors (e.g., job loss, bereavement); 4) cultural/religious factors (e.g.,
inhibitions related to prohibitions against sexual activity; attitudes toward sexuality); and 5)
medical factors relevant to prognosis, course, or treatment. Each of these factors may contribute
differently to the presenting symptoms of different men with this disorder.
Prevalence
The prevalence of male hypoactive sexual desire disorder varies depending on country of origin
and method of assessment. Estimates of prevalence in representative samples range
from 3% to 17%. Sexual desire problems are less common in younger men (ages 16–24), with
prevalence rates between 3% and 14%, compared with older men (ages 60–74 years), with
prevalence rates between 16% and 28%. However, a persistent lack of interest in sex, lasting 6
months or more, affects a smaller proportion of men (6%). Moreover, less than 2% of men report
clinically significant distress associated with low desire. Studies on help-seeking behavior
indicate that only 10.5% of men with sexual problems in the previous year sought help.
Development and Course
By definition, lifelong male hypoactive sexual desire disorder indicates that low or no sexual
desire has always been present, whereas the acquired subtype would be assigned if the man’s low
desire developed after a period of normal sexual desire. There is a requirement that low desire
persist for approximately 6 months or more; thus, short-term changes in sexual desire should not
be diagnosed as male hypoactive sexual desire disorder.
There is a normative age-related decline in sexual desire. The prevalence of low sexual desire
in men increases with age, from approximately 5.2% prevalence at age 27 years to 18.5% at age

Temperamental.
Environmental.
Genetic and physiological.
50 years. Like women, men identify a variety of triggers for their sexual desire, and they
describe a wide range of reasons that they choose to engage in sexual activity. Although erotic
visual cues may be more potent elicitors of desire in younger men, the potency of sexual cues
may decrease with age and must be considered when evaluating men for hypoactive sexual
desire disorder.
Risk and Prognostic Factors
Mood and anxiety symptoms appear to be strong predictors of low desire in men.
Up to half of men with a past history of psychiatric symptoms may have moderate or severe loss
of desire, compared with only 15% of those without such a history. A man’s feelings about
himself, his perception of his partner’s sexual desire toward him, feelings of being emotionally
connected, and contextual variables may all negatively (as well as positively) affect sexual
desire.
Beliefs about sexuality (particularly restrictive sexual attitudes and conservative beliefs) are
commonly associated with low sexual desire in men. Moreover, lack of erotic thoughts and
concerns about erection during sexual activity are significant predictors of low sexual desire, as
well as low confidence levels in erectile function.
Alcohol use may increase the occurrence of low desire. Other environmental
determinants of low sexual desire include problematic dyadic relationships, reduced attraction
toward the partner, living in a long-term relationship, sexual boredom, and professional stress. At
the larger societal level, cohort studies in a few high-income countries indicate a trend toward the
decrease of sexual desire in men in recent decades.
Endocrine disorders such as hyperprolactinemia and hypogonadism
significantly affect sexual desire in men. Age is a significant risk factor for low desire in men. It
is unclear whether or not men with low desire also have abnormally low levels of testosterone;
however, among hypogonadal men, low desire is common. There also may be a critical threshold
below which testosterone will affect sexual desire in men and above which there is little effect of
testosterone on men’s desire.
Culture-Related Diagnostic Issues
There is marked variability in prevalence rates of low desire across world regions, ranging from
12.5% in Northern European men to 28% in Southeast Asian men ages 40–80 years. Distress
about lack of sexual desire was significantly associated with sociocultural contexts (e.g.,
occupational stress) in a web-based survey across three European countries (Portugal, Croatia,
and Norway).
Sex- and Gender-Related Diagnostic Issues
In contrast to the classification of sexual dysfunctions in women, desire and arousal disorders
have been retained as separate constructs in men. Despite some similarities in the experience of
desire across men and women, and the fact that desire fluctuates over time and is dependent on
contextual factors, men do report a significantly higher intensity and frequency of sexual desire

Nonsexual mental disorders.
Substance/medication use.
Another medical condition.
Interpersonal factors.
Other sexual dysfunctions.
F52.4
compared with women. However, preliminary data suggest that the overlap between sexual
desire and sexual arousal (erectile function) is also very common in men, particularly when they
present for help regarding sexual problems. Regarding sexual orientation, data suggest that low
sexual desire is more commonly reported by gay men (19%) than by heterosexual men (9%).
Differential Diagnosis
Nonsexual mental disorders, such as major depressive disorder,
which is characterized by “markedly diminished interest or pleasure in all, or almost all,
activities,” may explain the lack of sexual desire. If the lack of desire is better explained by
another mental disorder, then a diagnosis of male hypoactive sexual desire disorder would not be
made.
An onset of male hypoactive sexual desire that coincides with the
beginning of substance/medication use and that dissipates with discontinuation of the
substance/medication or dose reduction is suggestive of a substance/medication-induced sexual
dysfunction, which should be diagnosed instead of male hypoactive sexual desire disorder.
If the low/absent desire and deficient/absent erotic thoughts or
fantasies are better explained by the effects of another medical condition (e.g., hypogonadism,
diabetes mellitus, thyroid dysfunction, central nervous system disease), then a diagnosis of male
hypoactive sexual desire disorder would not be made.
If interpersonal or significant contextual factors, such as severe relationship
distress or other significant stressors, are associated with the loss of desire in the man, then a
diagnosis of male hypoactive sexual desire disorder would not be made.
The presence of another sexual dysfunction does not rule out a
diagnosis of male hypoactive sexual desire disorder; there is some evidence that up to one-half of
men with low sexual desire also have erectile difficulties, and slightly fewer may also have early
ejaculation difficulties. If the man’s low desire is explained by self-identification as an asexual,
then a diagnosis of male hypoactive sexual desire disorder is not made.
Comorbidity
Male hypoactive sexual desire disorder is rarely the sole sexual diagnosis in men. Erectile
dysfunction, delayed ejaculation, and premature (early) ejaculation are often comorbid
diagnoses. Depression and other mental disorders, as well as endocrinological factors, are often
comorbid with male hypoactive sexual desire disorder.
Premature (Early) Ejaculation
Diagnostic Criteria
A. A persistent or recurrent pattern of ejaculation occurring during partnered sexual
activity within approximately 1 minute following vaginal penetration and before
the individual wishes it.

502
Note: Although the diagnosis of premature (early) ejaculation may be applied to
individuals engaged in nonvaginal sexual activities, specific duration criteria have
not been established for these activities.
B. The symptom in Criterion A must have been present for at least 6 months and
must be experienced on almost all or all (approximately 75%–100%) occasions
of sexual activity (in identified situational contexts or, if generalized, in all
contexts).
C. The symptom in Criterion A causes clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexual mental disorder or
as a consequence of severe relationship distress or other significant stressors
and is not attributable to the effects of a substance/medication or another
medical condition.
Specify whether:
Lifelong: The disturbance has been present since the individual became
sexually active.
Acquired: The disturbance began after a period of relatively normal sexual
function.
Specify whether:
Generalized: Not limited to certain types of stimulation, situations, or partners.
Situational: Only occurs with certain types of stimulation, situations, or partners.
Specify current severity:
Mild: Ejaculation occurring within approximately 30 seconds to 1 minute of
vaginal penetration.
Moderate: Ejaculation occurring within approximately 15–30 seconds of vaginal
penetration.
Severe: Ejaculation occurring prior to sexual activity, at the start of sexual
activity, or within approximately 15 seconds of vaginal penetration.
Diagnostic Features
Premature (early) ejaculation is manifested by ejaculation that occurs prior to or shortly after
vaginal penetration, operationalized by an individual’s estimate of ejaculatory latency (i.e.,
elapsed time before ejaculation) after vaginal penetration. Although the diagnostic criteria
specify penile-vaginal sex, it is reasonable to assume that similar estimates of ejaculatory latency
apply to males having sex with males, as well as to other sexual behaviors. Estimated and
measured intravaginal ejaculatory latencies are highly correlated as long as the ejaculatory
latency is of short duration; therefore, self-reported estimates of ejaculatory latency are sufficient
for diagnostic purposes. A 60-second intravaginal ejaculatory latency time was previously
considered to be an appropriate cutoff for the diagnosis of lifelong premature (early) ejaculation
in men; however, expert consensus now considers this latency time to be too brief and instead

Temperamental.
Genetic and physiological.
recommends a 120-second threshold.
Associated Features
Many males with premature (early) ejaculation complain of a sense of lack of control over
ejaculation and report apprehension about their anticipated inability to delay ejaculation on
future sexual encounters.
The following factors may be relevant in the evaluation of any sexual dysfunction: 1) partner
factors (e.g., partner’s sexual problems, partner’s health status); 2) relationship factors (e.g., poor
communication, discrepancies in desire for sexual activity); 3) individual vulnerability factors
(e.g., history of sexual or emotional abuse), psychiatric comorbidity (e.g., depression, anxiety),
and stressors (e.g., job loss, bereavement); 4) cultural/religious factors (e.g., lack of privacy,
inhibitions related to prohibitions against sexual activity; attitudes toward sexuality); and 5)
medical factors relevant to prognosis, course, or treatment.
Prevalence
Estimates of the prevalence of premature (early) ejaculation vary widely depending on the
definition utilized. Internationally, a prevalence range of 8%–30% has been reported across all
ages, with even lower and higher rates in other studies. Prevalence of premature (early)
ejaculation may increase with age. For example, the prevalence among males ages 18–30 in
Switzerland and Turkey is about 9%–11%, while the reported prevalence of concern among
males ages 50–59 in the United States about how rapidly they ejaculate may be as high as 55%.
When premature (early) ejaculation is defined as ejaculation occurring within approximately 1
minute of vaginal penetration, only 1%–3% of males would be diagnosed with the disorder.
Development and Course
By definition, lifelong premature (early) ejaculation starts during a male’s initial sexual
experiences and persists thereafter. Some males may experience premature (early) ejaculation
during their initial sexual encounters but gain ejaculatory control over time. It is the persistence
of ejaculatory problems for longer than 6 months that determines the diagnosis of premature
(early) ejaculation. In contrast, some males develop the disorder after a period of having a
normal ejaculatory latency, known as acquired premature (early) ejaculation. There is far less
known about acquired premature (early) ejaculation than about lifelong premature (early)
ejaculation. The acquired form likely has a later onset, usually appearing during or after the
fourth decade of life. Lifelong is relatively stable throughout life.
Risk and Prognostic Factors
Premature (early) ejaculation may be more common in males with anxiety
disorders, especially social anxiety disorder.
There is a moderate genetic contribution to lifelong premature (early)
ejaculation. Premature (early) ejaculation may be associated with dopamine transporter gene
polymorphism or serotonin transporter gene polymorphism. Thyroid disease, prostatitis, and

Substance/medication-induced sexual dysfunction.
drug withdrawal are associated with acquired premature (early) ejaculation. Positron emission
tomography measures of regional cerebral blood flow during ejaculation have shown primary
activation in the mesocephalic transition zone, including the ventral tegmental area.
Culture-Related Diagnostic Issues
Perception of what constitutes a normal ejaculatory latency differs cross-culturally and may be
related to varying awareness of sexual dysfunction, concern about sexual failure, and perceptions
about the importance of sex. Measured ejaculatory latencies may differ in some countries.
Cultural or religious factors may contribute to these differences. For example, reports of
premature (early) ejaculation were more common in arranged marriages, because of factors such
as anxiety over family pressures and lack of premarital sexual experience.
Sex- and Gender-Related Diagnostic Issues
Premature (early) ejaculation is a sexual dysfunction in men. Men and their sexual partners may
differ in their perception of what constitutes an acceptable ejaculatory latency. There may be
increasing concerns in women about early ejaculation in their sexual partners, which may be a
reflection of changing societal attitudes concerning women’s sexual activity.
Diagnostic Markers
Ejaculatory latency is usually monitored in research settings by the sexual partner utilizing a
timing device (e.g., stopwatch), though this is not ideal in real-life sexual situations. In clinical
settings, the man’s estimate of the time between intravaginal penetration and ejaculation should
be accepted in lieu of stopwatch measurements.
Association With Suicidal Thoughts or Behavior
Among males receiving treatment for premature (early) ejaculation with comorbid depression,
elevated rates of suicidal thoughts or behavior have been observed; although the affected males
attributed the suicidal symptoms to their premature (early) ejaculation, the presence of
depression was also a likely contributing factor.
Functional Consequences of Premature (Early) Ejaculation
A pattern of premature (early) ejaculation may be associated with decreased self-esteem and selfconfidence, a sense of lack of control, and adverse consequences for partner relationships. It may
also cause personal distress and decreased sexual satisfaction in the sexual partner. Single males
are more bothered than partnered males by premature (early) ejaculation because of its
interference with seeking and maintaining new relationships. Ejaculation prior to penetration
may be associated with difficulties in conception.
Differential Diagnosis
When 
problems 
with 
premature 
(early)
ejaculation are attributable exclusively to substance use, intoxication, or withdrawal,

Ejaculatory concerns that do not meet diagnostic criteria.
substance/medication-induced sexual dysfunction should be diagnosed.
It is necessary to identify males with normal
ejaculatory latencies who desire longer ejaculatory latencies and males who have episodic
premature (early) ejaculation (e.g., during the first sexual encounter with a new partner when a
short ejaculatory latency may be common or normative). Neither of these situations would lead
to a diagnosis of premature (early) ejaculation, even though these situations may be distressing to
some males.
Comorbidity
Premature (early) ejaculation may be associated with erectile problems. In many cases, it may be
difficult to determine which difficulty preceded the other. Lifelong premature (early) ejaculation
may be associated with certain anxiety disorders. Acquired premature (early) ejaculation may be
associated with prostatitis, thyroid disease, or drug withdrawal (e.g., during opioid withdrawal).
Substance/Medication-Induced Sexual Dysfunction
Diagnostic Criteria
A. A clinically significant disturbance in sexual function is predominant in the clinical
picture.
B. There is evidence from the history, physical examination, or laboratory findings
of both (1) and (2):
1. The symptoms in Criterion A developed during or soon after substance
intoxication or withdrawal or after exposure to or withdrawal from a
medication.
2. The involved substance/medication is capable of producing the symptoms in
Criterion A.
C. The disturbance is not better explained by a sexual dysfunction that is not
substance/medication-induced. Such evidence of an independent sexual
dysfunction could include the following:
The symptoms precede the onset of the substance/medication use; the
symptoms persist for a substantial period of time (e.g., about 1 month) after
the cessation of acute withdrawal or severe intoxication; or there is other
evidence 
suggesting 
the 
existence 
of 
an 
independent 
nonsubstance/medication-induced sexual dysfunction (e.g., a history of recurrent
non-substance/medication-related episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress in the individual.

Note: This diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the symptoms in Criterion A
predominate in the clinical picture and are sufficiently severe to warrant clinical
attention.
Coding note: The ICD-10-CM codes for the [specific substance/medication]-induced
sexual dysfunctions are indicated in the table below. Note that the ICD-10-CM code
depends on whether or not there is a comorbid substance use disorder present for
the same class of substance. In any case, an additional separate diagnosis of a
substance use disorder is not given. If a mild substance use disorder is comorbid
with the substance-induced sexual dysfunction, the 4th position character is “1,” and
the clinician should record “mild [substance] use disorder” before the substanceinduced sexual dysfunction (e.g., “mild cocaine use disorder with cocaine-induced
sexual dysfunction”). If a moderate or severe substance use disorder is comorbid
with the substance-induced sexual dysfunction, the 4th position character is “2,” and
the clinician should record “moderate [substance] use disorder” or “severe
[substance] use disorder,” depending on the severity of the comorbid substance use
disorder. If there is no comorbid substance use disorder (e.g., after a one-time heavy
use of the substance), then the 4th position character is “9,” and the clinician should
record only the substance-induced sexual dysfunction.
ICD-10-CM
With mild use
disorder
With moderate or
severe use disorder
Without use
disorder
Alcohol
F10.181
F10.281
F10.981
Opioid
F11.181
F11.281
F11.981
Sedative, hypnotic, or anxiolytic
F13.181
F13.281
F13.981
Amphetamine-type substance (or other
stimulant)
F15.181
F15.281
F15.981
Cocaine
F14.181
F14.281
F14.981
Other (or unknown) substance
F19.181
F19.281
F19.981
Specify (see Table 1 in the chapter “Substance-Related and Addictive Disorders,”
which indicates whether “with onset during intoxication” and/or “with onset during
withdrawal” applies to a given substance class; or specify “with onset after
medication use”):
With onset during intoxication: If criteria are met for intoxication with the
substance and the symptoms develop during intoxication.
With onset during withdrawal: If criteria are met for withdrawal from the
substance and the symptoms develop during, or shortly after, withdrawal.
With onset after medication use: If symptoms developed at initiation of
medication, with a change in use of medication, or during withdrawal of
medication.

Specify current severity:
Mild: Occurs on 25%–50% of occasions of sexual activity.
Moderate: Occurs on 50%–75% of occasions of sexual activity.
Severe: Occurs on 75% or more of occasions of sexual activity.
Recording Procedures
The name of the substance/medication-induced sexual dysfunction begins with the specific
substance (e.g., alcohol) that is presumed to be causing the sexual dysfunction. The ICD-10-CM
code that corresponds to the applicable drug class is selected from the table included in the
criteria set. For substances that do not fit into any of the classes (e.g., fluoxetine), the ICD-10CM code for the other (or unknown) substance class should be used and the name of the specific
substance recorded (e.g., F19.981 fluoxetine-induced sexual dysfunction). In cases in which a
substance is judged to be an etiological factor but the specific substance is unknown, the ICD-10CM code for the other (or unknown) substance class is used and the fact that the substance is
unknown is recorded (e.g., F19.981 unknown substance-induced sexual dysfunction).
When recording the name of the disorder, the comorbid substance use disorder (if any) is
listed first, followed by the word “with,” followed by the name of the substance-induced sexual
dysfunction, followed by the specification of onset (i.e., onset during intoxication, onset during
withdrawal, with onset after medication use), followed by the severity specifier (e.g., mild,
moderate, severe). For example, in the case of erectile dysfunction occurring during intoxication
in a man with a severe alcohol use disorder, the diagnosis is F10.281 severe alcohol use disorder
with alcohol-induced sexual dysfunction, with onset during intoxication, moderate. A separate
diagnosis of the comorbid severe alcohol use disorder is not given. If the substance-induced
sexual dysfunction occurs without a comorbid substance use disorder (e.g., after a one-time
heavy use of the substance), no accompanying substance use disorder is noted (e.g., F15.981
amphetamine-induced sexual dysfunction, with onset during intoxication). When more than one
substance is judged to play a significant role in the development of the sexual dysfunction, each
should be listed separately (e.g., F14.181 mild cocaine use disorder with cocaine-induced sexual
dysfunction, with onset during intoxication, moderate; F19.981 fluoxetine-induced sexual
dysfunction, with onset after medication use, moderate).
Diagnostic Features
The essential features of substance/medication-induced sexual dysfunction are clinically
significant disturbances in sexual function that are predominant in the clinical picture (Criterion
A) that are judged to be due to the effects of a substance (e.g., a drug of abuse or medication).
The sexual dysfunction must have developed during or soon after substance intoxication or
withdrawal or after exposure to or withdrawal from a medication, and the substances or
medications must be capable of producing the symptoms (Criterion B2). Substance/medicationinduced sexual dysfunction due to a prescribed treatment for a
mental disorder or another medical condition must have its onset while the individual is

receiving the medication (or during withdrawal, if a withdrawal is associated with the
medication). Once the treatment is discontinued, the sexual dysfunction will usually improve or
remit within days to several weeks (depending on the half-life of the substance/medication and
the presence of withdrawal). The diagnosis of substance/medication-induced sexual dysfunction
should not be given if the onset of the sexual dysfunction precedes the substance/medication
intoxication or withdrawal, or if the symptoms persist for a substantial period of time (i.e.,
usually longer than 1 month) from the time of severe intoxication or withdrawal.
Associated Features
Sexual dysfunctions can occur in association with intoxication with the following classes of
substances: alcohol; opioids; sedatives, hypnotics, or anxiolytics; stimulants (including cocaine);
and other (or unknown) substances. Sexual dysfunctions can occur in association with
withdrawal from the following classes of substances: alcohol; opioids; sedatives, hypnotics, or
anxiolytics; and other (or unknown) substances. Medications that can induce sexual dysfunctions
include antidepressants, antipsychotics, and hormonal contraceptives.
The most commonly reported side effect of antidepressant drugs is difficulty with orgasm or
ejaculation in men, and with arousal in women. Problems with desire and erection are less
frequent. There is evidence that the effects of antidepressant medications on sexual dysfunction
occur regardless of levels of depression. Approximately 30% of sexual complaints are clinically
significant. Certain agents (i.e., bupropion, mirtazapine, nefazodone, and vilazodone) appear to
have lower rates of sexual side effects than other antidepressants.
The sexual problems associated with antipsychotic drugs, including problems with sexual
desire, erection, lubrication, ejaculation, or orgasm, have occurred with typical as well as
atypical agents. However, problems are less common with prolactin-sparing antipsychotics or
those that do not block dopamine receptors.
Although the effects of mood stabilizers on sexual function are unclear, it is possible that
lithium and anticonvulsants, with the possible exception of lamotrigine, have adverse effects on
sexual desire. Problems with orgasm may occur with gabapentin. Similarly, there may be a
higher prevalence of erectile and orgasm problems associated with benzodiazepines. There have
not been such reports with buspirone.
Many nonpsychiatric medications, such as cardiovascular, cytotoxic, gastrointestinal, and
hormonal agents, are associated with disturbances in sexual function. Use of 5-α-reductase
inhibitors (e.g., dutasteride, finasteride) may reduce erectile function, ejaculatory function, and
libido in men.
Illicit substance use is associated with decreased sexual desire, erectile dysfunction, and
difficulty reaching orgasm. Sexual dysfunctions are also seen in individuals receiving methadone
but are seldom reported by individuals receiving buprenorphine. Chronic nicotine or chronic
alcohol abuse are associated with erectile problems. Cannabis, like alcohol, is a central nervous
system depressant, and its use may be a risk factor for sexual dysfunction; however, it has also
been suggested to potentially improve satisfaction with orgasm.
Prevalence
The prevalence and the incidence of substance/medication-induced sexual dysfunction are
unclear, likely because of underreporting of treatment-emergent sexual side effects. Data on

substance/medication-induced sexual dysfunction typically concern the effects of antidepressant
drugs. The prevalence of antidepressant-induced sexual dysfunction varies in part depending on
the specific agent. Approximately 25%–80% of individuals taking monoamine oxidase
inhibitors, tricyclic antidepressants, serotonergic antidepressants, and combined serotonergicadrenergic antidepressants report sexual side effects. There
are differences in the incidence of sexual side effects between some serotonergic and combined
adrenergic-serotonergic antidepressants, with medications such as citalopram, fluoxetine,
fluvoxamine, paroxetine, sertraline, and venlafaxine having the highest rates of sexual
dysfunction.
Approximately 50% of individuals taking antipsychotic medications will experience adverse
sexual side effects, including problems with sexual desire, erection, lubrication, ejaculation, or
orgasm. The incidence of these side effects among different antipsychotic agents is unclear.
Exact prevalence and incidence of sexual dysfunctions among users of nonpsychiatric
medications such as cardiovascular, cytotoxic, gastrointestinal, and hormonal agents are
unknown. Elevated rates of sexual dysfunction have been reported high-dose opioid drugs for
pain. There are increased rates of decreased sexual desire, erectile dysfunction, and difficulty
reaching orgasm associated with illicit substance use. The prevalence of sexual problems appears
related to chronic drug abuse and appears higher in individuals who abuse heroin (approximately
60%–70%) than in individuals who abuse amphetamine-type substances or 3,4methylenedioxymethamphetamine (i.e., MDMA, ecstasy). Elevated rates of sexual dysfunction
are also seen in individuals receiving methadone but are seldom reported by individuals
receiving buprenorphine. Chronic alcohol abuse and chronic nicotine abuse are related to higher
rates of erectile problems.
Development and Course
The onset of antidepressant-induced sexual dysfunction may be as early as 8 days after the agent
is first taken. Approximately 30% of individuals with mild to moderate orgasm delay will
experience spontaneous remission of the dysfunction within 6 months. In some cases, serotonin
reuptake inhibitor–induced sexual dysfunction may persist after the agent is discontinued. The
time to onset of sexual dysfunction after initiation of antipsychotic drugs or drugs of abuse is
unknown. It is probable that the adverse effects of nicotine and alcohol may not appear until after
years of use. Premature (early) ejaculation can sometimes occur after cessation of opioid use.
There is some evidence that disturbances in sexual function related to substance/medication use
increase with age.
Culture-Related Diagnostic Issues
There may be an interaction among cultural factors, the influence of medications on sexual
functioning, and the response of the individual to those changes.
Sex- and Gender-Related Diagnostic Issues
Some gender differences in sexual side effects from substances and medications may exist, such

Non-substance/medication-induced sexual dysfunctions.
that men may more often report impairments with desire and orgasm following antidepressant
use, and women may more often report difficulties with sexual arousal.
Functional Consequences of Substance/Medication-Induced Sexual
Dysfunction
Medication-induced sexual dysfunction may result in medication noncompliance, such as
stopping medications or using them irregularly, which could contribute to the lack of efficacy for
antidepressants.
Differential Diagnosis
Many mental disorders, such as depressive,
bipolar, anxiety, and psychotic disorders, are associated with disturbances of sexual function.
Thus, differentiating a substance/medication-induced sexual
dysfunction from a manifestation of the underlying mental disorder can be quite difficult. The
diagnosis is usually established if a close relationship between substance/medication initiation or
discontinuation is observed. A clear diagnosis can be established if the problem occurs after
substance/medication initiation, dissipates with substance/medication discontinuation, and recurs
with introduction of the same agent. Most substance/medication-induced side effects occur
shortly after initiation or discontinuation. Sexual side effects that only occur after chronic use of
a substance/medication may be extremely difficult to diagnose with certainty.
Other Specified Sexual Dysfunction
F52.8
This category applies to presentations in which symptoms characteristic of a sexual
dysfunction that cause clinically significant distress in the individual predominate but
do not meet the full criteria for any of the disorders in the sexual dysfunctions
diagnostic class. The other specified sexual dysfunction category is used in
situations in which the clinician chooses to communicate the specific reason that the
presentation does not meet the criteria for any specific sexual dysfunction. This is
done by recording “other specified sexual dysfunction” followed by the specific
reason (e.g., “sexual aversion”).
Unspecified Sexual Dysfunction
F52.9
This category applies to presentations in which symptoms characteristic of a sexual

dysfunction that cause clinically significant distress in the individual predominate but
do not meet the full criteria for any of the disorders in the sexual dysfunctions
diagnostic class. The unspecified sexual dysfunction category is used in situations in
which the clinician chooses not to specify the reason that the criteria are not met for
a specific sexual dysfunction, and includes presentations for which there is
insufficient information to make a more specific diagnosis.

# 14 - Gender Dysphoria

# Gender Dysphoria

511

Gender Dysphoria
In this chapter, there is one overarching diagnosis of gender dysphoria, with separate
developmentally appropriate criteria sets for children and for adolescents and adults. The area of
sex and gender is highly controversial and has led to a proliferation of terms whose meanings
vary over time and within and between disciplines. An additional source of confusion is that in
English “sex” connotes both male/female and sexuality. This chapter employs constructs and
terms as they are widely used by clinicians from various disciplines with specialization in
treating gender dysphoria. In this chapter, sex and sexual refer to the biological indicators of
male and female (understood in the context of reproductive capacity), such as in sex
chromosomes, gonads, sex hormones, and nonambiguous internal and external genitalia.
Disorders of sex development or differences of sex development (DSDs) included the historical
terms hermaphroditism and pseudohermaphroditism. DSDs include somatic intersex conditions
such as congenital development of ambiguous genitalia (e.g., clitoromegaly, micropenis),
congenital disjunction of internal and external sex anatomy (e.g., complete androgen insensitivity
syndrome), incomplete development of sex anatomy (e.g., gonadal agenesis), sex chromosome
anomalies (e.g., Turner syndrome; Klinefelter syndrome), or disorders of gonadal development
(e.g., ovotestes).
Gender is used to denote the public, sociocultural (and usually legally recognized) lived role
as boy or girl, man or woman, or other gender. Biological factors are seen as contributing, in
interaction with social and psychological factors, to gender development. Gender assignment
refers to the assignment as male or female. This occurs usually at birth based on phenotypic sex
and, thereby, yields the birth-assigned gender, historically referred to as “biological sex” or,
more recently, “natal gender.” Birth-assigned sex is often used interchangeably with birthassigned gender. The terms assigned sex and assigned gender encompass birth-assigned
sex/gender but also include gender/sex assignments and reassignments made after birth but
during infancy or early childhood, usually in the case of intersex conditions. Gender-atypical
refers to somatic features or behaviors that are not typical (in a statistical sense) of individuals
with the same assigned gender in a given society and historical era; gender-nonconforming,
gender variant, and gender diverse are alternative nondiagnostic terms. Gender reassignment
denotes an official (and sometimes legal) change of gender. Gender-affirming treatments are
medical procedures (hormones or surgeries or both) that aim to align an individual’s physical
characteristics with their experienced gender. Gender identity is a category of social identity and
refers to an individual’s identification as male, female, some category in between (i.e., gender
fluid), or a category other than male or female (i.e., gender neutral). There has been a
proliferation of gender identities in recent years. Gender dysphoria as a general descriptive term
refers to the distress that may accompany the incongruence between one’s experienced or
expressed gender and one’s assigned gender. However, it is more specifically defined when used
as a diagnostic category. It does not refer to distress related to stigma, a distinct although

F64.2
possibly co-occurring source of distress. Transgender refers to the broad spectrum of individuals
whose gender identity is different from their birth-assigned gender. Cisgender describes
individuals whose gender expression is congruent with their birth-assigned gender (also
nontransgender). Transsexual, a historic term, denotes an individual who seeks, is undergoing,
or has undergone a social transition from male to female or female to male, which in many,
but not all, cases also involves a somatic transition by gender-affirming hormone treatment and
genital, breast, or other gender-affirming surgery (historically referred to as sex reassignment
surgery).
Although not all individuals will experience distress from incongruence, many are distressed
if the desired physical interventions using hormones and/or surgery are not available. The current
term is more descriptive than the previous DSM-IV term gender identity disorder and focuses on
dysphoria as the clinical problem, not identity per se.
Gender Dysphoria
Diagnostic Criteria
Gender Dysphoria in Children
A. A marked incongruence between one’s experienced/expressed gender and
assigned gender, of at least 6 months’ duration, as manifested by at least six of
the following (one of which must be Criterion A1):
1. A strong desire to be of the other gender or an insistence that one is the other
gender (or some alternative gender different from one’s assigned gender).
2. In boys (assigned gender), a strong preference for cross-dressing or
simulating female attire; or in girls (assigned gender), a strong preference for
wearing only typical masculine clothing and a strong resistance to the
wearing of typical feminine clothing.
3. A strong preference for cross-gender roles in make-believe play or fantasy
play.
4. A strong preference for the toys, games, or activities stereotypically used or
engaged in by the other gender.
5. A strong preference for playmates of the other gender.
6. In boys (assigned gender), a strong rejection of typically masculine toys,
games, and activities and a strong avoidance of rough-and-tumble play; or in
girls (assigned gender), a strong rejection of typically feminine toys, games,
and activities.
7. A strong dislike of one’s sexual anatomy.
8. A strong desire for the primary and/or secondary sex characteristics that

F64.0
match one’s experienced gender.
B. The condition is associated with clinically significant distress or impairment in
social, school, or other important areas of functioning.
Specify if:
With a disorder/difference of sex development (e.g., a congenital
adrenogenital disorder such as E25.0 congenital adrenal hyperplasia or E34.50
androgen insensitivity syndrome).
Coding note: Code the disorder/difference of sex development as well as
gender dysphoria.
Gender Dysphoria in Adolescents and Adults
A. A marked incongruence between one’s experienced/expressed gender
and assigned gender, of at least 6 months’ duration, as manifested by at least
two of the following:
1. A marked incongruence between one’s experienced/expressed gender and
primary and/or secondary sex characteristics (or in young adolescents, the
anticipated secondary sex characteristics).
2. A strong desire to be rid of one’s primary and/or secondary sex
characteristics 
because 
of 
a 
marked 
incongruence 
with 
one’s
experienced/expressed gender (or in young adolescents, a desire to prevent
the development of the anticipated secondary sex characteristics).
3. A strong desire for the primary and/or secondary sex characteristics of the
other gender.
4. A strong desire to be of the other gender (or some alternative gender different
from one’s assigned gender).
5. A strong desire to be treated as the other gender (or some alternative gender
different from one’s assigned gender).
6. A strong conviction that one has the typical feelings and reactions of the other
gender (or some alternative gender different from one’s assigned gender).
B. The condition is associated with clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
Specify if:
With a disorder/difference of sex development (e.g., a congenital
adrenogenital disorder such as E25.0 congenital adrenal hyperplasia or E34.50
androgen insensitivity syndrome).
Coding note: Code the disorder/difference of sex development as well as
gender dysphoria.
Specify if:

Posttransition: The individual has transitioned to full-time living in the
experienced gender (with or without legalization of gender change) and has
undergone (or is preparing to have) at least one gender-affirming medical
procedure or treatment regimen—namely, regular gender-affirming hormone
treatment or gender reassignment surgery confirming the experienced gender
(e.g., breast augmentation surgery and/or vulvovaginoplasty in an individual
assigned male at birth; transmasculine chest surgery and/or phalloplasty or
metoidioplasty in an individual assigned female at birth).
Specifiers
The specifier “with a disorder/difference of sex development” should be used in the context of
individuals who have a specific and codable disorder/difference of sex development documented
in their medical record.
The “posttransition” specifier may be used in the context of continuing treatment procedures
that serve to support the new gender assignment.
Diagnostic Features
Individuals with gender dysphoria have a marked incongruence between the gender to which
they have been assigned (usually based on phenotypic sex at birth, referred to as birth-assigned
gender) and their experienced/expressed gender. This discrepancy is the core component of the
diagnosis. There must also be evidence of distress about this incongruence. Experienced gender
may include alternative gender identities beyond binary stereotypes. Consequently, distress may
involve not only the experience that the individual is a male or female gender other than the one
assigned at birth but also an experience that the individual is an intermediate or alternative
gender that differs from the individual’s birth-assigned gender.
Gender dysphoria manifests itself differently in different age groups. The following examples
may be less prominent in children raised in surroundings with fewer gender stereotypes.
Prepubertal individuals assigned female at birth with gender dysphoria may express a
marked, persistent feeling or conviction that they are a boy, express aversion to the idea of
being a girl, or assert they will grow up to be a man. They often prefer boys’ clothing and
hairstyles, may be perceived by strangers as boys, and may ask to be called by a boy’s name.
Sometimes they display intense negative reactions to parental attempts to have them wear dresses
or other feminine attire. Some may refuse to attend school or social events where such clothes
are required. These children may demonstrate marked gender nonconformity in role-playing,
dreams, gender-typed play and toy preferences, styles, mannerisms, fantasies, and peer
preferences. Contact sports, rough-and-tumble play, traditional boyhood games, and boys as
playmates are most often preferred. They show little interest in stereotypically feminine toys
(e.g., dolls) or activities (e.g., feminine dress-up or role-play). Occasionally, they refuse to
urinate in a sitting position. Some may express a desire to have a penis or claim to have a penis
or that they will grow one when older. They may also state that they do not want to develop

breasts or menstruate.
Prepubertal individuals assigned male at birth with gender dysphoria may express a marked,
persistent feeling or conviction that they are a girl or assert that they will grow up to be a woman.
They may express aversion to the idea of being a boy. They often prefer dressing in girls’ or
women’s clothes or may improvise clothing from available materials (e.g., using towels, aprons,
and scarves for long hair or skirts). These children may demonstrate marked gender
nonconformity in gender-typed play and toy preferences, styles, mannerisms, and peer
preferences. They may role-play female figures (e.g., playing “mother”) and may be intensely
interested in female fantasy figures. Traditional feminine activities, stereotypical games, and
pastimes (e.g., “playing house”; drawing feminine pictures; watching television or videos of
favorite female characters) may be preferred. Stereotypical female-type dolls (e.g., Barbie) may
be favorite toys, and girls are their preferred playmates. They avoid rough-and-tumble play and
have little interest in stereotypically masculine toys (e.g., cars, trucks). They may state that they
find their penis or testes disgusting, that they wish them removed, or that they have, or wish to
have, a vagina.
Increasingly, parents are presenting to specialized clinics after their child with gender
dysphoria has already socially transitioned.
As the onset of puberty for individuals assigned female at birth is somewhere between ages 9
and 13, and between 11 and 14 for individuals assigned male at birth, their symptoms and
concerns may arise in a developmental phase somewhere between childhood and adolescence.
As secondary sex characteristics of younger adolescents are not yet fully developed, these
individuals may not state dislike of them, but they may be markedly distressed by imminent
physical changes.
In adolescents and adults with gender dysphoria, the discrepancy between experienced
gender and physical sex characteristics is often, but not always, accompanied by a desire to be
rid of primary and/or secondary sex characteristics and/or a strong desire to acquire some
primary and/or secondary sex characteristics of another gender. To varying degrees, older
adolescents and adults with gender dysphoria may adopt the behavior, clothing, and mannerisms
of their experienced gender. They feel uncomfortable being regarded by others, or functioning in
society, as members of their assigned gender. Some adults and adolescents may have a strong
desire to be of a different gender and treated as such, and they may have an inner certainty to feel
and respond as their experienced gender without seeking medical treatment to alter body
characteristics. They may find other ways to resolve the incongruence between
experienced/expressed and assigned gender by partially living in the desired role or by adopting
a gender role neither conventionally male nor conventionally female.
Associated Features
When visible signs of puberty develop, individuals assigned male at birth may shave their facial,
body, and leg hair at the first signs of growth. They sometimes bind their genitals to make
erections less visible. Individuals assigned female at birth may bind their breasts,
walk with a stoop, or use loose sweaters to make breasts less visible. Increasingly, adolescents

request, or may obtain without medical prescription and supervision, drugs that suppress
production of gonadal steroids (e.g., gonadotropin-releasing hormone [GnRH] agonists) or that
block gonadal hormone actions (e.g., spironolactone). Clinically referred adolescents often want
hormone treatment and many also wish for gender-affirming surgery. Adolescents living in an
accepting environment may openly express the desire to be and be treated as their experienced
gender and dress partly or completely as their experienced gender, have a hairstyle typical of
their experienced gender, preferentially seek friendships with peers of another gender, and/or
adopt a new first name consistent with their experienced gender. Older adolescents, when
sexually active, often do not show or allow partners to touch their sexual organs. For adults with
an aversion toward their genitals, sexual activity is constrained by the preference that their
genitals not be seen or touched by their partners. Not infrequently, adults may seek hormone
treatment (sometimes without medical prescription and supervision) and gender-affirming
surgery. Others are satisfied with either hormone treatment or surgery alone, or without any
gender-affirming medical treatment.
In children, adolescents, and adults with gender dysphoria, an overrepresentation of autism
spectrum traits has been observed. Also, individuals with autism spectrum disorder are more
likely to exhibit gender diversity.
Adolescents and adults with gender dysphoria before gender-affirming treatment and legal
gender change are at increased risk for mental health problems including suicidal ideation,
suicide attempts, and suicides. After gender reassignment, adjustment may vary, and suicide risk
and mental health problems may persist.
In prepubertal children, increasing age is associated with having more behavioral or
emotional problems; this is related to the increasing nonacceptance of gender-nonconforming
behavior by others. Children and adolescents who feel supported and accepted in their gender
nonconformity may show less or even no psychological problems.
Prevalence
There are no large-scale population studies of gender dysphoria. Based on gender-affirming
treatment–seeking populations, the prevalence for gender dysphoria diagnosis across populations
has been assessed to be less than 1/1,000 (i.e., < 0.1%) for both individuals assigned male at birth
and individuals assigned female at birth. Because many adults with gender dysphoria do not seek
care at specialty treatment programs, prevalence rates are likely underestimates. Prevalence
estimates based on surveys of self-reporting general population samples in the United States and
Europe suggest higher numbers, although varied methods of assessment make comparisons
difficult across studies. Self-identification as transgender ranges from 0.5% to 0.6%;
experiencing oneself as having an incongruent gender identity ranges from 0.6% to 1.1%; feeling
that one is a person of a different sex ranges from 2.1% to 2.6%; and the desire to undergo
medical treatment ranges from 0.2% to 0.6%.
Development and Course
Because expression of gender dysphoria varies with age, there are separate criteria sets for
children versus those for adolescents and adults. Criteria for children are defined in a more
concrete, behavioral manner than those for adolescents and adults. Young children are less likely
than older children, adolescents, and adults to express extreme and persistent anatomic

Gender dysphoria without a disorder of sex development.
dysphoria. In adolescents and adults, incongruence between experienced gender and assigned
gender is a central feature of the diagnosis. Factors related to distress and impairment also vary
with age. A very young child may show signs of distress (e.g., intense crying) only when parents
tell the child that he or she is “really” not a member of another gender but only “desires” to be.
Distress may not be manifest in social environments supportive of the child’s gender
nonconformity and may emerge only if there is
parental/social interference with the child’s gender variance. In adolescents and adults, distress
may manifest because of strong incongruence between experienced gender and birth-assigned
gender. Such distress may, however, be mitigated by supportive environments and knowledge
that biomedical treatments exist to reduce incongruence. Impairment (e.g., school refusal,
development of depression, anxiety, peer and behavioral problems, and substance abuse) may be
a correlate of gender dysphoria.
For clinic-referred children studied in
Canada and the Netherlands, onset of gender-nonconforming behaviors is usually between ages 2
and 4 years. This corresponds to the developmental time period in which most children begin
expressing gendered behaviors and interests. For some preschool-age children, both marked,
persistent gender-atypical behaviors and the expressed desire to be another gender may be
present, or labeling themselves as a member of another gender may occur. In other cases, the
gender expression appears later, usually at entry into elementary school. Children may
sometimes express discomfort with their sexual anatomy or will state the desire to have a sexual
anatomy corresponding to their experienced gender (“anatomic dysphoria”). Expressions of
anatomic dysphoria become more common as children with gender dysphoria approach and
anticipate puberty.
No general population studies exist of adolescent or adult outcomes of childhood gender
variance. Some prepubescent children expressing a desire to be another gender will not seek
gender-affirming somatic treatments when they reach puberty. They frequently report
nonheterosexual orientations and frequently marked gender-nonconforming behavior, although
not necessarily a transgender identity in adolescence/young adulthood. Some children with
gender dysphoria in childhood that remits in adolescence may experience a recurrence in
adulthood.
In individuals assigned male at birth, studies from North America and the Netherlands found
persistence ranged from 2% to 39%. In individuals assigned female at birth, persistence ranged
from 12% to 50%. Persistence of gender dysphoria is modestly correlated with dimensional
measures of severity ascertained at the time of a childhood baseline assessment. Early social
transition may also be a factor in persistence of gender dysphoria in adolescence.
Studies have shown a high incidence of sexual attraction to those of the individual’s birthassigned gender, regardless of the trajectory of the prepubescent child’s gender dysphoria. For
individuals whose gender dysphoria continues into adolescence and beyond, most self-identify as
heterosexual. In those who no longer have gender dysphoria by the time of adolescence, a
majority self-identify as gay, lesbian, or bisexual.
Two broad trajectories have been described for development of gender dysphoria in
individuals who identify as either male or female.

Gender dysphoria in association with a disorder of sex development.
Temperamental.
As opposed to gender-nonconforming children, individuals with prepubertal-onset gender
dysphoria have symptoms that meet diagnostic criteria for gender dysphoria in childhood. The
dysphoria can continue into adolescence and adulthood; alternatively, some individuals go
through a period in which the gender dysphoria either desists or is denied. At such times, these
individuals may self-identify as being gay or lesbian. Some may identify as heterosexual and
cisgender. However, it is possible that some of these individuals may experience a recurrence of
gender dysphoria later in life.
Regardless of whether the individual’s gender dysphoria persists or desists at a later date,
either the onset of puberty or the realization that puberty will begin with development of
secondary sex characteristics can prompt distressing feelings of gender incongruence that can
exacerbate the individual’s gender dysphoria.
The early/prepubertal-onset group often present for clinical, gender-affirming care during
childhood, during adolescence, or in young adulthood. This may reflect a more intense gender
dysphoria compared with individuals with late/postpubertal-onset gender dysphoria, whose
distress may be more variable and less intense.
Late-onset or pubertal/postpubertal-onset gender dysphoria occurs around puberty or even
much later in life. Some of these individuals report having had a desire to be of another gender in
childhood that was not expressed verbally to others or had gender-nonconforming behavior that
did not meet full criteria for gender dysphoria in childhood. Others have no recollection of any
signs of childhood gender dysphoria. Parents of individuals with gender dysphoria of
pubertal/postpubertal-onset often report surprise, as they saw no signs of gender dysphoria
during childhood.
Individuals 
with 
DSDs 
who
require early medical intervention or decisions about gender assignment come to clinical
attention at an early age. Depending on the condition, they may have been gonadectomized
(often because of risk of future malignancy) before puberty so that administration of exogenous
hormones is part of routine care to induce puberty. Infertility is common whether due to the
condition itself or to gonadectomy, and genital surgery may have been done in infancy or
childhood with the intent of affirming the assigned gender to both the affected individual and
caregivers.
Affected individuals may exhibit gender-nonconforming behavior starting in early childhood
in a manner that is predictable depending on the specific DSD syndrome and the gender
assignment, and thresholds for supporting social and medical gender transition in minors have
traditionally been much lower for those with compared to those without DSDs. As individuals
with some DSD syndromes become aware of their condition and medical history, many
experience uncertainty about their gender, as opposed to developing a firm conviction that they
are of another gender. The proportion who develop gender dysphoria and progress to gender
transition varies markedly depending on the particular syndrome and gender assignment.
Risk and Prognostic Factors
Gender-variant behavior among individuals with prepubertal-onset gender

Environmental.
Genetic and physiological.
dysphoria can develop in early preschool age. Studies suggest that a greater intensity of gender
nonconformity and an older age at presentation make persistence of gender dysphoria into
adolescence and adulthood more likely. A predisposing factor under consideration, especially in
individuals with postpubertal-onset gender dysphoria (adolescence, adulthood), includes history
of transvestism that may develop into autogynephilia (i.e., sexual arousal associated with the
thought or image of oneself as a woman).
Individuals assigned male at birth with gender dysphoria without a DSD (in both
childhood and adolescence) more commonly have older brothers when compared with cisgender
males.
For individuals with gender dysphoria without a DSD, some genetic
contribution is suggested by evidence for (weak) familiality of gender dysphoria among nontwin
siblings, increased concordance for gender dysphoria in monozygotic compared with dizygotic
same-sex twins, and some degree of heritability of gender dysphoria. Research suggests that
gender dysphoria has a polygenetic basis involving interactions of several genes and
polymorphisms that may affect in utero sexual differentiation of the brain, contributing to gender
dysphoria in individuals assigned male at birth.
As to endocrine findings in individuals with gender dysphoria, no endogenous systemic
abnormalities in sex-hormone levels have been found in 46,XY individuals, whereas there appear
to be increased androgen levels (in the range found in hirsute women but far below normal male
levels) in 46,XX individuals. Overall, current evidence is insufficient to label gender dysphoria
without a DSD as a form of intersexuality limited to the central nervous system.
In gender dysphoria associated with a DSD, the likelihood of later gender dysphoria is
increased if prenatal production and utilization (via receptor sensitivity) of androgens are grossly
variant relative to what is usually seen in individuals with the same assigned
gender. Examples include 46,XY individuals with a history of normal male prenatal hormone
milieu but inborn nonhormonal genital defects (as in cloacal bladder exstrophy or penile
agenesis) and who have been assigned to the female gender. The likelihood of gender dysphoria
is further enhanced by additional, prolonged, highly gender-variant postnatal androgen exposure
with somatic virilization as may occur in female-raised and noncastrated 46,XY individuals with
5-alpha reductase-2 deficiency or 17-beta-hydroxysteroid dehydrogenase-3 deficiency or in
female-raised 46,XX individuals with classical congenital adrenal hyperplasia with prolonged
periods of nonadherence to glucocorticoid replacement therapy. However, the prenatal androgen
milieu is more closely related to gendered behavior than to gender identity. Many individuals
with DSDs and markedly gender-variant behavior do not develop gender dysphoria. Thus,
gender-nonconforming behavior by itself should not be interpreted as an indicator of current or
future gender dysphoria. There appears to be a higher rate of gender dysphoria and patientinitiated gender change from assigned female to male than from assigned male to female in
individuals prenatally exposed to a full complement of masculinizing hormonal influences.
Culture-Related Diagnostic Issues
Individuals with gender dysphoria have been reported across many countries and cultural

contexts around the world. The equivalent of gender dysphoria has also been reported in
individuals living in cultural contexts with institutionalized gender identity categories other than
men/boys or women/girls that sanction gender nonconforming development. These include India,
Sri Lanka, Myanmar, Oman, Samoa, Thailand, and Indigenous Peoples of North America. It is
unclear however, in such cultural contexts, whether the diagnostic criteria for gender dysphoria
would be met with these individuals.
The prevalence of coexisting mental health problems differs among cultures; these
differences may also be related to differences in attitudes toward gender nonconformity in
children, adolescents, and adults. However, also in some non-Western cultures, anxiety has been
found to be relatively common in individuals with gender dysphoria, even in cultures with
accepting attitudes toward gender-variant behavior.
Sex- and Gender-Related Diagnostic Issues
Sex differences in rate of referrals to specialty clinics vary by age group. In children, sex ratios
of individuals assigned male at birth to individuals assigned female at birth range from 1.25:1 to
4.3:1. Studies show increasing numbers of children and adolescents presenting to specialty
clinics, presentation at younger ages, more frequent early social transition, and a shift to a greater
number of individuals assigned female at birth in adolescents and young adults than individuals
assigned male at birth. In adults, estimates generally suggest more individuals assigned male at
birth seek gender-affirming treatment, with ratios ranging from 1:1 to 6.1:1 in most studies in the
United States and Europe.
Association With Suicidal Thoughts or Behavior
Rates of suicidality and suicide attempts for transgender individuals are reported to range from
30% to 80%, with risk factors including past maltreatment, gender victimization, depression,
substance abuse, and younger age. Transgender adolescents referred to gender clinics have
substantially higher rates of suicidal thoughts and behaviors when compared with nonreferred
adolescents. Prior to receiving gender-affirming treatment and legal gender reassignment,
adolescents and adults with gender dysphoria are at increased risk for suicidal thoughts and
suicide attempts. After gender-affirming treatment, adjustment varies, and while improvement in
coexisting symptoms is often seen, some individuals continue to experience prominent anxiety
and affective symptoms and remain at increased risk for suicide.
A study of 572 children referred for gender identity concerns in Canada and several
comparison groups (siblings, other referred children, and nonreferred children) largely from
other high-income countries found that gender-referred children were 8.6 times more likely to
self-harm or attempt suicide than comparison children, even after adjustment for overall behavior
and peer relationship problems, and particularly in the second half of childhood. Among
adolescents, the highest rate of suicide attempt is among transgender young men, followed by
those defining themselves as neither male nor female.
Functional Consequences of Gender Dysphoria

Nonconformity to gender roles.
Transvestic disorder.
Body dysmorphic disorder.
Autism spectrum disorder.
Gender nonconformity may appear at all ages after the first 2–3 years of childhood and may
interfere with daily activities. In older children, gender nonconformity may affect peer
relationships and may lead to isolation from peer groups and to distress. Many children
experience teasing and harassment or pressure to dress in attire associated with their birthassigned sex, especially when growing up in a nonsupportive and nonaccepting environment.
Also in adolescents and adults, the distress resulting from gender incongruence often interferes
with daily activities. Relationship difficulties, including sexual relationship problems, are
common, and functioning at school or at work may be impaired. Gender dysphoria is associated
with high levels of stigmatization, discrimination, and victimization, leading to negative selfconcept, increased rates of depression, suicidality, and other mental disorder co-occurrence,
school dropout, and economic marginalization, including unemployment, with attendant social
and mental health risks, especially in individuals who lack family or social support. In addition,
these individuals’ access to health services and mental health services may be impeded by
structural barriers, such as institutional discomfort about, inexperience with, or hostility toward
working with this patient population.
Differential Diagnosis
Gender 
dysphoria 
should 
be 
distinguished 
from 
simple
nonconformity to stereotypical gender role behavior by the strong desire to be of another gender
than the assigned one and by the extent and pervasiveness of gender-variant activities and
interests. The diagnosis is not meant to merely describe nonconformity to stereotypical gender
role behavior (e.g., “tomboyism” in girls, “girly-boy” behavior in boys, occasional cross-dressing
in adult men). Given the increased openness of gender-diverse expressions by individuals across
the entire range of the transgender spectrum, it is important that the clinical diagnosis be limited
to those individuals whose distress and impairment meet the specified criteria.
Transvestic disorder is diagnosed in heterosexual (or bisexual) adolescent
and adult males (rarely in females) for whom women’s clothing generates sexual excitement and
causes distress and/or impairment without drawing their assigned gender into question. It is
occasionally accompanied by gender dysphoria. An individual with transvestic disorder who also
has clinically significant gender dysphoria can be given both diagnoses. In some cases of
postpubertal-onset gender dysphoria in individuals assigned male at birth who are attracted to
women, cross-dressing with sexual excitement is a precursor to the diagnosis of gender
dysphoria.
An individual with body dysmorphic disorder focuses on the alteration
or removal of a specific body part because it is perceived as abnormally formed, not because it
represents a repudiated assigned gender. When an individual’s presentation meets criteria for
both gender dysphoria and body dysmorphic disorder, both diagnoses can be given. Individuals
wishing to have a healthy limb amputated (termed by some body integrity identity disorder)
because it makes them feel more “complete” usually do not wish to change gender, but rather
desire to live as an amputee or a disabled person.
In individuals with autism spectrum disorder, diagnosing gender
dysphoria can be challenging. It can be difficult to differentiate potential co-occurring

Schizophrenia and other psychotic disorders.
Other clinical presentations.
gender dysphoria from an autistic preoccupation because of the concrete and rigid thinking
around gender roles and/or poor understanding of social relationships characteristic of autism
spectrum disorder.
In schizophrenia, there may rarely be delusions of
belonging to some other gender. In the absence of psychotic symptoms, insistence by an
individual with gender dysphoria that he or she is another gender is not considered a delusion.
Schizophrenia (or other psychotic disorders) and gender dysphoria may co-occur. Genderthemed delusions may occur in up to 20% of individuals with schizophrenia. They can usually be
differentiated from gender dysphoria by their bizarre content and by waxing and waning with
remissions and exacerbations of psychotic episodes.
Some individuals with an emasculinization desire who develop an
alternative, nonmale/nonfemale gender identity do have a presentation that meets criteria for
gender dysphoria. However, some males seek genital surgery for either aesthetic reasons or to
remove psychological effects of androgens without changing male identity; in these cases, the
criteria for gender dysphoria are not met.
Comorbidity
Clinically referred children with gender dysphoria show elevated levels of anxiety, disruptive,
impulse-control, and depressive disorders. Autism spectrum disorder is more prevalent in
clinically referred adolescents and adults with gender dysphoria than in the general population.
Clinically referred adolescents and adults with gender dysphoria often have high rates of
associated mental disorders, with anxiety and depressive disorders being the most common.
Individuals who have experienced harassment and violence may also develop posttraumatic
stress disorder.
Other Specified Gender Dysphoria
F64.8
This category applies to presentations in which symptoms characteristic of gender
dysphoria that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for gender
dysphoria. The other specified gender dysphoria category is used in situations in which the
clinician chooses to communicate the specific reason that the presentation does not meet the
criteria for gender dysphoria. This is done by recording “other specified gender dysphoria”
followed by the specific reason (e.g., “brief gender dysphoria,” in which symptoms meet full
criteria for gender dysphoria but the duration is less than the required 6 months).
Unspecified Gender Dysphoria
F64.9

This category applies to presentations in which symptoms characteristic of gender
dysphoria that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for gender dysphoria. The unspecified gender dysphoria category is
used in situations in which the clinician chooses not to specify the reason that the
criteria are not met for gender dysphoria, and includes presentations in which there
is insufficient information to make a more specific diagnosis.

# 15 - Disruptive, Impulse Control, and Conduct Diso

# Disruptive, Impulse-Control, and Conduct Disorders

521

Disruptive, Impulse-Control, and Conduct
Disorders
Disruptive, impulse-control, and conduct disorders include conditions
involving problems in the self-control of emotions and behaviors. While other disorders in DSM5 may also involve problems in emotional and/or behavioral regulation, the disorders in this
chapter are unique in that these problems are manifested in behaviors that violate the rights of
others (e.g., aggression, destruction of property) and/or that bring the individual into significant
conflict with societal norms or authority figures. The underlying causes of the problems in the
self-control of emotions and behaviors can vary greatly across the disorders in this chapter and
among individuals within a given diagnostic category.
The chapter includes oppositional defiant disorder, intermittent explosive disorder, conduct
disorder, antisocial personality disorder (which is described in the chapter “Personality
Disorders”), pyromania, kleptomania, and other specified and unspecified disruptive, impulsecontrol, and conduct disorders. Although all the disorders in the chapter involve problems in both
emotional and behavioral regulation, the source of variation among the disorders is the relative
emphasis on problems in the two types of self-control. For example, the criteria for conduct
disorder focus largely on poorly controlled behaviors that violate the rights of others or that
violate major societal norms. These behaviors may or may not result from poorly controlled
emotions. Some symptoms of conduct disorder (e.g., certain forms of aggression) can be
attributable to constricted emotional responses. At the other extreme, the criteria for intermittent
explosive disorder focus largely on poorly controlled emotion, outbursts of anger that are
disproportionate to the interpersonal or other provocation or to other psychosocial stressors.
Intermediate in impact to these two disorders is oppositional defiant disorder, in which the
criteria are more evenly distributed between emotions (anger and irritation) and behaviors
(argumentativeness and defiance). Pyromania and kleptomania are characterized by poor impulse
control related to specific behaviors (fire setting or stealing) that relieve internal tension. Other
specified disruptive, impulse-control, and conduct disorder is a category for conditions in which
there are symptoms of conduct disorder, oppositional defiant disorder, or other disruptive,
impulse-control, and conduct disorders, but the number or type of symptoms does not meet the
diagnostic threshold for any of the disorders in this chapter, even though there is evidence of
clinically significant impairment associated with the symptoms.
The disruptive, impulse-control, and conduct disorders all tend to be more common in boys
and men than in girls and women, although the relative degree of male predominance may differ
both across disorders and within a disorder at different ages. The disorders in this chapter tend to
have first onset in childhood or adolescence. In fact, it is very rare for either conduct disorder or
oppositional defiant disorder to first emerge in adulthood. There is a developmental relationship
between oppositional defiant disorder and conduct disorder, in that most cases of conduct

F91.3
disorder previously would have had symptoms that met criteria for oppositional defiant disorder,
at least in those cases in which conduct disorder emerges prior to adolescence. However, most
children with oppositional defiant disorder do not eventually develop conduct disorder.
Furthermore, children with
oppositional defiant disorder are at risk for eventually developing other problems besides
conduct disorder, including anxiety and depressive disorders.
Many of the symptoms that define the disruptive, impulse-control, and conduct disorders are
behaviors that can occur to some degree in typically developing persons. Thus, it is critical that
the frequency, persistence, pervasiveness across situations, and impairment associated with the
behaviors indicative of the diagnosis be considered relative to what is normative for a person’s
age, gender, and culture when determining if they are symptomatic of a disorder.
The disruptive, impulse-control, and conduct disorders have been linked to a common
externalizing spectrum associated with the personality dimensions of disinhibition and negative
emotionality (some facets); and inversely with constraint and agreeableness. These shared
personality dimensions could account for the high level of comorbidity among these disorders
and their frequent comorbidity with substance use disorders and antisocial personality disorder.
However, the specific nature of the shared diathesis that constitutes the externalizing spectrum
remains unknown.
Oppositional Defiant Disorder
Diagnostic Criteria
A. A 
pattern 
of 
angry/irritable 
mood, 
argumentative/defiant 
behavior, 
or
vindictiveness lasting at least 6 months as evidenced by at least four symptoms
from any of the following categories, and exhibited during interaction with at least
one individual who is not a sibling.
Angry/Irritable Mood
1. Often loses temper.
2. Is often touchy or easily annoyed.
3. Is often angry and resentful.
Argumentative/Defiant Behavior
4. Often argues with authority figures or, for children and adolescents, with
adults.
5. Often actively defies or refuses to comply with requests from authority figures
or with rules.
6. Often deliberately annoys others.
7. Often blames others for his or her mistakes or misbehavior.

Vindictiveness
8. Has been spiteful or vindictive at least twice within the past 6 months.
Note: The persistence and frequency of these behaviors should be used to
distinguish a behavior that is within normal limits from a behavior that is
symptomatic. For children younger than 5 years, the behavior should occur on
most days for a period of at least 6 months unless otherwise noted (Criterion
A8). For individuals 5 years or older, the behavior should occur at least once
per week for at least 6 months, unless otherwise noted (Criterion A8). While
these frequency criteria provide guidance on a minimal level of frequency to
define symptoms, other factors should also be considered, such as whether the
frequency and intensity of the behaviors are outside a range that is normative
for the individual’s developmental level, gender, and culture.
B. The disturbance in behavior is associated with distress in the individual or others
in his or her immediate social context (e.g., family, peer group, work colleagues),
or it impacts negatively on social, educational, occupational, or other important
areas of functioning.
C. The behaviors do not occur exclusively during the course of a psychotic,
substance use, depressive, or bipolar disorder. Also, the criteria are not met for
disruptive mood dysregulation disorder.
Specify current severity:
Mild: Symptoms are confined to only one setting (e.g., at home, at school, at
work, with peers).
Moderate: Some symptoms are present in at least two settings.
Severe: Some symptoms are present in three or more settings.
Specifiers
It is not uncommon for individuals with oppositional defiant disorder to show symptoms only at
home and only with family members. However, the pervasiveness of the symptoms is an
indicator of the severity of the disorder.
Diagnostic Features
The essential feature of oppositional defiant disorder is a frequent and persistent pattern of
angry/irritable mood, argumentative/defiant behavior, or vindictiveness (Criterion A). It is not
unusual for individuals with oppositional defiant disorder to show the behavioral features of the
disorder without problems of negative mood. However, individuals with the disorder who show
the angry/irritable mood symptoms typically show the behavioral features as well.
The symptoms of oppositional defiant disorder may be confined to only one setting, and this
is most frequently the home. Individuals who show enough symptoms to meet the diagnostic
threshold, even if it is only at home, may be significantly impaired in their social functioning.

However, in more severe cases, the symptoms of the disorder are present in multiple settings.
Given that the pervasiveness of symptoms is an indicator of the severity of the disorder, it is
critical that the individual’s behavior be assessed across multiple settings and relationships.
Because these behaviors are common among siblings, they must be observed during interactions
with persons other than siblings. Also, because symptoms of the disorder are typically more
evident in interactions with adults or peers whom the individual knows well, they may not be
apparent during a clinical examination.
The symptoms of oppositional defiant disorder can occur to some degree in persons without
this disorder. There are several key considerations for determining if the behaviors are
symptomatic of oppositional defiant disorder. First, the diagnostic threshold of four or more
symptoms within the preceding 6 months must be met. Second, the persistence and frequency of
the symptoms should exceed what is normative for an individual’s age, gender, and culture.
Temper outbursts for a preschool child would be considered a symptom of oppositional defiant
disorder only if they occurred on most days for the preceding 6 months, if they occurred with at
least three other symptoms of the disorder, and if the temper outbursts contributed to the
significant impairment associated with the disorder (e.g., led to destruction of property during
outbursts, resulted in the child being asked to leave a preschool). It should be noted that temper
loss need not always involve tantrum behavior and can be displayed by angry facial expressions,
verbal expressions of anger, and subjective feelings of anger that would not typically be
considered a tantrum.
The symptoms of the disorder often are part of a pattern of problematic interactions with
others. Furthermore, individuals with this disorder typically do not regard themselves as angry,
oppositional, or defiant. Instead, they often justify their behavior as a response to unreasonable
demands or circumstances. Thus, it can be difficult to disentangle the relative contribution of the
individual with the disorder to the problematic interactions he or she experiences. For example,
children with oppositional defiant disorder may have
experienced a history of hostile parenting, and it is often impossible to determine if the
child’s behavior caused the parents to act in a more hostile manner toward the child, if the
parents’ hostility led to the child’s problematic behavior, or if there was some combination of
both. Whether or not the clinician can separate the relative contributions of potential causal
factors should not influence whether the diagnosis is made. In the event that the child may be
living in particularly poor conditions where neglect or mistreatment may occur (e.g., in
institutional settings), clinical attention to reducing the contribution of the environment may be
helpful.
Associated Features
Two of the most common co-occurring conditions with oppositional defiant disorder are
attention-deficit/hyperactivity disorder (ADHD) and conduct disorder (see the section
“Comorbidity” for this disorder). Oppositional defiant disorder has been associated with
increased risk for suicide attempts, even after comorbid disorders are controlled for.

Temperamental.
Environmental.
Prevalence
The cross-national prevalence of oppositional defiant disorder ranges from 1% to 11%, with an
average prevalence estimate of around 3.3%. The rate of oppositional defiant disorder may vary
depending on the age and gender of the child. The disorder appears to be somewhat more
prevalent in boys than in girls (1.59:1) prior to adolescence. This male predominance is not
consistently found in samples of adolescents or adults.
Development and Course
The first symptoms of oppositional defiant disorder usually appear during the preschool years
and rarely later than early adolescence. Oppositional defiant disorder often precedes the
development of conduct disorder, especially for those with the childhood-onset type of conduct
disorder. However, many children and adolescents with oppositional defiant disorder do not
subsequently develop conduct disorder. Oppositional defiant disorder also conveys risk for the
development of anxiety disorders and major depressive disorder, even in the absence of conduct
disorder. The defiant, argumentative, and vindictive symptoms carry most of the risk for conduct
disorder, whereas the angry/irritable mood symptoms carry most of the risk for mood and
anxiety disorders.
Manifestations of the disorder across development appear consistent. Children and
adolescents with oppositional defiant disorder are at increased risk for a number of problems in
adjustment as adults, including functional impairments (e.g., problems in relationships with
family, peers, and romantic partners; lower educational attainment; more workplace stress), the
persistence of oppositional defiant disorder, and other psychopathology, such as antisocial
behavior, impulse-control problems, substance misuse, anxiety, and depression.
Many of the behaviors associated with oppositional defiant disorder increase in frequency
during the preschool period and in adolescence. Thus, it is especially critical during these
development periods that the frequency and intensity of these behaviors be evaluated against
normative levels before it is decided that they are symptoms of oppositional defiant disorder. For
example, it is not unusual for preschool children to show temper tantrums on a weekly basis, but
daily tantrums occur in only about 10% of preschool children.
Risk and Prognostic Factors
Temperamental factors related to problems in emotional regulation (e.g., high
levels of emotional reactivity, poor frustration tolerance) have been predictive of the disorder.
Children with oppositional defiant disorder influence their environments, which
in turn can influence them. For example, harsh, inconsistent, or neglectful child-rearing practices
predict increases in symptoms, and oppositional symptoms predict increases in harsh and
inconsistent parenting. In children and adolescents, oppositional defiant disorder is more
prevalent in families in which childcare is disrupted by a succession of different caregivers.
Children with oppositional defiant disorder are also at greater risk for both bullying peers and
being bullied by peers.

Genetic and physiological.
Conduct disorder.
Adjustment disorder.
A number of neurobiological markers (e.g., lower heart rate and skin
conductance reactivity; reduced basal cortisol reactivity; abnormalities in the prefrontal cortex
and amygdala) have been associated with oppositional defiant disorder. Studies have
demonstrated overlapping genetic influences for the irritability and anger symptoms of
oppositional defiant disorder with depression and generalized anxiety disorder. To date, the vast
majority of studies have not separated children with oppositional defiant disorder from those
with conduct disorder. Further study of markers specific to oppositional defiant disorder is
needed.
Culture-Related Diagnostic Issues
The reported prevalence of oppositional defiant disorder or other disruptive disorders may be
affected by misdiagnosis or overdiagnosis of individuals from some cultural backgrounds. Social
norms may affect the prevalence of the disorder and its male gender predominance in children
and adolescents. A meta-analysis of prevalence rates in middle childhood found that the disorder
is more common in boys compared with girls in Western cultures, but that the prevalence is
similar across genders in non-Western cultures. Also, despite adverse experiences, firstgeneration migrants and refugees may be at decreased risk of developing oppositional defiant
disorder symptoms.
Sex- and Gender-Related Diagnostic Issues
Some studies find few sex or gender differences for this disorder compared with, for example,
conduct disorder. There may be slight differences in risk factors with harsh parenting more
highly associated with oppositional defiant disorder in girls but not boys.
Functional Consequences of Oppositional Defiant Disorder
When oppositional defiant disorder is persistent throughout development, individuals with the
disorder experience frequent conflicts with parents, teachers, supervisors, peers, and romantic
partners. Such problems often result in significant impairments in the individual’s emotional,
social, academic, and occupational adjustment.
Differential Diagnosis
Conduct disorder and oppositional defiant disorder are both related to conduct
problems that bring the individual in conflict with adults and other authority figures (e.g.,
teachers, work supervisors). The behaviors of oppositional defiant disorder are typically of a less
severe nature than those of conduct disorder and do not include aggression toward people or
animals, destruction of property, or a pattern of theft or deceit. However, evidence suggests that
oppositional defiant disorder is associated with equivalent or even greater levels of impairment
than conduct disorder. Furthermore, oppositional defiant disorder includes problems of emotion
dysregulation (i.e., angry and irritable mood) that are not included in the definition of conduct
disorder.
Environmental and family stressors may be associated with externalizing
manifestations of emotion dysregulation. In children, these may manifest as

Posttraumatic stress disorder.
Attention-deficit/hyperactivity disorder.
Depressive and bipolar disorders.
Disruptive mood dysregulation disorder.
Intermittent explosive disorder.
Intellectual developmental disorder (intellectual disability).
Language disorder.
Social anxiety disorder.
tantrums and oppositional behavior; and in adolescents, as aggressive behaviors (e.g., rebellion
and defiance). Temporal association with a stressor and symptom duration of less than 6 months
after the resolution of the stressor may help distinguish adjustment disorder from oppositional
defiant disorder.
In children younger than 6 years, posttraumatic stress disorder may
manifest initially as dysregulated behaviors, opposition, and tantrums; the association with a
traumatic event and with other specific symptoms (traumatic play) are key to establishing the
diagnosis. In adolescents, traumatic reenactment and risk-taking may be misinterpreted as
defiance and opposition or as conduct problems.
ADHD is often comorbid with oppositional defiant disorder.
To make the additional diagnosis of oppositional defiant disorder, it is important to determine
that the individual’s failure to conform to requests of others is not solely in situations that
demand sustained effort and attention or demand that the individual sit still.
Depressive and bipolar disorders often involve negative affect
and irritability. As a result, a diagnosis of oppositional defiant disorder should not be made if the
symptoms occur exclusively during the course of a mood disorder.
Oppositional defiant disorder shares with disruptive mood
dysregulation disorder the symptoms of chronic irritable mood and temper outbursts. However, if
the irritable mood and other symptoms meet criteria for disruptive mood dysregulation disorder,
a diagnosis of oppositional defiant disorder is not given, even if all criteria for oppositional
defiant disorder are met.
Intermittent explosive disorder also involves high rates of anger.
However, individuals with this disorder show serious aggression toward others that is not part of
the definition of oppositional defiant disorder.
In 
individuals 
with 
intellectual
developmental disorder, a diagnosis of oppositional defiant disorder is given only if the
oppositional behavior is markedly greater than is commonly observed among individuals of
comparable mental age and with comparable severity of intellectual disability.
Oppositional defiant disorder must also be distinguished from a failure to
follow directions that is the result of impaired language comprehension (e.g., hearing loss).
Oppositional defiant disorder must also be distinguished from defiance
because of fear of negative evaluation associated with social anxiety disorder.
Comorbidity
Rates of oppositional defiant disorder are much higher in samples of children, adolescents, and
adults with ADHD, and this may be the result of shared temperamental risk factors. Also,
oppositional defiant disorder often precedes conduct disorder, although this appears to be most
common in children with the childhood-onset subtype. Individuals with oppositional defiant
disorder are also at increased risk for anxiety disorders and major depressive disorder, and this
seems largely attributable to the presence of the angry-irritable mood symptoms. Extremely high

F63.81
rates of comorbidity between disruptive mood dysregulation disorder and symptoms
characteristic of oppositional defiant disorder have been reported, with most individuals with
disruptive mood dysregulation disorder having symptoms that meet criteria for oppositional
defiant disorder (such as showing argumentative/defiant symptoms); but because oppositional
defiant disorder cannot be diagnosed if criteria are also met for disruptive mood dysregulation
disorder, only disruptive mood dysregulation disorder would be diagnosed in such cases.
Adolescents and adults with oppositional defiant disorder also show a higher rate of substance
use disorders,
although it is unclear if this association is independent of the comorbidity with conduct disorder.
Intermittent Explosive Disorder
Diagnostic Criteria
A. Recurrent behavioral outbursts representing a failure to control aggressive
impulses as manifested by either of the following:
1. Verbal aggression (e.g., temper tantrums, tirades, verbal arguments or fights)
or physical aggression toward property, animals, or other individuals,
occurring twice weekly, on average, for a period of 3 months. The physical
aggression does not result in damage or destruction of property and does not
result in physical injury to animals or other individuals.
2. Three behavioral outbursts involving damage or destruction of property
and/or physical assault involving physical injury against animals or other
individuals occurring within a 12-month period.
B. The magnitude of aggressiveness expressed during the recurrent outbursts is
grossly out of proportion to the provocation or to any precipitating psychosocial
stressors.
C. The recurrent aggressive outbursts are not premeditated (i.e., they are impulsive
and/or anger-based) and are not committed to achieve some tangible objective
(e.g., money, power, intimidation).
D. The recurrent aggressive outbursts cause either marked distress in the individual
or impairment in occupational or interpersonal functioning, or are associated with
financial or legal consequences.
E. Chronological age is at least 6 years (or equivalent developmental level).
F. The recurrent aggressive outbursts are not better explained by another mental
disorder (e.g., major depressive disorder, bipolar disorder, disruptive mood
dysregulation disorder, a psychotic disorder, antisocial personality disorder,
borderline personality disorder) and are not attributable to another medical
condition (e.g., head trauma, Alzheimer’s disease) or to the physiological effects

of a substance (e.g., a drug of abuse, a medication). For children ages 6–18
years, aggressive behavior that occurs as part of an adjustment disorder should
not be considered for this diagnosis.
Note: This diagnosis can be made in addition to the diagnosis of attentiondeficit/hyperactivity disorder, conduct disorder, oppositional defiant disorder, or
autism spectrum disorder when recurrent impulsive aggressive outbursts are in
excess of those usually seen in these disorders and warrant independent clinical
attention.
Diagnostic Features
The impulsive (or anger-based) aggressive outbursts in intermittent explosive disorder have a
rapid onset and, typically, little or no prodromal period. Outbursts typically last for less than 30
minutes and commonly occur in response to a minor provocation by a close intimate or associate.
Individuals with intermittent explosive disorder often have less severe episodes of verbal or
nondamaging, nondestructive, or noninjurious physical assault (Criterion A1) in between more
severe destructive/assaultive episodes (Criterion A2). Criterion A1 defines frequent (i.e., twice
weekly, on average, for a period of 3 months) aggressive outbursts characterized by temper
tantrums, tirades, verbal arguments or fights, or assault without damage to objects or without
injury to animals or other individuals. Criterion A2 defines infrequent (i.e., three in a 1-year
period) impulsive aggressive outbursts characterized by damaging or destroying an object,
regardless of its tangible value, or by
assaulting/striking or otherwise causing physical injury to an animal or to another individual.
Regardless of the nature of the impulsive aggressive outburst, the core feature of intermittent
explosive disorder is failure to control impulsive aggressive behavior in response to subjectively
experienced provocation (i.e., psychosocial stressor) that would not typically result in an
aggressive outburst (Criterion B). The aggressive outbursts are generally impulsive or angerbased rather than premeditated or instrumental (Criterion C) and cause significant distress or
impairment in occupational or interpersonal functioning or are associated with financial or legal
consequences (Criterion D). A diagnosis of intermittent explosive disorder should not be given to
individuals younger than 6 years, or the equivalent developmental level (Criterion E), or to
individuals whose aggressive outbursts are better explained by another mental disorder (Criterion
F). A diagnosis of intermittent explosive disorder should not be given to individuals with
disruptive mood dysregulation disorder or to individuals whose impulsive aggressive outbursts
are attributable to another medical condition or to the physiological effects of a substance
(Criterion F). In addition, children ages 6–18 years should not receive this diagnosis when
impulsive aggressive outbursts occur in the context of an adjustment disorder (Criterion F).
Associated Features
Depressive disorders, anxiety disorders, and substance use disorders are associated with
intermittent explosive disorder, although onset of these disorders is typically later than that of
intermittent explosive disorder.

Environmental.
Genetic and physiological.
Research provides neurobiological support for the presence of serotonergic abnormalities,
globally and in the brain, specifically in areas of the limbic system (anterior cingulate) and
orbitofrontal cortex in individuals with intermittent explosive disorder. Amygdala responses to
anger stimuli, during functional magnetic resonance imaging scanning, are greater in individuals
with intermittent explosive disorder compared with healthy persons. In addition, the volume of
gray matter in several frontolimbic regions is reduced and correlates inversely with measures of
aggression in individuals with intermittent explosive disorder, although these brain differences
are not always seen.
Prevalence
The 1-year prevalence for intermittent explosive disorder in the United States is about 2.6%, with
a lifetime prevalence of 4.0%. Higher 1-year prevalences of 3.9% and 6.9% (narrow definition)
are present among African Americans and Caribbean Black adolescents, respectively, in the
United States, especially among males. This is consistent with higher 12-month rates of
psychiatric disorder among immigrant Caribbean Black men and their second- and thirdgeneration offspring, possibly associated with downward social mobility and the effects of
racism. However, the reported prevalence of conduct disorder or other disruptive disorders may
be affected by misdiagnosis or overdiagnosis of individuals from some cultural backgrounds.
Intermittent explosive disorder is more prevalent among younger individuals (e.g., younger than
35–40 years), compared with individuals older than 50 years, and individuals with a high school
education or less. In some studies, the prevalence of intermittent explosive disorder is greater in
men and boys than in women and girls; other studies have found no sex or gender differences.
Development and Course
The onset of recurrent, problematic, impulsive aggressive behavior is most common in late
childhood or adolescence and rarely begins for the first time after age 40 years. The course of the
disorder may be episodic, with recurrent periods of impulsive aggressive outbursts. Intermittent
explosive disorder appears to follow a chronic and persistent course over many years. It also
appears to be quite common regardless of the presence or absence of
attention-deficit/hyperactivity disorder (ADHD) or other disruptive, impulse-control, and
conduct disorders (e.g., conduct disorder, oppositional defiant disorder).
Risk and Prognostic Factors
Individuals with a history of physical and emotional trauma during the first 20
years of life are at increased risk for intermittent explosive disorder. Long-term displacement
from home and separation from family members are risk factors in some refugee population
settings.
First-degree relatives of individuals with intermittent explosive
disorder are at increased risk for intermittent explosive disorder, and twin studies have
demonstrated a substantial genetic influence for impulsive aggression.

Disruptive mood dysregulation disorder.
Antisocial personality disorder or borderline personality disorder.
Culture-Related Diagnostic Issues
The lower prevalence of intermittent explosive disorder in some regions (Asia, Middle East) or
countries (Romania, Nigeria), compared with the United States, suggests that information about
recurrent, problematic, impulsive aggressive behaviors either is not elicited on questioning or is
less likely to be present, because of cultural factors.
Association With Suicidal Thoughts or Behavior
A study of 1,460 research volunteers found that intermittent explosive disorder comorbid with
posttraumatic stress disorder was associated with a markedly elevated rate of lifetime suicide
attempt (41%). Posttraumatic stress disorder and intermittent explosive disorder were the only
disorders associated with suicide attempt among soldiers with suicidal ideation, although the role
of intermittent explosive disorder was less clear in multivariate analyses.
Functional Consequences of Intermittent Explosive Disorder
Social (e.g., loss of friends, relatives, marital instability), occupational (e.g., demotion, loss of
employment), financial (e.g., because of value of objects destroyed), and legal (e.g., civil suits as
a result of aggressive behavior against person or property; criminal charges for assault) problems
often develop as a result of intermittent explosive disorder.
Differential Diagnosis
A diagnosis of intermittent explosive disorder should not be made when Criteria A1 and/or A2
are only met during an episode of another mental disorder (e.g., major depressive disorder,
bipolar disorder, psychotic disorder), or when impulsive aggressive outbursts are attributable to
another medical condition or to the physiological effects of a substance or medication. This
diagnosis also should not be made, particularly in children and adolescents ages 6–18 years,
when the impulsive aggressive outbursts occur in the context of an adjustment disorder.
In contrast to intermittent explosive disorder, disruptive
mood dysregulation disorder is characterized by a persistently negative mood state (i.e.,
irritability, anger) most of the day, nearly every day, between impulsive aggressive outbursts. A
diagnosis of disruptive mood dysregulation disorder can only be given when the onset of
recurrent, problematic, impulsive aggressive outbursts is before age 10 years. Finally, a diagnosis
of disruptive mood dysregulation disorder should not be made for the first time after age 18
years. Otherwise, these diagnoses are mutually exclusive.
Individuals 
with 
antisocial
personality disorder or borderline personality disorder often display recurrent,
problematic impulsive aggressive outbursts. However, the level of impulsive aggression in
individuals with antisocial personality disorder or borderline personality disorder is lower than
that in individuals with intermittent explosive disorder.

Delirium, major neurocognitive disorder, and personality change due to another medical
condition, aggressive type.
Substance intoxication or substance withdrawal.
Attention-deficit/hyperactivity disorder, conduct disorder, oppositional defiant disorder, or
autism spectrum disorder.
A diagnosis of intermittent explosive disorder should not be made when aggressive outbursts are
judged to result from the physiological effects of another diagnosable medical condition (e.g.,
brain injury associated with a change in personality characterized by aggressive outbursts;
complex partial epilepsy). Nonspecific abnormalities on neurological examination (e.g., “soft
signs”) and nonspecific electroencephalographic changes are compatible with a diagnosis of
intermittent explosive disorder unless there is a diagnosable medical condition that better
explains the impulsive aggressive outbursts.
A diagnosis of intermittent explosive disorder
should not be made when impulsive aggressive outbursts are nearly always associated with
intoxication with or withdrawal from substances (e.g., alcohol, phencyclidine, cocaine and other
stimulants, barbiturates, inhalants). However, when a sufficient number of impulsive aggressive
outbursts also occur in the absence of substance intoxication or withdrawal, and these warrant
independent clinical attention, a diagnosis of intermittent explosive disorder may be given.
Individuals with any of these childhood-onset disorders may exhibit impulsive aggressive
outbursts. Individuals with ADHD are typically impulsive and, as a result, may also exhibit
impulsive aggressive outbursts. While individuals with conduct disorder can exhibit impulsive
aggressive outbursts, the form of aggression characterized by the diagnostic criteria is proactive
and predatory. Aggression in oppositional defiant disorder is typically characterized by temper
tantrums and verbal arguments with authority figures, whereas impulsive aggressive outbursts in
intermittent explosive disorder are in response to a broader array of provocation and include
physical assault. The level of impulsive aggression in individuals with a history of one or more
of these disorders has been reported as lower than that in comparable individuals whose
symptoms also meet intermittent explosive disorder Criteria A through E. Accordingly, if
Criteria A through E are also met, and the impulsive aggressive outbursts warrant independent
clinical attention, a diagnosis of intermittent explosive disorder may be given.
Comorbidity
Depressive disorders, anxiety disorders, posttraumatic stress disorder, bulimia nervosa, bingeeating disorder, and substance use disorders are most commonly comorbid with intermittent
explosive disorder in community samples. In addition, individuals with antisocial personality
disorder or borderline personality disorder, and individuals with a history of disorders with
disruptive behaviors (e.g., ADHD, conduct disorder, oppositional defiant disorder), are at greater
risk for comorbid intermittent explosive disorder.
Conduct Disorder
Diagnostic Criteria
A. A repetitive and persistent pattern of behavior in which the basic rights of others

or major age-appropriate societal norms or rules are violated, as manifested by
the presence of at least three of the following 15 criteria in the past 12 months
from any of the categories below, with at least one criterion present in the past 6
months:
Aggression to People and Animals
1. Often bullies, threatens, or intimidates others.
2. Often initiates physical fights.
3. Has used a weapon that can cause serious physical harm to others (e.g., a
bat, brick, broken bottle, knife, gun).
4. Has been physically cruel to people.
5. Has been physically cruel to animals.
6. Has stolen while confronting a victim (e.g., mugging, purse snatching,
extortion, armed robbery).
7. Has forced someone into sexual activity.
Destruction of Property
8. Has deliberately engaged in fire setting with the intention of causing serious
damage.
9. Has deliberately destroyed others’ property (other than by fire setting).
Deceitfulness or Theft
10. Has broken into someone else’s house, building, or car.
11. Often lies to obtain goods or favors or to avoid obligations (i.e., “cons”
others).
12. Has stolen items of nontrivial value without confronting a victim (e.g.,
shoplifting, but without breaking and entering; forgery).
Serious Violations of Rules
13. Often stays out at night despite parental prohibitions, beginning before age 13
years.
14. Has run away from home overnight at least twice while living in the parental
or parental surrogate home, or once without returning for a lengthy period.
15. Is often truant from school, beginning before age 13 years.
B. The disturbance in behavior causes clinically significant impairment in social,
academic, or occupational functioning.
C. If the individual is age 18 years or older, criteria are not met for antisocial
personality disorder.
Specify whether:
F91.1 Childhood-onset type: Individuals show at least one symptom
characteristic of conduct disorder prior to age 10 years.
F91.2 Adolescent-onset type: Individuals show no symptom characteristic of

conduct disorder prior to age 10 years.
F91.9 Unspecified onset: Criteria for a diagnosis of conduct disorder are met,
but there is not enough information available to determine whether the onset of
the first symptom was before or after age 10 years.
Specify if:
With limited prosocial emotions: To qualify for this specifier, an individual
must have displayed at least two of the following characteristics persistently over
at least 12 months and in multiple relationships and settings. These
characteristics reflect the individual’s typical pattern of interpersonal and
emotional functioning over this period and not just occasional occurrences in
some situations. Thus, to assess the criteria for the specifier, multiple information
sources are necessary. In addition to the individual’s self-report, it is necessary
to consider reports by others who have known the individual for extended
periods of time (e.g., parents, teachers, co-workers, extended family members,
peers).
Lack of remorse or guilt: Does not feel bad or guilty when he or she does
something wrong (exclude remorse when expressed only when caught and/or
facing punishment). The individual shows a general lack of concern about the
negative consequences of his or her actions. For example, the individual is not
remorseful after hurting someone or does not care about the consequences of
breaking rules.
Callous—lack of empathy: Disregards and is unconcerned about the feelings
of others. The individual is described as cold and uncaring. The individual
appears more concerned about the effects of his or her actions on himself or
herself, rather than their effects on others, even when they result in substantial
harm to others.
Unconcerned about performance: Does not show concern about
poor/problematic performance at school, at work, or in other important
activities. The individual does not put forth the effort necessary to perform well,
even when expectations are clear, and typically blames others for his or her
poor performance.
Shallow or deficient affect: Does not express feelings or show emotions to
others, except in ways that seem shallow, insincere, or superficial (e.g.,
actions contradict the emotion displayed; can turn emotions “on” or “off”
quickly) or when emotional expressions are used for gain (e.g., emotions
displayed to manipulate or intimidate others).
Specify current severity:
Mild: Few if any conduct problems in excess of those required to make the
diagnosis are present, and conduct problems cause relatively minor harm to
others (e.g., lying, truancy, staying out after dark without permission, other rule

breaking).
Moderate: The number of conduct problems and the effect on others are
intermediate between those specified in “mild” and those in “severe” (e.g.,
stealing without confronting a victim, vandalism).
Severe: Many conduct problems in excess of those required to make the
diagnosis are present, or conduct problems cause considerable harm to others
(e.g., forced sex, physical cruelty, use of a weapon, stealing while confronting a
victim, breaking and entering).
Subtypes
Three subtypes of conduct disorder are provided based on the age at onset of the disorder. Both
childhood-onset and adolescent-onset subtypes can occur in a mild, moderate, or severe form. An
unspecified-onset subtype is designated when there is insufficient information to determine age
at onset.
In childhood-onset conduct disorder, individuals are usually male, have disturbed peer
relationships, may have had oppositional defiant disorder during early childhood, and usually
have symptoms that meet full criteria for conduct disorder prior to puberty. Individuals with the
childhood-onset type may be more likely to display aggression toward others than individuals
with the adolescent-onset type. Many children with this subtype also have concurrent attentiondeficit/hyperactivity disorder (ADHD) or other neurodevelopmental difficulties. Individuals with
childhood-onset type are more likely to have persistent conduct disorder into adulthood than are
those with adolescent-onset type. Individuals with adolescent-onset conduct disorder tend to
have more normative peer relationships (although they often display conduct problems in the
company of others).
Specifiers
A minority of individuals with conduct disorder exhibit characteristics that qualify for the “with
limited prosocial emotions” specifier. The indicators of this specifier are those that have often
been labeled as callous and unemotional traits in research. Other personality features, such as
thrill seeking, fearlessness, and insensitivity to punishment, may also distinguish those with
characteristics described in the specifier. Individuals with
characteristics described in this specifier may be more likely than other individuals with conduct
disorder to engage in aggression that is planned for instrumental gain. Individuals with conduct
disorder of any subtype or any level of severity can have characteristics that qualify for the
specifier “with limited prosocial emotions,” although individuals with the specifier are more
likely to have childhood-onset type and a severity specifier rating of severe.
Although the validity of self-report to assess the presence of the specifier has been supported
in some research contexts, individuals with conduct disorder with this specifier may not readily
admit to the traits in a clinical interview. Thus, to assess the criteria for the specifier, multiple
information sources are necessary. Also, because the indicators of the specifier are characteristics

that reflect the individual’s typical pattern of interpersonal and emotional functioning, it is
important to consider reports by others who have known the individual for extended periods of
time and across relationships and settings (e.g., parents, teachers, co-workers, extended family
members, peers).
Diagnostic Features
The essential feature of conduct disorder is a repetitive and persistent pattern of behavior in
which the basic rights of others or major age-appropriate societal norms or rules are violated
(Criterion A). These behaviors fall into four main groupings: aggressive conduct that causes or
threatens physical harm to other people or animals (Criteria A1–A7); nonaggressive conduct that
causes property loss or damage (Criteria A8–A9); deceitfulness or theft (Criteria A10–A12); and
serious violations of rules (Criteria A13–A15). Three or more characteristic behaviors must have
been present during the past 12 months, with at least one behavior present in the past 6 months.
The disturbance in behavior causes clinically significant impairment in social, academic, or
occupational functioning (Criterion B). The behavior pattern is usually present in a variety of
settings, such as home, at school, or in the community. Because individuals with conduct
disorder are likely to minimize their conduct problems, the clinician often must rely on additional
informants. However, informants’ knowledge of the individual’s conduct problems may be
limited if they have inadequately supervised the individual or the individual has concealed
symptom behaviors.
Individuals with conduct disorder often initiate aggressive behavior and react aggressively to
others. They may display bullying, threatening, or intimidating behavior (including bullying via
messaging on web-based social media) (Criterion A1); initiate frequent physical fights (Criterion
A2); use a weapon that can cause serious physical harm (e.g., a bat, brick, broken bottle, knife,
gun) (Criterion A3); be physically cruel to people (Criterion A4) or animals (Criterion A5); steal
while confronting a victim (e.g., mugging, purse snatching, extortion, armed robbery) (Criterion
A6); or force someone into sexual activity (Criterion A7). Physical violence may take the form
of rape, assault, or, in rare cases, homicide. Deliberate destruction of others’ property may
include deliberate fire setting with the intention of causing serious damage (Criterion A8) or
deliberate destroying of other people’s property in other ways (e.g., smashing car windows,
vandalizing school property) (Criterion A9). Acts of deceitfulness or theft may include breaking
into someone else’s house, building, or car (Criterion A10); frequently lying or breaking
promises to obtain goods or favors or to avoid debts or obligations (e.g., “conning” other
individuals) (Criterion A11); or stealing items of nontrivial value without confronting the victim
(e.g., shoplifting, forgery, fraud) (Criterion A12).
Individuals with conduct disorder may also frequently commit serious violations of rules
(e.g., school, parental, workplace). Children with conduct disorder often have a pattern,
beginning before age 13 years, of staying out late at night despite parental prohibitions (Criterion
A13). Children may also show a pattern of running away from home overnight (Criterion A14).
To be considered a symptom of conduct disorder, the running away must have occurred at least
twice (or only once if the individual did not return for a lengthy period). Runaway episodes that
occur as a direct consequence of physical or sexual abuse do not typically qualify for this
criterion. Children with conduct disorder may often be truant from school, beginning prior to age
13 years (Criterion A15).

534
Associated Features
Especially in ambiguous situations, aggressive individuals with conduct disorder frequently
misperceive the intentions of others as more hostile and threatening than is the case and respond
with aggression that they then feel is reasonable and justified. Personality features of trait
negative emotionality and poor self-control, including poor frustration tolerance, irritability,
temper outbursts, suspiciousness, insensitivity to punishment, thrill seeking, and recklessness,
frequently co-occur with conduct disorder. Substance misuse is often an associated feature,
particularly in adolescent girls.
Prevalence
One-year population prevalence estimates in the United States and other largely high-income
countries range from 2% to more than 10%, with a median of 4%. In the United States, the
lifetime prevalence was found to be 12.0% among men and 7.1% among women. The prevalence
of conduct disorder in largely Western samples appears to be fairly consistent across various
countries. Prevalence rates rise from childhood to adolescence. Prevalence of adolescent-onset
conduct disorder is more frequently associated with psychosocial stressors—for example, being a
member of a socially oppressed ethnic group facing discrimination. Few children with impairing
conduct disorder receive treatment.
Development and Course
The onset of conduct disorder may occur as early as the preschool years, but the first significant
symptoms usually emerge during the period from middle childhood through middle adolescence.
Oppositional defiant disorder is a common precursor to the childhood-onset type of conduct
disorder. Physically aggressive symptoms are more common than nonaggressive symptoms
during childhood, but nonaggressive symptoms become more common than aggressive
symptoms during adolescence.
Conduct disorder may be diagnosed in adults; however, symptoms of conduct disorder
usually emerge in childhood or adolescence, and onset is rare after age 16 years. The course of
conduct disorder after onset is variable. In a majority of individuals, the disorder remits by
adulthood. Many individuals with conduct disorder—particularly those with adolescent-onset
type and those with few and milder symptoms—achieve adequate social and occupational
adjustment as adults. However, the childhood-onset type predicts a worse prognosis and an
increased risk of criminal behavior, conduct disorder, and substance-related disorders in
adulthood. Individuals with conduct disorder are at risk for later mood disorders, anxiety
disorders, posttraumatic stress disorder, impulse-control disorders, psychotic disorders, somatic
symptom disorders, and substance-related disorders as adults.
Symptoms of the disorder vary with age as the individual develops increased physical
strength, cognitive abilities, and sexual maturity. Symptom behaviors that emerge first tend to be
less serious (e.g., lying, shoplifting), whereas conduct problems that emerge last tend to be more
severe (e.g., rape, theft while confronting a victim). However, there are wide differences among
individuals, with some engaging in the more damaging behaviors at an early age (which is

Temperamental.
Environmental.
Genetic and physiological.
Course modifiers.
predictive of a worse prognosis). When individuals with conduct disorder reach adulthood,
symptoms of aggression, property destruction, deceitfulness, and rule violation, including
violence against co-workers, partners, and children, may be exhibited in the workplace and the
home, such that antisocial personality disorder may be considered.
Risk and Prognostic Factors
Temperamental risk factors include a difficult undercontrolled infant
temperament and lower-than-average intelligence, particularly with regard to verbal IQ.
Family-level risk factors include parental rejection and neglect, inconsistent
child-rearing practices, harsh discipline, physical or sexual abuse, lack of supervision,
early institutional living, frequent changes of caregivers, large family size, parental criminality,
and certain kinds of familial psychopathology (e.g., substance-related disorders). Communitylevel risk factors include peer rejection, association with a delinquent peer group, neighborhood
disadvantage, and exposure to violence. Both types of risk factors tend to be more common and
severe among individuals with the childhood-onset subtype of conduct disorder. On the other
hand, parental migration is a risk factor for children who are left in the country of origin as well
as for those who migrated with their parents, with conduct problems being attributable to
acculturation processes. Nevertheless, first-generation immigrants and refugees often have fewer
conduct problems than their peers.
Conduct disorder is influenced by both genetic and environmental
factors. Genetic associations may be stronger for aggressive symptoms. The risk is increased in
children with a biological or adoptive parent or a sibling with conduct disorder. The disorder also
appears to be more common in children of biological parents with severe alcohol use disorder,
depressive and bipolar disorders, or schizophrenia or biological parents who have a history of
ADHD or conduct disorder. Family history particularly characterizes individuals with the
childhood-onset subtype of conduct disorder. Slower resting heart rate has been reliably noted in
individuals with conduct disorder compared with those without the disorder, and this marker is
not characteristic of any other mental disorder. Reduced autonomic fear conditioning,
particularly low skin conductance, is also well documented. However, these psychophysiological
findings are not diagnostic of the disorder. Structural and functional differences in brain areas
associated with affect regulation and affect processing, particularly frontotemporal-limbic
connections involving the brain’s ventral prefrontal cortex and amygdala, have been consistently
noted in individuals with conduct disorder compared with those without the disorder. However,
neuroimaging findings are not diagnostic of the disorder.
Persistence is more likely for individuals with behaviors that meet criteria for
the childhood-onset subtype and qualify for the specifier “with limited prosocial emotions.” The
risk that conduct disorder will persist is also increased by co-occurring ADHD and by substance
abuse.
Culture-Related Diagnostic Issues

Oppositional defiant disorder.
Conduct disorder diagnosis may at times be misapplied to individuals in settings where patterns
of disruptive behavior are viewed as near-normative (e.g., in very threatening, high-crime areas
or war zones). Therefore, the context in which the undesirable behaviors have occurred should be
considered. In youth from underserved ethnic and racialized groups, reactions to racism that
involve anger and resistance-based coping may be misdiagnosed as conduct disorder by
uninformed practitioners, as suggested by the association between experiences of discrimination
and adolescent-onset conduct disorder in these groups.
Sex- and Gender-Related Diagnostic Issues
Boys and men with a diagnosis of conduct disorder frequently exhibit fighting, stealing,
vandalism, and school discipline problems. Girls and women with a diagnosis of conduct
disorder are more likely to exhibit lying, truancy, running away, and prostitution. Whereas boys
and men and girls and women exhibit relational aggression (behavior that harms social
relationships of others), girls and women exhibit considerably less physical aggression than do
boys and men.
Association With Suicidal Thoughts or Behavior
Suicidal thoughts, suicide attempts, and suicide occur at a higher-than-expected rate in
individuals with conduct disorder. A large study conducted in Taiwan that followed adolescents
with conduct disorder over 10 years found that conduct disorder was associated
with a higher rate of suicide attempts even after adjustment for comorbid mood, anxiety, and
substance use disorders.
Functional Consequences of Conduct Disorder
Conduct disorder behaviors may lead to school suspension or expulsion, problems in work
adjustment, legal difficulties, sexually transmitted diseases, unplanned pregnancy, and physical
injury from accidents or fights. These problems may preclude attendance in ordinary schools or
living in a parental or foster home. Conduct disorder is often associated with an early onset of
sexual behavior, alcohol use, tobacco smoking, use of illegal substances, and reckless and risktaking acts. Accident rates appear to be higher among individuals with conduct disorder
compared with those without the disorder. These functional consequences of conduct disorder
may increase the risk for health difficulties when individuals reach midlife. It is not uncommon
for individuals with conduct disorder to come into contact with the criminal justice system for
engaging in illegal behavior. Conduct disorder is a common reason for treatment referral and is
frequently diagnosed in mental health facilities for children, especially in forensic practice. It is
associated with impairment that is more severe and chronic than that experienced by other clinicreferred children.
Differential Diagnosis
Conduct disorder and oppositional defiant disorder are both related

Attention-deficit/hyperactivity disorder.
Depressive and bipolar disorders.
Intermittent explosive disorder.
Adjustment disorders.
to symptoms that bring the individual in conflict with adults and other authority figures (e.g.,
parents, teachers, work supervisors). The behaviors of oppositional defiant disorder are typically
of a less severe nature than those of individuals with conduct disorder and do not include
aggression toward people or animals, destruction of property, or a pattern of theft or deceit.
Furthermore, oppositional defiant disorder includes problems of emotion dysregulation (i.e.,
angry and irritable mood) that are not included in the definition of conduct disorder. When
criteria are met for both oppositional defiant disorder and conduct disorder, both diagnoses can
be given.
Although children with ADHD often exhibit hyperactive
and impulsive behavior that may be disruptive, this behavior does not by itself violate societal
norms or the rights of others and therefore does not usually meet criteria for conduct disorder.
When criteria are met for both ADHD and conduct disorder, both diagnoses should be given.
Irritability, aggression, and conduct problems can occur in
children or adolescents with major depressive disorder, bipolar disorder, or disruptive mood
dysregulation disorder. The behavioral problems associated with these mood disorders can
usually be distinguished from the pattern of conduct problems seen in conduct disorder based on
their course. Specifically, individuals with conduct disorder will display substantial levels of
aggressive or nonaggressive conduct problems during periods in which there is no mood
disturbance, either historically (i.e., a history of conduct problems predating the onset of the
mood disturbance) or concurrently (i.e., display of some conduct problems that are premeditated
and do not occur during periods of intense emotional arousal). In those cases in which criteria for
conduct disorder and a mood disorder are met, both diagnoses can be given.
Both conduct disorder and intermittent explosive disorder involve
high rates of aggression. However, the aggression in individuals with intermittent explosive
disorder is limited to impulsive aggression and is not premeditated, and it is not committed in
order to achieve some tangible objective (e.g., money, power, intimidation). Also, the definition
of intermittent explosive disorder does not include the non-aggressive symptoms of conduct
disorder. If criteria for both disorders are met, the diagnosis of intermittent explosive disorder
should be given only when the recurrent impulsive aggressive outbursts warrant independent
clinical attention.
The diagnosis of an adjustment disorder (with disturbance of conduct or
with mixed disturbance of emotions and conduct) should be considered if clinically significant
conduct problems that do not meet the criteria for another specific disorder develop in clear
association with the onset of a psychosocial stressor and do not resolve within 6 months of the
termination of the stressor (or its consequences). Conduct disorder is diagnosed only when the
conduct problems represent a repetitive and persistent pattern that is associated with impairment
in social, academic, or occupational functioning.
Comorbidity
ADHD and oppositional defiant disorder are both common in individuals with conduct disorder,
and this comorbid presentation predicts worse outcomes. Individuals who show the personality

F63.1
features associated with antisocial personality disorder often violate the basic rights of others or
violate major age-appropriate societal norms, and as a result their pattern of behavior often meets
criteria for conduct disorder. Conduct disorder may also co-occur with one or more of the
following mental disorders: specific learning disorder, anxiety disorders, depressive or bipolar
disorders, and substance-related disorders. Academic achievement, particularly in reading and
other verbal skills, is often below the level expected on the basis of age and intelligence and may
justify the additional diagnosis of specific learning disorder or a communication disorder.
Antisocial Personality Disorder
Criteria and text for antisocial personality disorder can be found in the chapter “Personality
Disorders.” Because this disorder is closely connected to the spectrum of “externalizing” conduct
disorders in this chapter, as well as to the disorders in the adjoining chapter “Substance-Related
and Addictive Disorders,” it is listed here as well as in the chapter “Personality Disorders.”
Pyromania
Diagnostic Criteria
A. Deliberate and purposeful fire setting on more than one occasion.
B. Tension or affective arousal before the act.
C. Fascination with, interest in, curiosity about, or attraction to fire and its situational
contexts (e.g., paraphernalia, uses, consequences).
D. Pleasure, gratification, or relief when setting fires or when witnessing or
participating in their aftermath.
E. The fire setting is not done for monetary gain, as an expression of sociopolitical
ideology, to conceal criminal activity, to express anger or vengeance, to improve
one’s living circumstances, in response to a delusion or hallucination, or as a
result of impaired judgment (e.g., in major neurocognitive disorder, intellectual
developmental disorder [intellectual disability], substance intoxication).
F. The fire setting is not better explained by conduct disorder, a manic episode, or
antisocial personality disorder.
Diagnostic Features
The essential feature of pyromania is the presence of multiple episodes of deliberate and
purposeful fire setting (Criterion A). Individuals with this disorder experience tension or
affective arousal before setting a fire (Criterion B). There is a fascination with, interest in,
curiosity about, or attraction to fire and its situational contexts (e.g., paraphernalia, uses,

consequences) (Criterion C). Individuals with this disorder are often regular “watchers” at fires
in their neighborhoods, may set off false alarms, and derive pleasure from institutions,
equipment, and personnel associated with fire. They may spend time at the local fire department,
set fires to be affiliated with the fire department, or even become firefighters. Individuals with
this disorder experience pleasure, gratification, or relief when setting the fire, witnessing its
effects, or participating in its aftermath (Criterion D). The fire setting is not done for monetary
gain, as an expression of sociopolitical ideology, to conceal criminal activity, to express anger or
vengeance, to improve one’s living circumstances, or in response to a delusion or a hallucination
(Criterion E). The fire setting does not result from impaired judgment (e.g., in major
neurocognitive disorder or intellectual developmental disorder [intellectual disability]). The
diagnosis is not made if the fire setting is better explained by conduct disorder, a manic episode,
or antisocial personality disorder (Criterion F).
Associated Features
Individuals with pyromania may make considerable advance preparation for starting a fire. They
may be indifferent to the consequences to life or property caused by the fire, or they may derive
satisfaction from the resulting property destruction. The behaviors may lead to property damage,
legal consequences, or injury or loss of life to the fire setter or to others. Individuals who
impulsively set fires (who may or may not have pyromania) often have a current or past history
of alcohol use disorder.
Prevalence
The population prevalence of pyromania is not known. The lifetime prevalence of fire-setting
behavior, which is just one component of pyromania and not sufficient for a diagnosis by itself,
was reported as 1.0%–1.1% in a population sample. Fire-setting behavior occurs more often in
men than in women (lifetime prevalence 1.7% vs. 0.4%); however, whether this also holds true
for pyromania is unknown. The most common comorbidities of fire-setting behavior were
antisocial personality disorder, substance use disorder, bipolar disorder, and gambling disorder.
In contrast to fire setting, pyromania as a primary diagnosis appears to be very rare. Among a
sample of persons in a Finnish hospital reaching the criminal system because of repeated fire
setting, only 3.3% had symptoms that met full criteria for pyromania. In a U.S. study, 3.4% of a
sample of adults hospitalized for psychiatric reasons had symptoms that met full criteria for
current pyromania.
Development and Course
Although data are limited, some research suggests that late adolescence may be the typical age at
onset of pyromania. The relationship between fire setting in childhood and pyromania in
adulthood has not been documented. In individuals with pyromania, fire-setting incidents are
episodic and may wax and wane in frequency. Longitudinal course is unknown. Although fire
setting is a major problem in children and adolescents (over 40% of those arrested for arson
offenses in the United States are younger than 18 years), pyromania in childhood appears to be
rare. Juvenile fire setting is usually associated with conduct disorder, attentiondeficit/hyperactivity disorder, or an adjustment disorder.

Other causes of intentional fire setting.
Other mental disorders.
F63.2
Sex- and Gender-Related Diagnostic Issues
While fire setting is associated with antisocial behavior in men and women, they differ on some
of the antisocial behaviors that accompany fire setting. Whether this holds for pyromania, which
is a subset of those with fire setting, is unknown.
Association With Suicidal Thoughts or Behavior
A study of a consecutive sample of male fire setters who had a forensic assessment compared
each case with four age-, sex-, and place of birth–matched controls and found that
fire setting was associated during follow-up with higher rates of suicide and also suicide attempt.
Whether these differences apply to pyromania is unknown.
Differential Diagnosis
It is important to rule out other causes of fire setting before
giving the diagnosis of pyromania. Intentional fire setting may occur for profit, sabotage, or
revenge; to conceal a crime; to make a political statement (e.g., an act of terrorism or protest); or
to attract attention or recognition (e.g., setting a fire in order to discover it and save the day). Fire
setting may also occur as part of developmental experimentation in childhood (e.g., playing with
matches, lighters, or fire).
A separate diagnosis of pyromania is not given when fire setting occurs as
part of conduct disorder, a manic episode, or antisocial personality disorder, or if it occurs in
response to a delusion or a hallucination (e.g., in schizophrenia) or is attributable to the
physiological effects of another medical condition (e.g., epilepsy). The diagnosis of pyromania
should also not be given when fire setting results from impaired judgment associated with major
neurocognitive disorder, intellectual developmental disorder, or substance intoxication.
Comorbidity
There appears to be a high co-occurrence of substance use disorders, gambling disorder,
depressive and bipolar disorders, and other disruptive, impulse-control, and conduct disorders
with pyromania.
Kleptomania
Diagnostic Criteria
A. Recurrent failure to resist impulses to steal objects that are not needed for
personal use or for their monetary value.
B. Increasing sense of tension immediately before committing the theft.
C. Pleasure, gratification, or relief at the time of committing the theft.

D. The stealing is not committed to express anger or vengeance and is not in
response to a delusion or a hallucination.
E. The stealing is not better explained by conduct disorder, a manic episode, or
antisocial personality disorder.
Diagnostic Features
The essential feature of kleptomania is the recurrent failure to resist impulses to steal items even
though the items are not needed for personal use or for their monetary value (Criterion A). The
individual experiences a rising subjective sense of tension before the theft (Criterion B) and feels
pleasure, gratification, or relief when committing the theft (Criterion C). The stealing is not
committed to express anger or vengeance, is not done in response to a delusion or hallucination
(Criterion D), and is not better explained by conduct disorder, a manic episode, or antisocial
personality disorder (Criterion E). The objects are stolen despite the fact that they are typically of
little value to the individual, who could have afforded to pay for them and often gives them away
or discards them. Occasionally the individual may hoard the stolen objects or surreptitiously
return them. Although individuals with this disorder will generally avoid stealing when
immediate arrest is probable (e.g., in full view of a police officer), they usually do not preplan
the thefts or fully take
into account the chances of apprehension. The stealing is done without assistance from, or
collaboration with, others.
Associated Features
Individuals with kleptomania typically attempt to resist the impulse to steal, and they are aware
that the act is wrong and senseless. The individual frequently fears being apprehended and often
feels depressed or guilty about the thefts. Neurotransmitter pathways associated with behavioral
addictions, including those associated with the serotonin, dopamine, and opioid systems, appear
to play a role in kleptomania as well.
Prevalence
In the United States and Canada, kleptomania occurs in about 4%–24% of individuals arrested
for shoplifting. Its prevalence in the U.S. general population is very rare, at approximately 0.3%–
0.6%. Women outnumber men at a ratio of 3:1.
Development and Course
Age at onset of kleptomania is variable, but the disorder often begins in adolescence. However,
the disorder may begin in childhood, adolescence, or adulthood, and in rare cases in late
adulthood. There is little systematic information on the course of kleptomania, but three typical
courses have been described: sporadic with brief episodes and long periods of remission;
episodic with protracted periods of stealing and periods of remission; and chronic with some
degree of fluctuation. The disorder may continue for years, despite multiple convictions for

Genetic and physiological.
Ordinary theft.
Malingering.
Antisocial personality disorder and conduct disorder.
Manic episodes, psychotic episodes, and major neurocognitive disorder.
shoplifting.
Risk and Prognostic Factors
There appears to be a higher rate of alcohol use disorders in first-degree
relatives of individuals with kleptomania than in the general population.
Association With Suicidal Thoughts or Behavior
Kleptomania has been associated with an increased risk for suicide attempts.
Functional Consequences of Kleptomania
The disorder may cause legal, family, career, and personal difficulties.
Differential Diagnosis
Kleptomania should be distinguished from ordinary acts of theft or shoplifting.
Ordinary theft (whether planned or impulsive) is deliberate and is motivated by the usefulness of
the object or its monetary worth. Some persons, especially adolescents, may also steal on a dare,
as an act of rebellion, or as a rite of passage. The diagnosis is not made unless other
characteristic features of kleptomania are also present. Kleptomania is rare, whereas shoplifting
is relatively common.
In malingering, individuals may simulate the symptoms of kleptomania to avoid
criminal prosecution.
Antisocial personality disorder and conduct
disorder are distinguished from kleptomania by a general pattern of antisocial behavior.
Kleptomania 
should 
be
distinguished from intentional or inadvertent stealing that may occur during a
manic episode, in response to delusions or hallucinations (e.g., in schizophrenia), or as a result of
a major neurocognitive disorder.
Comorbidity
Kleptomania may be associated with compulsive buying as well as with depressive and bipolar
disorders (especially major depressive disorder), anxiety disorders, eating disorders (particularly
bulimia nervosa), personality disorders, substance use disorders (especially alcohol use disorder),
and other disruptive, impulse-control, and conduct disorders.
Other Specified Disruptive, Impulse-Control, and Conduct
Disorder
F91.8

This category applies to presentations in which symptoms characteristic of a
disruptive, impulse-control, and conduct disorder that cause clinically significant
distress or impairment in social, occupational, or other important areas of functioning
predominate but do not meet the full criteria for any of the disorders in the disruptive,
impulse-control, and conduct disorders diagnostic class. The other specified
disruptive, impulse-control, and conduct disorder category is used in situations in
which the clinician chooses to communicate the specific reason that the presentation
does not meet the criteria for any specific disruptive, impulse-control, and conduct
disorder. This is done by recording “other specified disruptive, impulse-control, and
conduct disorder” followed by the specific reason (e.g., “recurrent behavioral
outbursts of insufficient frequency”).
Unspecified Disruptive, Impulse-Control, and Conduct
Disorder
F91.9
This category applies to presentations in which symptoms characteristic of a
disruptive, impulse-control, and conduct disorder that cause clinically significant
distress or impairment in social, occupational, or other important areas of functioning
predominate but do not meet the full criteria for any of the disorders in the disruptive,
impulse-control, and conduct disorders diagnostic class. The unspecified disruptive,
impulse-control, and conduct disorder category is used in situations in which the
clinician chooses not to specify the reason that the criteria are not met for a specific
disruptive, impulse-control, and conduct disorder, and includes presentations in
which there is insufficient information to make a more specific diagnosis (e.g., in
emergency room settings).

# 16 - Substance Related and Addictive Disorders

# Substance-Related and Addictive Disorders

543

Substance-Related and Addictive Disorders
The substance-related disorders encompass 10 separate classes of drugs:
alcohol; caffeine; cannabis; hallucinogens (with separate categories for phencyclidine [or
similarly acting arylcyclohexylamines] and other hallucinogens); inhalants; opioids; sedatives,
hypnotics, or anxiolytics; stimulants (amphetamine-type substances, cocaine, and other
stimulants); tobacco; and other (or unknown) substances. These 10 classes are not fully distinct.
All drugs that are taken in excess have in common the ability to directly activate the brain reward
systems, which are involved in the reinforcement of behaviors and establishment of memories.
Instead of achieving reward system activation through adaptive behaviors, these substances
produce such an intense activation of the reward system that normal activities may be neglected.
The pharmacological mechanisms by which each class of drugs produces reward are different,
but the drugs typically activate the system and produce feelings of pleasure, often referred to as a
“high.” Furthermore, studies suggest that the neurobiological roots of substance use disorders for
some individuals can be seen in their behaviors long before the onset of actual substance use
(e.g., lower levels of self-control may reflect impairments of brain inhibitory mechanisms);
research also suggests the negative impact of substance use itself on brain inhibitory
mechanisms.
Note that the phrase “drug addiction” is not applied as a diagnostic term in this classification,
although it is in common usage in many countries to describe severe problems related to
compulsive and habitual use of substances. The more neutral term substance use disorder is used
to describe the wide range of the disorder, from a mild form to a severe state of chronically
relapsing, compulsive pattern of drug taking. Some clinicians will choose to use the phrase “drug
addiction” to describe more severe presentations, but that wording is omitted from the official
DSM-5 substance use disorder diagnostic terminology because of its uncertain definition and its
potentially negative connotation.
In addition to the substance-related disorders, this chapter also includes gambling disorder,
reflecting evidence that gambling behaviors activate reward systems similar to those activated by
drugs of abuse and that produce some behavioral symptoms that appear comparable to those
produced by the substance use disorders. Other excessive behavioral patterns, such as Internet
gaming (see “Conditions for Further Study”), have also been described, but the research on these
and other behavioral syndromes is less clear. Thus, groups of repetitive behaviors, sometimes
termed behavioral addictions (with subcategories such as “sex addiction,” “exercise addiction,”
and “shopping addiction”), are not included because there is insufficient peer-reviewed evidence
to establish the diagnostic criteria and course descriptions needed to identify these behaviors as
mental disorders.
The substance-related disorders are divided into two groups: substance use disorders and
substance-induced disorders. The following conditions may be classified as substance-induced:
substance intoxication, substance withdrawal, and substance/medication-induced mental

disorders (diagnostic criteria and text are provided in this manual for substance/medicationinduced psychotic disorders, bipolar and related disorders, depressive disorders, anxiety
disorders, obsessive-compulsive and related disorders, sleep disorders, sexual dysfunctions,
delirium, and neurocognitive disorders in their respective chapters). The term
substance/medication-induced mental disorder refers to symptomatic presentations that are
due to the physiological effects of an exogenous substance on the central nervous system and
includes typical intoxicants (e.g., alcohol, inhalants, cocaine), psychotropic medications (e.g.,
stimulants, sedative-hypnotics), other medications, (e.g., steroids), and environmental toxins
(e.g., organophosphate insecticides).
The current section begins with a general discussion of criteria sets for substance use
disorder, substance intoxication, substance withdrawal, and substance/medication-induced
mental disorders, at least some of which are applicable across classes of substances. Reflecting
some unique aspects of the 10 substance classes relevant to this chapter, the remainder of the
chapter is organized by substance class. To facilitate differential diagnosis, the diagnostic criteria
and text for the substance/medication-induced mental disorders are included with disorders with
which they share phenomenology (e.g., substance/medication-induced depressive disorder is in
the chapter “Depressive Disorders”). Note that only certain classes of drugs are capable of
causing particular types of substance-induced disorders. The substance-related diagnostic
categories associated with specific drug classes are shown in Table 1.
TABLE 1 Diagnoses associated with substance class
Psychotic
disorders
Bipolar
and
related
disorders
Depressive
disorders
Anxiety
disorders
Obsessivecompulsive
and related
disorders
Sleep
disorders dy
Alcohol
I/W
I/W
I/W
I/W
I/W
Caffeine
I
I/W
Cannabis
I
I
I/W
Hallucinogens
Phencyclidine
I
I
I
I
Other
hallucinogens
I*
I
I
I
Inhalants
I
I
I
Opioids
I/W
W
I/W
Sedatives,
hypnotics, or
anxiolytics
I/W
I/W
I/W
W
I/W
Stimulants**
I
I/W
I/W
I/W
I/W
I/W
Tobacco
W

Other (or
unknown)
I/W
I/W
I/W
I/W
I/W
I/W
Note. X = The category is recognized in DSM-5.
I = The specifier “with onset during intoxication” may be noted for the category.
W = The specifier “with onset during withdrawal” may be noted for the category.
I/W = Either “with onset during intoxication” or “with onset during withdrawal” may be noted for the category. Major = major
neurocognitive disorder; mild = mild neurocognitive disorder.
*Also hallucinogen persisting perception disorder (flashbacks).
**Includes amphetamine-type substances, cocaine, and other or unspecified stimulants.
Substance-Related Disorders
Substance Use Disorders
Diagnostic Features
The essential feature of a substance use disorder is a cluster of cognitive, behavioral, and
physiological symptoms indicating that the individual continues using the substance despite
significant substance-related problems. As seen in Table 1, the diagnosis of a substance use
disorder can be applied to all 10 substance classes included in this chapter except caffeine. For
certain classes, some symptoms are less salient, and in a few instances not all symptoms apply
(e.g., withdrawal symptoms are not specified for phencyclidine use disorder, other hallucinogen
use disorder, or inhalant use disorder). Of note, the consumption of substances, including
prescribed medications, may depend in part on cultural background, substance availability, and
specific local drug regulations. Thus, there can be significant local or cultural variation in
exposure (e.g., countries with cultural prohibitions against alcohol or other substance use may
have a lower prevalence of substance-related disorders).
An important characteristic of substance use disorders is an underlying change in brain
circuits that may persist beyond detoxification, particularly in individuals with severe disorders.
The behavioral effects of these brain changes may be exhibited in the repeated relapses and
intense drug craving when the individuals are exposed to drug-related stimuli. These persistent
drug effects may benefit from long-term approaches to treatment.
Overall, the diagnosis of a substance use disorder is based on a pathological pattern of
behaviors related to use of the substance. To assist with organization, the diagnostic items
making up Criterion A can be considered to fit within overall groupings of impaired control,
social impairment, risky use, and pharmacological criteria. Impaired control over substance use
is the first criteria grouping (Criteria 1–4). The individual may take the substance in larger
amounts or over a longer period than was originally intended (Criterion 1). The individual may
express a persistent desire to cut down or regulate substance use and may report
multiple unsuccessful efforts to decrease or discontinue use (Criterion 2). The individual may
spend a great deal of time obtaining the substance, using the substance, or recovering from its

effects (Criterion 3). In some instances of more severe substance use disorders, virtually all of
the individual’s daily activities revolve around the substance. Craving (Criterion 4) is manifested
by an intense desire or urge for the drug that may occur at any time but is more likely when in an
environment where the drug previously was obtained or used. Craving has also been shown to
involve classical conditioning and is associated with activation of specific reward structures in
the brain. Craving might be queried by asking if there has ever been a time when there were such
strong urges to take the drug that the individual could not think of anything else. Current craving
is often used as a treatment outcome measure because it may be a signal of impending relapse.
Social impairment is the second grouping of criteria (Criteria 5–7). Recurrent substance use
may result in a failure to fulfill major role obligations at work, school, or home (Criterion 5). The
individual may continue substance use despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of the substance (Criterion 6).
Important social, occupational, or recreational activities may be given up or reduced because of
substance use (Criterion 7). The individual may withdraw from family activities and hobbies in
order to use the substance.
Risky use of the substance is the third grouping of criteria (Criteria 8–9). This may take the
form of recurrent substance use in situations in which it is physically hazardous (Criterion 8).
The individual may continue substance use despite knowledge of having a persistent or recurrent
physical or psychological problem that is likely to have been caused or exacerbated by the
substance (Criterion 9). The key issue in evaluating this criterion is not the existence of the
problem, but rather the individual’s failure to abstain from using the substance despite the
difficulty it is causing.
Pharmacological criteria are the final grouping (Criteria 10 and 11). Tolerance (Criterion 10)
is signaled by requiring a markedly increased dose of the substance to achieve the desired effect
or a markedly reduced effect when the usual dose is consumed. The degree to which tolerance
develops varies greatly across different individuals as well as across substances and may involve
a variety of central nervous system effects. For example, tolerance to respiratory depression and
tolerance to sedating and motor coordination may develop at different rates, depending on the
substance. Tolerance may be difficult to determine by history alone, and laboratory tests may be
helpful (e.g., high blood levels of the substance coupled with little evidence of intoxication
suggest that tolerance is likely). Tolerance must also be distinguished from individual variability
in the initial sensitivity to the effects of particular substances. For example, some first-time
alcohol drinkers show very little evidence of intoxication with three or four drinks, whereas
others of similar weight and drinking histories have slurred speech and incoordination.
Withdrawal (Criterion 11) is a syndrome that occurs when blood or tissue concentrations of a
substance decline in an individual who had maintained prolonged, heavy use of the substance.
After developing withdrawal symptoms, the individual is likely to consume the substance to
relieve the symptoms. Withdrawal symptoms vary greatly across the classes of substances, and
separate criteria sets for withdrawal are provided for the drug classes. Marked and generally
easily measured physiological signs of withdrawal are common with alcohol, opioids, and
sedatives, hypnotics, and anxiolytics. Withdrawal signs and symptoms with stimulants
(amphetamine-type substances, cocaine, other or unspecified stimulants), as well as tobacco and
cannabis, are often present but may be less apparent. Significant withdrawal has not been
documented in humans after repeated use of phencyclidine, other hallucinogens, and inhalants;
therefore, this criterion is not included for these substances. Neither tolerance nor withdrawal is

necessary for a diagnosis of a substance use disorder. However, for most classes of substances, a
past history of withdrawal is associated with a
more severe clinical course (i.e., an earlier onset of a substance use disorder, higher levels of
substance intake, and a greater number of substance-related problems).
Symptoms of tolerance and withdrawal occurring during appropriate use of prescribed
medications given as part of medical treatment (e.g., opioid analgesics, sedatives, stimulants) are
specifically not counted when diagnosing a substance use disorder. The appearance of normal,
expected pharmacological tolerance and withdrawal during the course of medical treatment has
been known to lead to an erroneous diagnosis of “addiction” even when these were the only
symptoms present. Individuals whose only symptoms are those that occur as a result of medical
treatment (i.e., tolerance and withdrawal as part of medical care when the medications are taken
as prescribed) should not receive a diagnosis solely on the basis of these symptoms. However,
prescription medications can be used inappropriately, and a substance use disorder can be
correctly diagnosed when there are other symptoms of compulsive, drug-seeking behavior.
Severity and Specifiers
Substance use disorders occur in a broad range of severity, from mild to severe, with severity
based on the number of symptom criteria endorsed. As a general estimate of severity, a mild
substance use disorder is suggested by the presence of two to three symptoms, moderate by four
to five symptoms, and severe by six or more symptoms. Changing severity across time is also
reflected by reductions or increases in the frequency and/or dose of substance use, as assessed by
the individual’s own report, report of knowledgeable others, clinician’s observations, and
biological testing. The following course specifiers and descriptive features specifiers are also
available for substance use disorders: “in early remission,” “in sustained remission,” “on
maintenance therapy,” and “in a controlled environment.” Definitions of each are provided
within respective criteria sets.
Recording Procedures
The clinician should use the code that applies to the substance class but record the name of the
specific substance. For example, the clinician should record F13.20 moderate alprazolam use
disorder (rather than moderate sedative, hypnotic, or anxiolytic use disorder) or F15.10 mild
methamphetamine use disorder (rather than mild amphetamine-type substance use disorder). For
substances that do not fit into any of the classes (e.g., anabolic steroids), the ICD-10-CM code
for other (or unknown) substance use disorder should be used and the specific substance
indicated (e.g., F19.10 mild anabolic steroid use disorder). If the substance taken by the
individual is unknown, the same ICD-10-CM code (i.e., for “other [or unknown] substance use
disorder”) should be used (e.g., F19.20 severe unknown substance use disorder). If criteria are
met for more than one substance use disorder, each should be diagnosed (e.g., F11.20 severe
heroin use disorder; F14.20 moderate cocaine use disorder).
The appropriate ICD-10-CM code for a substance use disorder depends on whether there is a

comorbid substance-induced disorder (including substance intoxication and substance
withdrawal). In the first example in the paragraph above, the diagnostic code for moderate
alprazolam use disorder, F13.20, reflects the absence of a comorbid alprazolam-induced mental
disorder. Because ICD-10-CM codes for substance-induced disorders indicate both the presence
(or absence) and the severity of the substance use disorder, ICD-10-CM codes for substance use
disorders can be used only in the absence of a substance-induced disorder. See the individual
substance-specific sections for additional coding information.
Substance-Induced Disorders
The overall category of substance-induced disorders includes substance intoxication, substance
withdrawal, and substance/medication-induced mental disorders (e.g., substance-induced
psychotic disorder, substance-induced depressive disorder). While substance intoxication and
substance withdrawal are recognized as mental disorders, for purposes of clarity of reference in
discussions across this chapter, the term substance/medication-induced mental disorder (e.g.,
alcohol-induced depressive disorder, methamphetamine-induced anxiety disorder) is used to
distinguish these disorders from substance intoxication and substance withdrawal.
Substance Intoxication and Substance Withdrawal
Criteria for the substance-specific intoxication syndromes are included within the substancespecific sections of this chapter. The essential feature is the development of a reversible
substance-specific syndrome due to the recent ingestion of a substance (Criterion A). The
clinically significant problematic behavioral or psychological changes associated with
intoxication (e.g., belligerence, mood lability, impaired judgment) are attributable to the
physiological effects of the substance on the central nervous system (CNS) and develop during
or shortly after use of the substance (Criterion B) and are accompanied by substance-specific
signs and symptoms (Criterion C). The symptoms are not attributable to another medical
condition and are not better explained by another mental disorder (Criterion D). Substance
intoxication is common among individuals with a substance use disorder but also occurs
frequently in persons who use substances but do not have a substance use disorder. This category
does not apply to tobacco.
The most common changes in substance intoxication involve disturbances of perception,
wakefulness, attention, thinking, judgment, psychomotor behavior, and interpersonal behavior.
Short-term, or “acute,” substance intoxications may have different signs and symptoms from
sustained, or “chronic,” substance intoxications. For example, moderate cocaine doses may
initially produce gregariousness, but social withdrawal may develop if such doses are frequently
repeated over days or weeks.
When used in the physiological sense, the term intoxication is broader than the diagnosis of
substance intoxication as defined in this manual. Many substances may produce physiological or
psychological changes that are not necessarily problematic. For example, an individual with
tachycardia from substance use is experiencing a physiological effect from the substance, but if

this is the only symptom in the absence of problematic behavior, the diagnosis of substance
intoxication would not apply. Intoxication may sometimes persist beyond the time when the
substance is detectable in the body. This may be attributable to enduring CNS effects, from
which the recovery takes longer than the time for elimination of the substance. These longer-term
effects of intoxication must be distinguished from withdrawal (i.e., symptoms initiated by a
decline in blood or tissue concentrations of a substance).
Criteria for substance withdrawal are also included within the substance-specific sections of
this chapter. The essential feature is the development of a substance-specific problematic
behavioral change, with physiological and cognitive concomitants, that is due to the cessation of,
or reduction in, heavy and prolonged substance use (Criterion A). The substance-specific
syndrome (Criterion B) causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning (Criterion C). The symptoms are not due to
another medical condition and are not better explained by another mental disorder (Criterion D).
Withdrawal is usually, but not always, associated with a substance use disorder. Also, it is
important to emphasize that symptoms of withdrawal occurring during appropriate use of
medications given as part of medical treatment with
prescribed medications (e.g., opioid analgesics, sedatives, stimulants) are specifically not
counted when diagnosing a substance use disorder. Most individuals with withdrawal have an
urge to readminister the substance to reduce the symptoms.
Route of Administration and Speed of Substance Effects
Routes of administration that produce more rapid and efficient absorption into the bloodstream
(e.g., intravenous, smoking, intranasal “snorting”) tend to result in a more intense intoxication
and an increased likelihood of an escalating pattern of substance use leading to withdrawal.
Similarly, rapidly acting substances are more likely than slower-acting substances to produce
immediate intoxication.
Duration of Effects
Within the same drug category, relatively short-acting substances tend to have a higher potential
for the development of withdrawal than do those with a longer duration of action. However,
longer-acting substances tend to have longer duration of withdrawal symptoms. The half-life of
the substance parallels aspects of withdrawal: the longer the duration of action, the longer the
time between cessation and the onset of withdrawal symptoms and the longer the withdrawal
duration. In general, the longer the acute withdrawal period, the less intense the syndrome tends
to be.
Use of Multiple Substances
Substance intoxication and withdrawal often involve several substances used simultaneously or
sequentially. In these cases, each diagnosis should be recorded separately.
Associated Laboratory Findings

Laboratory analyses of blood and urine samples can help determine recent use and the specific
substances involved. However, a positive laboratory test result does not by itself indicate that the
individual has a pattern of substance use that meets criteria for a substance-induced or substance
use disorder, and a negative test result does not by itself rule out a diagnosis.
Laboratory tests can be useful in identifying withdrawal. If the individual presents with
withdrawal from an unknown substance, laboratory tests may help identify the substance and
may also be helpful in differentiating withdrawal from other mental disorders. In addition,
normal functioning in the presence of high blood levels of a substance suggests considerable
tolerance.
Development and Course
Individuals ages 18–24 years have relatively high prevalence rates for the use of virtually every
substance. Intoxication is usually the initial substance-related disorder and often begins in the
teens. Withdrawal can occur at any age as long as the relevant drug has been taken in sufficient
doses over an extended period of time.
Recording Procedures for Substance Intoxication and Substance
Withdrawal
The clinician should use the code that applies to the class of substances but record the name of
the specific substance. For example, the clinician should record F13.230 secobarbital withdrawal
(rather than sedative, hypnotic, or anxiolytic withdrawal) or F15.120 methamphetamine
intoxication (rather than amphetamine-type substance intoxication). Note that
the appropriate ICD-10-CM diagnostic codes for substance intoxication and substance
withdrawal depend on whether there is a comorbid substance use disorder. In this case, the
F15.120 code for methamphetamine intoxication indicates the presence of a comorbid mild
methamphetamine use disorder. If there had been no comorbid methamphetamine use disorder
(and no perceptual disturbances), the diagnostic code would have been F15.920. See the coding
note for the substance-specific intoxication and withdrawal syndromes for the actual coding
options.
For substances that do not fit into any of the classes (e.g., anabolic steroids), the ICD-10-CM
code for other (or unknown) substance intoxication or other (or unknown) substance withdrawal
should be used and the specific substance indicated (e.g., F19.920 anabolic steroid intoxication).
If the substance taken by the individual is unknown, the same code (i.e., for the class “other [or
unknown] substance”) should be used (e.g., F19.920 unknown substance intoxication). If there
are symptoms or problems associated with a particular substance but criteria are not met for any
of the substance-specific disorders, the unspecified category can be used (e.g., F12.99
unspecified cannabis-related disorder).
As noted above, the substance-related codes in ICD-10-CM combine the substance use
disorder aspect of the clinical picture and the substance-induced aspect into a single combined
code. Thus, if both heroin withdrawal and moderate heroin use disorder are present, the single
code F11.23 for heroin withdrawal is given to cover both presentations. See the individual

substance-specific sections for additional coding information.
Substance/Medication-Induced Mental Disorders
The substance/medication-induced mental disorders are potentially severe, usually temporary,
but sometimes persisting CNS syndromes that develop in the context of the effects of substances
of abuse, medications, and some toxins. They are distinguished from the substance use disorders,
in which a cluster of cognitive, behavioral, and physiological symptoms contribute to the
continued use of a substance despite significant substance-related problems. The
substance/medication-induced mental disorders may be induced by any of the 10 classes of
substances that produce substance use disorders, or by a great variety of other medications used
in medical treatment. Each substance/medication-induced mental disorder is described in the
relevant chapter (e.g., substance/medication-induced depressive disorder is located in
“Depressive Disorders”), and therefore, only a brief description is offered here. All
substance/medication-induced disorders share common characteristics. It is important to
recognize these common features to aid in the detection of these disorders. These features are
described as follows:
A. A clinically significant presentation of symptoms characteristic of disorders in the relevant
diagnostic class predominates in the clinical picture.
B. There is evidence from the history, physical examination, or laboratory findings of both of
the following:
1. The symptoms in Criterion A developed during or soon after substance intoxication,
substance withdrawal, or exposure to or withdrawal from a medication; and
2. The involved substance/medication is capable of producing the symptoms in Criterion A.
C. The disturbance is not better explained by an independent mental disorder (i.e., one that is
not substance- or medication-induced). Such evidence of an independent mental disorder
could include the following:
1. The disturbance preceded the onset of severe intoxication or withdrawal or exposure to the
medication; or
2. The disturbance persisted for a substantial period of time (e.g., at least 1 month) after the
cessation of acute withdrawal or severe intoxication or taking the
medication. This criterion does not apply to substance-induced neurocognitive disorders
or hallucinogen persisting perception disorder, which persist beyond the cessation of acute
intoxication or withdrawal.
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social, occupational,
or other important areas of functioning.
Diagnostic and Associated Features

Some generalizations can be made regarding the categories of substances capable of producing
clinically relevant substance-induced mental disorders. In general, the more sedating drugs
(sedative, hypnotics, or anxiolytics, and alcohol) can produce prominent and clinically
significant depressive disorders during intoxication, while anxiety conditions are likely to be
observed during withdrawal syndromes from these substances. Also, during intoxication, the
more stimulating substances (e.g., amphetamines and cocaine) are likely to be associated with
substance-induced psychotic disorders and substance-induced anxiety disorders, and with
substance-induced major depressive episodes observed during withdrawal. Both the more
sedating and the more stimulating drugs are likely to produce significant but temporary sleep and
sexual disturbances. An overview of the relationship between specific categories of substances
and specific psychiatric syndromes is presented in Table 1.
The medication-induced conditions include what are often idiosyncratic CNS reactions or
relatively extreme examples of side effects for a wide range of medications taken for a variety of
medical concerns. These include neurocognitive complications of anesthetics, antihistamines,
antihypertensives, and a variety of other medications and toxins (e.g., organophosphates,
insecticides, carbon monoxide), as described in the chapter on neurocognitive disorders.
Psychotic syndromes may be temporarily experienced in the context of anticholinergic,
cardiovascular, and steroid drugs, as well as during use of stimulant-like and depressant-like
prescription or over-the-counter drugs. Temporary but severe mood disturbances can be observed
with a wide range of medications, including steroids, antihypertensives, disulfiram, and any
prescription or over-the-counter depressant or stimulant-like substances. A similar range of
medications can be associated with temporary anxiety syndromes, sexual dysfunctions, and
conditions of disturbed sleep.
In general, to be considered a substance/medication-induced mental disorder, there must be
evidence that the symptoms being observed are not likely to be better explained by an
independent mental disorder. The latter is more likely to be the case if the symptoms were
present before the severe intoxication or withdrawal or medication administration, or, with the
exception of several substance-induced persisting disorders listed in 1, continued more than 1
month after cessation of acute withdrawal, severe intoxication, or use of the medications. When
symptoms are only observed during a substance-induced delirium (e.g., alcohol withdrawal
delirium), only the delirium should be diagnosed, and other psychiatric symptoms occurring
during the delirium should not also be diagnosed separately, as many of these symptoms (e.g.,
disturbances in mood, anxiety, reality testing) are commonly seen during agitated, confused
states. The features associated with each relevant major mental disorder are similar whether
observed with independent or substance/medication-induced mental disorders. However,
individuals with substance/medication-induced mental disorders are likely to also demonstrate
the associated features seen with the specific category of substance or medication, as listed in
other subsections of this chapter.
Development and Course
Substance-induced mental disorders develop in the context of intoxication with or withdrawal
from substances of abuse, whereas medication-induced mental disorders can be seen with
prescribed or over-the-counter medications that are taken at the suggested doses.

552
Both conditions are usually temporary and likely to disappear within 1 month or so of cessation
of acute withdrawal, severe intoxication, or use of the medication. Exceptions to these
generalizations occur for certain long-duration substance-induced disorders: substance-associated
neurocognitive disorders that relate to conditions such as alcohol-induced neurocognitive
disorder, inhalant-induced neurocognitive disorder, and sedative-, hypnotic-, or anxiolyticinduced neurocognitive disorder; and hallucinogen persisting perception disorder (“flashbacks”;
see the section “Hallucinogen-Related Disorders” later in this chapter). However, most
substance/medication-induced mental disorders, regardless of the severity of the symptoms, are
likely to improve relatively quickly with abstinence and unlikely to remain clinically relevant for
more than 1 month after complete cessation of use.
As is true of many consequences of heavy substance use, some individuals are more and
others less prone toward developing specific substance-induced disorders. Similar types of
predispositions may make some individuals more likely to develop psychiatric side effects of
some types of medications, but not others. However, it is unclear whether individuals with
family histories or personal prior histories of independent psychiatric syndromes are more likely
to develop the induced syndrome once the consideration is made as to whether the quantity and
frequency of the substance were sufficient to lead to the development of a substance-induced
syndrome.
There are indications that the intake of substances of abuse or some medications with
psychiatric side effects in the context of a preexisting mental disorder is likely to result in an
intensification of the symptoms of the preexisting mental disorder. The risk for
substance/medication-induced mental disorders is likely to increase with both the quantity and
the frequency of consumption of the relevant substance.
The symptom profiles for the substance/medication-induced mental disorders resemble
independent mental disorders. While the symptoms of substance/medication-induced mental
disorders can be identical to those of independent mental disorders (e.g., delusions,
hallucinations, psychoses, major depressive episodes, anxiety syndromes), and although they can
have the same severe consequences (e.g., suicide), most induced mental disorders are likely to
improve in a matter of days to weeks of abstinence.
The substance/medication-induced mental disorders are an important part of the differential
diagnoses for the independent psychiatric conditions. The importance of recognizing an induced
mental disorder is similar to the relevance of identifying the possible role of some medical
conditions and medication reactions before diagnosing an independent mental disorder.
Symptoms of substance- and medication-induced mental disorders may be identical crosssectionally to those of independent mental disorders but have different treatments and prognoses
from the independent condition.
Functional Consequences of Substance/Medication-Induced Mental
Disorders
The same consequences related to the relevant independent mental disorder (e.g., suicide
attempts) are likely to apply to the substance/medication-induced mental disorders, but these are
likely to disappear within 1 month after abstinence. Similarly, the same functional consequences

associated with the relevant substance use disorder are likely to be seen for the substanceinduced mental disorders.
Recording Procedures for Substance/Medication-Induced Mental
Disorders
Diagnostic 
criteria, 
coding 
notes, 
and 
recording 
procedures 
for 
the 
specific
substance/medication-induced mental disorders are provided in chapters of the manual
corresponding with disorders of shared phenomenology (see the substance/medication-induced
mental disorders in these chapters: “Schizophrenia Spectrum and Other Psychotic Disorders,”
“Bipolar and Related Disorders,” “Depressive Disorders,” “Anxiety Disorders,” “ObsessiveCompulsive and Related Disorders,” “Sleep-Wake Disorders,” “Sexual Dysfunctions,” and
“Neurocognitive Disorders”). When recording a substance/medication-induced mental disorder
that is comorbid with a substance use disorder, only a single diagnosis is given that reflects both
the type of substance and the type of mental disorder induced by the substance, as well as the
severity of the comorbid substance use disorder (e.g., cocaine-induced psychotic disorder with
severe cocaine use disorder). For a substance-induced mental disorder occurring in the absence
of comorbid substance use disorder (e.g., when the disorder is induced by one-time use of a
substance or medication), only the substance/medication-induced mental disorder is recorded
(e.g., corticosteroid-induced depressive disorder). Additional information needed to record the
diagnostic name of the substance/medication-induced mental disorder is provided in the section
“Recording Procedures” for each substance/medication-induced mental disorder in its respective
chapter.
Alcohol-Related Disorders
Alcohol Use Disorder
Alcohol Intoxication
Alcohol Withdrawal
Alcohol-Induced Mental Disorders
Unspecified Alcohol-Related Disorder
Alcohol Use Disorder
Diagnostic Criteria
A. A problematic pattern of alcohol use leading to clinically significant impairment or

distress, as manifested by at least two of the following, occurring within a 12month period:
1. Alcohol is often taken in larger amounts or over a longer period than was
intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control
alcohol use.
3. A great deal of time is spent in activities necessary to obtain alcohol, use
alcohol, or recover from its effects.
4. Craving, or a strong desire or urge to use alcohol.
5. Recurrent alcohol use resulting in a failure to fulfill major role obligations at
work, school, or home.
6. Continued alcohol use despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of alcohol.
7. Important social, occupational, or recreational activities are given up or
reduced because of alcohol use.
8. Recurrent alcohol use in situations in which it is physically hazardous.
9. Alcohol use is continued despite knowledge of having a persistent or
recurrent physical or psychological problem that is likely to have been caused
or exacerbated by alcohol.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of alcohol to achieve intoxication
or desired effect.
b. A markedly diminished effect with continued use of the same amount of
alcohol.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for alcohol (refer to Criteria A and
B of the criteria set for alcohol withdrawal).
b. Alcohol (or a closely related substance, such as a benzodiazepine) is
taken to relieve or avoid withdrawal symptoms.
Specify if:
In early remission: After full criteria for alcohol use disorder were previously
met, none of the criteria for alcohol use disorder have been met for at least 3
months but for less than 12 months (with the exception that Criterion A4,
“Craving, or a strong desire or urge to use alcohol,” may be met).
In sustained remission: After full criteria for alcohol use disorder were
previously met, none of the criteria for alcohol use disorder have been met at
any time during a period of 12 months or longer (with the exception that Criterion
A4, “Craving, or a strong desire or urge to use alcohol,” may be met).

Specify if:
In a controlled environment: This additional specifier is used if the individual is
in an environment where access to alcohol is restricted.
Code based on current severity/remission: If an alcohol intoxication, alcohol
withdrawal, or another alcohol-induced mental disorder is also present, do not use
the codes below for alcohol use disorder. Instead, the comorbid alcohol use disorder
is indicated in the 4th character of the alcohol-induced disorder code (see the coding
note for alcohol intoxication, alcohol withdrawal, or a specific alcohol-induced mental
disorder). For example, if there is comorbid alcohol intoxication and alcohol use
disorder, only the alcohol intoxication code is given, with the 4th character indicating
whether the comorbid alcohol use disorder is mild, moderate, or severe: F10.129 for
mild alcohol use disorder with alcohol intoxication or F10.229 for a moderate or
severe alcohol use disorder with alcohol intoxication.
Specify current severity/remission:
F10.10 Mild: Presence of 2–3 symptoms.
F10.11 Mild, In early remission
F10.11 Mild, In sustained remission
F10.20 Moderate: Presence of 4–5 symptoms.
F10.21 Moderate, In early remission
F10.21 Moderate, In sustained remission
F10.20 Severe: Presence of 6 or more symptoms.
F10.21 Severe, In early remission
F10.21 Severe, In sustained remission
Specifiers
“In a controlled environment” applies as a further specifier of remission if the individual is both
in remission and in a controlled environment (i.e., in early remission in a controlled environment
or in sustained remission in a controlled environment). Examples of these environments are
closely supervised and substance-free jails, therapeutic communities, and locked hospital units.
Severity of the disorder is based on the number of diagnostic criteria endorsed. For a given
individual, changes in severity of alcohol use disorder across time are also reflected by
reductions in the frequency (e.g., days of use per month) or dose (e.g., number of standard drinks
consumed per day) of alcohol used, as assessed by the individual’s self-report, report of
knowledgeable others, clinician observations, and, when practical, biological testing (e.g.,
elevations in blood tests as described in the section “Diagnostic Markers” for this disorder).
Diagnostic Features
Alcohol use disorder is defined by a cluster of behavioral and physical symptoms, such as
withdrawal, tolerance, and craving. Alcohol withdrawal is characterized by withdrawal

symptoms that develop approximately 4–12 hours after the reduction of intake following
prolonged, heavy alcohol ingestion. Because withdrawal from alcohol can be unpleasant and
intense, individuals may continue to consume alcohol despite adverse consequences, often to
avoid or to relieve withdrawal symptoms. Some withdrawal symptoms (e.g., sleep problems) can
persist at lower intensities for months and can contribute to relapse. Once a pattern of repetitive
and intense use develops, individuals with alcohol use disorder may devote substantial periods of
their time to obtaining and consuming alcoholic beverages.
Craving for alcohol is indicated by a strong desire to drink that makes it difficult to think of
anything else and that often results in the onset of drinking. School and job performance may
also suffer either from the aftereffects of drinking or from actual intoxication at school or on the
job; child care or household responsibilities may be neglected; and alcohol-related absences may
occur from school or work. The individual may use alcohol in physically hazardous
circumstances (e.g., driving an automobile, swimming, operating machinery while intoxicated).
Finally, individuals with an alcohol use disorder may continue to consume alcohol despite the
knowledge that continued consumption poses significant physical (e.g., blackouts, liver disease),
psychological (e.g., depression), social, or interpersonal problems (e.g., violent arguments with
spouse while intoxicated, child abuse).
Associated Features
Alcohol use disorder is often associated with problems similar to those associated with other
substances (e.g., cannabis; cocaine; heroin; amphetamines; sedatives, hypnotics, or anxiolytics).
Alcohol may be used to alleviate the unwanted effects of these other substances or to substitute
for them when they are not available. Symptoms of conduct problems, depression, anxiety, and
insomnia frequently accompany heavy drinking and sometimes precede it.
Repeated intake of high doses of alcohol can affect nearly every organ system, especially the
gastrointestinal tract, cardiovascular system, and the central and peripheral nervous systems.
Gastrointestinal effects include gastritis, stomach or duodenal ulcers, and, in about 15% of
individuals who use alcohol heavily, liver cirrhosis and/or pancreatitis. There is also an increased
rate of cancer of the esophagus, stomach, and other parts of the gastrointestinal tract. One of the
most commonly associated conditions is low-grade hypertension. Cardiomyopathy and other
myopathies are less common but occur at an increased rate among those who drink very heavily.
These factors, along with marked
increases in levels of triglycerides and low-density lipoprotein cholesterol, contribute to an
elevated risk of heart disease. Peripheral neuropathy may be evidenced by muscular weakness,
paresthesias, and decreased peripheral sensation. More persistent central nervous system effects
include cognitive deficits, such as severe memory impairment and degenerative changes in the
cerebellum. These effects are related to the direct effects of alcohol, trauma, or vitamin
deficiencies (particularly of the B vitamins, including thiamine). One devastating central nervous
system effect is the relatively rare alcohol-induced persisting amnestic disorder, or WernickeKorsakoff syndrome, in which the ability to encode new memory is severely impaired. This
condition would now be described within the chapter “Neurocognitive Disorders” and would be

termed a substance/medication-induced neurocognitive disorder.
Alcohol use disorder is an important contributor to suicide risk during severe intoxication
and in the context of a temporary alcohol-induced depressive or bipolar disorder. There is an
increased rate of suicidal behavior as well as of suicide among individuals with the disorder.
Prevalence
Alcohol use disorder is common. In the United States, lifetime prevalence rates of DSM-5
alcohol use disorder among adults were estimated to be 29.1% overall with severity specified as
follows: 8.6% mild, 6.6% moderate, and 13.9% severe. Among Australian adults, the estimated
lifetime prevalence of DSM-5 alcohol use disorder was 31.0%.
Rates of disorder vary by gender and age. In the United States, rates were greater among men
(36.0% lifetime prevalence) than among women (22.7%). Twelve-month prevalence of DSM-IV
alcohol use disorders in the United States was 4.6% among individuals ages 12–17 years, 16.2%
among individuals ages 18–29 years, and 1.5% among individuals 65 years and older.
Twelve-month prevalence of alcohol use disorders varies across U.S. ethnoracial groups as
well. For individuals ages 12–17 years, prevalence of DSM-IV alcohol use disorders was
greatest among Native Americans (2.8%) and non-Latinx Whites (2.2%), relative to Asian
Americans (1.6%), individuals reporting two or more racialized backgrounds (1.6%), Hispanics
(1.5%), and African Americans (0.8%). Among adults, data from a large U.S. population-based
study indicated that the 12-month prevalence of DSM-5 alcohol use disorder was 14.4% in
African Americans, 14.0% in non-Hispanic Whites, 13.6% in Hispanics, and 10.6% in Asian
Americans and Pacific Islanders. Data from a large community-based survey of Native
Americans from Southwestern and Northern Plains tribal nations showed that the 12-month
prevalence of DSM-IV alcohol abuse and dependence ranged from 4.1% to 9.8%. There is
extensive diversity in the rates and patterns of alcohol abuse and dependence across the more
than 570 American Indian and Alaska Native communities in the United States, as well as high
rates of abstinence from alcohol use in some of these communities. Historical experiences of
dispossession and subjugation and ongoing discrimination have been associated with increased
risk of symptom onset. Given the diversity of tribal communities, prevalence estimates for
alcohol use disorder among Native Americans should be interpreted with caution.
Development and Course
The first episode of alcohol intoxication is likely to occur during the mid-teens. Alcohol-related
problems that do not meet full criteria for a use disorder or isolated problems may occur before
age 20 years, but the age at onset of an alcohol use disorder with two or more of the criteria
clustered together peaks in the late teens or early to mid 20s. The large majority of individuals
who develop alcohol-related disorders do so by their late 30s. The first evidence of withdrawal is
not likely to appear until after many other aspects of an alcohol use disorder have developed. An
earlier onset of alcohol use disorder is observed in adolescents with preexisting conduct
problems and those with an earlier onset of intoxication.
Alcohol use disorder has a variable course that is characterized by periods of remission and

Environmental.
Genetic and physiological.
relapse. A decision to stop drinking, often in response to a crisis, is likely to be followed by a
period of weeks or more of abstinence, which is often followed by limited periods of controlled
or nonproblematic drinking. However, once alcohol intake resumes, it is highly likely that
consumption will rapidly escalate and that severe problems will once again develop.
Alcohol use disorder is often erroneously perceived as an intractable condition, perhaps
based on the fact that individuals who present for treatment typically have a history of many
years of severe alcohol-related problems. However, these most severe cases represent only a
minority of individuals with this disorder, and the typical individual with the disorder has a much
more promising prognosis.
Among adolescents, conduct disorder and repeated antisocial behavior often co-occur with
alcohol- and with other substance-related disorders. While most individuals with alcohol use
disorder develop the condition before age 40 years, perhaps 10% have later onset, as suggested
by a prospective study in California. Age-related physical changes in older individuals result in
increased brain susceptibility to the depressant effects of alcohol; decreased rates of liver
metabolism of a variety of substances, including alcohol; and decreased percentages of body
water. These changes can cause older people to develop more severe intoxication and subsequent
problems at lower levels of consumption. Alcohol-related problems in older people are also
especially likely to be associated with other medical complications.
Risk and Prognostic Factors
Environmental risk and prognostic factors may include poverty and
discrimination (including structural inequities such as differential incarceration rates and
differential access to medications for addiction treatment), unemployment and low levels of
education, cultural attitudes toward drinking and intoxication, the availability of alcohol
(including price), acquired personal experiences with alcohol, and stress levels. Additional
potential mediators of how alcohol problems develop in predisposed individuals include heavier
peer substance use, exaggerated positive expectations of the effects of alcohol, and suboptimal
ways of coping with stress.
Alcohol use disorder runs in families, with 40%–60% of the variance of
risk explained by genetic influences. The rate of this condition is three to four times higher in
close relatives of individuals with alcohol use disorder, with values highest for individuals with a
greater number of affected relatives, closer genetic relationships to the affected individual, and
higher severity of the alcohol-related problems in those relatives. A significantly higher rate of
alcohol use disorder exists in the monozygotic twin than in the dizygotic twin of an individual
with the condition. A three- to fourfold increase in risk has been observed in children of
individuals with alcohol use disorder, even when these children were given up for adoption at
birth and raised by adoptive parents who did not have the disorder.
Advances in understanding the genes that operate through intermediate characteristics (or
phenotypes) to affect the risk of alcohol use disorder can help to identify individuals who might
be at particularly low or high risk for alcohol use disorder. Among the low-risk phenotypes is the
acute alcohol-related skin flush (seen more commonly in persons of Asian descent). High
vulnerability is associated with preexisting schizophrenia or bipolar disorder, as well as
impulsivity (producing enhanced rates of all substance use disorders and gambling disorder), and
a high risk specifically for alcohol use disorder is associated with a low level of response (low

Course modifiers.
sensitivity) to alcohol. A number of gene variations may account for low response to alcohol or
modulate the dopamine reward systems; however, any single gene variant is likely to explain
only 1%–2% of the risk for these disorders. Gene-environment interactions modulate the impact
of genetic variations; for
example, genetic effects on alcohol use are more pronounced when social constraints are
minimized (e.g., low parental monitoring) or when the environment permits easy access to
alcohol or encourages its use (e.g., high peer deviance).
In general, high levels of impulsivity are associated with an earlier onset and
more severe alcohol use disorder.
Culture-Related Diagnostic Issues
In most cultures, alcohol is the most frequently used intoxicating substance and contributes to
considerable morbidity and mortality. Globally, 2.8 million deaths were attributed to alcohol use,
which corresponds to 2.2% of total age-standardized deaths among women and 6.8% among
men. Globally, an estimated 237 million men and 46 million women have alcohol use disorder,
with the highest prevalence being among men and women in the European Region (14.8% and
3.5%) and the Region of the Americas (11.5% and 5.1%); in general, high-income countries have
the highest prevalence. Greater acculturation to U.S. society among immigrants is associated
with rising prevalence of alcohol use disorder, especially among women. Ethnic density (greater
proportion of people from the same background) may decrease the risk of alcohol use disorder
because of greater social support and buffering against the effects of discrimination. However,
neighborhood segregation may increase the risk for disorders because of the association with
other risk factors, such as higher concentration of alcohol advertising and retail outlets in lowincome areas.
Genetic polymorphisms for the alcohol-metabolizing enzymes alcohol dehydrogenase and
aldehyde dehydrogenase may affect the response to alcohol. When consuming alcohol,
individuals with certain polymorphisms can experience a flushed face and palpitations, reactions
that can be so severe as to limit or preclude future alcohol consumption and diminish the risk for
alcohol use disorder. For example, these gene variations are seen in as many as 40% of Japanese,
Chinese, and Korean individuals and are related to lower risks for the disorder. However, this
protective effect may be modulated by sociocultural factors, as shown by rising prevalence of
alcohol use disorder in Japan, China, and South Korea over the last decades associated with
increasing westernization and changing cultural attitudes about women’s drinking.
Despite small variations regarding individual criterion items, the diagnostic criteria perform
equally well across most race/ethnicity groups.
Sex- and Gender-Related Diagnostic Issues
Men have higher rates of drinking and alcohol use disorder than women, although the gender gap
is narrowing as women are initiating alcohol use at a younger age. Because females generally
weigh less than males, have more fat and less water in their bodies, and metabolize less alcohol
in their esophagus and stomach, they are likely to develop higher blood alcohol levels per drink

than males. Females who drink heavily may also be more vulnerable than males to some of the
physical consequences associated with alcohol, including alcohol-related blackouts and liver
disease. Additionally, while genetic-related mechanisms for alcohol risk overlap for males and
females, the specific environmental components that add to the risk may differ across sexes,
especially during adolescence. Drinking during pregnancy, which tends to decrease overall, may
be a sign of an alcohol use disorder.
Diagnostic Markers
Individuals whose heavier drinking places them at elevated risk for alcohol use disorder can be
identified both through standardized questionnaires and by elevations in blood test results likely
to be seen with regular heavier drinking. These measures do not establish a diagnosis of an
alcohol-related disorder but can be useful in highlighting individuals for
whom more information should be gathered. The most direct test available to measure alcohol
consumption cross-sectionally is blood alcohol concentration, which can also be used to judge
tolerance to alcohol. For example, an individual with a concentration of 150 mg of ethanol per
deciliter (dL) of blood who does not show signs of intoxication can be presumed to have
acquired at least some degree of tolerance to alcohol. At 200 mg/dL, most nontolerant
individuals demonstrate severe intoxication.
Regarding laboratory tests, one sensitive laboratory indicator of heavy drinking is a modest
elevation or high-normal levels (>35 units) of gamma-glutamyltransferase (GGT). This may be
the only laboratory finding. At least 70% of individuals with a high GGT level are persistent
heavy drinkers (i.e., consuming eight or more drinks daily on a regular basis). A second test with
comparable or even higher levels of sensitivity and specificity is carbohydrate-deficient
transferrin (CDT), with levels of 20 units or higher useful in identifying individuals who
regularly consume eight or more drinks daily. Given that both GGT and CDT levels return
toward normal within days to weeks of stopping drinking, both state markers may be useful in
monitoring abstinence, especially when the clinician observes increases, rather than decreases, in
these values over time—a finding indicating that the individual is likely to have returned to
heavy drinking. The combination of tests for CDT and GGT may have even higher levels of
sensitivity and specificity than either test used alone. Additional useful tests include the mean
corpuscular volume (MCV), which may be elevated to high-normal values in individuals who
drink heavily—a change that is due to the direct toxic effects of alcohol on erythropoiesis.
Although the MCV can be used to help identify those who drink heavily, it is a poor method of
monitoring abstinence because of the long half-life of red blood cells. Liver function tests (e.g.,
alanine aminotransferase and alkaline phosphatase) can reveal liver injury that is a consequence
of heavy drinking. Other potential markers of heavy drinking that are more nonspecific for
alcohol but can help the clinician think of the possible effects of alcohol include elevations in
blood levels or lipids (e.g., triglycerides and high-density lipoprotein cholesterol) and highnormal levels of uric acid.
Additional diagnostic markers relate to signs and symptoms that reflect the consequences
often associated with persistent heavy drinking. For example, dyspepsia, nausea, and bloating

can accompany gastritis, and hepatomegaly, esophageal varices, and hemorrhoids may reflect
alcohol-induced changes in the liver. Other physical signs of heavy drinking include tremor,
unsteady gait, insomnia, and erectile dysfunction. Males with chronic alcohol use disorder may
exhibit decreased testicular size and feminizing effects associated with reduced testosterone
levels. Repeated heavy drinking in females is associated with menstrual irregularities and, during
pregnancy, spontaneous abortion and fetal alcohol syndrome. Individuals with preexisting
histories of epilepsy or severe head trauma are more likely to develop alcohol-related seizures.
Alcohol withdrawal may be associated with nausea, vomiting, gastritis, hematemesis, dry mouth,
puffy blotchy complexion, and mild peripheral edema.
Association With Suicidal Thoughts or Behavior
Most studies on suicidality and alcohol address alcohol consumption rather than alcohol use
disorder. However, a psychological autopsy study in Australia found that aggression, psychiatric
comorbidity, and recent interpersonal conflicts are suicide risk factors in individuals with alcohol
use disorder. A review of studies from 1999 through 2014 conducted in several countries,
including the United States, reported that both intoxication and chronic heavy alcohol use are
associated with suicide, extensive population-level data link alcohol with suicide, and there is
evidence suggesting that restrictive alcohol policies may help prevent suicide on a general
population level. A meta-analysis of studies conducted in the United States and several other
countries from 1996 through 2015 found that compared with nondrinking individuals, the acute
use of alcohol was associated with a nearly
sevenfold increase in risk of suicide attempt. Moreover, in this meta-analysis, as well as in U.S.-
based case-control crossover studies, heavier alcohol use within 24 hours was a much more
potent risk factor for suicide attempt than lower alcohol use. In a cohort of patients in
Mississippi, acute co-use of alcohol and sedatives had an even stronger association with suicide
attempt compared with alcohol use alone. A systematic review and meta-analysis of studies from
1975 through 2014 in several countries, including the United States, found that alcohol use is
associated with possession of firearms, that alcohol drinkers are four to six times more likely to
die by suicide with a gun than nondrinkers, and that heavy drinkers are more likely to choose
firearms over other suicide methods compared with nondrinkers.
Functional Consequences of Alcohol Use Disorder
The diagnostic features of alcohol use disorder highlight major areas of life functioning likely to
be impaired. These include driving and operating machinery, school and work, interpersonal
relationships and communication, and health. Alcohol-related disorders contribute to
absenteeism from work, job-related accidents, and low employee productivity. Rates are elevated
in homeless individuals, perhaps reflecting a downward spiral in social and occupational
functioning, although most individuals with alcohol use disorder continue to live with their
families and function within their jobs.
Alcohol use disorder is associated with a significant increase in the risk of accidents,
violence, and suicide. It is estimated that one in five intensive care unit admissions in some urban

Nonpathological use of alcohol.
Alcohol intoxication, alcohol withdrawal, and alcohol-induced mental disorders.
Sedative, hypnotic, or anxiolytic use disorder.
Conduct disorder in childhood and antisocial personality disorder.
hospitals is related to alcohol and that 40% of individuals in the United States experience an
alcohol-related adverse event at some time in their lives, with alcohol accounting for up to 55%
of fatal driving events. Severe alcohol use disorder, especially in individuals with antisocial
personality disorder, is associated with the commission of criminal acts, including homicide.
Severe problematic alcohol use also contributes to disinhibition and feelings of sadness and
irritability, which contribute to suicide attempts and suicide.
Unanticipated alcohol withdrawal in hospitalized individuals for whom a diagnosis of
alcohol use disorder has been overlooked can add to the risks and costs of hospitalization and to
time spent in the hospital.
Differential Diagnosis
The key element of alcohol use disorder is the use of heavy doses
of alcohol with resulting repeated and significant distress or impaired functioning. While most
drinkers sometimes consume enough alcohol to feel intoxicated, only a minority (< 20%) ever
develop alcohol use disorder. Therefore, drinking, even daily, in low doses and occasional
intoxication do not by themselves make this diagnosis.
Alcohol use disorder is
differentiated from alcohol intoxication, alcohol withdrawal, and alcohol induced mental
disorders (e.g., alcohol-induced depressive disorder) in that alcohol use disorder describes a
problematic pattern of alcohol use that involves impaired control over alcohol use, social
impairment due to alcohol use, risky alcohol use (e.g., driving while intoxicated), and
pharmacological symptoms (the development of tolerance or withdrawal), whereas alcohol
intoxication, alcohol withdrawal, and alcohol-induced mental disorders describe psychiatric
syndromes that develop in the context of heavy use. Alcohol intoxication, alcohol withdrawal,
and alcohol-induced mental disorders occur frequently in individuals with alcohol use disorder.
In such cases, a diagnosis of alcohol intoxication, alcohol withdrawal, or an alcohol-induced
mental disorder should be given in addition to
a diagnosis of alcohol use disorder, the presence of which is indicated in the diagnostic code.
The signs and symptoms of alcohol use disorder are
similar to those seen in sedative, hypnotic, or anxiolytic use disorder. The two must be
distinguished, however, because the course may be different, especially in relation to medical
problems.
Alcohol use disorder, along with
other substance use disorders, is seen in the majority of individuals with antisocial personality
disorder and preexisting conduct disorder. Because these diagnoses are associated with an early
onset of alcohol use disorder as well as a worse prognosis, it is important to establish both
conditions.
Comorbidity
Bipolar disorders, schizophrenia, and antisocial personality disorder are associated with alcohol

use disorder, and most anxiety and depressive disorders are associated with alcohol use disorder
as well. At least a part of the reported association between depression and moderate to severe
alcohol use disorder may be attributable to temporary, alcohol-induced comorbid depressive
symptoms resulting from the acute effects of intoxication or withdrawal, although this point has
long been debated. Severe, repeated alcohol intoxication may also suppress immune mechanisms
and predispose individuals to infections and increase the risk for cancers.
Alcohol Intoxication
Diagnostic Criteria
A. Recent ingestion of alcohol.
B. Clinically significant problematic behavioral or psychological changes (e.g.,
inappropriate sexual or aggressive behavior, mood lability, impaired judgment)
that developed during, or shortly after, alcohol ingestion.
C. One (or more) of the following signs or symptoms developing during, or shortly
after, alcohol use:
1. Slurred speech.
2. Incoordination.
3. Unsteady gait.
4. Nystagmus.
5. Impairment in attention or memory.
6. Stupor or coma.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication with
another substance.
Coding note: The ICD-10-CM code depends on whether there is a comorbid alcohol
use disorder. If a mild alcohol use disorder is comorbid, the ICD-10-CM code is
F10.120, and if a moderate or severe alcohol use disorder is comorbid, the ICD-10CM code is F10.220. If there is no comorbid alcohol use disorder, then the ICD-10CM code is F10.920.
Diagnostic Features
The essential feature of alcohol intoxication is the presence of clinically significant and
sometimes life-threatening problematic behavioral or psychological changes (e.g., inappropriate
sexual or aggressive behavior, mood lability, impaired judgment and decision-making,
difficulties with complex tasks such as driving, and impaired social or occupational functioning)
that develop during, or shortly after, alcohol ingestion (Criterion B). These changes are

accompanied by evidence of impaired functioning and judgment and, if intoxication is intense,
can result in a life-threatening coma. The symptoms must not be attributable to another medical
condition (e.g., diabetic ketoacidosis), are not a reflection of conditions such as delirium, and are
not related to intoxication with other depressant drugs (e.g., benzodiazepines) (Criterion D). The
levels of incoordination can interfere with driving abilities and performance of usual activities to
the point of causing vehicle crashes or other events resulting in injury. Evidence of alcohol use
can be obtained by smelling alcohol on the individual’s breath, eliciting a history from the
individual or another observer, and, when needed, having the individual provide breath, blood, or
urine samples for toxicology analyses.
Associated Features
Signs and symptoms of intoxication are likely to be more intense when the blood alcohol level is
rising than when it is falling. The duration of intoxication depends on how much alcohol was
consumed over what period of time. In general, the body is able to metabolize approximately one
drink per hour, so that the blood alcohol level generally decreases at a rate of 15–20 mg/dL per
hour.
During even mild alcohol intoxication, different symptoms are likely to be observed at
different time points. Evidence of mild intoxication with alcohol can be seen in most individuals
after approximately two drinks (each standard drink is approximately 10–12 grams of ethanol
and raises the blood alcohol concentration approximately 20 mg/dL). Early in the drinking
period, when blood alcohol levels are rising, symptoms often reflect stimulation (e.g.,
talkativeness, a sensation of well-being, a bright, expansive mood). Later, especially when blood
alcohol levels are falling, the individual is likely to become progressively more depressed,
withdrawn, and cognitively impaired.
Alcohol intoxication is sometimes associated with amnesia for the events that occurred
during the course of the intoxication (“blackouts”). This phenomenon is related to a relatively
high blood alcohol level and, perhaps, to the rapidity with which this level is reached. Acute
alcohol intoxication may cause metabolic alterations (e.g., hypoglycemia, electrolyte
disturbances) and may have severe cardiovascular, respiratory, and/or gastrointestinal effects. At
very high blood alcohol levels (e.g., 200–300 mg/dL), an individual who has not developed
tolerance for alcohol is likely to fall asleep and enter a first stage of anesthesia. Higher blood
alcohol levels (e.g., in excess of 300–400 mg/dL) can cause inhibition of respiration and pulse
and even death in nontolerant individuals.
Alcohol intoxication is an important contributor to interpersonal violence and suicidal
behavior. Among individuals intoxicated by alcohol, there appears to be an increased rate of
accidental injury (including death due to behaviors associated with altered judgment, self-harm,
and violence), suicidal behavior, and suicide.
Prevalence
The large majority of alcohol consumers are likely to have been intoxicated to some degree at
some point in their lives. For example, in 2018, 43% of 12th-grade students in the United States
reported having “been drunk” at least once in their lifetime, and 17.5% of them reported that they
had gotten drunk at least once in the prior 30 days. Using a definition of intoxication of four or
more standard drinks on any day for women and five or more

563
standard drinks on any day for men, the 12-month prevalence of high-risk drinking in U.S. adults
is 17.4% for Native Americans, 15.1% for African Americans, 13.5% for Latinx, 12.3% for nonLatinx Whites, and 7.2% for Asians and Pacific Islanders.
Development and Course
Intoxication usually occurs as an episode developing over minutes to hours and typically lasting
several hours. In the United States, the average age at first intoxication is approximately 15
years, with the highest prevalence at approximately 18–25 years. Frequency and intensity usually
decrease with further advancing age. The earlier the onset of regular intoxication, the greater the
likelihood the individual will go on to develop alcohol use disorder.
Risk and Prognostic Factors
Temperamental.
Episodes of alcohol intoxication increase with personality characteristics of sensation seeking
and impulsivity.
Environmental.
Episodes of alcohol intoxication increase with having heavy-drinking peers, holding beliefs that
heavy drinking is an important component of having fun, and using alcohol to cope with stress.
Culture-Related Diagnostic Issues
The major issues parallel the cultural differences regarding the use of alcohol overall. For
example, some college fraternities and sororities encourage alcohol intoxication. This condition
is also frequent on certain dates of cultural significance (e.g., New Year’s Eve) and, for some
subgroups, during specific events (e.g., wakes following funerals). Other subgroups encourage
drinking at religious celebrations (e.g., Jewish and Catholic holidays), while still others strongly
discourage all drinking or intoxication (e.g., some religious groups, such as Mormons,
fundamentalist Christians, and Muslims).
Sex- and Gender-Related Diagnostic Issues
Historically, in many Western societies, acceptance of drinking and drunkenness is more
tolerated for men, but such gender differences may be much less prominent in recent years,
especially during adolescence and young adulthood. In general, women are less tolerant of the
same amount of alcohol than men.
Diagnostic Markers
Intoxication is usually established by observing an individual’s behavior and smelling alcohol on
the breath. The degree of intoxication increases with an individual’s blood or breath alcohol level
and with the ingestion of other substances, especially those with sedating effects.

Other medical conditions.
Alcohol-induced mental disorders.
Sedative, hypnotic, or anxiolytic intoxication.
Association With Suicidal Thoughts or Behavior
A collaborative, international study in emergency departments in 17 countries found that acute
alcohol use, independent of chronic use, increases the risk of suicide attempt, with each drink
raising the risk by 30%. For more information, see “Association With Suicidal Thoughts or
Behavior” in the Alcohol Use Disorder section.
Functional Consequences of Alcohol Intoxication
Alcohol intoxication contributed to the more than 95,000 deaths and 2.8 million years of
potential life lost each year in the United States from 2011 through 2015, shortening the
lives of those who died by an average of 30 years. In addition, intoxication with this drug
contributes to huge costs associated with drunk driving and lost time from school or work, as
well as interpersonal arguments and physical fights.
Differential Diagnosis
Several medical (e.g., diabetic acidosis) and neurological conditions
(e.g., cerebellar ataxia, multiple sclerosis) can temporarily resemble alcohol intoxication.
Alcohol intoxication is distinguished from alcohol-induced
mental disorders (e.g., alcohol-induced depressive disorder, with onset during intoxication)
because the symptoms (e.g., depressed mood) in these latter disorders are in excess of those
usually associated with alcohol intoxication, predominate in the clinical presentation, and are
severe enough to warrant clinical attention.
Intoxication with sedative, hypnotic, or anxiolytic
drugs or with other sedating substances (e.g., antihistamines, anticholinergic drugs) can be
mistaken for alcohol intoxication. The differential requires observing alcohol on the breath,
measuring blood or breath alcohol levels, ordering a medical workup, and gathering a good
history. The signs and symptoms of sedative-hypnotic intoxication are very similar to those
observed with alcohol and include similar problematic behavioral or psychological changes.
These changes are accompanied by evidence of impaired functioning and judgment—which, if
intense, can result in a life-threatening coma—and levels of incoordination that can interfere with
driving abilities and with performing usual activities. However, there is no smell as there is with
alcohol, but there is likely to be evidence of misuse of the depressant drug in the blood or urine
toxicology analyses.
Comorbidity
Alcohol intoxication may occur comorbidly with other substance intoxication, especially in
individuals with conduct disorder or antisocial personality disorder. Given the typical overlap of
alcohol intoxication with alcohol use disorder, see “Comorbidity” under Alcohol Use Disorder
for more details about co-occurring conditions that are likely to be encountered.

Alcohol Withdrawal
Diagnostic Criteria
A. Cessation of (or reduction in) alcohol use that has been heavy and prolonged.
B. Two (or more) of the following, developing within several hours to a few days
after the cessation of (or reduction in) alcohol use described in Criterion A:
1. Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 bpm).
2. Increased hand tremor.
3. Insomnia.
4. Nausea or vomiting.
5. Transient visual, tactile, or auditory hallucinations or illusions.
6. Psychomotor agitation.
7. Anxiety.
8. Generalized tonic-clonic seizures.
C. The signs or symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication or
withdrawal from another substance.
Specify if:
With perceptual disturbances: This specifier applies in the rare instance when
hallucinations (usually visual or tactile) occur with intact reality testing, or
auditory, visual, or tactile illusions occur in the absence of a delirium.
Coding note: The ICD-10-CM code depends on whether or not there is a comorbid
alcohol use disorder and whether or not there are perceptual disturbances.
For alcohol withdrawal, without perceptual disturbances: If a mild alcohol
use disorder is comorbid, the ICD-10-CM code is F10.130, and if a moderate or
severe alcohol use disorder is comorbid, the ICD-10-CM code is F10.230. If
there is no comorbid alcohol use disorder, then the ICD-10-CM code is F10.930.
For alcohol withdrawal, with perceptual disturbances: If a mild alcohol use
disorder is comorbid, the ICD-10-CM code is F10.132, and if a moderate or
severe alcohol use disorder is comorbid, the ICD-10-CM code is F10.232. If
there is no comorbid alcohol use disorder, then the ICD-10-CM code is F10.932.
Specifiers

When hallucinations occur in the absence of delirium (i.e., in a clear sensorium), a diagnosis of
substance/medication-induced psychotic disorder should be considered.
Diagnostic Features
The essential feature of alcohol withdrawal is the presence of a characteristic withdrawal
syndrome that develops within several hours to a few days after the cessation of (or reduction in)
heavy and prolonged alcohol use (Criteria A and B). The withdrawal syndrome includes two or
more of the symptoms reflecting autonomic hyperactivity and anxiety listed in Criterion B, along
with gastrointestinal symptoms.
Withdrawal symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning (Criterion C). The symptoms must not be
attributable to another medical condition and are not better explained by another mental disorder
(e.g., generalized anxiety disorder), including intoxication or withdrawal from another substance
(e.g., sedative, hypnotic, or anxiolytic withdrawal) (Criterion D).
Symptoms can be relieved by administering alcohol or benzodiazepines (e.g., diazepam). The
withdrawal symptoms typically begin when blood concentrations of alcohol decline sharply (i.e.,
within 4–12 hours) after alcohol use has been stopped or reduced. Reflecting the relatively fast
metabolism of alcohol, symptoms of alcohol withdrawal usually peak in intensity during the
second day of abstinence and are likely to improve markedly by the fourth or fifth day.
Following acute withdrawal, however, symptoms of anxiety, insomnia, and autonomic
dysfunction may persist for up to 3–6 months at lower levels of intensity.
Fewer than 10% of individuals who develop alcohol withdrawal will ever develop dramatic
symptoms (e.g., severe autonomic hyperactivity, tremors, alcohol withdrawal delirium). Tonicclonic seizures occur in fewer than 3% of individuals.
Associated Features
Although confusion and changes in consciousness are not core criteria for alcohol withdrawal,
alcohol withdrawal delirium (see “Delirium” in the chapter “Neurocognitive Disorders”) may
occur in the context of withdrawal. As is true for any agitated, confused state, regardless of the
cause, in addition to a disturbance of consciousness and cognition, withdrawal delirium can
include visual, tactile, or (rarely) auditory hallucinations
(delirium tremens). When alcohol withdrawal delirium develops, it is likely that a clinically
relevant medical condition may be present (e.g., liver failure, pneumonia, gastrointestinal
bleeding, sequelae of head trauma, hypoglycemia, an electrolyte imbalance, postoperative
status).
Prevalence
It is estimated that approximately 50% of middle-class, highly functional individuals with
alcohol use disorder in the United States have ever experienced a full alcohol withdrawal
syndrome. Among individuals with alcohol use disorder who are hospitalized or homeless, the
rate of alcohol withdrawal may be greater than 80%. Less than 10% of individuals in withdrawal

Environmental.
Other medical conditions.
ever demonstrate alcohol withdrawal delirium or withdrawal seizures. The prevalence of alcohol
withdrawal symptoms does not seem to vary across U.S. ethnoracial groups.
Development and Course
Acute alcohol withdrawal occurs as an episode usually lasting 4–5 days and only after extended
periods of heavy drinking. Withdrawal is relatively rare in individuals younger than 30 years,
and the risk and severity increase with increasing age.
Risk and Prognostic Factors
Alcohol withdrawal is more likely to occur with heavier alcohol intake, and that might be most
often observed in individuals with conduct disorder and antisocial personality disorder.
Withdrawal states are also more severe in individuals who are also dependent on other
depressant drugs (sedative-hypnotics) and individuals who have had more alcohol withdrawal
experiences in the past. Predictors of severe alcohol withdrawal include alcohol withdrawal
delirium, prior histories of severe withdrawal syndromes, low blood potassium levels, decreased
platelet counts, and systolic hypertension.
The probability of developing alcohol withdrawal increases with the quantity and
frequency of alcohol consumption. Most individuals with this condition are drinking daily,
consuming large amounts (approximately more than eight drinks per day) for multiple days.
However, there are large inter-individual differences, with enhanced risks for individuals with
concurrent medical conditions, those with family histories of alcohol withdrawal (i.e., a genetic
component), those with prior withdrawals, and individuals who consume sedative, hypnotic, or
anxiolytic drugs.
Diagnostic Markers
Autonomic hyperactivity in the context of moderately high but falling blood alcohol levels and a
history of prolonged, heavy drinking indicate a likelihood of alcohol withdrawal.
Functional Consequences of Alcohol Withdrawal
Symptoms of withdrawal may serve to perpetuate drinking behaviors and contribute to relapse,
resulting in persistently impaired social and occupational functioning. Symptoms requiring
medically supervised detoxification result in hospital utilization and loss of work productivity.
Overall, the presence of withdrawal is associated with greater functional impairment and poor
prognosis among individuals with alcohol use disorder.
Differential Diagnosis
The symptoms of alcohol withdrawal can also be mimicked by some
medical conditions (e.g., hypoglycemia and diabetic ketoacidosis). Essential tremor,
a disorder that frequently runs in families, may erroneously suggest the tremulousness associated
with alcohol withdrawal.

Alcohol-induced mental disorders.
Sedative, hypnotic, or anxiolytic withdrawal.
Alcohol withdrawal is distinguished from alcohol-induced
mental disorders (e.g., alcohol-induced anxiety disorder, with onset during withdrawal) because
the symptoms (e.g., anxiety) in these latter disorders are in excess of those usually associated
with alcohol withdrawal, predominate in the clinical presentation, and are severe enough to
warrant clinical attention.
Sedative, hypnotic, or anxiolytic withdrawal produces a
syndrome very similar to that of alcohol withdrawal.
Comorbidity
Given the typical overlap of alcohol withdrawal with alcohol use disorder, see “Comorbidity”
under Alcohol Use Disorder for more details about co-occurring conditions that are likely to be
encountered.
Alcohol-Induced Mental Disorders
The following alcohol-induced mental disorders are described in other chapters of the manual
with disorders with which they share phenomenology (see the substance/medication-induced
mental disorders in these chapters): alcohol-induced psychotic disorder (“Schizophrenia
Spectrum and Other Psychotic Disorders”); alcohol-induced bipolar and related disorder
(“Bipolar and Related Disorders”); alcohol-induced depressive disorder (“Depressive
Disorders”); alcohol-induced anxiety disorder (“Anxiety Disorders”); alcohol-induced sleep
disorder 
(“Sleep-Wake 
Disorders”); 
alcohol-induced 
sexual 
dysfunction 
(“Sexual
Dysfunctions”); and alcohol-induced major or mild neurocognitive disorder (“Neurocognitive
Disorders”). For alcohol intoxication delirium and alcohol withdrawal delirium, see the criteria
and discussion of delirium in the chapter “Neurocognitive Disorders.” These alcohol-induced
mental disorders are diagnosed instead of alcohol intoxication or alcohol withdrawal only when
the symptoms are sufficiently severe to warrant independent clinical attention.
Diagnostic and Associated Features
The symptom profiles for an alcohol-induced condition resemble the corresponding independent
mental disorders as described elsewhere in this manual. Moreover, while alcohol-induced
conditions can have the same severe consequences as independent mental disorders (e.g., suicide
attempts), they are likely to improve without formal treatment in a matter of days to weeks after
cessation of severe intoxication and/or withdrawal.
Each alcohol-induced mental disorder is listed in the relevant diagnostic section and therefore
only a brief description is offered here. These alcohol-induced mental disorders must have
developed in the context of severe alcohol intoxication and/or alcohol withdrawal.
Given that the presentation of an alcohol-induced mental disorder symptomatically resembles
the presentations of independent mental disorders from the same diagnostic class, they must be
differentiated based on the temporal relationship between the alcohol use and the psychiatric
symptoms. Individuals with alcohol-induced mental disorders are likely to also demonstrate the
associated features seen with an alcohol use disorder, as listed in that subsection.
There must be evidence that the disorder being observed is not likely to be better explained

by an independent mental disorder. The latter is likely to occur if the mental
disorder was present before the severe intoxication or withdrawal, or continued for more than
1 month after the cessation of severe intoxication or withdrawal. When symptoms are observed
only during a delirium, they should be considered part of the delirium and not diagnosed
separately, as many symptoms (including disturbances in mood, anxiety, and reality testing) are
commonly seen during agitated, confused states. The alcohol-induced mental disorder must be
clinically relevant, causing significant distress or significant functional impairment. Finally, there
are indications that the intake of substances of abuse in the context of a preexisting mental
disorder are likely to result in an intensification of the preexisting independent syndrome.
Rates of alcohol-induced mental disorders vary somewhat by diagnostic category. For
example, the lifetime risk for major depressive episodes in individuals with alcohol use disorder
is approximately 40%, but only about one-third to one-half of these represent independent major
depressive syndromes observed outside the context of intoxication. Similar rates of alcoholinduced sleep and anxiety disorders are likely, but alcohol-induced psychotic episodes are
estimated to be seen in less than 5% of individuals with alcohol use disorder.
Development and Course
Once present, the symptoms of an alcohol-induced mental disorder are likely to remain clinically
relevant as long as the individual continues to experience severe intoxication or withdrawal.
While the symptoms may be identical to those of independent mental disorders (e.g., psychoses,
major depressive disorder), and while they can have the same severe consequences (e.g., suicide
attempts), all alcohol-induced mental disorders other than alcohol-induced neurocognitive
disorder, amnestic confabulatory type (alcohol-induced persisting amnestic disorder), regardless
of the severity of the symptoms, are likely to improve relatively quickly and unlikely to remain
clinically relevant for more than 1 month after cessation of severe intoxication and/or
withdrawal.
The alcohol-induced mental disorders are an important part of the differential diagnoses for
the independent mental conditions. Independent schizophrenia, major depressive disorder,
bipolar disorder, and anxiety disorders, such as panic disorder, are likely to be associated with
much longer-lasting periods of symptoms and often require longer-term medications to optimize
the probability of improvement or recovery. The alcohol-induced mental disorders, on the other
hand, are likely to be much shorter in duration and disappear within several days to 1 month after
cessation of severe intoxication and/or withdrawal, even without psychotropic medications.
The importance of recognizing an alcohol-induced mental disorder is similar to the relevance
of identifying the possible role of some endocrine conditions and medication reactions before
diagnosing an independent mental disorder. In light of the high prevalence of alcohol use
disorders worldwide, it is important that these alcohol-induced diagnoses be considered before
independent mental disorders are diagnosed.
Unspecified Alcohol-Related Disorder

F15.920
F10.99
This category applies to presentations in which symptoms characteristic of an
alcohol-related disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for any specific alcohol-related disorder or any of the disorders
in the substance-related and addictive disorders diagnostic class.
Caffeine-Related Disorders
Caffeine Intoxication
Caffeine Withdrawal
Caffeine-Induced Mental Disorders
Unspecified Caffeine-Related Disorder
Caffeine Intoxication
Diagnostic Criteria
A. Recent consumption of caffeine (typically a high dose well in excess of 250 mg).
B. Five (or more) of the following signs or symptoms developing during, or shortly
after, caffeine use:
1. Restlessness.
2. Nervousness.
3. Excitement.
4. Insomnia.
5. Flushed face.
6. Diuresis.
7. Gastrointestinal disturbance.
8. Muscle twitching.
9. Rambling flow of thought and speech.
10. Tachycardia or cardiac arrhythmia.
11. Periods of inexhaustibility.
12. Psychomotor agitation.

C. The signs or symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication with
another substance.
Diagnostic Features
Caffeine can be consumed from a number of different sources, including coffee, tea, caffeinated
soda, “energy” drinks, over-the-counter analgesics and cold remedies, weight-loss aids, and
chocolate. Caffeine is also increasingly being used as an additive to vitamins and to food
products. More than 85% of children and adults in the United States consume caffeine. Some
caffeine users display symptoms consistent with problematic use, including tolerance and
withdrawal (see “Caffeine Withdrawal” later in this chapter); the data are not available at this
time to determine the clinical significance of a caffeine use disorder and its prevalence. In
contrast, there is evidence that caffeine withdrawal and caffeine intoxication are clinically
significant and sufficiently prevalent.
The essential feature of caffeine intoxication is recent consumption of caffeine and five or
more signs or symptoms that develop during or shortly after caffeine use (Criteria A and B).
Symptoms include restlessness, nervousness, excitement, insomnia, flushed face, diuresis, and
gastrointestinal complaints, which can occur with low doses (e.g., 200 mg) in
vulnerable individuals such as children, the elderly, or individuals who have not been
exposed to caffeine previously. Symptoms that generally appear at levels of more than 1 g/day
include muscle twitching, rambling flow of thought and speech, tachycardia or cardiac
arrhythmia, periods of inexhaustibility, and psychomotor agitation. Caffeine intoxication may
not occur despite high caffeine intake because of the development of tolerance. The signs or
symptoms must cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning (Criterion C). The signs or symptoms must not be
attributable to another medical condition and are not better explained by another mental disorder
(e.g., an anxiety disorder) or intoxication with another substance (Criterion D).
Associated Features
Mild sensory disturbances (e.g., ringing in the ears and flashes of light) may occur with high
doses of caffeine. Although large doses of caffeine can increase heart rate, typical dietary doses
can slow heart rate. Whether excess caffeine intake can cause headaches is unclear. On physical
examination, agitation, restlessness, sweating, tachycardia, flushed face, and increased bowel
motility may be seen. Caffeine blood levels may provide important information for diagnosis,
particularly when the individual is a poor historian, although these levels are not diagnostic by
themselves in view of the individual variation in response to caffeine.
Prevalence

Environmental.
Genetic and physiological.
Independent mental disorders.
The prevalence of caffeine intoxication in the general population is unclear. In the United States,
approximately 7% of individuals in the population may experience five or more symptoms along
with functional impairment consistent with a diagnosis of caffeine intoxication.
Consumption of caffeinated energy drinks, often together with alcohol, leading to caffeine
intoxication, has increased among adolescents and young adults in high-income countries,
resulting in the doubling of U.S. emergency department visits related to caffeinated energy
drinks between 2007 and 2011.
Development and Course
Consistent with a half-life of caffeine of approximately 4–6 hours, caffeine intoxication
symptoms usually remit within the first day or so and do not have any known long-lasting
consequences. However, individuals who consume very high doses of caffeine (i.e., 5–10 g) may
require immediate medical attention, as such doses can be lethal.
With advancing age, individuals are likely to demonstrate increasingly intense reactions to
caffeine, with greater complaints of interference with sleep or feelings of hyperarousal. Caffeine
intoxication among young individuals after consumption of highly caffeinated products,
including energy drinks, has been observed. Children and adolescents may be at increased risk
for caffeine intoxication because of low body weight, lack of tolerance, and lack of knowledge
about the pharmacological effects of caffeine.
Risk and Prognostic Factors
Caffeine intoxication is often seen among individuals who use caffeine less
frequently or in those who have recently increased their caffeine intake by a substantial amount.
Furthermore, oral contraceptives significantly decrease the elimination of caffeine and
consequently may increase the risk of intoxication.
Genetic factors may affect risk of caffeine intoxication.
Functional Consequences of Caffeine Intoxication
Impairment from caffeine intoxication may have serious consequences, including dysfunction at
work or school, social indiscretions, or failure to fulfill role obligations. Moreover, extremely
high doses of caffeine can be fatal. In some cases, caffeine intoxication may precipitate a
caffeine-induced disorder.
Differential Diagnosis
Caffeine intoxication may be characterized by symptoms (e.g.,
panic attacks) that resemble independent mental disorders. To meet criteria for caffeine
intoxication, the symptoms must not be associated with another medical condition or another
mental disorder, such as an anxiety disorder, that could better explain them. Manic episodes;
panic disorder; generalized anxiety disorder; amphetamine intoxication; sedative, hypnotic, or
anxiolytic withdrawal or tobacco withdrawal; sleep disorders; and medication-induced side
effects (e.g., akathisia) can cause a clinical picture that is similar to that of caffeine intoxication.

Caffeine-induced mental disorders.
F15.93
The temporal relationship of the symptoms to increased
caffeine use or to abstinence from caffeine helps to establish the diagnosis. Caffeine intoxication
is differentiated from caffeine-induced anxiety disorder, with onset during intoxication (see
“Substance/Medication-Induced Anxiety Disorder” in the chapter “Anxiety Disorders”), and
caffeine-induced sleep disorder, with onset during intoxication (see “Substance/MedicationInduced Sleep Disorder” in the chapter “Sleep-Wake Disorders”), because the symptoms (e.g.,
anxiety and insomnia, respectively) in these latter disorders are in excess of those usually
associated with caffeine intoxication, predominate in the clinical presentation, and are severe
enough to warrant independent clinical attention.
Comorbidity
Typical dietary doses of caffeine have not been consistently associated with medical problems.
However, heavy use (e.g., > 400 mg) can cause or exacerbate anxiety and somatic symptoms and
gastrointestinal distress. With acute, extremely high doses of caffeine, grand mal seizures and
respiratory failure may result in death. Excessive caffeine use is associated with depressive
disorders, bipolar disorders, eating disorders, psychotic disorders, sleep disorders, and substancerelated disorders, whereas individuals with anxiety disorders are more likely to avoid caffeine.
Caffeine Withdrawal
Diagnostic Criteria
A. Prolonged daily use of caffeine.
B. Abrupt cessation of or reduction in caffeine use, followed within 24 hours by
three (or more) of the following signs or symptoms:
1. Headache.
2. Marked fatigue or drowsiness.
3. Dysphoric mood, depressed mood, or irritability.
4. Difficulty concentrating.
5. Flu-like symptoms (nausea, vomiting, or muscle pain/stiffness).
C. The signs or symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not associated with the physiological effects of
another medical condition (e.g., migraine, viral illness) and are not better
explained by another mental disorder, including intoxication or withdrawal from
another substance.

Diagnostic Features
The essential feature of caffeine withdrawal is the presence of a characteristic withdrawal
syndrome that develops after the abrupt cessation of (or substantial reduction in) prolonged daily
caffeine ingestion (Criterion B). Because individuals may be unaware of the wide array of
sources of caffeine beyond coffee, colas, and energy drinks (e.g., over-the-counter analgesics and
cold remedies, weight loss aids, chocolate), they may not connect ingestion of these substances
with symptoms of caffeine withdrawal. The caffeine withdrawal syndrome is indicated by three
or more of the following (Criterion B): headache; marked fatigue or drowsiness; dysphoric
mood, depressed mood, or irritability; difficulty concentrating; and flu-like symptoms (nausea,
vomiting, or muscle pain/stiffness). The withdrawal syndrome causes clinically significant
distress or impairment in social, occupational, or other important areas of functioning (Criterion
C). The symptoms must not be associated with the physiological effects of another medical
condition and are not better explained by another mental disorder (Criterion D).
Headache is the hallmark feature of caffeine withdrawal and may be diffuse, gradual in
development, throbbing, severe, and sensitive to movement. However, other symptoms of
caffeine withdrawal can occur in the absence of headache. Caffeine is the most widely used
behaviorally active drug in the world and is present in many different types of beverages (e.g.,
coffee, tea, mate, soft drinks, energy drinks), foods, energy aids, medications, and dietary
supplements. Because caffeine ingestion is often integrated into social customs and daily rituals
(e.g., coffee break, tea time), some caffeine consumers may be unaware of their physical
dependence on caffeine. Thus, caffeine withdrawal symptoms could be unexpected and
misattributed to other causes (e.g., the flu, migraine). Furthermore, caffeine withdrawal
symptoms may occur when individuals are required to abstain from foods and beverages prior to
medical procedures or when a usual caffeine dose is missed because of a change in routine (e.g.,
during travel, weekends).
The probability and severity of caffeine withdrawal generally increase as a function of usual
daily caffeine dose. However, there is large variability among individuals and within individuals
across different episodes in the incidence, severity, and time course of withdrawal symptoms.
Caffeine withdrawal symptoms may occur after abrupt cessation of relatively low chronic daily
doses of caffeine (i.e., 100 mg).
Associated Features
Caffeine abstinence has been shown to be associated with impaired behavioral and cognitive
performance (e.g., sustained attention), as well as with increased total sleep time, sleep
efficiency, and slow-wave sleep. Electroencephalographic studies have shown that caffeine
withdrawal symptoms are significantly associated with increases in theta power and decreases in
beta-2 power. Decreased motivation to work and decreased sociability have also been reported
during caffeine withdrawal. Increased analgesic use during caffeine withdrawal has been
documented.
Prevalence
More than 85% of adults and children in the United States regularly consume caffeine, with adult
caffeine consumers ingesting about 280 mg/day on average. The incidence and prevalence of the

Temperamental.
Environmental.
Genetic and physiological.
caffeine withdrawal syndrome in the general population are unclear. In the United States,
headache may occur in approximately 50% of cases of caffeine abstinence.
In attempts to permanently stop caffeine use, more than 70% of individuals in a U.S.
metropolitan county reported at least one caffeine withdrawal symptom (47% experienced
headache), and 24% experienced headache plus one or more other symptoms as well as
functional impairment due to withdrawal. Among individuals who abstained from caffeine for at
least 24 hours but were not trying to permanently stop caffeine use, 11% experienced headache
plus one or more other symptoms as well as functional impairment. Caffeine consumers can
decrease the incidence of caffeine withdrawal by using caffeine daily or only infrequently (e.g.,
no more than 2 consecutive days). Gradual reduction in caffeine over a period of days or weeks
may decrease the incidence and severity of caffeine withdrawal.
Development and Course
Symptoms usually begin 12–24 hours after the last caffeine dose and peak after 1–2 days of
abstinence. Caffeine withdrawal symptoms last for 2–9 days, with the possibility of withdrawal
headaches occurring for up to 21 days. Symptoms usually remit rapidly (within 30–60 minutes)
after re-ingestion of caffeine. Doses of caffeine significantly less than the individual’s usual daily
dose may be sufficient to prevent or attenuate caffeine withdrawal symptoms (e.g., consumption
of 25 mg by an individual who typically consumes 300 mg).
Caffeine is unique in that it is a behaviorally active drug that is consumed by individuals of
nearly all ages, with rates of caffeine consumption and overall level of caffeine consumption
increasing with age. Although caffeine withdrawal among children and adolescents has been
documented, relatively little is known about risk factors for caffeine withdrawal among this age
group. The use of highly caffeinated energy drinks is increasing in young people, which could
increase the risk for caffeine withdrawal.
Risk and Prognostic Factors
Heavy caffeine use has been observed among individuals with mental disorders,
including eating disorders and alcohol and other substance use disorders, as well as among
individuals who smoke cigarettes and those who are incarcerated. Thus, these individuals could
be at higher risk for caffeine withdrawal upon acute caffeine abstinence.
The unavailability of caffeine is an environmental risk factor for incipient
withdrawal symptoms. While caffeine is legal and usually widely available, there are conditions
in which caffeine use may be restricted, such as during medical procedures, pregnancy,
hospitalizations, religious observances, wartime, travel, and research participation. These
external environmental circumstances may precipitate a withdrawal syndrome in vulnerable
individuals.
Genetic factors appear to increase vulnerability to caffeine withdrawal,
but no specific genes have been identified.
Culture-Related Diagnostic Issues

Other medical conditions and medication side effects.
Caffeine-induced sleep disorder.
Habitual caffeine consumers who fast for religious reasons may be at increased risk for caffeine
withdrawal.
Sex- and Gender-Related Diagnostic Issues
Metabolism of caffeine is slower in females who use oral contraceptives and in the luteal phase
of the menstrual cycle, and caffeine metabolism becomes progressively slower in the second and
third trimesters of pregnancy compared with the first trimester and the nonpregnant state. These
features reduce the rate of clearance and may diminish withdrawal, although they can also
lengthen the duration of caffeine-associated adverse symptoms. It is unlikely that doses < 300
mg/day are associated with adverse reproductive outcomes in pregnancy.
Functional Consequences of Caffeine Withdrawal
Caffeine withdrawal symptoms can vary from mild to extreme, at times causing functional
impairment in normal daily activities. Rates of functional impairment in studies conducted
largely in the United States range from 10% to 55% (median 13%), with rates as high as 73%
found among individuals who also show other problematic features of caffeine use. Examples of
functional impairment include being unable to work, exercise, or care for children; staying in bed
all day; missing religious services; ending a vacation early; and canceling a social gathering.
Caffeine withdrawal headaches may be described by individuals as “the worst headaches” ever
experienced. Decrements in cognitive and motor performance have also been observed.
Differential Diagnosis
Caffeine withdrawal can mimic migraine and
other headache disorders, viral illnesses, sinus conditions, tension, other drug withdrawal states
(e.g., from amphetamines, cocaine), and medication side effects. The final determination of
caffeine withdrawal should rest on a determination of the pattern and amount consumed, the time
interval between caffeine abstinence and onset of symptoms, and the particular clinical features
presented by the individual. A challenge dose of caffeine followed by symptom remission may
be used to confirm the diagnosis.
Caffeine withdrawal is distinguished from caffeine-induced sleep
disorder (e.g., caffeine-induced sleep disorder, insomnia type, with onset during withdrawal)
because the sleep symptoms are in excess of those usually associated caffeine withdrawal,
predominate in the clinical presentation, and are severe enough to warrant clinical attention.
Comorbidity
Caffeine withdrawal may be associated with major depressive disorder, generalized anxiety
disorder, panic disorder, antisocial personality disorder, moderate to severe alcohol use disorder,
and cannabis and cocaine use.
Caffeine-Induced Mental Disorders

The following caffeine-induced mental disorders are described in other chapters of the manual
with disorders with which they share phenomenology (see the substance/medication-induced
mental disorders in these chapters): caffeine-induced anxiety disorder (“Anxiety Disorders”) and
caffeine-induced sleep disorder (“Sleep-Wake Disorders”). These caffeine-induced mental
disorders are diagnosed instead of caffeine intoxication or caffeine withdrawal only when the
symptoms are sufficiently severe to warrant independent clinical attention.
Unspecified Caffeine-Related Disorder
F15.99
This category applies to presentations in which symptoms characteristic of a
caffeine-related disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for any specific caffeine-related disorder or any of the disorders
in the substance-related and addictive disorders diagnostic class.
Cannabis-Related Disorders
Cannabis Use Disorder
Cannabis Intoxication
Cannabis Withdrawal
Cannabis-Induced Mental Disorders
Unspecified Cannabis-Related Disorder
Cannabis Use Disorder
Diagnostic Criteria
A. A problematic pattern of cannabis use leading to clinically significant impairment
or distress, as manifested by at least two of the following, occurring within a 12month period:
1. Cannabis is often taken in larger amounts or over a longer period than was
intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control
cannabis use.

3. A great deal of time is spent in activities necessary to obtain cannabis, use
cannabis, or recover from its effects.
4. Craving, or a strong desire or urge to use cannabis.
5. Recurrent cannabis use resulting in a failure to fulfill major role obligations at
work, school, or home.
6. Continued cannabis use despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of cannabis.
7. Important social, occupational, or recreational activities are given up or
reduced because of cannabis use.
8. Recurrent cannabis use in situations in which it is physically hazardous.
9. Cannabis use is continued despite knowledge of having a persistent or
recurrent physical or psychological problem that is likely to have been caused
or exacerbated by cannabis.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of cannabis to achieve
intoxication or desired effect.
b. Markedly diminished effect with continued use of the same amount of
cannabis.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for cannabis (refer to Criteria A
and B of the criteria set for cannabis withdrawal).
b. Cannabis (or a closely related substance) is taken to relieve or avoid
withdrawal symptoms.
Specify if:
In early remission: After full criteria for cannabis use disorder were previously
met, none of the criteria for cannabis use disorder have been met for at least 3
months but
for less than 12 months (with the exception that Criterion A4, “Craving, or a
strong desire or urge to use cannabis,” may be met).
In sustained remission: After full criteria for cannabis use disorder were
previously met, none of the criteria for cannabis use disorder have been met at
any time during a period of 12 months or longer (with the exception that Criterion
A4, “Craving, or a strong desire or urge to use cannabis,” may be present).
Specify if:
In a controlled environment: This additional specifier is used if the individual is
in an environment where access to cannabis is restricted.
Code based on current severity/remission: If a cannabis intoxication, cannabis
withdrawal, or another cannabis-induced mental disorder is also present, do not use

the codes below for cannabis use disorder. Instead, the comorbid cannabis use
disorder is indicated in the 4th character of the cannabis-induced disorder code (see
the coding note for cannabis intoxication, cannabis withdrawal, or a specific
cannabis-induced mental disorder). For example, if there is comorbid cannabisinduced anxiety disorder and cannabis use disorder, only the cannabis-induced
anxiety disorder code is given, with the 4th character indicating whether the
comorbid cannabis use disorder is mild, moderate, or severe: F12.180 for mild
cannabis use disorder with cannabis-induced anxiety disorder or F12.280 for a
moderate or severe cannabis use disorder with cannabis-induced anxiety disorder.
Specify current severity/remission:
F12.10 Mild: Presence of 2–3 symptoms.
F12.11 Mild, In early remission
F12.11 Mild, In sustained remission
F12.20 Moderate: Presence of 4–5 symptoms.
F12.21 Moderate, In early remission
F12.21 Moderate, In sustained remission
F12.20 Severe: Presence of 6 or more symptoms.
F12.21 Severe, In early remission
F12.21 Severe, In sustained remission
Specifiers
“In a controlled environment” applies as a further specifier of remission if the individual is both
in remission and in a controlled environment (i.e., in early remission in a controlled environment
or in sustained remission in a controlled environment). Examples of these environments are
closely supervised and substance-free jails, therapeutic communities, and locked hospital units.
Changing severity across time in an individual may also be reflected by changes in the
frequency (e.g., days of use per month or times used per day) and/or dose (e.g., amount used per
episode) of cannabis, as assessed by individual self-report, report of knowledgeable others,
clinician’s observations, and biological testing.
Diagnostic Features
Cannabis use disorder includes problems associated with use of substances derived from the
cannabis plant and chemically similar synthetic compounds. In these substances, the primary
component with psychoactive effects (and hence, addiction potential) is the cannabinoid delta-9tetrahydrocannabinol (delta-9-THC or THC). Cannabinoids have diverse effects in the brain,
prominent among which are actions on CB1 and CB2 cannabinoid receptors found throughout the
central nervous system.
Cannabis is used in many forms. It is most commonly smoked in a cigarette-like form (often

called “joints” or “reefers”), and also in pipes, water pipes (bongs or hookahs), or hollowed-out
cigars (“blunts”). More recently developed methods include “vaping” (vaporizing) by heating
without combustion plant cannabis material to release psychoactive components for inhalation,
and “dabbing,” in which a concentrated cannabis product (butane hash oil, known as “dabs”),
created through butane extraction of THC from cannabis plant material, is heated and inhaled.
Vaping and dabbing are gaining popularity, particularly among youth. Cannabis can also be
ingested orally in food (edibles) or beverages. Inhalation typically produces more rapid and
intense onset of effects than oral administration. Hashish or hash oil, a concentrated extraction of
the cannabis plant, is also used. Across products, cannabis potency (THC concentration) varies
greatly, averaging 10%–15% in typical cannabis plant material, 30%–40% in hashish, and 50%–
55% in hash oil. During the past two decades, the potency of seized illegal plant cannabis has
steadily increased, and legal cannabis products may have even higher THC potency (e.g., 20%
for plant material and 68% for cannabis extracts). Synthetic oral THC formulations
(pill/capsules/sprays) are also available for various medical uses (e.g., chronic pain; nausea and
vomiting caused by chemotherapy or ano-rexia; weight loss among those with AIDS). Other
entirely illicit synthetic cannabinoid compounds (e.g., K2, Spice, JWH-018, JWH-073) are in the
form of plant material sprayed with a cannabinoid formulation. Although such synthetic
cannabinoids are designed to mimic cannabis effects, their chemical composition, potency,
effects, and duration of action are unpredictable, and they may cause more severe adverse effects
than cannabis plant products, including seizures, cardiac conditions, psychosis, and even death.
In the United States, cannabis remains an illegal substance under federal law, while the legal
status of cannabis varies by state. Thus, cannabis use under state law can involve an illicit
product, a product authorized for medical purposes, or a completely legal product. The most
common medical purpose for cannabis use is chronic pain, and the conditions approved for
medicinal cannabis use vary from state to state. When cannabis or a cannabinoid is taken as
indicated for a medical condition, tolerance and withdrawal (physiological dependence) may
occur but should not be the primary basis for diagnosing cannabis use disorder. The efficacy of
cannabis for different medical conditions continues to be debated, and cannabis use as medically
advised should be taken into account when a cannabis use disorder diagnosis is being considered.
Patterns of cannabis use can range from light, infrequent use to heavy, frequent use.
Individuals with DSM-5 cannabis use disorder use cannabis frequently (on average, 4 or more
days a week), and some individuals may use cannabis throughout the day over a period of
months or years. Because of the increasingly common perception that cannabis use is harmless,
individuals may not recognize that symptoms of cannabis use disorder (e.g., withdrawal
symptoms) are cannabis related. Additionally, among individuals with multiple substance use
disorders, lack of clarity about whether symptoms are caused by cannabis or by other substances
may lead to underreporting of cannabis use disorder symptoms.
Cannabis use disorder is defined by the same 11 criteria that define the other substance use
disorders, as supported by considerable empirical evidence. These criteria, a cluster of behavioral
and physical symptoms, lead to clinically significant impairment or distress and can include
withdrawal, tolerance, craving, spending a great deal of time in activities related to the substance,
and hazardous use (e.g., driving while under its influence). Some individuals who use cannabis
multiple times per day do not perceive themselves as spending excessive time under the
influence of cannabis or recovering from its effects, despite being intoxicated from cannabis or
coming down from its effects most of the time, most days. An important marker of a severe

cannabis use disorder is continued use despite negative effects on other important activities or
relationships (e.g., school, work, sports, partner or parent relationship).
Regular cannabis users become tolerant to many acute cannabis effects, and cessation of
regular cannabis use generally leads to a cannabis withdrawal syndrome. Cannabis withdrawal
can cause significant distress, leading to continued use to relieve the symptoms and difficulty
quitting use or relapse.
Associated Features
Individuals who regularly use cannabis often report using it to cope with mood, insomnia, anger,
pain, or other physiological or psychological problems, and individuals diagnosed with cannabis
use disorder frequently have other concurrent mental disorders. Careful assessment can reveal
that cannabis use contributes to exacerbation of these symptoms, as well as other reasons for
frequent use (e.g., the coping motives listed above; to experience euphoria; as an enjoyable
social activity). Chronic intake of cannabis can produce a lack of motivation that resembles
persistent depressive disorder.
Because some individuals may underreport the amount or frequency of their cannabis use,
provider awareness of common signs and symptoms of cannabis use and intoxication facilitates
better assessment of cannabis use disorder. Some additional signs of acute and chronic use are
red eyes (conjunctival injection), cannabis odor on clothing, yellowing of fingertips (from
smoking joints), chronic cough, burning of incense (to hide the odor), and exaggerated craving
and impulse for specific foods, sometimes at odd times of the day or night.
Prevalence
Cannabinoids, especially cannabis, are the most widely used illicit psychoactive substances in
the United States. The following prevalence data are drawn from U.S.-based studies, unless
otherwise noted. Among youth (ages 12–17 years), the past-year prevalence of DSM-IV
cannabis use disorder is 2.7%–3.1%. Among adults age 18 years and older, the prevalence is
1.5%–2.9%. Among cannabis users, the prevalence of DSM-IV cannabis use disorder is 20.4%
among youth and 30.6% among adults. For DSM-5 cannabis use disorder, 12-month prevalence
is approximately 2.5% among adults (1.4%, 0.6%, and 0.6% at mild, moderate, and severe
levels, respectively). During the past decade, the prevalence of cannabis use disorder has
decreased among adolescents. In contrast, among adults, some studies suggest that the
prevalence of cannabis use disorder has either remained stable or increased—for example,
among adults in the general population, patients in inpatient settings, and patients in the Veterans
Health Administration. Globally, the age-standardized rate of cannabis use disorders was 289.7
per 100,000 people in 2016, a 25.6% increase over 1990. Prevalence varies widely across
geographic regions, being lowest in Western Sub-Saharan Africa and highest in North America.
According to age, the prevalence of cannabis use disorder in the United States is highest
among individuals ages 18–29 years (6.9%) and lowest among individuals age 45 years and
older (0.8%). Rates of cannabis use disorder are greater in men than in women (3.5% vs. 1.7%)
and in boys than in girls ages 12–17 years (3.4% vs. 2.8%), although gender differences have

been narrowing in recent birth cohorts across several countries. Regarding ethnoracial
differences, for adolescents ages 12–17 years, rates are highest among Hispanics (3.8%),
followed by Whites (3.1%), African Americans (2.9%), and other ethnoracial groups (2.3%).
Among adults, the prevalence of cannabis use disorder is 5.3% in American Indians and Alaska
Natives, 4.5% in African Americans, 2.6% in Hispanics, 2.2% in Whites, and 1.3% in Asians
and Pacific Islanders. In the United States and other high-income countries, the number of
individuals seeking treatment for cannabis-related problems has increased since the 1990s.
However, among adults with cannabis use disorder, only 7%–8% received any type of cannabisspecific treatment in the past year, indicating that cannabis use disorder is a seriously
undertreated condition.
Development and Course
The onset of cannabis use disorder can occur at any age but is most common during adolescence
or young adulthood. The increasing acceptability and availability of medical and recreational
marijuana may impact the development and course of cannabis use disorder, with increased onset
among older adults.
Generally, cannabis use disorder develops over an extended period of time, although the
progression may be more rapid in adolescents, particularly in those with conduct problems. Most
individuals who develop a cannabis use disorder establish a pattern of cannabis use that
gradually increases in frequency and amount. Beginning around 2010, cannabis has increasingly
displaced alcohol and tobacco in the United States as the first psychoactive substance used
during adolescence. This may be attributable to the decrease in perceived harmfulness of
cannabis use among adolescents and adults and the fact that many now perceive cannabis use as
less harmful than alcohol or tobacco use.
Cannabis use disorder among preteens, adolescents, and young adults is associated with
preferences for novelty-seeking and risk-taking, norm-violating or other illegal behaviors, and
conduct disorder. Milder cases of cannabis use disorder in youth primarily reflect continued use
despite problems related to disapproval of use by peers, school administration, or family, and can
place youths at risk for physical or behavioral consequences. In more severe cases, progression
to using alone or using throughout the day interferes with daily functioning and takes the place of
previously established, prosocial activities.
Cannabis use disorder among adults typically involves well-established patterns of daily
cannabis use that continue despite clear psychosocial or medical problems. Many adults
experience repeated desire to stop or have failed at repeated cessation attempts. Milder adult
cases may resemble mild adolescent cases in that cannabis use is not as frequent or heavy but
continues despite potential significant consequences of sustained use. The rate of use among U.S.
middle-age and older adults is increasing, which may be atributable to increased availability and
acceptability, along with a possible “baby boomer” cohort effect resulting from high prevalence
of use among those who were young adults in the late 1960s and the 1970s.
Early onset of cannabis use (e.g., prior to age 15 years) is a robust predictor of the
development of cannabis use disorder and other types of substance use disorders and mental
disorders during young adulthood. Such early onset is often concurrent with other externalizing

Temperamental.
Environmental.
Genetic and physiological.
problems (e.g., symptoms of conduct disorder). However, early onset is also a predictor of
internalizing problems and as such may reflect a general risk factor for the development of
mental disorders.
Risk and Prognostic Factors
A history of conduct disorder in childhood or adolescence and antisocial
personality disorder are risk factors for the development of many substance use disorders,
including cannabis use disorder. Other risk factors include externalizing or internalizing
disorders during childhood or adolescence. Youth with high behavioral disinhibition scores show
early-onset substance use disorders, including cannabis use disorder and multiple substance
involvement, and early conduct problems.
Risk factors include unstable or abusive family situations, use of cannabis among
immediate family members, a childhood history of emotional or physical abuse or the violent
death of a close family member or friend, a family history of substance use disorders, and low
socioeconomic status. As with all substances of abuse, the ease of availability of the substance is
a risk factor; cannabis is relatively easy to obtain in most cultures, which increases the risk of
developing a cannabis use disorder. Increasingly permissive U.S. state medical and recreational
marijuana laws have reduced barriers to obtaining cannabis in about two-thirds of U.S. states.
Living in a U.S. state that has legalized recreational
marijuana use increases the risk for adult cannabis use disorder. The risk of the disorder among
past-year cannabis users is higher among Black, Native American, Hispanic, and Asian
American adults and adolescents, relative to non-Hispanic Whites.
Genetic influences contribute to the development of cannabis use
disorders. Heritable factors contribute between 30% and 80% of the total variance in risk of
cannabis use disorders, although studies have not yet definitively identified the specific genetic
variants involved. Genetic and environmental influences shared between cannabis and other
types of substance use disorders suggest a general common basis for substance use disorders that
includes cannabis use disorder.
Culture-Related Diagnostic Issues
The acceptability of cannabis for medical and recreational use has varied widely over time and
across cultural contexts. Currently, cannabis is one of the world’s most commonly used
psychoactive substances. In some cultural settings, cannabis use is influenced by ethnicity,
religion, and sociocultural practices, such as political movements.
Sex- and Gender-Related Diagnostic Issues
Compared with men, women report more severe cannabis withdrawal symptoms, especially
mood symptoms such as irritability, restlessness, and anger, and gastrointestinal symptoms such
as stomachache and nausea, which may contribute to potential telescoping (faster transition from
first cannabis use to cannabis use disorder).

Past-month cannabis use was reported by 7.0% of pregnant women in a nationally
representative U.S. survey in 2016–2017. The rate of cannabis use is lower in pregnant compared
with nonpregnant women, but resumption of use following delivery occurs in the majority who
attain abstinence in pregnancy.
Diagnostic Markers
Detection of 11-nor-9-carboxy-delta-9-tetrahydrocannabinol (THCCOOH) in urine is often used
as a biological marker of cannabis use. In frequent users, urine tests for THCCOOH often remain
positive for weeks after last use, limiting the uses for these tests (e.g., remission status), and
expertise in urine testing methods is needed to reliably interpret results. However, a positive
result can be useful in working with individuals who deny all use despite concerns of family or
friends. Tests for the presence of cannabinoids in blood that give more fine-grained results are
under active development, and the development of detection using oral fluids may eventually
offer the possibility of roadside tests to use in driving safety efforts.
Association With Suicidal Thoughts or Behavior
In a study of Iraq/Afghanistan-era veterans, after adjustment for multiple sociodemographic
factors, psychiatric and other substance comorbidities, and past trauma, including combat,
cannabis use disorder was still associated with increased risk of both suicidal and nonsuicidal
self-injury. In a study of all U.S. Veterans Health Administration patients in 2005, any current
substance use disorder was associated with increased suicide risk in both sexes but especially
among women. In particular, men with cannabis use disorder had a suicide rate of 79 per
100,000 person-years, and women with cannabis use disorder had a suicide rate of 47 per
100,000 person-years. A review and meta-analysis of the international literature from 1990
through 2015 found evidence that chronic cannabis use, but not acute cannabis use, is associated
with suicidal thoughts and behavior.
Functional Consequences of Cannabis Use Disorder
Functional consequences of cannabis use disorder are part of the diagnostic criteria. Many areas
of psychosocial, cognitive, and health functioning may be compromised in relation to
cannabis use disorder. Although it can be difficult to distinguish the short-term impairments due
to cannabis intoxication from the longer-term functional consequences of cannabis use disorder,
cognitive function (particularly higher executive function) even while unintoxicated may become
compromised in cannabis users in a cumulative dose-dependent relationship, which may
contribute to difficulty at school or work. Accidents due to potentially dangerous activities while
under the influence (e.g., driving, sports, at work) are also of concern. In particular, placebocontrolled studies and large-scale epidemiological studies show that cannabis use impairs driver
reaction time, spatial perceptions, and decision-making. Cannabis use has also been linked to a
reduction in goal-directed activity and decreased self-efficacy, labeled an amotivational
syndrome, that manifests itself in poor school or work performance. Similarly, cannabisassociated problems with social relationships are commonly reported in those with cannabis use

Nonproblematic use of cannabis.
Cannabis intoxication, cannabis withdrawal, and cannabis-induced mental disorders.
disorder. Cannabis use is associated with poorer life satisfaction and increased treatment and
hospitalization for mental health problems.
Differential Diagnosis
Although the majority of individuals who use cannabis do not
have problems related to its use, 20%–30% of cannabis users do experience symptoms and
associated consequences consistent with a cannabis use disorder. Differentiating nonproblematic
use of cannabis and cannabis use disorder can be challenging because individuals may not
attribute cannabis-related social, behavioral, or psychological problems to the substance,
especially in the context of polysubstance use. Also, failure to acknowledge heavy cannabis use
and its role in associated problems is common among individuals referred to treatment by others
(i.e., school, family, employer, criminal justice system).
Cannabis 
use
disorder is differentiated from cannabis intoxication, cannabis withdrawal, and cannabis-induced
mental disorders (e.g., cannabis-induced anxiety disorder) in that cannabis use disorder describes
a problematic pattern of cannabis use that involves impaired control over cannabis use, social
impairment due to cannabis use, risky cannabis use (e.g., driving while intoxicated), and
pharmacological symptoms (the development of tolerance or withdrawal), whereas cannabis
intoxication, cannabis withdrawal, and cannabis-induced mental disorders describe psychiatric
syndromes that develop in the context of heavy use. Cannabis intoxication, cannabis withdrawal,
and cannabis-induced mental disorders occur frequently in individuals with cannabis use
disorder. In such cases, a diagnosis of cannabis intoxication, cannabis withdrawal, or a cannabisinduced mental disorder should be given in addition to a diagnosis of cannabis use disorder, the
presence of which is indicated in the diagnostic code.
Comorbidity
Cannabis use disorder is highly comorbid with other substance use disorders (e.g., alcohol,
cocaine, opioids). For example, compared with adults without cannabis use disorder, having a
cannabis use disorder multiplies the risk for any other substance disorder by a factor of about
nine. Cannabis has been commonly considered as a “gateway” drug because individuals who use
cannabis have a substantially greater lifetime probability than nonusers of subsequently using
other, more risky substances (e.g., opioids or cocaine). Among adults seeking treatment for a
cannabis use disorder, many (63%) report problematic use of secondary or tertiary substances,
including alcohol, cocaine, methamphetamine/amphetamine, and heroin or other opiates, and
cannabis use disorder is often a secondary or tertiary problem among those with a primary
diagnosis of other substance use disorders. Among adolescents in treatment, cannabis is
frequently the primary substance of abuse (76%).
Among adults with DSM-5 cannabis use disorder, 64% had a past-year tobacco use disorder,
and the odds of a comorbid tobacco disorder increased sharply as the severity of cannabis use
disorder increased.
Co-occurring mental disorders are also common among those with cannabis use disorder and

include major depressive disorder, bipolar I and II disorders, anxiety disorders, posttraumatic
stress disorder, and personality disorders. In a Minnesota twin study, about half of adolescents
with cannabis use disorder had internalizing disorders (e.g., anxiety, depression, posttraumatic
stress disorder), and 64% had externalizing disorders (e.g., conduct disorder, attentiondeficit/hyperactivity disorder).
Considerable concern has been raised about cannabis use as a risk factor in schizophrenia and
other psychotic disorders. Cannabis use in critical periods is consistently associated with a
threefold increase in the risk for psychosis. Differences in frequency of daily cannabis use and
use of high-potency varieties of cannabis may have contributed to the striking variation in the
incidence of psychotic disorder across 11 European sites. The population attributable fraction
from regular cannabis in explaining hospital admissions for psychosis was estimated to be 17.7%
(95% CI: 1.2%–45.5%) in Chile. On the other hand, some data suggest that childhood abuse may
be the determining factor that increases the risk for cannabis abuse and for psychosis. Overall,
cannabis use may contribute to the onset of an acute psychotic episode, can exacerbate some
symptoms, and can adversely affect treatment of a major psychotic illness.
Regarding medical conditions, cannabinoid hyperemesis syndrome is a syndrome of nausea
and cyclic vomiting associated with regular cannabis use that is increasingly seen in emergency
departments as the prevalence of cannabis use increases. In addition, respiratory disorders (e.g.,
asthma, chronic obstructive pulmonary disease, pneumonia) are associated with regular cannabis
use (by smoking, vaping, or e-cigarettes) regardless of tobacco co-use, as are some adverse
cardiovascular outcomes.
Cannabis Intoxication
Diagnostic Criteria
A. Recent use of cannabis.
B. Clinically significant problematic behavioral or psychological changes (e.g.,
impaired motor coordination, euphoria, anxiety, sensation of slowed time,
impaired judgment, social withdrawal) that developed during, or shortly after,
cannabis use.
C. Two (or more) of the following signs or symptoms developing within 2 hours of
cannabis use:
1. Conjunctival injection.
2. Increased appetite.
3. Dry mouth.
4. Tachycardia.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication with
another substance.
Specify if:

With perceptual disturbances: Hallucinations with intact reality testing or
auditory, visual, or tactile illusions occur in the absence of a delirium.
Coding note: The ICD-10-CM code depends on whether or not there is a comorbid
cannabis use disorder and whether or not there are perceptual disturbances.
For cannabis intoxication, without perceptual disturbances: If a mild
cannabis use disorder is comorbid, the ICD-10-CM code is F12.120, and if a
moderate or severe cannabis use disorder is comorbid, the ICD-10-CM code is
F12.220. If there is no comorbid cannabis use disorder, then the ICD-10-CM
code is F12.920.
For cannabis intoxication, with perceptual disturbances: If a mild cannabis
use disorder is comorbid, the ICD-10-CM code is F12.122, and if a moderate or
severe cannabis use disorder is comorbid, the ICD-10-CM code is F12.222. If
there is no comorbid cannabis use disorder, then the ICD-10-CM code is
F12.922.
Specifiers
When hallucinations occur in the absence of intact reality testing, a diagnosis of
substance/medication-induced psychotic disorder should be considered.
Diagnostic Features
The essential feature of cannabis intoxication is the presence of clinically significant problematic
behavioral or psychological changes that develop during, or shortly after, cannabis use (Criterion
B). Intoxication typically begins with a “high” feeling followed by symptoms that include
euphoria with inappropriate laughter and grandiosity, sedation, lethargy, impairment in shortterm memory, difficulty carrying out complex mental processes, impaired judgment, distorted
sensory perceptions, impaired motor performance, and the sensation that time is passing slowly.
Occasionally, anxiety (which can be severe), dysphoria, or social withdrawal occurs. These
psychoactive effects are accompanied by two or more of the following signs, developing within
2 hours of cannabis use: conjunctival injection, increased appetite, dry mouth, and tachycardia
(Criterion C).
Intoxication develops within minutes if plant cannabis is smoked, and may take a few hours
to develop when the cannabis is ingested orally. The effects usually last 3–4 hours, with duration
longer when the substance is ingested orally. The magnitude of the behavioral and physiological
changes depends on the dose, the method of administration, and the characteristics of the
individual using the substance, such as rate of absorption, tolerance, and sensitivity to the effects
of the substance. Because most cannabinoids, including delta-9-tetrahydrocannabinol (delta-9THC), are fat soluble, the effects of cannabis or hashish may occasionally persist or reoccur for
12–24 hours because of the slow release of psychoactive substances from fatty tissue or to
enterohepatic circulation.
Synthetic cannabinoids (e.g., Spice), whose use has become more common in recent years,

Other substance intoxication.
Cannabis-induced mental disorders.
also produce rapid effects, including euphoria, talkativeness, feelings of joy and laughter, and
relaxation. In terms of psychoactive effects, low doses of synthetic cannabinoids and other
cannabis products are similar. At higher doses of synthetic cannabinoids, delusional and
hallucinatory symptoms are more likely to occur.
Prevalence
The prevalence of episodes of cannabis intoxication in the general population is unknown.
However, it is probable that most individuals using cannabis would at some time experience
symptoms that meet criteria for cannabis intoxication. Given this, the prevalence of individuals
using cannabis and the prevalence of individuals experiencing cannabis intoxication are likely
similar.
Functional Consequences of Cannabis Intoxication
Impairment from cannabis intoxication may have serious consequences, including dysfunction at
work or school, social indiscretions, failure to fulfill role obligations, traffic accidents, and
having unprotected sex. In rare cases, cannabis intoxication may precipitate a psychosis that may
vary in duration.
Differential Diagnosis
Note that if the clinical presentation includes hallucinations in the absence of intact reality
testing, a diagnosis of substance/medication-induced psychotic disorder should be considered.
Cannabis intoxication may resemble intoxication with other types of
substances. However, in contrast to cannabis intoxication, alcohol intoxication and sedative,
hypnotic, or anxiolytic intoxication frequently decrease appetite, increase aggressive behavior,
and produce nystagmus or ataxia. Hallucinogens in low doses may cause a clinical picture that
resembles cannabis intoxication. Phencyclidine, like cannabis, can be smoked and also causes
perceptual changes, but phencyclidine intoxication is much more likely to cause ataxia and
aggressive behavior.
Cannabis intoxication is distinguished from cannabis-induced
mental disorders (e.g., cannabis-induced anxiety disorder, with onset during intoxication)
because the symptoms (e.g., anxiety) in these latter disorders are in excess of those usually
associated with cannabis intoxication, predominate in the clinical presentation, and are severe
enough to warrant independent clinical attention.
Comorbidity
Given the typical overlap of cannabis intoxication with cannabis use disorder, see “Comorbidity”
under Cannabis Use Disorder for more details about co-occurring conditions that are likely to be
encountered.
Cannabis Withdrawal

Diagnostic Criteria
A. Cessation of cannabis use that has been heavy and prolonged (i.e., usually daily
or almost daily use over a period of at least a few months).
B. Three (or more) of the following signs and symptoms develop within
approximately 1 week after Criterion A:
1. Irritability, anger, or aggression.
2. Nervousness or anxiety.
3. Sleep difficulty (e.g., insomnia, disturbing dreams).
4. Decreased appetite or weight loss.
5. Restlessness.
6. Depressed mood.
7. At least one of the following physical symptoms causing significant
discomfort: abdominal pain, shakiness/tremors, sweating, fever, chills, or
headache.
C. The signs or symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication or
withdrawal from another substance.
Coding note: The ICD-10-CM code depends on whether or not there is a comorbid
cannabis use disorder. If a mild cannabis use disorder is comorbid, the ICD-10-CM
code is F12.13, and if a moderate or severe cannabis use disorder is comorbid, the
ICD-10-CM code is F12.23. For cannabis withdrawal occurring in the absence of a
cannabis use disorder (e.g., in a patient taking cannabis solely under appropriate
medical supervision), the ICD-10-CM code is F12.93.
Diagnostic Features
The essential feature of cannabis withdrawal is the presence of a characteristic withdrawal
syndrome that develops after the cessation of regular cannabis use. Regular users become
tolerant to many acute cannabis effects, and cessation of regular use can lead to a cannabis
withdrawal syndrome. Common cannabis withdrawal symptoms include irritability, depressed
mood, anxiety, restlessness, sleep difficulty, and decreased appetite or weight loss. Cannabis
withdrawal can cause significant distress, leading to continued use to relieve the symptoms,
difficulty in quitting, and relapse. Unlike withdrawal from other substances (i.e., opioids,
alcohol, sedatives), behavioral and emotional symptoms (e.g., nervousness, irritability, sleep
difficulty) are often more common than physical symptoms (e.g., shakiness, sweating).
Associated Features

Cannabis withdrawal may be accompanied by observed fatigue, yawning, difficulty
concentrating, and rebound periods of increased appetite and hypersomnia that follow initial
periods of loss of appetite and insomnia.
Prevalence
Among adult and adolescent cannabis users, prevalence estimates of cannabis withdrawal
symptoms vary widely, from 35% to 95%, based on research in the United States and other
countries. Some of the variation in rates is likely attributable to assessment methods, and some to
differences between samples. Among adult regular cannabis users in the general population, 12%
reported signs and symptoms that met criteria for the full syndrome of DSM-5 cannabis
withdrawal, with substantial differences in prevalence among non-Latinx Whites (10%), African
Americans (15.3%), and Asian Americans, Native Hawaiians, and Pacific Islanders (31%).
Among adults and adolescents who are enrolled in treatment or are heavy cannabis users, 50%–
95% report cannabis withdrawal. These findings indicate that cannabis withdrawal occurs among
a substantial subset of regular cannabis users who try to quit.
Development and Course
Withdrawal onset typically occurs within 24–48 hours after cessation of use. It peaks within 2–5
days and resolves within 1–2 weeks, although sleep disturbance can persist longer. The amount,
duration, and frequency of cannabis smoking required to produce cannabis withdrawal are
unknown, but more chronic and frequent cannabis use is associated with greater quantity and
severity of withdrawal symptoms. Cannabis withdrawal can occur in adults and adolescents.
Women may experience more severe cannabis withdrawal symptoms than men.
Risk and Prognostic Factors
Among cannabis users, the propensity to experience cannabis withdrawal is moderately
heritable, indicating genetic influences. The prevalence and severity of cannabis withdrawal are
greater among heavier cannabis users, particularly those seeking treatment for cannabis use
disorder. Withdrawal severity may also be related to the presence and severity of comorbid
symptoms of mental disorders.
Functional Consequences of Cannabis Withdrawal
Cannabis users report using cannabis to relieve withdrawal symptoms, making cannabis
withdrawal a contributor to the persistence of cannabis use disorder. This makes cannabis
withdrawal a current target for medication development. Worse outcomes may be
associated with greater withdrawal. Sleep difficulty has been reported as the withdrawal
symptom most often associated with relapse to cannabis use. Cannabis users report having
relapsed to cannabis use or initiating use of other drugs (e.g., tranquilizers) to provide relief from
cannabis withdrawal symptoms.

Differential Diagnosis
Because many of the symptoms of cannabis withdrawal are also symptoms of other substance
withdrawal syndromes or of depressive or bipolar disorders, careful evaluation should focus on
ensuring that the symptoms are not better explained by cessation of another substance (e.g.,
tobacco or alcohol withdrawal), another mental disorder (generalized anxiety disorder, major
depressive disorder), or another medical condition. Given the increasingly common belief that
cannabis use is harmless, regular cannabis users experiencing cannabis withdrawal may not
realize that their withdrawal symptoms are due to the effects of cannabis wearing off, and
continue to use cannabis as a form of self-medication.
Comorbidity
Among adult frequent cannabis users, cannabis withdrawal is associated with comorbid
depression, anxiety, and antisocial personality disorder. Given the typical overlap of cannabis
withdrawal with cannabis use disorder, see “Comorbidity” under Cannabis Use Disorder for
more details about co-occurring conditions that are likely to be encountered.
Cannabis-Induced Mental Disorders
The following cannabis-induced mental disorders are described in other chapters of the manual
with disorders with which they share phenomenology (see the substance/medication-induced
mental disorders in these chapters): cannabis-induced psychotic disorder (“Schizophrenia
Spectrum and Other Psychotic Disorders”); cannabis-induced anxiety disorder (“Anxiety
Disorders”); and cannabis-induced sleep disorder (“Sleep-Wake Disorders”). For cannabis
intoxication delirium and delirium induced by pharmaceutical cannabis receptor agonists taken
as prescribed, see the criteria and discussion of delirium in the chapter “Neurocognitive
Disorders.” These cannabis-induced mental disorders are diagnosed instead of cannabis
intoxication or cannabis withdrawal when the symptoms are sufficiently severe to warrant
independent clinical attention.
Unspecified Cannabis-Related Disorder
F12.99
This category applies to presentations in which symptoms characteristic of a
cannabis-related disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for any specific cannabis-related disorder or any of the disorders
in the substance-related and addictive disorders diagnostic class.

Hallucinogen-Related Disorders
Phencyclidine Use Disorder
Other Hallucinogen Use Disorder
Phencyclidine Intoxication
Other Hallucinogen Intoxication
Hallucinogen Persisting Perception Disorder
Phencyclidine-Induced Mental Disorders
Hallucinogen-Induced Mental Disorders
Unspecified Phencyclidine-Related Disorder
Unspecified Hallucinogen-Related Disorder
Phencyclidine Use Disorder
Diagnostic Criteria
A. A pattern of phencyclidine (or a pharmacologically similar substance) use
leading to clinically significant impairment or distress, as manifested by at least
two of the following, occurring within a 12-month period:
1. Phencyclidine is often taken in larger amounts or over a longer period than
was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control
phencyclidine use.
3. A great deal of time is spent in activities necessary to obtain phencyclidine,
use the phencyclidine, or recover from its effects.
4. Craving, or a strong desire or urge to use phencyclidine.
5. Recurrent phencyclidine use resulting in a failure to fulfill major role
obligations at work, school, or home (e.g., repeated absences from work or
poor work performance related to phencyclidine use; phencyclidine-related
absences, suspensions, or expulsions from school; neglect of children or
household).
6. Continued phencyclidine use despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of the
phencyclidine (e.g., arguments with a spouse about consequences of
intoxication; physical fights).
7. Important social, occupational, or recreational activities are given up or
reduced because of phencyclidine use.

8. Recurrent phencyclidine use in situations in which it is physically hazardous
(e.g., driving an automobile or operating a machine when impaired by a
phencyclidine).
9. Phencyclidine use is continued despite knowledge of having a persistent or
recurrent physical or psychological problem that is likely to have been caused
or exacerbated by the phencyclidine.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of the phencyclidine to achieve
intoxication or desired effect.
b. A markedly diminished effect with continued use of the same amount of
the phencyclidine.
Note: Withdrawal symptoms and signs are not established for phencyclidines, and
so this criterion does not apply. (Withdrawal from phencyclidines has been reported
in animals but not documented in human users.)
Specify if:
In early remission: After full criteria for phencyclidine use disorder were
previously met, none of the criteria for phencyclidine use disorder have been met
for at least 3 months but for less than 12 months (with the exception that
Criterion A4, “Craving, or a strong desire or urge to use the phencyclidine,” may
be met).
In sustained remission: After full criteria for phencyclidine use disorder were
previously met, none of the criteria for phencyclidine use disorder have been met
at any time during a period of 12 months or longer (with the exception that
Criterion A4, “Craving, or a strong desire or urge to use the phencyclidine,” may
be met).
Specify if:
In a controlled environment: This additional specifier is used if the individual is
in an environment where access to phencyclidines is restricted.
Code based on current severity/remission: If a phencyclidine intoxication or
another phencyclidine-induced mental disorder is also present, do not use the codes
below for phencyclidine use disorder. Instead, the comorbid phencyclidine use
disorder is indicated in the 4th character of the phencyclidine-induced disorder code
(see the coding note for phencyclidine intoxication or a specific phencyclidineinduced mental disorder). For example, if there is comorbid phencyclidine-induced
psychotic disorder, only the phencyclidine-induced psychotic disorder code is given,
with the 4th character indicating whether the comorbid phencyclidine use disorder is
mild, moderate, or severe: F16.159 for mild phencyclidine use disorder with
phencyclidine-induced psychotic disorder or F16.259 for a moderate or severe
phencyclidine use disorder with phencyclidine-induced psychotic disorder.

Specify current severity/remission:
F16.10 Mild: Presence of 2–3 symptoms.
F16.11 Mild, In early remission
F16.11 Mild, In sustained remission
F16.20 Moderate: Presence of 4–5 symptoms.
F16.21 Moderate, In early remission
F16.21 Moderate, In sustained remission
F16.20 Severe: Presence of 6 or more symptoms.
F16.21 Severe, In early remission
F16.21 Severe, In sustained remission
Specifiers
“In a controlled environment” applies as a further specifier of remission if the individual is both
in remission and in a controlled environment (i.e., in early remission in a controlled environment
or in sustained remission in a controlled environment). Examples of these environments are
closely supervised and substance-free jails, therapeutic communities, and locked hospital units.
Diagnostic Features
The phencyclidines (or phencyclidine-like substances) include phencyclidine (e.g., PCP, “angel
dust”) and less potent but similarly acting compounds such as ketamine,
cyclohexamine, and dizocilpine. These substances were first developed as dissociative
anesthetics in the 1950s and became street drugs in the 1960s. They produce feelings of
separation from mind and body (hence “dissociative”) in low doses, and at high doses, stupor
and coma can result. These substances are most commonly smoked or taken orally, but they may
also be snorted or injected. Although the primary psychoactive effects of phencyclidine last for a
few hours, the total elimination rate of this drug from the body typically extends 8 days or
longer. The hallucinogenic effects in vulnerable individuals may last for weeks and may
precipitate a persistent psychotic episode resembling schizophrenia. Ketamine has been observed
to have utility in the treatment of major depressive disorder. Withdrawal symptoms have not
been clearly established in humans, and therefore the withdrawal criterion is not included in the
diagnosis of phencyclidine use disorder.
Associated Features
Phencyclidine may be detected in urine for up to 8 days or even longer at very high doses. In
addition to laboratory tests to detect its presence, characteristic symptoms resulting from
intoxication with phencyclidine or related substances may aid in its diagnosis. Phencyclidine is
likely to produce dissociative symptoms, analgesia, nystagmus, risk of hypertension/hypotension
and shock, euphoria, visual/auditory hallucinations, derealization, and unusual thought content.

Other substance use disorders.
Phencyclidine intoxication and phencyclidine-induced mental disorders.
Violent behavior can also occur with phencyclidine use, as intoxicated individuals may believe
that they are being attacked.
Prevalence
Data on the prevalence of phencyclidine use disorder are not available, but rates appear to be low
(based on rates of the overall category of hallucinogen use disorder, which includes
phencyclidine, of about 0.1% among individuals age 12 and older in the United States).
Furthermore, among U.S. substance use treatment facility admissions, only 0.3% of the admitted
individuals endorsed phencyclidine as their primary drug.
Risk and Prognostic Factors
In a general population study in Australia, ketamine users were more likely to be men and to
have consumed more than 11 standard drinks per day.
Sex- and Gender-Related Diagnostic Issues
The gender ratio for phencyclidine use disorder is not known, but among U.S. substance use
treatment facility admissions endorsing phencyclidine as the primary drug, 62% were men.
Diagnostic Markers
Laboratory testing may be useful, as phencyclidine is present in the urine in intoxicated
individuals up to 8 days after ingestion. The individual’s history along with certain physical
signs (e.g., nystagmus, analgesia, prominent hypertension) may aid in distinguishing the
phencyclidine clinical picture from that of other hallucinogens.
Functional Consequences of Phencyclidine Use Disorder
In individuals with phencyclidine use disorder, there may be physical evidence of injuries from
accidents, fights, and falls. Chronic use of phencyclidine can lead to acute and persistent
cognitive impairment; urinary tract and intestinal symptoms; abdominal pain, chest pain,
palpitations, and tachycardia; respiratory depression; sleep disorders; and depression.
Differential Diagnosis
Distinguishing the effects of phencyclidine from those of other
substances may be important, because phencyclidine can be an additive to other substances (e.g.,
cannabis, cocaine).
Phencyclidine use disorder is
differentiated from phencyclidine intoxication and phencyclidine-induced mental disorders (e.g.,
phencyclidine-induced psychotic disorder) in that phencyclidine use disorder describes a
problematic pattern of phencyclidine use that involves impaired control over phencyclidine use,
social impairment attributable to phencyclidine use, risky phencyclidine use (e.g., driving while
intoxicated), and pharmacological symptoms (the development of tolerance), whereas

Independent mental disorders.
phencyclidine intoxication and phencyclidine-induced mental disorders describe psychiatric
syndromes that occur in the context of heavy use. Phencyclidine intoxication and phencyclidineinduced mental disorders occur frequently in individuals with phencyclidine use disorder. In
such cases, a diagnosis of phencyclidine intoxication or a phencyclidine-induced mental disorder
should be given in addition to a diagnosis of phencyclidine use disorder, the presence of which is
indicated in the diagnostic code.
Some of the effects of phencyclidine use may resemble symptoms
of independent mental disorders, such as psychosis (schizophrenia); low mood (major depressive
disorder); and violent, aggressive behaviors (conduct disorder, antisocial personality disorder).
Discerning whether these behaviors occurred before the intake of the drug is important in the
differentiation of acute drug effects from a preexisting mental disorder.
Comorbidity
Conduct disorder in adolescents and antisocial personality disorder may be associated with
phencyclidine use. Other substance use disorders, especially alcohol, cocaine, and amphetamine
use disorders, are common among those with phencyclidine use disorder.
Other Hallucinogen Use Disorder
Diagnostic Criteria
A. A problematic pattern of hallucinogen (other than phencyclidine) use leading to
clinically significant impairment or distress, as manifested by at least two of the
following, occurring within a 12-month period:
1. The hallucinogen is often taken in larger amounts or over a longer period than
was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control
hallucinogen use.
3. A great deal of time is spent in activities necessary to obtain the hallucinogen,
use the hallucinogen, or recover from its effects.
4. Craving, or a strong desire or urge to use the hallucinogen.
5. Recurrent hallucinogen use resulting in a failure to fulfill major role obligations
at work, school, or home (e.g., repeated absences from work or poor work
performance related to hallucinogen use; hallucinogen-related absences,
suspensions, or expulsions from school; neglect of children or household).
6. Continued hallucinogen use despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of the
hallucinogen (e.g., arguments with a spouse about consequences of
intoxication; physical fights).

7. Important social, occupational, or recreational activities are given up or
reduced because of hallucinogen use.
8. Recurrent hallucinogen use in situations in which it is physically hazardous
(e.g., driving an automobile or operating a machine when impaired by the
hallucinogen).
9. Hallucinogen use is continued despite knowledge of having a persistent or
recurrent physical or psychological problem that is likely to have been caused
or exacerbated by the hallucinogen.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of the hallucinogen to achieve
intoxication or desired effect.
b. A markedly diminished effect with continued use of the same amount of
the hallucinogen.
Note: Withdrawal symptoms and signs are not established for hallucinogens, and so
this criterion does not apply.
Specify the particular hallucinogen.
Specify if:
In early remission: After full criteria for other hallucinogen use disorder were
previously met, none of the criteria for other hallucinogen use disorder have
been met for at least 3 months but for less than 12 months (with the exception
that Criterion A4, “Craving, or a strong desire or urge to use the hallucinogen,”
may be met).
In sustained remission: After full criteria for other hallucinogen use disorder
were previously met, none of the criteria for other hallucinogen use disorder
have been met at any time during a period of 12 months or longer (with the
exception that Criterion A4, “Craving, or a strong desire or urge to use the
hallucinogen,” may be met).
Specify if:
In a controlled environment: This additional specifier is used if the individual is
in an environment where access to hallucinogens is restricted.
Code based on current severity/remission: If a hallucinogen intoxication or
another hallucinogen-induced mental disorder is also present, do not use the codes
below for hallucinogen use disorder. Instead, the comorbid hallucinogen use
disorder is indicated in the 4th character of the hallucinogen-induced disorder code
(see the coding note for hallucinogen intoxication or specific hallucinogen-induced
mental disorder). For example, if there is comorbid hallucinogen-induced psychotic
disorder and hallucinogen use disorder, only the hallucinogen-induced psychotic
disorder code is given, with the 4th character indicating whether the comorbid
hallucinogen use disorder is mild, moderate, or severe: F16.159 for mild
hallucinogen use disorder with hallucinogen-induced psychotic disorder or F16.259
for a moderate or severe hallucinogen use disorder with hallucinogen-induced
psychotic disorder.

Specify current severity/remission:
F16.10 Mild: Presence of 2–3 symptoms.
F16.11 Mild, In early remission
F16.11 Mild, In sustained remission
F16.20 Moderate: Presence of 4–5 symptoms.
F16.21 Moderate, In early remission
F16.21 Moderate, In sustained remission
F16.20 Severe: Presence of 6 or more symptoms.
F16.21 Severe, In early remission
F16.21 Severe, In sustained remission
Specifiers
“In a controlled environment” applies as a further specifier of remission if the individual is both
in remission and in a controlled environment (i.e., in early remission in a controlled environment
or in sustained remission in a controlled environment). Examples of these environments are
closely supervised and substance-free jails, therapeutic communities, and locked hospital units.
Diagnostic Features
Hallucinogens comprise a diverse group of substances that despite having different chemical
structures and possibly involving different molecular mechanisms, produce similar alterations of
perception, mood, and cognition in users. Hallucinogens included are phenylalkylamines (e.g.,
mescaline, 
DOM 
[2,5-dimethoxy-4-methylamphetamine], 
and 
MDMA 
[3,4methylenedioxymethamphetamine; also called “ecstasy” or “molly”]); the indoleamines,
including psilocybin (and its metabolite psilocin, the compound primarily responsible for the
psychedelic effects of hallucinogenic mushrooms) and dimethyltryptamine (DMT); and the
ergolines, such as LSD (lysergic acid diethylamide) and morning glory seeds. In addition,
miscellaneous other ethnobotanical compounds are classified as hallucinogens, of which Salvia
divinorum and jimsonweed are two examples. Excluded from the hallucinogen group are
cannabis and its active compound, delta-9-tetrahydrocannabinol (THC) (see the section
“Cannabis-Related Disorders”). These substances can have hallucinogenic effects but are
diagnosed separately because of significant differences in their psychological and behavioral
effects.
Hallucinogens are usually taken orally, although some forms are smoked (e.g., DMT, salvia)
or (rarely) taken intranasally or by injection (e.g., ecstasy). Duration of effects varies across
types of hallucinogens. Some of these substances (i.e., LSD, MDMA) have a long half-life and
extended duration such that users may spend hours to days using and/or recovering from the
effects of these drugs. However, other hallucinogenic drugs (e.g., DMT, salvia) are short acting.
Tolerance to hallucinogens develops with repeated use and has been reported to have both
autonomic and psychological effects.

Temperamental.
MDMA/ecstasy as a hallucinogen may have distinctive effects attributable to both its
hallucinogenic and its stimulant properties. Ecstasy users have a higher risk of developing a
hallucinogen use disorder than those using other hallucinogens. Among both adolescent and
adult ecstasy users and users of other hallucinogens, the most frequently reported hallucinogen
use disorder criteria are tolerance, hazardous use, use despite emotional or health problems,
giving up activities in favor of use, and spending a lot of time obtaining, using, or recovering
from the effects of use. As found for other substances, diagnostic criteria for other hallucinogen
use disorder are arrayed along a single continuum of severity.
Given that a clinically significant withdrawal syndrome has not been consistently
documented in humans, the diagnosis of hallucinogen withdrawal syndrome is not included in
this manual and therefore is not part of the hallucinogen use disorder diagnostic criteria.
However, there may be evidence of withdrawal from MDMA, with endorsement of any two or
more withdrawal symptoms (e.g., malaise, appetite disturbance, mood changes [anxious,
depressed, irritable], poor concentration, sleep disruption) or withdrawal avoidance observed in
more than half of individuals in diverse samples of ecstasy users in the United States and
internationally.
Associated Features
The characteristic symptom features of use of some hallucinogens can aid in diagnosis if urine or
blood toxicology results are not available. For example, individuals who use LSD tend to
experience visual hallucinations that can be frightening.
Prevalence
Other hallucinogen use disorder is rare. In the U.S. general population, about 0.1% of individuals
age 12 or older endorsed the symptoms of past 12-month hallucinogen use disorder in 2018. The
rate was 0.2% among those ages 12–17, 0.4% among those ages 18–25,
and < 0.1% among those age 26 and older. Prevalence is higher in U.S. clinical samples (e.g.,
19% in adolescents in treatment), and among select groups of individuals who use hallucinogens
frequently (e.g., recent heavy ecstasy use) in the United States and Australia, 73.5% of adults and
77% of adolescents have a problematic pattern of use that may meet other hallucinogen use
disorder criteria.
Development and Course
Prevalence of other hallucinogen use disorder by age among adolescents is unknown. Among
U.S. adults age 18 years and older, most (90%) of those with other hallucinogen use disorder are
ages 18–29, suggesting that the disorder is not often persistent and is concentrated in young
adults.
Risk and Prognostic Factors
The use of specific hallucinogens (i.e., ecstasy, salvia) has been linked with high

Environmental.
Genetic and physiological.
sensation-seeking.
On the basis of research in the United States, environmental risk factors of other
hallucinogen use disorder include higher income, lower education, being never married, and
residing in urban areas. Early onset of hallucinogen use has also been linked to transition to
hallucinogen use disorder. Peer use of other drugs is also highly associated with ecstasy and
salvia use.
Among male twins, total variance due to additive genetics has been
estimated to range from 26% to 79%, with inconsistent evidence for shared environmental
influences.
Culture-Related Diagnostic Issues
Historically, hallucinogens have been used as part of established religious or spiritual practices,
such as the use of peyote in the Native American Church and in Mexico. Ritual use by
Indigenous populations of psilocybin obtained from certain types of mushrooms has occurred in
South America, Mexico, and some areas in the United States, or of ayahuasca in the Santo
Daime and União de Vegetal religious groups.
Sex- and Gender-Related Diagnostic Issues
Among U.S. adolescents, boys have greater 12-month prevalence rates of other hallucinogen use
than girls, and these gender differences extend to specific hallucinogens, including LSD,
MDMA, psilocybin, and salvia divinorum. Among U.S. adults, 60% of individuals with other
hallucinogen use disorder are men. International research suggests that women administered
MDMA may have greater subjective effects, such as altered state of consciousness, anxiety, and
depression. No information from international studies is available regarding gender differences
for other hallucinogen use disorder.
Diagnostic Markers
Laboratory testing can be useful in distinguishing among the different hallucinogens. However,
because some agents (e.g., LSD) are so potent that as little as 75 micrograms can produce severe
reactions, typical toxicological examination will not always reveal which substance has been
used.
Functional Consequences of Other Hallucinogen Use Disorder
Although insufficient information exists to clearly note the functional consequences of other
hallucinogen use disorder, complications of use of these substances have been
identified. Adverse effects of other hallucinogen use include those related to intoxication, such as
hyperthermia, cardiac tachyarrhythmias, pneumothorax hypernatremia, motor incoordination,
nystagmus, restlessness, hallucinations/delusions, mydriasis, increased alertness, and high blood
pressure. Other more serious reactions related to consequences of repeated use of other
hallucinogens include renal failure, hepatic failure, seizures, cerebral infarction, rhabdomyolysis,

Other substance disorders.
Hallucinogen intoxication and hallucinogen-induced mental disorders.
Independent mental disorders.
cardiac complications, and hepatotoxicity.
There is evidence for persisting neurotoxic effects of MDMA/ecstasy use, including
impairments in memory, psychological function, and neuroendocrine function; serotonin system
dysfunction; and sleep disturbance; as well as adverse effects on brain microvasculature, white
matter maturation, and damage to axons.
Differential Diagnosis
The effects of hallucinogen use must be distinguished from those of
other substances (e.g., amphetamine use disorder, alcohol or sedative withdrawal), especially
because contamination of the hallucinogens with other drugs is relatively common.
Hallucinogen use disorder is
differentiated from hallucinogen intoxication and hallucinogen-induced mental disorders (e.g.,
hallucinogen-induced psychotic disorder) in that hallucinogen use disorder describes a
problematic pattern of hallucinogen use that involves impaired control over hallucinogen use,
social impairment attributable to hallucinogen use, risky hallucinogen use (e.g., driving while
intoxicated), and pharmacological symptoms (the development of tolerance), whereas
hallucinogen intoxication and hallucinogen-induced mental disorders describe psychiatric
syndromes that occur in the context of heavy use. Hallucinogen intoxication and hallucinogeninduced mental disorders occur frequently in individuals with hallucinogen use disorder. In such
cases, a diagnosis of hallucinogen intoxication or a hallucinogen-induced mental disorder should
be given in addition to a diagnosis of hallucinogen use disorder, the presence of which is
indicated in the diagnostic code.
Some of the effects of hallucinogen use may resemble symptoms of
independent psychiatric disorders, such as schizophrenia and depressive and bipolar disorders.
Discerning whether symptoms occurred before the intake of the drug is important in the
differentiation of acute drug effects from a preexisting mental disorder. In particular,
schizophrenia should be ruled out, as some affected individuals (e.g., individuals with
schizophrenia who exhibit paranoia) may falsely attribute their symptoms to use of
hallucinogens.
Comorbidity
Other hallucinogen use disorder is highly associated with cocaine use disorder, stimulant use
disorder, other substance use disorder, tobacco (nicotine) use disorder, any personality disorder,
posttraumatic stress disorder, and panic attacks.
Phencyclidine Intoxication
Diagnostic Criteria
A. Recent use of phencyclidine (or a pharmacologically similar substance).
B. Clinically significant problematic behavioral changes (e.g., belligerence,

assaultiveness, impulsiveness, unpredictability, psychomotor agitation, impaired
judgment) that developed during, or shortly after, phencyclidine use.
C. Within 1 hour, two (or more) of the following signs or symptoms:
Note: When the drug is smoked, “snorted,” or used intravenously, the onset may
be particularly rapid.
1. Vertical or horizontal nystagmus.
2. Hypertension or tachycardia.
3. Numbness or diminished responsiveness to pain.
4. Ataxia.
5. Dysarthria.
6. Muscle rigidity.
7. Seizures or coma.
8. Hyperacusis.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication with
another substance.
Coding note: The ICD-10-CM code depends on whether there is a comorbid
phencyclidine use disorder. If a mild phencyclidine use disorder is comorbid, the
ICD-10-CM code is F16.120, and if a moderate or severe phencyclidine use disorder
is comorbid, the ICD-10-CM code is F16.220. If there is no comorbid phencyclidine
use disorder, then the ICD-10-CM code is F16.920.
Note: In addition to the section “Functional Consequences of Phencyclidine
Intoxication,” see the corresponding section in Phencyclidine Use Disorder.
Diagnostic Features
Phencyclidine intoxication reflects the clinically significant behavioral changes that occur shortly
after ingestion of this substance (or a pharmacologically similar substance). The most common
clinical presentations of phencyclidine intoxication include disorientation; confusion without
hallucinations; nystagmus; numbness or diminished responsiveness to pain; ataxia; dysarthria;
muscle rigidity; hyperacusis; and coma of varying severity. Other clinically significant
behavioral changes associated with phencyclidine intoxication include violent behavior, extreme
agitation, persecutory delusions, euphoria, retrograde amnesia, and hypertension.
Prevalence
Use of phencyclidine or related substances (e.g., ketamine) may be taken as an estimate of the
prevalence of intoxication. Phencyclidine use is rare, with < 0.1% of the U.S. population age 12
and older reporting past 12-month use in 2018. In surveys of U.S. students and young adults
followed up from high school, past 12-month prevalence of ketamine use, which is assessed

Other substance intoxication.
Phencyclidine-induced mental disorders.
Other medical conditions.
separately from other substances, was estimated at about 1.2% among 12th graders and 0.5%
among young adults, ages 19–28 years.
Diagnostic Markers
Laboratory testing may be useful, as phencyclidine is detectable in urine for up to 8 days
following use, although the levels are only weakly associated with an individual’s clinical
presentation and may therefore not be useful for case management. Creatine phosphokinase and
aspartate aminotransferase levels may be elevated.
Functional Consequences of Phencyclidine Intoxication
Phencyclidine intoxication produces extensive cardiovascular and neurological (e.g., seizures,
dystonias, dyskinesias, catalepsy, hypothermia or hyperthermia) toxicity.
Differential Diagnosis
In particular, in the absence of intact reality testing (i.e., without insight that the perceptual
abnormalities are drug induced), an additional diagnosis of phencyclidine-induced psychotic
disorder should be considered.
Phencyclidine intoxication should be differentiated from intoxication
due to other substances, including other hallucinogens; amphetamine, cocaine, or other
stimulants; and anticholinergics, as well as withdrawal from benzodiazepines. Nystagmus and
bizarre and violent behavior may distinguish intoxication due to phencyclidine from that due to
other substances. Toxicological tests may be useful in making this distinction. However, the
weak correlation between quantitative toxicology levels of phencyclidine and clinical
presentation may diminish the utility of the laboratory findings for patient management.
Phencyclidine 
intoxication 
is 
distinguished 
from
phencyclidine-induced mental disorders (e.g., phencyclidine-induced depressive disorder, with
onset during intoxication) because the symptoms (e.g., depressed mood) in the latter disorders
are in excess of those usually associated with phencyclidine intoxication, predominate in the
clinical presentation, and are severe enough to warrant clinical attention.
Medical conditions to be considered include certain metabolic disorders
like hypoglycemia and hyponatremia, central nervous system tumors, seizure disorders, sepsis,
neuroleptic malignant syndrome, and vascular insults.
Comorbidity
Given the typical overlap of phencyclidine intoxication with phencyclidine use disorder, see
“Comorbidity” under Phencyclidine Use Disorder for more details about co-occurring conditions
that are likely to be encountered.
Other Hallucinogen Intoxication

Diagnostic Criteria
A. Recent use of a hallucinogen (other than phencyclidine).
B. Clinically significant problematic behavioral or psychological changes (e.g.,
marked anxiety or depression, ideas of reference, fear of “losing one’s mind,”
paranoid ideation, impaired judgment) that developed during, or shortly after,
hallucinogen use.
C. Perceptual changes occurring in a state of full wakefulness and alertness (e.g.,
subjective intensification of perceptions, depersonalization, derealization,
illusions, hallucinations, synesthesias) that developed during, or shortly after,
hallucinogen use.
D. Two (or more) of the following signs developing during, or shortly after,
hallucinogen use:
1. Pupillary dilation.
2. Tachycardia.
3. Sweating.
4. Palpitations.
5. Blurring of vision.
6. Tremors.
7. Incoordination.
E. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication with
another substance.
Coding note: The ICD-10-CM code depends on whether there is a comorbid
hallucinogen use disorder. If a mild hallucinogen use disorder is comorbid, the ICD10-CM code is F16.120, and if a moderate or severe hallucinogen use disorder is
comorbid, the ICD-10-CM code is F16.220. If there is no comorbid hallucinogen use
disorder, then the ICD-10-CM code is F16.920.
Note: For information on Associated Features and Culture-Related Diagnostic Issues,
see the corresponding sections in Other Hallucinogen Use Disorder.
Diagnostic Features
Other hallucinogen intoxication reflects the clinically significant behavioral or psychological
changes that occur shortly after ingestion of a hallucinogen. Depending on the specific
hallucinogen, the intoxication may last only minutes (e.g., for salvia) or several hours or longer
(e.g., for LSD [lysergic acid diethylamide] or MDMA [3,4-methylenedioxymethamphetamine]).
Prevalence

Other substance intoxication.
Other conditions.
Hallucinogen persisting perception disorder.
The prevalence of other hallucinogen intoxication is not fully known but may be approximated
based on the prevalence of use of the substances. In 2018, 1.5% of individuals ages 12–17 years
in the United States reported use of hallucinogens in the past year; among individuals ages 18–
25, the rate was 6.9%, and among those age 26 or older, the rate was 1.3%. Rates were
consistently higher for boys and men than for girls and women in every age group.
Association With Suicidal Thoughts or Behavior
Other hallucinogen intoxication may lead to increased suicidal thoughts or behavior, although
suicide is rare among individuals who use hallucinogens. Of note, a study of more than 135,000
randomly selected U.S. adults, including more than 19,000 individuals who use psychedelics, did
not find evidence, after adjustment for sociodemographics, other drug use, and childhood
depression, that lifetime psychedelic use is an independent risk factor for mental health
problems, suicidal thoughts, or suicide attempts. In addition, one large U.S. population survey
found that a lifetime history of hallucinogen use was associated with lower odds of mental
distress and suicidal thoughts or behavior, although a causal relationship between hallucinogenic
drugs and lower distress cannot be inferred from this study. On the basis of these findings, the
relationship of other hallucinogen use to suicidal thoughts and behaviors is uncertain.
Functional Consequences of Other Hallucinogen Intoxication
Other hallucinogen intoxication can have serious consequences. The perceptual disturbances and
impaired judgment associated with other hallucinogen intoxication can result in injuries or
fatalities from automobile crashes, physical fights, or unintentional self-injury (e.g., cuts or falls
from impaired depth perception). When other hallucinogens are consumed in combination with
other drugs (including alcohol), coma can occur, with the duration and profundity of coma
greater than when other hallucinogens are taken alone. Continued use of hallucinogens,
particularly MDMA, has also been linked with neurotoxic effects. Adverse effects of other
hallucinogen use include hyperthermia, cardiac tachyarrhythmias, pneumothorax hypernatremia,
motor incoordination, nystagmus, restlessness, hallucinations/delusions, mydriasis, increased
alertness, and high blood pressure. More serious reactions include renal failure, hepatic failure,
seizures, cerebral infarction, rhabdomyolysis, cardiac complications, and hepatotoxicity.
Differential Diagnosis
Other hallucinogen intoxication should be differentiated from
intoxication with amphetamine-type substances, cocaine, or other stimulants; anticholinergics,
inhalants, and phencyclidine. Toxicological tests are useful in making this distinction, and
determining the route of administration may also be useful.
Other disorders and conditions to be considered include schizophrenia,
depression, withdrawal from other drugs (e.g., sedatives, alcohol), certain metabolic disorders
(e.g., hypoglycemia), seizure disorders, tumors of the central nervous system, and vascular
insults.
Other hallucinogen intoxication is distinguished from

Hallucinogen-induced mental disorders.
F16.983
hallucinogen persisting perception disorder because the symptoms in the latter continue
episodically or continuously for weeks (or longer) after the most recent intoxication.
Other hallucinogen intoxication is distinguished from
hallucinogen-induced mental disorders (e.g., hallucinogen-induced anxiety disorder, with onset
during intoxication) because the symptoms (e.g., anxiety) in these latter disorders are in excess
of those usually associated with other hallucinogen intoxication, predominate in the clinical
presentation, and are severe enough to warrant independent clinical attention.
Comorbidity
Given the typical overlap of other hallucinogen intoxication with other hallucinogen use
disorder, see “Comorbidity” under Other Hallucinogen Use Disorder for more details about cooccurring conditions that are likely to be encountered.
Hallucinogen Persisting Perception Disorder
Diagnostic Criteria
A. Following cessation of use of a hallucinogen, the reexperiencing of one or more
of the perceptual symptoms that were experienced while intoxicated with the
hallucinogen (e.g., geometric hallucinations, false perceptions of movement in
the peripheral visual fields, flashes of color, intensified colors, trails of images of
moving objects, positive afterimages, halos around objects, macropsia and
micropsia).
B. The symptoms in Criterion A cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
C. The symptoms are not attributable to another medical condition (e.g., anatomical
lesions and infections of the brain, visual epilepsies) and are not better explained
by another mental disorder (e.g., delirium, major neurocognitive disorder,
schizophrenia) or hypnopompic hallucinations.
Diagnostic Features
The hallmark of hallucinogen persisting perception disorder is the reexperiencing, when the
individual is sober, of the perceptual disturbances that were experienced while the individual was
intoxicated with the hallucinogen (Criterion A). The symptoms may include any perceptual
perturbations, but visual disturbances tend to be predominant. Typical of the abnormal visual
perceptions are geometric hallucinations, false perceptions of
movement in the peripheral visual fields, flashes of color, intensified colors, trails of images of
moving objects (i.e., images left suspended in the path of a moving object as seen in stroboscopic

photography), perceptions of entire objects, visual snow, positive afterimages (i.e., a samecolored or complementary-colored “shadow” of an object remaining after removal of the object),
halos around objects, or misperception of images as too large (macropsia) or too small
(micropsia). Duration of the visual disturbances may be episodic or nearly continuous and must
cause clinically significant distress or impairment in social, occupational, or other important
areas of functioning (Criterion B). The disturbances may last for weeks, months, or years. Other
explanations for the disturbances (e.g., brain lesions, preexisting psychosis, seizure disorders,
migraine aura without headaches) must be ruled out (Criterion C).
Hallucinogen persisting perception disorder occurs primarily after LSD (lysergic acid
diethylamide) use, but not exclusively. There does not appear to be a strong correlation between
hallucinogen persisting perception disorder and number of occasions of hallucinogen use, with
some instances of hallucinogen persisting perception disorder occurring in individuals with
minimal exposure to hallucinogens. Some instances of hallucinogen persisting perception
disorder may be triggered by use of other substances (e.g., cannabis or alcohol), adaptation to
dark environments, exercise, and exposure to noise and photophobia.
Associated Features
Reality testing remains intact in individuals with hallucinogen persisting perception disorder
(i.e., the individual is aware that the disturbance is linked to the effect of the drug). If this is not
the case, another disorder might better explain the abnormal perceptions.
Prevalence
Prevalence estimates of hallucinogen persisting perception disorder are unknown. Initial
prevalence estimates of the disorder among individuals who use hallucinogens is approximately
4.2%.
Development and Course
Little is known about the development of hallucinogen persisting perception disorder. Its course,
as suggested by its name, is persistent, lasting for weeks, months, or even years in certain
individuals.
Risk and Prognostic Factors
There is little evidence regarding risk factors for hallucinogen persisting perception disorder,
although genetic factors have been suggested as a possible explanation underlying the
susceptibility to LSD effects in this condition.
Functional Consequences of Hallucinogen Persisting Perception
Disorder
Although hallucinogen persisting perception disorder remains a chronic condition in some cases,
many individuals with the disorder are able to suppress the disturbances and continue to function
normally.
Differential Diagnosis

Conditions to be ruled out include schizophrenia, other drug effects, neurodegenerative
disorders, stroke, brain tumors, infections, and head trauma. Neuroimaging results in
hallucinogen persisting perception disorder cases are typically negative. As noted earlier, reality
testing remains intact (i.e., the individual is aware that the disturbance is linked to the
effect of the drug); if this is not the case, another disorder (e.g., psychotic disorder, another
medical condition) might better explain the abnormal perceptions.
Comorbidity
Common comorbid mental disorders accompanying hallucinogen persisting perception disorder
are panic disorder, alcohol use disorder, major depressive disorder, bipolar I disorder, and
schizophrenia spectrum disorders.
Phencyclidine-Induced Mental Disorders
Other phencyclidine-induced mental disorders are described in other chapters of the manual with
disorders with which they share phenomenology (see the substance/medication-induced mental
disorders in these chapters): phencyclidine-induced psychotic disorder (“Schizophrenia Spectrum
and Other Psychotic Disorders”); phencyclidine-induced bipolar and related disorder (“Bipolar
and Related Disorders”); phencyclidine-induced depressive disorder (“Depressive Disorders”);
and phencyclidine-induced anxiety disorder (“Anxiety Disorders”). For phencyclidine-induced
intoxication delirium and delirium induced by ketamine taken as prescribed, see the criteria and
discussion of delirium in the chapter “Neurocognitive Disorders.” These phencyclidine-induced
mental disorders are diagnosed instead of phencyclidine intoxication only when the symptoms
are sufficiently severe to warrant independent clinical attention.
Hallucinogen-Induced Mental Disorders
The following other hallucinogen-induced mental disorders are described in other chapters of the
manual with disorders with which they share phenomenology (see the substance/medicationinduced mental disorders in these chapters): other hallucinogen–induced psychotic disorder
(“Schizophrenia Spectrum and Other Psychotic Disorders”); other hallucinogen–induced bipolar
and related disorder (“Bipolar and Related Disorders”); other hallucinogen–induced depressive
disorder (“Depressive Disorders”); and other hallucinogen–induced anxiety disorder (“Anxiety
Disorders”). For other hallucinogen intoxication delirium and delirium induced by other
hallucinogens taken as prescribed, see the criteria and discussion of delirium in the chapter
“Neurocognitive Disorders.” These hallucinogen-induced mental disorders are diagnosed instead
of other hallucinogen intoxication only when the symptoms are sufficiently severe to warrant
independent clinical attention.
Unspecified Phencyclidine-Related Disorder

F16.99
This category applies to presentations in which symptoms characteristic of a
phencyclidine-related disorder that cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning predominate but do
not meet the full criteria for any specific phencyclidine-related disorder or any of the
disorders in the substance-related and addictive disorders diagnostic class.
Unspecified Hallucinogen-Related Disorder
F16.99
This category applies to presentations in which symptoms characteristic of a
hallucinogen-related disorder that cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning predominate but do
not meet the full criteria for any specific hallucinogen-related disorder or any of the
disorders in the substance-related and addictive disorders diagnostic class.
Inhalant-Related Disorders
Inhalant Use Disorder
Inhalant Intoxication
Inhalant-Induced Mental Disorders
Unspecified Inhalant-Related Disorder
Inhalant Use Disorder
Diagnostic Criteria
A. A problematic pattern of use of a hydrocarbon-based inhalant substance leading
to clinically significant impairment or distress, as manifested by at least two of
the following, occurring within a 12-month period:
1. The inhalant substance is often taken in larger amounts or over a longer
period than was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control use

of the inhalant substance.
3. A great deal of time is spent in activities necessary to obtain the inhalant
substance, use it, or recover from its effects.
4. Craving, or a strong desire or urge to use the inhalant substance.
5. Recurrent use of the inhalant substance resulting in a failure to fulfill major
role obligations at work, school, or home.
6. Continued use of the inhalant substance despite having persistent or
recurrent social or interpersonal problems caused or exacerbated by the
effects of its use.
7. Important social, occupational, or recreational activities are given up or
reduced because of use of the inhalant substance.
8. Recurrent use of the inhalant substance in situations in which it is physically
hazardous.
9. Use of the inhalant substance is continued despite knowledge of having a
persistent or recurrent physical or psychological problem that is likely to have
been caused or exacerbated by the substance.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of the inhalant substance to
achieve intoxication or desired effect.
b. A markedly diminished effect with continued use of the same amount of
the inhalant substance.
Specify the particular inhalant: When possible, the particular substance involved
should be named (e.g., “solvent use disorder”).
Specify if:
In early remission: After full criteria for inhalant use disorder were previously
met, none of the criteria for inhalant use disorder have been met for at least 3
months but for less than 12 months (with the exception that Criterion A4,
“Craving, or a strong desire or urge to use the inhalant substance,” may be met).
In sustained remission: After full criteria for inhalant use disorder were
previously met, none of the criteria for inhalant use disorder have been met at
any time during a period of 12 months or longer (with the exception that Criterion
A4, “Craving, or a strong desire or urge to use the inhalant substance,” may be
met).
Specify if:
In a controlled environment: This additional specifier is used if the individual is
in an environment where access to inhalant substances is restricted.
Code based on current severity/remission: If an inhalant intoxication or another
inhalant-induced mental disorder is also present, do not use the codes below for
inhalant use disorder. Instead, the comorbid inhalant use disorder is indicated in the

4th character of the inhalant-induced disorder code (see the coding note for inhalant
intoxication or a specific inhalant-induced mental disorder). For example, if there is
comorbid inhalant-induced depressive disorder and inhalant use disorder, only the
inhalant-induced depressive disorder code is given, with the 4th character indicating
whether the comorbid inhalant use disorder is mild, moderate, or severe: F18.14 for
mild inhalant use disorder with inhalant-induced depressive disorder or F18.24 for a
moderate or severe inhalant use disorder with inhalant-induced depressive disorder.
Specify current severity/remission:
F18.10 Mild: Presence of 2–3 symptoms.
F18.11 Mild, In early remission
F18.11 Mild, In sustained remission
F18.20 Moderate: Presence of 4–5 symptoms.
F18.21 Moderate, In early remission
F18.21 Moderate, In sustained remission
F18.20 Severe: Presence of 6 or more symptoms.
F18.21 Severe, In early remission
F18.21 Severe, In sustained remission
Specifiers
“In a controlled environment” applies as a further specifier of remission if the individual is both
in remission and in a controlled environment (i.e., in early remission in a controlled environment
or in sustained remission in a controlled environment). Examples of these environments are
closely supervised and substance-free jails, therapeutic communities, and locked hospital units.
The severity of individuals’ inhalant use disorder is assessed by the number of diagnostic
criteria endorsed. Changing severity of individuals’ inhalant use disorder across time is reflected
by reductions in the frequency (e.g., days used per month) and/or dose (e.g., tubes of glue per
day) used, as assessed by the individual’s self-report, report of others, clinician’s observations,
and biological testing (when practical).
Diagnostic Features
Examples of inhalant substances include volatile hydrocarbons, which comprise toxic gases from
glues, fuels, paints, and other volatile compounds. When possible, the
particular substance involved should be named (e.g., “toluene use disorder”). However, most
compounds that are inhaled are a mixture of several substances that can produce psychoactive
effects, and it is often difficult to ascertain the exact substance responsible for the disorder.
Unless there is clear evidence that a single, unmixed substance has been used, the general term
inhalant should be used in recording the diagnosis. Disorders arising from inhalation of nitrous
oxide or of amyl-, butyl-, or isobutylnitrite are considered as other (or unknown) substance use

disorder.
Features of inhalant use disorder include repeated use of an inhalant substance despite the
individual’s knowing that the substance is causing serious problems for the individual (Criterion
A9). Those problems are reflected in the diagnostic criteria.
Missing work or school or inability to perform typical responsibilities at work or school
(Criterion A5), and continued use of the inhalant substance even though it causes arguments with
family or friends, fights, and other social or interpersonal problems (Criterion A6), may be seen
in inhalant use disorder. Limiting family contact, work or school obligations, or recreational
activities (e.g., sports, games, hobbies) may also occur (Criterion A7). Use of inhalants when
driving or operating dangerous equipment (Criterion A8) is also seen.
Tolerance (Criterion A10) is reported by about 10% of individuals who use inhalants.
Because a clinically significant withdrawal syndrome has not been established with inhalant use,
neither a diagnosis of inhalant withdrawal nor a corresponding diagnostic criterion for
withdrawal complaints for inhalant use disorder is included. However, withdrawal symptoms
may occur among inhalant users and individuals with moderate to severe inhalant use disorder,
and these symptoms appear to be similar in frequency to withdrawal symptoms among those
with moderate to severe cocaine use disorder.
Associated Features
A diagnosis of inhalant use disorder is supported by recurring episodes of intoxication with
negative results in standard drug screens (which do not detect inhalants); possession, or lingering
odors, of inhalant substances; peri-oral or peri-nasal “glue-sniffer’s rash”; association with other
individuals known to use inhalants; membership in groups with prevalent inhalant use (e.g.,
some native or aboriginal communities, homeless children in street gangs); easy access to certain
inhalant substances; paraphernalia possession; presence of the disorder’s characteristic medical
complications (e.g., brain white matter pathology, rhabdomyolysis); and the presence of multiple
other substance use disorders. Individuals with inhalant use disorder may present with symptoms
of pernicious anemia, subacute combined degeneration of the spinal cord, major or mild
neurocognitive disorder, brain atrophy, leukoencephalopathy, and many other nervous system
disorders.
Prevalence
About 2.3% of American youth ages 12–17 years have used inhalants in the past 12 months, with
0.1% having a pattern of use that meets criteria for inhalant use disorder. Among U.S. adults, age
18 years and older, past 12-month prevalence of inhalant use is about 0.21%, with 0.04% having
a pattern of use that meets criteria for an inhalant use disorder. Among youth, the prevalence of
past 12-month inhalant use is highest among non-Hispanic Whites and individuals reporting
more than one racialized identity and lowest among American Indians/Alaska Natives. Twelvemonth prevalence rates of inhalant use and inhalant use disorder among adults are highest among
non-Hispanic Whites and lowest among non-Hispanic Blacks and American Indians/Alaska
Natives.
Development and Course

Temperamental.
Environmental.
Genetic and physiological.
The declining prevalence in the United States of inhalant use and inhalant use disorder after
adolescence (from 2.3% during adolescence to 0.1% in early adulthood for inhalant use and from
0.1% to 0.04% for inhalant use disorder) indicates that the disorder usually
remits in early adulthood. Inhalant use disorder is rare in prepubertal children, most common in
adolescents and young adults, and uncommon in older persons. Calls to poison-control centers
for “intentional abuse” of inhalants peak with calls involving individuals at age 14 years. Those
with inhalant use disorder extending into adulthood demonstrate earlier onset of inhalant use, use
of multiple inhalants, and more frequent inhalant use.
Risk and Prognostic Factors
Predictors of inhalant use disorder include sensation seeking and impulsivity.
Inhalant gases are widely and legally available, increasing the risk of misuse.
Childhood maltreatment or trauma also is associated with youthful progression from inhalant
non-use to inhalant use disorder.
Behavioral disinhibition is a highly heritable general propensity to not
constrain behavior in socially acceptable ways, to break social norms and rules, and to take
dangerous risks, pursuing rewards excessively despite dangers of adverse consequences. Youths
with strong behavioral disinhibition show risk factors for inhalant use disorder: early-onset
substance use disorder, multiple substance involvement, and early conduct problems. Because
behavioral disinhibition is under strong genetic influence, youths in families with substance use
and antisocial behaviors are at elevated risk for inhalant use disorder.
Culture-Related Diagnostic Issues
Internationally, certain isolated Indigenous communities have experienced a high prevalence of
inhalant problems. Also, in some low- and middle-income countries, groups of homeless
children living on the streets have extensive inhalant use problems because of the effects of
poverty and the availability and affordability of the substances, and as a way to cope with
homelessness.
Sex- and Gender-Related Diagnostic Issues
Although the past 12-month prevalence of inhalant use disorder in the United States is almost
identical among adolescent boys and girls, the disorder is very rare among adult women.
Diagnostic Markers
Urine, breath, or saliva tests may be valuable for assessing concurrent use of non-inhalant
substances by individuals with inhalant use disorder. However, technical problems and the
considerable expense of analyses make frequent biological testing for inhalants themselves
impractical.
Association With Suicidal Thoughts or Behavior

Inhalant exposure (unintentional) from industrial or other accidents.
Inhalant intoxication, without meeting criteria for inhalant use disorder.
Inhalant intoxication meeting criteria for inhalant use disorder, and inhalant-induced mental
disorders.
Other substance use disorders, especially those involving sedating substances (e.g., alcohol,
benzodiazepines, barbiturates).
In the United States, adolescent and adult inhalant use and inhalant use disorder are associated
with suicidal thoughts and behavior, especially among individuals reporting symptoms of anxiety
and depression and histories of trauma.
Functional Consequences of Inhalant Use Disorder
Because of inherent toxicity, use of inhalants can be fatal. Death can occur from anoxia, cardiac
dysfunction, extreme allergic reaction, severe injury to the lungs, vomiting, accidents or injury,
or central nervous system depression. Moreover, any inhaled volatile hydrocarbons may produce
“sudden sniffing death” from cardiac arrhythmia. Inhalant use impairs neurobehavioral function
and causes various neurological, gastrointestinal, cardiovascular, and pulmonary problems.
Long-term inhalant users are at increased risk for tuberculosis, HIV/AIDS, sexually
transmitted diseases, depression, anxiety, bronchitis, asthma, and sinusitis.
Differential Diagnosis
A diagnosis of inhalant use
disorder only applies if the inhalant exposure is intentional.
Inhalant 
intoxication 
occurs
frequently during inhalant use disorder but also may occur among individuals whose use does
not meet criteria for inhalant use disorder.
Inhalant use disorder is differentiated from inhalant intoxication and inhalant-induced mental
disorders (e.g., inhalant-induced depressive disorder) in that inhalant use disorder describes a
problematic pattern of inhalant use that involves impaired control over inhalant use, social
impairment attributable to inhalant use, risky inhalant use (e.g., inhalant use despite medical
complications), and pharmacological symptoms (the development of tolerance), whereas inhalant
intoxication and inhalant-induced mental disorders describe psychiatric syndromes that develop
in the context of heavy use. Inhalant intoxication and inhalant-induced mental disorders occur
frequently in individuals with inhalant use disorder. In such cases, a diagnosis of inhalant
intoxication or an inhalant-induced mental disorder should be given in addition to a diagnosis of
inhalant use disorder, the presence of which is indicated in the diagnostic code.
Inhalant use disorder commonly co-occurs with other substance use disorders, and the symptoms
of the disorders may be similar and overlapping. To disentangle symptom patterns, it is helpful
to inquire about which symptoms persisted during periods when some of the substances were not
being used.
Comorbidity
Individuals with inhalant use disorder receiving clinical care often have numerous other
substance use, mood, anxiety, and personality disorders. Inhalant use disorder commonly co-

occurs with conduct disorder in adolescents and with antisocial personality disorder. Individuals
with inhalant use disorder may have comorbid symptoms of hepatic or renal damage,
rhabdomyolysis, methemoglobinemia, or symptoms of other gastrointestinal, cardiovascular, or
pulmonary diseases.
Inhalant Intoxication
Diagnostic Criteria
A. Recent intended or unintended short-term, high-dose exposure to inhalant
substances, including volatile hydrocarbons such as toluene or gasoline.
B. Clinically significant problematic behavioral or psychological changes (e.g.,
belligerence, assaultiveness, apathy, impaired judgment) that developed during,
or shortly after, exposure to inhalants.
C. Two (or more) of the following signs or symptoms developing during, or shortly
after, inhalant use or exposure:
1. Dizziness.
2. Nystagmus.
3. Incoordination.
4. Slurred speech.
5. Unsteady gait.
6. Lethargy.
7. Depressed reflexes.
8. Psychomotor retardation.
9. Tremor.
10. Generalized muscle weakness.
11. Blurred vision or diplopia.
12. Stupor or coma.
13. Euphoria.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication with
another substance.
Coding note: The ICD-10-CM code depends on whether there is a comorbid
inhalant use disorder. If a mild inhalant use disorder is comorbid, the ICD-10-CM
code is F18.120, and if a moderate or severe inhalant use disorder is comorbid, the
ICD-10-CM code is F18.220. If there is no comorbid inhalant use disorder, then the
ICD-10-CM code is F18.920.

Note: For information on Development and Course, Risk and Prognostic Factors,
Culture-Related Diagnostic Issues, and Diagnostic Markers, see the corresponding
sections in Inhalant Use Disorder.
Diagnostic Features
The essential feature of inhalant intoxication is the presence of clinically significant problematic
behavioral or psychological changes that develop during, or immediately after, intended or
unintended inhalation of a volatile hydrocarbon substance. When possible, the particular
substance involved should be named (e.g., toluene intoxication). Intoxication clears within a few
minutes to a few hours after the exposure ends. Thus, inhalant intoxication usually occurs in
brief episodes that may recur with further inhalant use.
Associated Features
Inhalant intoxication may be indicated by evidence of possession, or lingering odors, of inhalant
substances (e.g., glue, paint thinner, gasoline, butane lighters); other features may include
euphoria, relaxation, headache, rapid heartbeat, confusion, talkativeness, blurred vision, amnesia,
slurred speech, irritability, nausea, fatigue, burning in eyes or throat, grandiosity, chest pain,
auditory or visual hallucinations, and dissociation.
Prevalence
The prevalence of actual episodes of inhalant intoxication in the general population is unknown,
but it is probable that a majority of inhalant users would at some time exhibit behavioral or
psychological changes and symptoms that would meet criteria for inhalant intoxication.
Therefore, the prevalence of inhalant use and the prevalence of inhalant intoxication are likely
similar. In 2017, inhalant use in the past year was reported by 0.6% of all Americans older than
12 years; the prevalence was highest in younger age groups (2.3% for individuals ages 12 –17
years, 1.6% for individuals ages 18–25 years, and 0.3% for individuals age 26 and older).
Sex- and Gender-Related Diagnostic Issues
Gender differences in the prevalence of inhalant intoxication in the general population are
unknown. Regarding gender differences in the prevalence of inhalant use in the United
States, 0.8% of boys/men older than 12 years and 0.5% of girls/women older than 12 years have
used inhalants in the previous year, but in the younger age groups differences are minimal or
girls may have slightly higher prevalence (e.g., among adolescents ages 12–17 years, 2.4% of
girls and 2.2% of boys have used inhalants in the past year).
Functional Consequences of Inhalant Intoxication
Use of inhaled substances in a closed container, such as a plastic bag over the head, may lead to
unconsciousness, anoxia, and death. Separately, “sudden sniffing death,” likely from cardiac
arrhythmia or arrest, may occur with various volatile inhalants. The enhanced toxicity of certain

Intoxication from other substances, especially from sedating substances (e.g., alcohol,
benzodiazepines, barbiturates).
Inhalant-induced mental disorders.
Other toxic, metabolic, traumatic, neoplastic, or infectious disorders that impair brain function
and cognition.
volatile inhalants, such as butane or propane, also causes fatalities. Although inhalant
intoxication itself is of short duration, it may produce persisting medical and neurological
problems, especially if the intoxications are frequent. Clinically significant correlates of inhalant
intoxication include reckless behaviors (e.g., taking foolish risks, getting into fights, having
unprotected sex), antisocial behaviors (cruelty, damaging property, arrests), and having serious
accidents.
Differential Diagnosis
These disorders may have similar signs and symptoms, but intoxication attributable to other
intoxicants may be identified via a toxicology screen. Differentiating the source of the
intoxication may involve discerning evidence of inhalant exposure as described for inhalant use
disorder. A diagnosis of inhalant intoxication may be suggested by possession or lingering odors
of inhalant substances (e.g., glue, paint thinner, gasoline, butane lighters); paraphernalia
possession (e.g., rags or bags for concentrating glue fumes); perioral or perinasal “glue-sniffer’s
rash”; reports from family or friends that the intoxicated individual possesses or uses inhalants;
or apparent intoxication despite negative results on standard drug screens (which usually fail to
identify inhalants).
Inhalant intoxication is distinguished from inhalant-induced
mental disorders (e.g., inhalant-induced anxiety disorder, with onset during intoxication) because
the symptoms (e.g., anxiety) in these latter disorders are in excess of those usually associated
with inhalant intoxication, predominate in the clinical presentation, and are severe enough to
warrant independent clinical attention.
Numerous neurological and other medical conditions may produce the clinically significant
behavioral or psychological changes (e.g., belligerence, assaultiveness, apathy, impaired
judgment) that also characterize inhalant intoxication.
Comorbidity
Given the typical overlap of inhalant intoxication with inhalant use disorder, see “Comorbidity”
under Inhalant Use Disorder for more details about co-occurring conditions that are likely to be
encountered.
Inhalant-Induced Mental Disorders
The following inhalant-induced mental disorders are described in other chapters of the manual
with disorders with which they share phenomenology (see the substance/medication-induced
mental disorders in these chapters): inhalant-induced psychotic disorder (“Schizophrenia
Spectrum and Other Psychotic Disorders”); inhalant-induced depressive
disorder (“Depressive Disorders”); inhalant-induced anxiety disorder (“Anxiety Disorders”); and

inhalant-induced major or mild neurocognitive disorder (“Neurocognitive Disorders”). For
inhalant intoxication delirium, see the criteria and discussion of delirium in the chapter
“Neurocognitive Disorders.” These inhalant-induced mental disorders are diagnosed instead of
inhalant intoxication only when symptoms are sufficiently severe to warrant independent clinical
attention.
Unspecified Inhalant-Related Disorder
F18.99
This category applies to presentations in which symptoms characteristic of an
inhalant-related disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for any specific inhalant-related disorder or any of the disorders
in the substance-related and addictive disorders diagnostic class.
Opioid-Related Disorders
Opioid Use Disorder
Opioid Intoxication
Opioid Withdrawal
Opioid-Induced Mental Disorders
Unspecified Opioid-Related Disorder
Opioid Use Disorder
Diagnostic Criteria
A. A problematic pattern of opioid use leading to clinically significant impairment or
distress, as manifested by at least two of the following, occurring within a 12month period:
1. Opioids are often taken in larger amounts or over a longer period than was
intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control
opioid use.
3. A great deal of time is spent in activities necessary to obtain the opioid, use
the opioid, or recover from its effects.

4. Craving, or a strong desire or urge to use opioids.
5. Recurrent opioid use resulting in a failure to fulfill major role obligations at
work, school, or home.
6. Continued opioid use despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of opioids.
7. Important social, occupational, or recreational activities are given up or
reduced because of opioid use.
8. Recurrent opioid use in situations in which it is physically hazardous.
9. Continued opioid use despite knowledge of having a persistent or recurrent
physical or psychological problem that is likely to have been caused or
exacerbated by the substance.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of opioids to achieve intoxication
or desired effect.
b. A markedly diminished effect with continued use of the same amount of
an opioid.
Note: This criterion is not considered to be met for those taking opioids solely
under appropriate medical supervision.
11. Withdrawal, as manifested by either of the following:
a. The characteristic opioid withdrawal syndrome (refer to Criteria A and B of
the criteria set for opioid withdrawal).
b. Opioids (or a closely related substance) are taken to relieve or avoid
withdrawal symptoms.
Note: This criterion is not considered to be met for those individuals taking
opioids solely under appropriate medical supervision.
Specify if:
In early remission: After full criteria for opioid use disorder were previously met,
none of the criteria for opioid use disorder have been met for at least 3 months
but for less than 12 months (with the exception that Criterion A4, “Craving, or a
strong desire or urge to use opioids,” may be met).
In sustained remission: After full criteria for opioid use disorder were previously
met, none of the criteria for opioid use disorder have been met at any time during
a period of 12 months or longer (with the exception that Criterion A4, “Craving, or
a strong desire or urge to use opioids,” may be met).
Specify if:
On maintenance therapy: This additional specifier is used if the individual is
taking a prescribed agonist medication such as methadone or buprenorphine
and none of the criteria for opioid use disorder have been met for that class of

medication (except tolerance to, or withdrawal from, the agonist). This category
also applies to those individuals being maintained on a partial agonist, an
agonist/antagonist, or a full antagonist such as oral naltrexone or depot
naltrexone.
In a controlled environment: This additional specifier is used if the individual is
in an environment where access to opioids is restricted.
Code based on current severity/remission: If an opioid intoxication, opioid
withdrawal, or another opioid-induced mental disorder is also present, do not use the
codes below for opioid use disorder. Instead, the comorbid opioid use disorder is
indicated in the 4th character of the opioid-induced disorder code (see the coding
note for opioid intoxication, opioid withdrawal, or a specific opioid-induced mental
disorder). For example, if there is comorbid opioid-induced depressive disorder and
opioid use disorder, only the opioid-induced depressive disorder code is given, with
the 4th character indicating whether the comorbid opioid use disorder is mild,
moderate, or severe: F11.14 for mild opioid use disorder with opioid-induced
depressive disorder or F11.24 for a moderate or severe opioid use disorder with
opioid-induced depressive disorder.
Specify current severity/remission:
F11.10 Mild: Presence of 2–3 symptoms.
F11.11 Mild, In early remission
F11.11 Mild, In sustained remission
F11.20 Moderate: Presence of 4–5 symptoms.
F11.21 Moderate, In early remission
F11.21 Moderate, In sustained remission
F11.20 Severe: Presence of 6 or more symptoms.
F11.21 Severe, In early remission
F11.21 Severe, In sustained remission
Specifiers
The “on maintenance therapy” specifier applies as a further specifier of remission if the
individual is both in remission and receiving maintenance therapy. “In a controlled environment”
applies as a further specifier of remission if the individual is both in remission and in a controlled
environment (i.e., in early remission in a controlled environment or in sustained remission in a
controlled environment). Examples of these environments are closely supervised and substancefree jails, therapeutic communities, and locked hospital units.
Changing severity across time in an individual is also reflected by reductions in the
frequency (e.g., days of use per month) and/or dose (e.g., injections or number of pills) of an
opioid, as assessed by the individual’s self-report, report of knowledgeable others, clinician’s

observations, and biological testing.
Diagnostic Features
The opioids include natural opioids (e.g., morphine, codeine), semisynthetics (e.g., heroin,
oxycodone, hydrocodone, hydromorphone, oxymorphone), and synthetics with morphine-like
action (e.g., methadone, meperidine, tramadol, fentanyl, carfentanil). Medications such as
pentazocine and buprenorphine that have both opiate agonist and antagonist effects are also
included in this class because, especially at lower doses, their agonist properties produce similar
physiological and behavioral effects as classic opioid agonists. Opioids are prescribed as
analgesics, anesthetics, antidiarrheal agents, or cough suppressants. Heroin is one of the most
commonly misused drugs of this class and is usually taken by injection, although it can be
smoked or “snorted,” especially when very pure heroin is available. Fentanyl is typically
injected, both medically and nonmedically, and is used medically in transdermal and
transmucosal formulations, whereas cough suppressants and antidiarrheal agents are taken orally.
The other opioids are generally taken both by injection and orally.
Opioid use disorder can arise from prescription opioids or illicit opioids (e.g., heroin and,
especially in recent years, fentanyl-related synthetic opioids). Opioid use disorder consists of
signs and symptoms reflecting compulsive, prolonged self-administration of opioid substances
either for a purpose other than a legitimate medical one or for use in a “non-medical” manner
(i.e., greatly exceeding the amount prescribed for a medical condition). For example, an
individual with adequate doses of prescribed analgesic opioid medication for pain relief who
uses significantly more of the medication than prescribed, and not only because of persistent
pain, is engaging in nonmedical opioid use and may have an opioid use disorder. Most
individuals with opioid use disorder have tolerance and experience withdrawal on abrupt
cessation or reduction in opioid use. Similar to processes that occur with other psychoactive
substances, individuals with opioid use disorder often develop conditioned responses to drugrelated stimuli (e.g., cue-reactive craving on seeing drug images or paraphernalia). These
responses probably contribute to relapse, are difficult to extinguish, and typically persist long
after withdrawal is completed.
Individuals with opioid use disorder tend to develop such regular patterns of compulsive drug
use that daily activities are planned around obtaining and administering
opioids. Prescription opioids used nonmedically can be obtained from family or friends, from
physicians by falsifying or exaggerating medical problems, by receiving simultaneous
prescriptions from several physicians, or via purchase on the illegal market. Health care
professionals with opioid use disorder can obtain opioids by writing prescriptions for themselves
or by diverting opioids that have been prescribed for individuals or from pharmacy supplies.
Associated Features
An attempt to achieve opioid intoxication may result in fatal or nonfatal opioid overdose. Opioid
overdose is characterized by unconsciousness, respiratory depression, and pinpoint pupils.
However, opioid overdoses can also occur in the absence of intoxication-seeking drug use.

Opioid overdoses have increased exponentially in the United States since 1999. Up to 2009,
opioid overdoses were mainly due to prescribed opioids, but since 2010, overdoses due to heroin
began a sharp rise, and additionally, since 2015, fatal overdoses due to synthetic opioids other
than methadone (generally fentanyl) have outnumbered overdoses due to prescribed opioids.
Opioid use disorder can be associated with a history of drug-related crimes (e.g., possession
or distribution of drugs, forgery, burglary, robbery, larceny, receiving stolen goods). Among
health care professionals and individuals who have ready access to controlled substances, a
different pattern of illegal activities may involve problems with state licensing boards,
professional staffs of hospitals, or other administrative agencies. Marital difficulties (including
divorce), unemployment, and irregular employment can be associated with opioid use disorder at
all socioeconomic levels.
Prevalence
The prevalence of nonmedical prescription opioid use among U.S. adults age 18 and older is
4.1%–4.7%, with rates of use higher in adults ages 18–25 than in those age 26 and older (5.5%
vs. 3.4%, respectively). The prevalence of heroin use in the United States is 0.3%–0.4% and is
higher among adults ages 18–25 (0.5%–0.7%) than in other age groups. In U.S. adolescents ages
12–17, 2.8%–3.9% use prescription opioids nonmedically, with higher rates in older adolescents
than in younger adolescents. Heroin use in adolescents is quite low (< 0.05%–0.1%).
The prevalence of prescription opioid use disorder among U.S. adults age 18 and older
(DSM-IV or DSM-5 criteria) is 0.6%–0.9%, and the prevalence of heroin use disorder (DSM-IV
or DSM-5 criteria) is 0.1%–0.3%. Among those ages 12–17, prevalence of prescription opioid
use disorder is 0.4%, and heroin use disorder is rare (essentially 0%). In the United States, rates
of opioid use disorder (prescription opioids and heroin) are higher among men than women,
among young adults than older adults, and among those with lower income or education. Among
U.S. adults in 2012–2013, the prevalence of nonmedical prescription opioid use disorder varied
by ethnoracial group: 1.42% in Native Americans, 1.04% in African Americans, 0.96% in nonLatinx Whites, 0.70% in Latinx, and 0.16% in Asian Americans or Pacific Islanders. Rates based
on household surveys may underestimate national prevalence by omitting individuals in
institutions and jail or prison, whose rates are likely to be much higher.
Globally in 2016, there were 26.8 million cases of DSM-IV opioid dependence, with an agestandardized prevalence of 353.0 cases per 100,000 people; prevalence of opioid dependence
across geographic regions ranged from 0.14% to 0.46%.
Development and Course
Opioid use disorder can begin at any age. In the United States, problems associated with opioid
use are most commonly first observed in the late teens or early 20s, with a longer interval
between first opioid use and onset of disorder for prescription opioids than for
heroin. Early use can reflect a desire for relief from life stressors or psychological pain. Longterm studies show that once an opioid use disorder that requires treatment develops, it can
continue over many years, with brief periods of abstinence in some individuals but long-term

abstinence only in a minority. An exception occurred among U.S. soldiers who became
dependent on opioids while serving in the Vietnam War; over 90% had long-term abstinence
from opioids after returning to the United States, although many subsequently experienced
problems with alcohol, amphetamines, or suicidal thoughts or behavior.
Risk and Prognostic Factors
In addition to an association with more frequent nonmedical prescription opioid use, adult
prescription opioid use disorder is associated with most other substance use disorders. Opioid use
disorder is highly associated with externalizing traits such as novelty-seeking, impulsivity, and
disinhibition. Family, peer, and social environmental factors all increase the risk for opioid use
disorder. Family and twin studies also indicate a strong genetic contribution to the risk for opioid
use disorders, although identifying the specific genetic variants contributing to genetic risk has
been slow. Peer factors may relate to genetic predisposition in terms of how individuals select
their environments, including their peers.
Culture-Related Diagnostic Issues
Individuals from socially oppressed ethnoracial groups were historically overrepresented among
individuals with opioid use disorder. However, over time, opioid use disorder has become more
common among White individuals, suggesting that the widespread availability of opioids and
other social factors (e.g., changes in rates of poverty and unemployment) have an impact on
prevalence. Consistent with these factors, despite small variations between ethnoracial groups in
the psychometric performance of opioid use disorder criterion items, the criteria for opioid use
disorder perform equally well across ethnoracial groups.
Sex- and Gender-Related Diagnostic Issues
Women with opioid use disorder appear more likely than men to have initiated opioid use in
response to sexual abuse and violence, and they are more likely than men to be introduced to the
drug by a partner. There is substantial evidence of telescoping among women in that they
progress to a use disorder more quickly than men after first use; women also appear to be more
ill when entering treatment facilities than are men, as noted in a large sample of heroin users in
Italy.
Diagnostic Markers
Routine urine toxicology test results are often positive for opioid drugs in individuals with opioid
use disorder. Urine test results remain positive for most opioids (e.g., heroin, morphine, codeine,
oxycodone, propoxyphene) for 12–36 hours after administration. Some opioids, such as fentanyl
and oxycodone, are not detected by standard urine tests (which test for morphine), but can be
identified by more specialized procedures for several days after use. Similarly, methadone and
buprenorphine (or buprenorphine/naloxone combinations) will not cause a positive result on
routine tests for opiates; they require specific tests that can detect these substances for several
days up to more than 1 week.
Although not specific markers of opioid use disorder, laboratory evidence of the presence of
other substances (e.g., cocaine, marijuana, alcohol, amphetamines, benzodiazepines) is common

in heroin users. In addition, screening test results for hepatitis A, B, and C virus are often
positive in injection opioid users, either for hepatitis antigen (signifying active infection) or for
hepatitis antibody (signifying past infection). Mildly elevated liver
function test results are common, either as a result of resolving hepatitis or from toxic injury
to the liver due to contaminants that have been mixed with the injected opioid. HIV is also
prevalent in injection opioid users. Subtle changes in cortisol secretion patterns and body
temperature regulation have been observed for up to 6 months following opioid withdrawal.
Association With Suicidal Thoughts or Behavior
Opioid use disorder is associated with a heightened risk for suicide attempts and suicide. Some
suicide risk factors overlap with risk factors for an opioid use disorder. In addition, repeated
opioid intoxication or withdrawal may be associated with severe depressions that although
temporary can be intense enough to lead to suicide attempts and suicide. Nonfatal accidental
opioid overdose and attempted suicide are distinct phenomena that can be difficult to
differentiate but should not be mistaken for each other, if possible.
Findings from the Global Burden of Disease Study 2010 showed that among drugs of abuse,
suicide is a common cause of death among regular users of opioids. Evidence suggests that
suicides are undercounted or often misclassified in opioid-poisoning data. In a study of the
Veterans Health Administration (VHA) national medical records, after adjustment for psychiatric
comorbidity, opioid use disorder elevated the risk for suicide mortality, with greater increase in
risk among women than among men. In another study also using VHA national medical records,
among veterans prescribed opioids for chronic pain, suicide mortality increased with higher
opioid doses, even after demographic and clinical factors were taken into account. A follow-up
of a U.S. national cohort of adults with a history of an opioid overdose found that the
standardized mortality ratio (SMR; the ratio between the observed number of deaths in a study
population and the number of deaths that would be expected) was 25.9 for suicide, with a higher
SMR for women than for men. A review posited that the reasons for the increased risk for
suicide among opioid users were related to shared risk factors, namely, comorbid mental
disorders and pain.
Functional Consequences of Opioid Use Disorder
Physiologically, opioid use is associated with a lack of mucous membrane secretions, causing
dry mouth and nose. Slowing of gastrointestinal activity and a decrease in gut motility can
produce severe constipation. Visual acuity may be impaired as a result of pupillary constriction
with acute administration. In individuals who inject opioids, sclerosed veins (“tracks”) and
puncture marks on the lower portions of the upper extremities are common. Veins sometimes
become so severely sclerosed that peripheral edema develops, and individuals switch to injecting
in veins in the legs, neck, or groin. When these veins become unusable, individuals often inject
directly into their subcutaneous tissue (“skin-popping”), resulting in cellulitis, abscesses, and
circular-appearing scars from healed skin lesions. Tetanus and Clostridium botulinum infections
are rare but serious consequences of injecting opioids, especially with contaminated needles.

Opioid intoxication, opioid withdrawal, and opioid-induced mental disorders.
Infections may also occur in other organs and include bacterial endocarditis, hepatitis, and HIV
infection. Hepatitis C infections, for example, may occur in up to 90% of individuals who inject
opioids. In addition, the prevalence of HIV infection is high among individuals who inject drugs,
a large proportion of whom are individuals with opioid use disorder. For example, HIV infection
rates are as high as 60% among heroin users in some areas of the United States and the Russian
Federation. However, the incidence may be much lower in areas where access to clean injection
material and paraphernalia is facilitated.
Tuberculosis is a particularly serious problem among individuals who use drugs
intravenously, especially those who are dependent on heroin; infection is usually asymptomatic
and evident only by the presence of a positive tuberculin skin test or tuberculosis blood test
(interferon gamma release assay). However, many cases of active tuberculosis have been found,
especially among those who are infected with HIV. These individuals
often have a newly acquired infection but also are likely to experience reactivation of a prior
infection because of impaired immune function.
Individuals who sniff heroin or other opioids into the nose (insufflation, or “snorting”) often
develop irritation of the nasal mucosa, sometimes accompanied by perforation of the nasal
septum. Difficulties in sexual functioning are common. Males often experience erectile
dysfunction during intoxication or chronic use. Females commonly have disturbances of
reproductive function and irregular menses.
Although acute opioid use produces analgesia, chronic use can produce hyperalgesia (opioidinduced hyperalgesia), a condition characterized by increased sensitivity to pain. Physiological
dependence on opioids may occur in about half of the infants born to females with opioid use
disorder. This can produce a severe withdrawal syndrome in the neonate requiring medical
treatment and has increased markedly in prevalence.
The mortality rate in individuals with opioid use disorder is 6–20 times greater than in the
general population. Fatal overdoses due to prescription opioids increased dramatically in the
United States since 1999, with almost 400,000 such deaths occurring since then, and the rate of
such overdoses is now five times higher than in 1999. Fatal overdoses due to heroin began a
sharp increase in 2010, and since 2013, fatal overdoses due to synthetic opioids (e.g., fentanyl)
increased so sharply that these rates were almost double the rates for prescription opioid or
heroin overdoses by 2017. Nonfatal opioid overdoses resulting in hospitalization and emergency
department visits have increased as well. Although not all risk factors for opioid use disorder and
opioid overdose are the same, substantial overlap exists, making the risk for overdose one of the
most serious potential consequences of opioid use disorder. Individuals with opioid use disorder
are also at increased risk for mortality from many medical conditions (e.g., hepatitis, HIV
infection, tuberculosis, cardiovascular disease). Death can also result from accidents, injuries, or
other general medical complications.
Differential Diagnosis
Opioid use disorder is
differentiated from opioid intoxication, opioid withdrawal, and opioid-induced mental disorders

Other substance intoxication.
Other withdrawal disorders.
Independent mental disorders.
(e.g., opioid-induced depressive disorder) in that opioid use disorder describes a problematic
pattern of opioid use that involves impaired control over opioid use, social impairment
attributable to opioid use, risky opioid use (e.g., continued opioid use despite medical
complications), and pharmacological symptoms (the development of tolerance or withdrawal),
whereas opioid intoxication, opioid withdrawal, and opioid-induced mental disorders describe
psychiatric syndromes that occur in the context of heavy use. Opioid intoxication, opioid
withdrawal, and opioid-induced mental disorders occur frequently in individuals with opioid use
disorder. In such cases, a diagnosis of opioid intoxication, opioid withdrawal, or opioid-induced
mental disorder should be given in addition to a diagnosis of opioid use disorder, the presence of
which is indicated in the diagnostic code.
Alcohol intoxication and sedative, hypnotic, or anxiolytic
intoxication can cause a clinical picture that resembles that of opioid intoxication. A diagnosis of
alcohol or sedative, hypnotic, or anxiolytic intoxication can usually be made based on the
absence of pupillary constriction or the lack of a response to naloxone challenge. In some cases,
intoxication may be due both to opioids and to alcohol or other sedatives. In these cases, the
naloxone challenge will not reverse all of the sedative effects.
The anxiety and restlessness associated with opioid withdrawal
resemble symptoms seen in sedative-hypnotic withdrawal. However, opioid withdrawal is also
accompanied by rhinorrhea, lacrimation, and pupillary dilation, which are not seen in sedativetype withdrawal. Dilated pupils are also seen in hallucinogen intoxication and stimulant
intoxication. However, other signs or symptoms of opioid
withdrawal, such as nausea, vomiting, diarrhea, abdominal cramps, rhinorrhea, or lacrimation,
are not present.
Some of the effects of opioid use may resemble symptoms (e.g.,
depressed mood) of an independent mental disorder (e.g., persistent depressive disorder).
Opioids are less likely to produce symptoms of mental disturbance than are most other drugs of
abuse.
Comorbidity
Other than overdose, the most common medical comorbidities associated with opioid use
disorder are viral (e.g., HIV, hepatitis C virus) and bacterial infections, particularly among
injection heroin users. These infections are less common in prescription opioid use disorder.
Research with nationally representative samples of the U.S. population has found that opioid
use disorder is often associated with other substance use disorders, especially those involving
tobacco, alcohol, cannabis, stimulants, and benzodiazepines. Individuals with opioid use disorder
are at risk for the development of persistent depressive disorder or major depressive disorder.
These symptoms may represent an opioid-induced depressive disorder or an exacerbation of a
preexisting independent depressive disorder. Periods of depression are especially common
during chronic intoxication or in association with physical or psychosocial stressors related to the
opioid use disorder. Insomnia is also common, especially during withdrawal. Opioid use disorder
is also associated with bipolar I disorder, posttraumatic stress disorder, and antisocial, borderline,

and schizotypal personality disorders. A history of conduct disorder in childhood or adolescence
has also been identified as a significant risk factor for substance-related disorders, especially
opioid use disorder. Further, prescription opioid use disorder and heroin use disorder are
generally associated with serious mental illness, defined as a mental disorder other than a
substance use disorder that results in serious functional impairment substantially limiting or
interfering with major life activities.
Opioid Intoxication
Diagnostic Criteria
A. Recent use of an opioid.
B. Clinically significant problematic behavioral or psychological changes (e.g., initial
euphoria followed by apathy, dysphoria, psychomotor agitation or retardation,
impaired judgment) that developed during, or shortly after, opioid use.
C. Pupillary constriction (or pupillary dilation due to anoxia from severe overdose)
and one (or more) of the following signs or symptoms developing during, or
shortly after, opioid use:
1. Drowsiness or coma.
2. Slurred speech.
3. Impairment in attention or memory.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication with
another substance.
Specify if:
With perceptual disturbances: This specifier may be noted in the rare instance
in which hallucinations with intact reality testing or auditory, visual, or tactile
illusions occur in the absence of a delirium.
Coding note: The ICD-10-CM code depends on whether or not there is a comorbid
opioid use disorder and whether or not there are perceptual disturbances.
For opioid intoxication, without perceptual disturbances: If a mild opioid use
disorder is comorbid, the ICD-10-CM code is F11.120, and if a moderate or
severe opioid use disorder is comorbid, the ICD-10-CM code is F11.220. If there
is no comorbid opioid use disorder, then the ICD-10-CM code is F11.920.
For opioid intoxication, with perceptual disturbances: If a mild opioid use
disorder is comorbid, the ICD-10-CM code is F11.122, and if a moderate or
severe opioid use disorder is comorbid, the ICD-10-CM code is F11.222. If there
is no comorbid opioid use disorder, then the ICD-10-CM code is F11.922.

Other substance intoxication.
Diagnostic Features
The essential feature of opioid intoxication is the presence of clinically significant problematic
behavioral or psychological changes (e.g., initial euphoria followed by apathy, dysphoria,
psychomotor agitation or retardation, impaired judgment) that develop during, or shortly after,
opioid use (Criteria A and B). Intoxication is accompanied by pupillary constriction (unless there
has been a severe overdose with consequent anoxia and pupillary dilation) and one or more of
the following signs: drowsiness (described as being “on the nod”), slurred speech, and
impairment in attention or memory (Criterion C); drowsiness may progress to coma. Individuals
with opioid intoxication may demonstrate inattention to the environment, even to the point of
ignoring potentially harmful events. The signs or symptoms of opioid intoxication must not be
attributable to another medical condition and are not better explained by another mental disorder
(Criterion D).
Up to 2009, opioid overdoses were mainly due to prescribed opioids, but starting in 2010,
overdoses due to heroin began a sharp rise, and additionally, since 2015, fatal overdoses due to
synthetic opioids other than methadone (generally fentanyl) have outnumbered overdoses due to
prescribed opioids.
Associated Features
Opioid intoxication can include decreases in respiratory rate and blood pressure, and mild
hypothermia. The duration of opioid intoxication can vary as a function of the pharmacokinetics
of the opioid ingested. Opioid intoxication may result in fatal or nonfatal opioid overdose.
Opioid overdose is characterized by unconsciousness, respiratory depression, and pinpoint
pupils. Fatal opioid overdoses have increased exponentially in the United States since 1999.
Development and Course
Opioid intoxication can occur in an individual who is opioid naïve, an individual who uses
opioids sporadically, and an individual who is physically dependent on opioids. The dose of
opioid consumed relative to the likelihood of experiencing opioid intoxication will vary as a
function of the status and history of the individual’s opioid exposure (i.e., tolerance). Individuals
often report that the qualitative pleasurable experience of opioid intoxication diminishes after
repeated use of an opioid.
Differential Diagnosis
Alcohol intoxication and sedative-hypnotic intoxication can cause a
clinical picture that resembles opioid intoxication. A diagnosis of alcohol or sedative-hypnotic
intoxication can usually be made based on the absence of pupillary constriction or the lack of a
response to a naloxone challenge. In some cases, intoxication may be due both to opioids and to
alcohol or other sedatives. In these cases, naloxone administration will not reverse all of the
sedative effects. While response to administration of

Opioid-induced mental disorders.
naloxone can support the diagnosis of opioid intoxication, nonresponse may be due to the coingestion of an opioid with another drug (e.g., a benzodiazepine, alcohol) or to ingestion of a
higher dose of and/or higher-potency opioid (e.g., fentanyl).
Opioid intoxication is distinguished from opioid-induced mental
disorders (e.g., opioid-induced depressive disorder, with onset during intoxication) because the
symptoms (e.g., depressed mood) in the latter disorders are in excess of those usually associated
with opioid intoxication, predominate in the clinical presentation, and are severe enough to
warrant clinical attention.
Comorbidity
Given the typical overlap of opioid intoxication with opioid use disorder, see “Comorbidity”
under Opioid Use Disorder for more details about co-occurring conditions that are likely to be
encountered.
Opioid Withdrawal
Diagnostic Criteria
A. Presence of either of the following:
1. Cessation of (or reduction in) opioid use that has been heavy and prolonged
(i.e., several weeks or longer).
2. Administration of an opioid antagonist after a period of opioid use.
B. Three (or more) of the following developing within minutes to several days after
Criterion A:
1. Dysphoric mood.
2. Nausea or vomiting.
3. Muscle aches.
4. Lacrimation or rhinorrhea.
5. Pupillary dilation, piloerection, or sweating.
6. Diarrhea.
7. Yawning.
8. Fever.
9. Insomnia.
C. The signs or symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication or
withdrawal from another substance.
Coding note: The ICD-10-CM code depends on whether or not there is a comorbid

opioid use disorder. If a mild opioid use disorder is comorbid, the ICD-10-CM code is
F11.13, and if a moderate or severe opioid use disorder is comorbid, the ICD-10-CM
code is F11.23. For opioid withdrawal occurring in the absence of an opioid use
disorder (e.g., in a patient taking opioids solely under appropriate medical
supervision), the ICD-10-CM code is F11.93.
Diagnostic Features
The essential feature of opioid withdrawal is the presence of a characteristic withdrawal
syndrome that develops after the cessation of (or reduction in) prolonged opioid use
(Criterion A1). The opioids used may be illicit or licitly obtained drugs prescribed to treat pain.
A withdrawal syndrome can also be precipitated by administration of an opioid antagonist (e.g.,
naloxone, naltrexone, nalmefene) after a period of opioid use (Criterion A2); it can also occur
after administration of an opioid partial agonist (e.g., buprenorphine) to an individual currently
using a full opioid agonist.
Opioid withdrawal has a characteristic pattern of signs and symptoms. The first of these are
subjective and consist of complaints of anxiety, restlessness, and an “achy feeling” that is often
located in the back and legs, along with irritability and increased sensitivity to pain. Three or
more of the following must be present to make a diagnosis of opioid withdrawal: dysphoric
mood; nausea or vomiting; muscle aches; lacrimation or rhinorrhea; pupillary dilation,
piloerection, or increased sweating; diarrhea; yawning; fever; and insomnia (Criterion B).
Piloerection and fever are associated with more severe withdrawal and are not often seen in
routine clinical practice because individuals with opioid use disorder usually obtain substances
before withdrawal becomes that far advanced. These symptoms of opioid withdrawal must cause
clinically significant distress or impairment in social, occupational, or other important areas of
functioning (Criterion C). The symptoms must not be attributable to another medical condition
and are not better explained by another mental disorder (Criterion D). Having symptoms that
meet diagnostic criteria for opioid withdrawal alone is not sufficient for a diagnosis of opioid use
disorder, but concurrent symptoms of craving and drug-seeking behavior are suggestive of
comorbid opioid use disorder.
Associated Features
Opioid withdrawal may occur in any individual after cessation of repeated use of an opioid,
whether in the setting of medical management of pain, during opioid agonist therapy for opioid
use disorder, in the context of illicit use, or following attempts to self-treat symptoms of mental
disorders with opioids. Opioid withdrawal is a distinct condition from opioid addiction or opioid
use disorder and does not necessarily require the drug-seeking behaviors associated with opioid
use disorder to be diagnosed. Thus, opioid withdrawal may occur in individuals without opioid
use disorder and should not be confused with it. Males with opioid withdrawal may experience
piloerection, sweating, and spontaneous ejaculations while awake.
Prevalence

Other withdrawal disorders.
Other substance intoxication.
Opioid-induced mental disorders.
Among individuals from various U.S. clinical settings, opioid withdrawal occurred in 60% of
individuals who had used heroin at least once in the prior 12 months. Individuals regularly using
opioids (e.g., prescription opioids for pain, illicit opioids) for a period of time are at risk for
developing physical dependence, including withdrawal, on cessation or marked reduction in use.
Development and Course
The speed and severity of withdrawal associated with opioids depend on the half-life of the
opioid used. Most individuals who are physiologically dependent on short-acting drugs such as
heroin begin to have withdrawal symptoms within 6–12 hours after the last dose. Symptoms may
take 2–4 days to emerge in the case of longer-acting drugs such as methadone or buprenorphine.
Acute withdrawal symptoms for a short-acting opioid such as heroin usually peak within 1–3
days and gradually subside over a period of 5–7 days. More chronic symptoms (e.g., anxiety,
dysphoria, anhedonia, craving, insomnia) can last for weeks to months. The severity of opioid
withdrawal also varies depending on the duration of opioid use. Opioid withdrawal symptoms
among individuals receiving long-term prescription opioid treatment for pain can be minimized
by tapering the drug slowly.
Among those with an opioid use disorder, opioid withdrawal and attempts to relieve
withdrawal are typical. The course of withdrawal can be part of an escalating pattern in which an
opioid is used to reduce withdrawal symptoms, in turn leading to recurrent episodes of
withdrawal at a later time.
Differential Diagnosis
The anxiety and restlessness associated with opioid withdrawal
resemble symptoms seen in sedative-hypnotic withdrawal. However, opioid withdrawal is also
accompanied by rhinorrhea, lacrimation, and pupillary dilation, which are not seen in sedativetype withdrawal.
Dilated pupils are also seen in hallucinogen intoxication and
stimulant intoxication. However, other signs or symptoms of opioid withdrawal, such as nausea,
vomiting, diarrhea, abdominal cramps, rhinorrhea, and lacrimation, are not present.
Opioid withdrawal is distinguished from opioid-induced mental
disorders (e.g., opioid-induced depressive disorder, with onset during withdrawal) because the
symptoms (e.g., depressed mood) in these latter disorders are in excess of those usually
associated with opioid withdrawal, predominate in the clinical presentation, and are severe
enough to warrant clinical attention.
Comorbidity
Given the typical overlap of opioid withdrawal with opioid use disorder, see “Comorbidity”
under Opioid Use Disorder for more details about co-occurring conditions that are likely to be
encountered.

Opioid-Induced Mental Disorders
The following opioid-induced mental disorders are described in other chapters of the manual
with disorders with which they share phenomenology (see the substance/medication-induced
mental disorders in these chapters): opioid-induced depressive disorder (“Depressive
Disorders”); opioid-induced anxiety disorder (“Anxiety Disorders”); opioid-induced sleep
disorder (“Sleep-Wake Disorders”); and opioid-induced sexual dysfunction (“Sexual
Dysfunctions”). For opioid intoxication delirium, opioid withdrawal delirium, and delirium
induced by opioids taken as prescribed, see the criteria and discussion of delirium in the chapter
“Neurocognitive Disorders.” These opioid-induced mental disorders are diagnosed instead of
opioid intoxication or opioid withdrawal only when the symptoms are sufficiently severe to
warrant independent clinical attention.
Unspecified Opioid-Related Disorder
F11.99
This category applies to presentations in which symptoms characteristic of an opioidrelated disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any specific opioid-related disorder or any of the disorders in the
substance-related and addictive disorders diagnostic class.
Sedative-, Hypnotic-, or Anxiolytic-Related
Disorders
Sedative, Hypnotic, or Anxiolytic Use Disorder
Sedative, Hypnotic, or Anxiolytic Intoxication
Sedative, Hypnotic, or Anxiolytic Withdrawal
Sedative-, Hypnotic-, or Anxiolytic-Induced Mental Disorders
Unspecified Sedative-, Hypnotic-, or Anxiolytic-Related Disorder
Sedative, Hypnotic, or Anxiolytic Use Disorder
Diagnostic Criteria

A. A problematic pattern of sedative, hypnotic, or anxiolytic use leading to clinically
significant impairment or distress, as manifested by at least two of the following,
occurring within a 12-month period:
1. Sedatives, hypnotics, or anxiolytics are often taken in larger amounts or over
a longer period than was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control
sedative, hypnotic, or anxiolytic use.
3. A great deal of time is spent in activities necessary to obtain the sedative,
hypnotic, or anxiolytic; use the sedative, hypnotic, or anxiolytic; or recover
from its effects.
4. Craving, or a strong desire or urge to use the sedative, hypnotic, or anxiolytic.
5. Recurrent sedative, hypnotic, or anxiolytic use resulting in a failure to fulfill
major role obligations at work, school, or home (e.g., repeated absences from
work or poor work performance related to sedative, hypnotic, or anxiolytic
use; sedative-, hypnotic-, or anxiolytic-related absences, suspensions, or
expulsions from school; neglect of children or household).
6. Continued sedative, hypnotic, or anxiolytic use despite having persistent or
recurrent social or interpersonal problems caused or exacerbated by the
effects of sedatives, hypnotics, or anxiolytics (e.g., arguments with a spouse
about consequences of intoxication; physical fights).
7. Important social, occupational, or recreational activities are given up or
reduced because of sedative, hypnotic, or anxiolytic use.
8. Recurrent sedative, hypnotic, or anxiolytic use in situations in which it is
physically hazardous (e.g., driving an automobile or operating a machine
when impaired by sedative, hypnotic, or anxiolytic use).
9. Sedative, hypnotic, or anxiolytic use is continued despite knowledge of having
a persistent or recurrent physical or psychological problem that is likely to
have been caused or exacerbated by the sedative, hypnotic, or anxiolytic.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of the sedative, hypnotic, or
anxiolytic to achieve intoxication or desired effect.
b. A markedly diminished effect with continued use of the same amount of
the sedative, hypnotic, or anxiolytic.
Note: This criterion is not considered to be met for individuals taking
sedatives, hypnotics, or anxiolytics under medical supervision.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for sedatives, hypnotics, or
anxiolytics (refer to Criteria A and B of the criteria set for sedative,
hypnotic, or anxiolytic withdrawal).

b. Sedatives, hypnotics, or anxiolytics (or a closely related substance, such
as alcohol) are taken to relieve or avoid withdrawal symptoms.
Note: This criterion is not considered to be met for individuals taking
sedatives, hypnotics, or anxiolytics under medical supervision.
Specify if:
In early remission: After full criteria for sedative, hypnotic, or anxiolytic use
disorder were previously met, none of the criteria for sedative, hypnotic, or
anxiolytic use disorder have been met for at least 3 months but for less than 12
months (with the exception that Criterion A4, “Craving, or a strong desire or urge
to use the sedative, hypnotic, or anxiolytic,” may be met).
In sustained remission: After full criteria for sedative, hypnotic, or anxiolytic
use disorder were previously met, none of the criteria for sedative, hypnotic, or
anxiolytic use disorder have been met at any time during a period of 12 months
or longer (with the exception that Criterion A4, “Craving, or a strong desire or
urge to use the sedative, hypnotic, or anxiolytic,” may be met).
Specify if:
In a controlled environment: This additional specifier is used if the individual is
in an environment where access to sedatives, hypnotics, or anxiolytics is
restricted.
Code based on current severity/remission: If a sedative, hypnotic, or anxiolytic
intoxication; sedative, hypnotic, or anxiolytic withdrawal; or another sedative-,
hypnotic-, or anxiolytic-induced mental disorder is also present, do not use the codes
below for sedative, hypnotic, or anxiolytic use disorder. Instead, the comorbid
sedative, hypnotic, or anxiolytic use disorder is indicated in the 4th character of the
sedative-, hypnotic-, or anxiolytic-induced disorder (see the coding note for sedative,
hypnotic, or anxiolytic intoxication; sedative, hypnotic, or anxiolytic withdrawal; or
specific sedative-, hypnotic-, or anxiolytic-induced mental disorder). For example, if
there is comorbid sedative-, hypnotic-, or anxiolytic-induced depressive disorder and
sedative, hypnotic, or anxiolytic use disorder, only the sedative-, hypnotic-, or
anxiolytic-induced depressive disorder code is given, with the 4th character
indicating whether the comorbid sedative, hypnotic, or anxiolytic use disorder is mild,
moderate, or severe: F13.14 for mild sedative, hypnotic, or anxiolytic use disorder
with sedative-, hypnotic-, or anxiolytic-induced depressive disorder or F13.24 for a
moderate or severe sedative, hypnotic, or anxiolytic use disorder with sedative-,
hypnotic-, or anxiolytic-induced depressive disorder.
Specify current severity/remission:
F13.10 Mild: Presence of 2–3 symptoms.
F13.11 Mild, In early remission
F13.11 Mild, In sustained remission
F13.20 Moderate: Presence of 4–5 symptoms.
F13.21 Moderate, In early remission

F13.21 Moderate, In sustained remission
F13.20 Severe: Presence of 6 or more symptoms.
F13.21 Severe, In early remission
F13.21 Severe, In sustained remission
Specifiers
“In a controlled environment” applies as a further specifier of remission if the individual is both
in remission and in a controlled environment (i.e., in early remission in a controlled environment
or in sustained remission in a controlled environment). Examples of these environments are
closely supervised and substance-free jails, therapeutic communities, and locked hospital units.
Diagnostic Features
Sedative, hypnotic, or anxiolytic substances include benzodiazepines, benzodiazepine-like drugs
(e.g., zolpidem, zaleplon), carbamates (e.g., glutethimide, meprobamate), barbiturates (e.g.,
secobarbital), and barbiturate-like hypnotics (e.g., glutethimide, methaqualone, propofol). This
class of substances includes most prescription sleeping medications and most prescription
antianxiety medications. Nonbenzodiazepine antianxiety agents (e.g., buspirone, gepirone) are
not included in this class because they do not appear to be associated with significant misuse.
Like 
alcohol, 
these 
agents 
are 
brain 
depressants 
and 
can 
produce 
similar
substance/medication-induced and substance use disorders. Sedative, hypnotic, or anxiolytic
substances are available both by prescription and illegally. Some individuals who obtain these
substances by prescription will develop a sedative, hypnotic, or anxiolytic use disorder, while
others who misuse these substances or use them for intoxication will not develop a use disorder.
In particular, sedatives, hypnotics, or anxiolytics with rapid onset or short to intermediate lengths
of action may be taken for intoxication purposes, although longer-acting substances in this class
may be taken for intoxication as well.
Craving (Criterion A4), either during periods of active use or during periods of abstinence, is
a typical feature of sedative, hypnotic, or anxiolytic use disorder. Misuse of substances from this
class may occur in conjunction with use of other substances. For example, individuals may use
intoxicating doses of sedatives or benzodiazepines to “come down” from cocaine or
amphetamines or use high doses of benzodiazepines in combination with methadone to “boost”
its effects.
Repeated absences or poor work performance, school absences, suspensions or expulsions,
and neglect of children or household (Criterion A5) may be related to sedative, hypnotic, or
anxiolytic use disorder; the continued use of the substances despite arguments with a spouse
about consequences of intoxication or despite physical fights (Criterion A6) may also occur.
Limiting contact with family or friends, avoiding work or school, or stopping participation in
hobbies, sports, or games (Criterion A7) and recurrent sedative, hypnotic, or anxiolytic use when
driving an automobile or operating machinery when impaired by such use (Criterion A8) are also
seen in sedative, hypnotic, or anxiolytic use disorder.
Very significant levels of tolerance and withdrawal can develop to sedative, hypnotic, or

anxiolytic substances. There may be evidence of tolerance and withdrawal in the absence of a
diagnosis of a sedative, hypnotic, or anxiolytic use disorder in an individual who has abruptly
discontinued use of benzodiazepines that were taken for long periods of time at prescribed and
therapeutic doses. In these cases, an additional diagnosis of sedative, hypnotic, or anxiolytic use
disorder is made only if other criteria are met. That is, sedative, hypnotic, or anxiolytic
medications may be prescribed for appropriate medical purposes, and depending on the dose
regimen, these drugs may then produce tolerance and withdrawal. If these drugs are prescribed or
recommended for appropriate medical purposes, and if they are used as prescribed, the resulting
tolerance or withdrawal does not count toward the diagnosis of a substance use disorder.
However, it is necessary to determine whether the drugs were inappropriately prescribed and
used (e.g., falsifying medical symptoms to obtain the medication; using more medication than
prescribed; obtaining the medication from several doctors without informing them).
Given the unidimensional nature of the symptoms of sedative, hypnotic, or anxiolytic use
disorder, severity is based on the number of criteria endorsed.
Associated Features
Research with nationally representative samples of the U.S. population has found that sedative,
hypnotic, or anxiolytic use disorder is often associated with other substance use disorders (e.g.,
alcohol, cannabis, opioid, stimulant use disorders). Sedatives are often used to alleviate the
unwanted effects of these other substances. With repeated use of the sedative, hypnotic, or
anxiolytic, tolerance develops to the sedative effects, and a progressively higher dose is used.
However, tolerance to brain stem depressant effects develops much more slowly, and as the
individual takes more substance to achieve euphoria or other desired effects, there may be a
sudden onset of respiratory depression and hypotension, which may result in death. Intense or
repeated sedative, hypnotic, or anxiolytic intoxication may be associated with severe depression
that although temporary can lead to suicide attempt and suicide.
Prevalence
The 12-month prevalence of DSM-IV sedative, hypnotic, or anxiolytic use disorder in the United
States is estimated to be 0.3% among adolescents ages 12–17 years and adults age 18 years and
older, and this prevalence has remained stable nationally despite increases in rates of prescription
of these medications. Rates of DSM-IV sedative, hypnotic, or anxiolytic use disorder in the
United States have not been shown to vary consistently by gender, but data from other countries
have generally found higher rates among girls and women than boys and men. The 12-month
prevalence of DSM-IV sedative, hypnotic, or anxiolytic use disorder in the United States
decreases as a function of age and is greatest among individuals ages 18–29 years (0.5%) and
lowest among individuals 65 years and older (0.04%).
Twelve-month prevalence of sedative, hypnotic, or anxiolytic use, misuse (e.g., use without a
prescription), or disorder varies across U.S. ethnoracial groups. For instance, 12-month
prevalence estimates for sedative, hypnotic, or anxiolytic misuse across ethnoracial groups range
from 0.6% to 2.5% for adolescents ages 12–17 years and 0.7% to 10.1% for adults.

Temperamental.
Environmental.
Development and Course
The usual course of sedative, hypnotic, or anxiolytic use disorder involves individuals in their
teens or 20s who escalate their occasional use of sedative, hypnotic, or anxiolytic agents to the
point at which they develop problems that meet criteria for a diagnosis. This pattern may be
especially likely among individuals who have other substance use disorders (e.g., alcohol,
opioids, stimulants). An initial pattern of intermittent use socially (e.g., at parties) can lead to
daily use and high levels of tolerance. Once this occurs, an increasing level of interpersonal
difficulties can be expected, as well as increasingly severe episodes of cognitive dysfunction and
physiological withdrawal.
The second and less frequently observed clinical course begins with an individual who
originally obtained the medication by prescription from a physician, usually for the treatment of
anxiety, insomnia, or somatic complaints. As either tolerance or a need for higher doses of the
medication develops, there is a gradual increase in the dose and frequency of self-administration.
The individual is likely to continue to justify use on the basis of original anxiety or insomnia
symptoms, but substance-seeking behavior becomes more prominent, and the individual may
seek out multiple physicians to obtain sufficient supplies of the medication. Tolerance can reach
high levels, and withdrawal (including seizures and withdrawal delirium) may occur.
As with many substance use disorders, sedative, hypnotic, or anxiolytic use disorder
generally has an onset during adolescence or early adult life. Although the risk for misuse and
use disorder decreases with age after about age 30, side effects associated with psychoactive
substances may increase as individuals age. In particular, cognitive impairment increases as a
side effect with age, and the metabolism of sedatives, hypnotics, or
anxiolytics decreases with age among older individuals. Both acute and chronic toxic effects
of these substances, especially effects on cognition, memory, and motor coordination, are likely
to increase with age as a consequence of pharmacodynamic and pharmacokinetic age-related
changes. Individuals with major neurocognitive disorder are more likely to develop intoxication
and impaired physiological functioning at lower doses. Because sedatives, hypnotics, and
anxiolytics are often used in combination with other psychoactive substances, it can be difficult
to ascertain whether the functional consequences are attributable to a single substance (e.g.,
sedative) or to the use of multiple substances.
Deliberate intoxication to achieve a “high” is most likely to be observed in teenagers and
individuals in their 20s. Problems associated with sedatives, hypnotics, or anxiolytics are also
seen in individuals in their 40s and older who escalate the dose of prescribed medications. In
older individuals, intoxication can resemble a progressive major neurocognitive disorder.
Risk and Prognostic Factors
Impulsivity and novelty seeking are individual temperaments that relate to the
propensity to develop a substance use disorder but may themselves be genetically determined.
Personality disorders can also increase the risk of sedative, hypnotic, or anxiolytic misuse or use
disorder.
Because sedatives, hypnotics, or anxiolytics are all medications, a key risk factor

Genetic and physiological.
Course modifiers.
relates to availability of the substances, both through an individual’s own prescriptions and from
prescriptions dispensed to family and friends. In the United States, the historical patterns of
sedative, hypnotic, or anxiolytic misuse relate to broad prescribing patterns. For instance, a
marked decrease in prescription of barbiturates was associated with an increase in
benzodiazepine prescriptions. Peer factors may relate to genetic predisposition in terms of how
individuals select their environment. Other individuals at heightened risk might include those
with alcohol use disorder who may receive repeated prescriptions in response to their complaints
of alcohol-related anxiety or insomnia.
As with other substance use disorders, the risk for sedative, hypnotic,
or anxiolytic use disorder has been found in U.S.-based twin registry studies to be related to
individual, family, peer, social, and environmental factors. Within these domains, genetic factors
play a particularly important role both directly and indirectly. Overall, across development,
genetic factors seem to play a larger role in the onset of sedative, hypnotic, or anxiolytic use
disorder as individuals age through puberty into adult life.
In nationally representative U.S. studies, early onset of use is associated with
greater likelihood for developing a sedative, hypnotic, or anxiolytic use disorder.
Culture-Related Diagnostic Issues
Prescription patterns (and availability) of this class of substances vary across countries and
populations, which may lead to variations in prevalence of sedative, hypnotic, or anxiolytic use
disorder. In the United States, use of benzodiazepines has been more frequently reported by nonLatinx Whites than Latinx or African Americans. However, risk of the disorder may vary within
populations exposed to these substances. For example, the 12-month prevalence of DSM-IV
benzodiazepine use disorder among U.S. individuals who used benzodiazepines was higher
among African Americans (3.0%) and non-Latinx “others” (2.6%) than among non-Latinx
Whites (1.3%).
Sex- and Gender-Related Diagnostic Issues
Although estimates from individual studies vary, there appear to be no gender differences in the
prevalence of sedative, hypnotic, or anxiolytic use disorder.
Diagnostic Markers
Almost all sedative, hypnotic, or anxiolytic substances can be identified through laboratory
evaluations of urine or blood (the latter of which can quantify the amounts of these agents in the
body). Urine test results are likely to remain positive for up to approximately 1 week after the
use of long-acting substances, such as diazepam or flurazepam.
Association With Suicidal Thoughts or Behavior
U.S. epidemiological studies show that hypnotics are associated with suicide, but it is unclear if
this association is attributable to underlying psychiatric conditions such as depression and
insomnia, which are themselves risk factors for suicide.

Sedative, hypnotic, or anxiolytic intoxication; sedative, hypnotic, or anxiolytic withdrawal; and
sedative-, hypnotic-, or anxiolytic-induced mental disorders.
Functional Consequences of Sedative, Hypnotic, or Anxiolytic Use
Disorder
The social and interpersonal consequences of sedative, hypnotic, or anxiolytic use disorder
mimic those of alcohol in terms of the potential for disinhibited behavior. Accidents,
interpersonal difficulties, and interference with work or school performance are common
outcomes. The disinhibiting effects of these agents, like alcohol, may potentially contribute to
overly aggressive behavior and arguments or fights, with subsequent interpersonal and legal
problems. Physical examination is likely to reveal evidence of a mild decrease in most aspects of
autonomic nervous system functioning, including a slower pulse, a slightly decreased respiratory
rate, and a slight drop in blood pressure (most likely to occur with postural changes).
Acute intoxication can result in accidental injuries and automobile accidents. There may be
consequences of trauma (e.g., internal bleeding, a subdural hematoma) from accidents that occur
while intoxicated. For elderly individuals, even short-term use of these sedating medications at
prescribed doses may be associated with an increased risk for cognitive problems and falls. The
association of sedative, hypnotic, or anxiolytic medications with increased risk of major
neurocognitive disorder remains unclear.
At high doses, sedative, hypnotic, or anxiolytic substances can be lethal, particularly when
mixed with other central nervous system depressants, such as opioids or alcohol, although the
lethal dosage varies considerably among the specific substances. Intravenous use of these
substances can result in medical complications related to the use of contaminated needles (e.g.,
hepatitis, HIV).
Accidental or deliberate overdoses, similar to those observed for alcohol use disorder or
repeated alcohol intoxication, can occur. Overdoses may be associated with a deterioration in
vital signs that signals an impending medical emergency (e.g., respiratory arrest from
barbiturates). In contrast to their wide margin of safety when used alone, benzodiazepines taken
in combination with opioids and alcohol can be particularly dangerous, and accidental overdoses
are reported commonly in U.S. data. Accidental overdoses have also been reported in individuals
who deliberately misuse barbiturates and other nonbenzodiazepine sedatives (e.g.,
methaqualone), but because these agents are much less available than the benzodiazepines, the
frequency of overdosing is low in most settings.
Differential Diagnosis
Sedative, hypnotic, or anxiolytic use disorder is differentiated from sedative, hypnotic, or
anxiolytic intoxication; sedative, hypnotic, or anxiolytic withdrawal; and sedative-, hypnotic-, or
anxiolytic-induced mental disorders (e.g., sedative-, hypnotic-, or anxiolytic-induced depressive
disorder) in that sedative, hypnotic, or anxiolytic use disorder describes a problematic pattern
of sedative, hypnotic, or anxiolytic use that involves impaired control over such use; social
impairment attributable to this use; risky sedative, hypnotic, or anxiolytic use (e.g., driving while
intoxicated); and pharmacological symptoms (the development of tolerance or withdrawal);
whereas sedative, hypnotic, or anxiolytic intoxication; sedative, hypnotic, or anxiolytic

Other medical conditions.
Alcohol use disorder.
Clinically appropriate use of sedative, hypnotic, or anxiolytic medications.
withdrawal; and sedative-, hypnotic-, or anxiolytic-induced mental disorders describe psychiatric
syndromes that occur in the context of heavy use. Sedative, hypnotic, or anxiolytic intoxication;
sedative, hypnotic, or anxiolytic withdrawal; and sedative-, hypnotic-, or anxiolytic-induced
mental disorders occur frequently in individuals with sedative, hypnotic, or anxiolytic use
disorder. In such cases, a diagnosis of sedative, hypnotic, or anxiolytic intoxication; sedative,
hypnotic, or anxiolytic withdrawal; or a sedative-, hypnotic-, or anxiolytic-induced mental
disorder should be given in addition to a diagnosis of sedative, hypnotic, and anxiolytic use
disorder, the presence of which is indicated in the diagnostic code.
The slurred speech, incoordination, and other associated features
characteristic of sedative, hypnotic, or anxiolytic intoxication could be the result of another
medical condition (e.g., multiple sclerosis) or of a prior head trauma (e.g., a subdural hematoma).
Sedative, hypnotic, or anxiolytic use disorder must be differentiated from
alcohol use disorder. The differential diagnosis is determined mostly through clinical history,
although liver damage and other potential signs of chronic alcohol toxicity (e.g.,
cardiomyopathy) can also be more suggestive of alcohol use disorder than of sedative, hypnotic,
or anxiolytic use disorder.
Individuals may continue to
take benzodiazepine medication according to a physician’s direction for a legitimate medical
indication over extended periods of time. Even if physiological signs of tolerance or withdrawal
are manifested, many of these individuals do not develop symptoms that meet the criteria for
sedative, hypnotic, or anxiolytic use disorder because they are not preoccupied with obtaining
the substance and its use does not interfere with their performance of usual social or occupational
roles.
Comorbidity
Nonmedical use of sedative, hypnotic, or anxiolytic agents is associated with alcohol use
disorder, tobacco use disorder, and, generally, illicit drug use. There may also be an overlap
between sedative, hypnotic, or anxiolytic use disorder and antisocial personality disorder;
depressive, bipolar, and anxiety disorders; and other substance use disorders, such as alcohol use
disorder and illicit drug use disorders. Antisocial behavior and antisocial personality disorder are
especially associated with sedative, hypnotic, or anxiolytic use disorder when the substances are
obtained illegally. Comorbidity with other substance use disorders and other psychiatric
disorders increases the risk of transition from sedative, hypnotic, or anxiolytic use to use disorder
and decreases the probability of remission.
Sedative, Hypnotic, or Anxiolytic Intoxication
Diagnostic Criteria
A. Recent use of a sedative, hypnotic, or anxiolytic.
B. Clinically significant maladaptive behavioral or psychological changes (e.g.,

inappropriate sexual or aggressive behavior, mood lability, impaired judgment)
that developed during, or shortly after, sedative, hypnotic, or anxiolytic use.
C. One (or more) of the following signs or symptoms developing during, or shortly
after, sedative, hypnotic, or anxiolytic use:
1. Slurred speech.
2. Incoordination.
3. Unsteady gait.
4. Nystagmus.
5. Impairment in cognition (e.g., attention, memory).
6. Stupor or coma.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication with
another substance.
Coding note: The ICD-10-CM code depends on whether there is a comorbid
sedative, hypnotic, or anxiolytic use disorder. If a mild sedative, hypnotic, or
anxiolytic use disorder is comorbid, the ICD-10-CM code is F13.120, and if a
moderate or severe sedative, hypnotic, or anxiolytic use disorder is comorbid, the
ICD-10-CM code is F13.220. If there is no comorbid sedative, hypnotic, or anxiolytic
use disorder, then the ICD-10-CM code is F13.920.
Note: For information on Development and Course; Risk and Prognostic Factors;
Culture-Related Diagnostic Issues; Diagnostic Markers; Functional Consequences of
Sedative, Hypnotic, or Anxiolytic Intoxication; and Comorbidity, see the corresponding
sections in Sedative, Hypnotic, or Anxiolytic Use Disorder.
Diagnostic Features
The essential feature of sedative, hypnotic, or anxiolytic intoxication is the presence of clinically
significant maladaptive behavioral or psychological changes (e.g., inappropriate sexual or
aggressive behavior, mood lability, impaired judgment, impaired social or occupational
functioning) that develop during, or shortly after, use of a sedative, hypnotic, or anxiolytic
(Criteria A and B). As with other brain depressants, such as alcohol, these behaviors may be
accompanied by slurred speech, incoordination (at levels that can interfere with driving abilities
and with performing usual activities to the point of causing falls or automobile accidents), an
unsteady gait, nystagmus, impairment in cognition (e.g., attentional or memory problems), and
stupor or coma (Criterion C). Memory impairment is a prominent feature of sedative, hypnotic,
or anxiolytic intoxication and is most often characterized by an anterograde amnesia that
resembles “alcoholic blackouts,” which can be disturbing to the individual. The symptoms must
not be attributable to another medical condition and are not better explained by another mental
disorder (Criterion D). Intoxication may occur in individuals who are receiving these substances
by prescription, are borrowing the medication from friends or relatives, or are deliberately taking

Alcohol use disorder.
Alcohol intoxication.
Sedative-, hypnotic-, or anxiolytic-induced mental disorders.
Neurocognitive disorders.
the substance to achieve intoxication. Because sedatives, hypnotics, and anxiolytics are often
used in combination with other psychoactive substances, it can be difficult to ascertain whether
the functional consequences are attributable to a sedative, hypnotic, or anxiolytic or to the use of
multiple substances.
Associated Features
Associated features include taking more medication than prescribed, taking multiple different
medications, or mixing sedative, hypnotic, or anxiolytic agents with alcohol, which can markedly
increase the effects of these agents.
Prevalence
The prevalence of sedative, hypnotic, or anxiolytic intoxication in the general population is
unknown. However, it is probable that most nonmedical users of sedatives, hypnotics,
or anxiolytics would at some time have signs or symptoms that meet criteria for sedative,
hypnotic, or anxiolytic intoxication; if so, then the prevalence of nonmedical sedative, hypnotic,
or anxiolytic use in the general population may be similar to the prevalence of sedative,
hypnotic, or anxiolytic intoxication. For example, in 2018, tranquilizers or sedative were used
nonmedically in the United States by 2.4% of individuals age 12 or older and 4.9% of those ages
18–25.
Differential Diagnosis
Because the clinical presentations may be identical, distinguishing sedative,
hypnotic, or anxiolytic intoxication from alcohol use disorder requires evidence for recent
ingestion of sedative, hypnotic, or anxiolytic medications by self-report, informant report, or
toxicological testing. Many individuals who misuse sedatives, hypnotics, or anxiolytics may also
misuse alcohol and other substances, and so multiple intoxication diagnoses are possible.
Alcohol intoxication may be distinguished from sedative, hypnotic, or
anxiolytic intoxication by the smell of alcohol on the breath. Otherwise, the features of the two
disorders may be similar.
Sedative, 
hypnotic, 
or 
anxiolytic
intoxication is distinguished from sedative-, hypnotic-, or anxiolytic-induced mental disorders
(e.g., sedative-, hypnotic-, or anxiolytic-induced anxiety disorder, with onset during withdrawal)
because the symptoms (e.g., anxiety) in the latter disorders are in excess of those usually
associated with sedative, hypnotic, or anxiolytic intoxication; predominate in the clinical
presentation; and are severe enough to warrant clinical attention.
In situations of cognitive impairment, traumatic brain injury, and
delirium from other causes, sedatives, hypnotics, or anxiolytics may be intoxicating at quite low
dosages. The differential diagnosis in these complex settings is based on the predominant
syndrome. An additional diagnosis of sedative, hypnotic, or anxiolytic intoxication may be
appropriate even if the substance has been ingested at a low dosage in the setting of these other

(or similar) co-occurring conditions.
Comorbidity
Given the typical overlap of sedative, hypnotic, or anxiolytic intoxication with sedative,
hypnotic, or anxiolytic use disorder, see “Comorbidity” under Sedative, Hypnotic, or Anxiolytic
Use Disorder for more details about co-occurring conditions that are likely to be encountered.
Sedative, Hypnotic, or Anxiolytic Withdrawal
Diagnostic Criteria
A. Cessation of (or reduction in) sedative, hypnotic, or anxiolytic use that has been
prolonged.
B. Two (or more) of the following, developing within several hours to a few days
after the cessation of (or reduction in) sedative, hypnotic, or anxiolytic use
described in Criterion A:
1. Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 bpm).
2. Hand tremor.
3. Insomnia.
4. Nausea or vomiting.
5. Transient visual, tactile, or auditory hallucinations or illusions.
6. Psychomotor agitation.
7. Anxiety.
8. Grand mal seizures.
C. The signs or symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication or
withdrawal from another substance.
Specify if:
With perceptual disturbances: This specifier may be noted when
hallucinations with intact reality testing or auditory, visual, or tactile illusions
occur in the absence of a delirium.
Coding note: The ICD-10-CM code depends on whether or not there is a comorbid
sedative, hypnotic, or anxiolytic use disorder and whether or not there are perceptual
disturbances.
For sedative, hypnotic, or anxiolytic withdrawal, without perceptual

disturbances: If a mild sedative, hypnotic, or anxiolytic use disorder is
comorbid, the ICD-10-CM code is F13.130, and if a moderate or severe
sedative, hypnotic, or anxiolytic use disorder is comorbid, the ICD-10-CM code is
F13.230. If there is no comorbid sedative, hypnotic, or anxiolytic use disorder
(e.g., in a patient taking sedatives, hypnotics, or anxiolytics solely under
appropriate medical supervision), then the ICD-10-CM code is F13.930.
For sedative, hypnotic, or anxiolytic withdrawal, with perceptual
disturbances: If a mild sedative, hypnotic, or anxiolytic use disorder is
comorbid, the ICD-10-CM code is F13.132, and if a moderate or severe
sedative, hypnotic, or anxiolytic use disorder is comorbid, the ICD-10-CM code is
F13.232. If there is no comorbid sedative, hypnotic, or anxiolytic use disorder
(e.g., in a patient taking sedatives, hypnotics, or anxiolytics solely under
appropriate medical supervision), then the ICD-10-CM code is F13.932.
Note: For information on Development and Course; Risk and Prognostic Factors;
Culture-Related Diagnostic Issues; Functional Consequences of Sedative, Hypnotic, or
Anxiolytic Withdrawal; and Comorbidity, see the corresponding sections in Sedative,
Hypnotic, or Anxiolytic Use Disorder.
Diagnostic Features
The essential feature of sedative, hypnotic, or anxiolytic withdrawal is the presence of a
characteristic syndrome that develops after a marked decrease in or cessation of intake after
several weeks or more of regular use (Criteria A and B). This withdrawal syndrome is
characterized by two or more symptoms (similar to alcohol withdrawal) that include autonomic
hyperactivity (e.g., increases in heart rate, respiratory rate, blood pressure, or body temperature,
along with sweating); a tremor of the hands; insomnia; nausea, sometimes accompanied by
vomiting; anxiety; and psychomotor agitation. A grand mal seizure may occur in perhaps as
many as 20%–30% of individuals undergoing untreated withdrawal from these substances. In
severe withdrawal, visual, tactile, or auditory hallucinations or illusions can occur but are usually
in the context of a withdrawal delirium. If the individual’s reality testing is intact (i.e., knows the
substance is causing the hallucinations) and the illusions occur in a clear sensorium, the specifier
“with perceptual disturbances”
can be noted. When hallucinations occur in the absence of intact reality testing, a diagnosis of
substance/medication-induced psychotic disorder should be considered. The symptoms cause
clinically significant distress or impairment in social, occupational, or other important areas of
functioning (Criterion C). The symptoms must not be attributable to another medical condition
and are not better explained by another mental disorder (e.g., alcohol withdrawal, generalized
anxiety disorder) (Criterion D). Relief of withdrawal symptoms with administration of any
sedative-hypnotic agent would support a diagnosis of sedative, hypnotic, or anxiolytic
withdrawal.

Other medical conditions.
Associated Features
The timing and severity of the withdrawal syndrome will differ depending on the specific
substance and its pharmacokinetics and pharmacodynamics. For example, withdrawal from
shorter-acting substances that are rapidly absorbed and that have no active metabolites (e.g.,
triazolam) can begin within hours after the substance is stopped; withdrawal from substances
with long-acting metabolites (e.g., diazepam) may not begin for 1–2 days or longer. The
withdrawal syndrome produced by substances in this class may be characterized by the
development of a delirium that can be life-threatening. There may be evidence of tolerance and
withdrawal in the absence of a diagnosis of a benzodiazepine use disorder in an individual who
has abruptly discontinued benzodiazepines that were taken for long periods of time at prescribed
and therapeutic doses.
The time course of the withdrawal syndrome is generally predicted by the half-life of the
substance. Medications whose actions typically last about 10 hours or less (e.g., lorazepam,
oxazepam, temazepam) produce withdrawal symptoms within 6–8 hours of decreasing blood
levels that peak in intensity on the second day and improve markedly by the fourth or fifth day.
For substances with longer half-lives (e.g., diazepam), symptoms may not develop for more than
1 week, peak in intensity during the second week, and decrease markedly during the third or
fourth week. There may be additional longer-term symptoms at a much lower level of intensity
that persist for several months.
The longer the substance has been taken and the higher the dosages used, the more likely
there will be severe withdrawal. However, withdrawal has been reported with as little as 15 mg
of diazepam (or its equivalent in other benzodiazepines) when taken daily for several months.
Doses of approximately 40 mg of diazepam (or its equivalent) daily are more likely to produce
clinically relevant withdrawal symptoms, and even higher doses (e.g., 100 mg of diazepam) are
more likely to be followed by withdrawal seizures or delirium. Sedative, hypnotic, or anxiolytic
withdrawal delirium is characterized by disturbances in consciousness and cognition, with visual,
tactile, or auditory hallucinations. When present, sedative, hypnotic, or anxiolytic withdrawal
delirium should be diagnosed instead of withdrawal.
Prevalence
The prevalence of sedative, hypnotic, or anxiolytic withdrawal is unknown.
Diagnostic Markers
Seizures and autonomic instability in the setting of a history of prolonged exposure to sedative,
hypnotic, or anxiolytic medications suggest a high likelihood of sedative, hypnotic, or anxiolytic
withdrawal.
Differential Diagnosis
The symptoms of sedative, hypnotic, or anxiolytic withdrawal may be
mimicked by other medical conditions (e.g., hypoglycemia, diabetic ketoacidosis). If seizures are
a feature of the sedative, hypnotic, or anxiolytic withdrawal, the

Essential tremor.
Alcohol withdrawal.
Sedative-, hypnotic-, or anxiolytic-induced mental disorders.
Anxiety disorders.
differential diagnosis includes the various causes of seizures (e.g., infections, head injury,
poisonings).
Essential tremor, a neurological condition that frequently runs in families, may
erroneously suggest the tremulousness associated with sedative, hypnotic, or anxiolytic
withdrawal.
Alcohol withdrawal produces a syndrome very similar to that of sedative,
hypnotic, or anxiolytic withdrawal. The differential diagnosis is determined mostly through
clinical history, although liver damage and other potential signs of chronic alcohol toxicity (e.g.,
cardiomyopathy) can also be more suggestive of alcohol withdrawal than of sedative, hypnotic,
or anxiolytic withdrawal.
Sedative, 
hypnotic, 
or 
anxiolytic
withdrawal is distinguished from sedative-, hypnotic-, or anxiolytic-induced mental disorders
(e.g., sedative-, hypnotic-, or anxiolytic-induced anxiety disorder, with onset during withdrawal)
because the symptoms (e.g., anxiety) in the latter disorders are in excess of those usually
associated with sedative, hypnotic, or anxiolytic withdrawal; predominate in the clinical
presentation; and are severe enough to warrant clinical attention.
Recurrence or worsening of an underlying anxiety disorder produces a
syndrome similar to sedative, hypnotic, or anxiolytic withdrawal, although the most extreme
manifestations of withdrawal, such as delirium tremens or true seizures, are not symptoms of any
anxiety disorder. Withdrawal would be suspected with an abrupt reduction in the dosage of a
sedative, hypnotic, or anxiolytic medication. When a taper is under way, distinguishing the
withdrawal syndrome from the underlying anxiety disorder can be difficult. As with alcohol,
lingering withdrawal symptoms (e.g., anxiety, moodiness, trouble sleeping) can be mistaken for
independent anxiety or depressive disorders (e.g., generalized anxiety disorder).
Comorbidity
Given the typical overlap of sedative, hypnotic, or anxiolytic withdrawal with sedative, hypnotic,
or anxiolytic use disorder, see “Comorbidity” under Sedative, Hypnotic, or Anxiolytic Use
Disorder for more details about co-occurring conditions that are likely to be encountered.
Sedative-, Hypnotic-, or Anxiolytic-Induced Mental
Disorders
The following sedative-, hypnotic-, or anxiolytic-induced mental disorders are described in other
chapters of the manual with disorders with which they share phenomenology (see the
substance/medication-induced mental disorders in these chapters): sedative-, hypnotic-, or
anxiolytic-induced psychotic disorder (“Schizophrenia Spectrum and Other Psychotic
Disorders”); sedative-, hypnotic-, or anxiolytic-induced bipolar and related disorder (“Bipolar
and Related Disorders”); sedative-, hypnotic-, or anxiolytic-induced depressive disorder
(“Depressive Disorders”); sedative-, hypnotic-, or anxiolytic-induced anxiety disorder (“Anxiety
Disorders”); sedative-, hypnotic-, or anxiolytic-induced sleep disorder (“Sleep-Wake
Disorders”); sedative-, hypnotic-, or anxiolytic-induced sexual dysfunction (“Sexual

Dysfunctions”); and sedative-, hypnotic-, or anxiolytic-induced major or mild neurocognitive
disorder (“Neurocognitive Disorders”). For sedative, hypnotic, or anxiolytic intoxication
delirium; sedative, hypnotic, or anxiolytic withdrawal delirium; and delirium induced by
sedatives, hypnotics, or anxiolytics taken as prescribed, see the
criteria and discussion of delirium in the chapter “Neurocognitive Disorders.” These sedative-,
hypnotic-, or anxiolytic-induced mental disorders are diagnosed instead of sedative, hypnotic, or
anxiolytic intoxication or sedative, hypnotic, or anxiolytic withdrawal only when the symptoms
are sufficiently severe to warrant independent clinical attention.
Unspecified Sedative-, Hypnotic-, or Anxiolytic-Related
Disorder
F13.99
This category applies to presentations in which symptoms characteristic of a sedative-,
hypnotic-, or anxiolytic-related disorder that cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning predominate but
do not meet the full criteria for any specific sedative-, hypnotic-, or anxiolytic-related
disorder or any of the disorders in the substance-related and addictive disorders diagnostic
class.
Stimulant-Related Disorders
Stimulant Use Disorder
Stimulant Intoxication
Stimulant Withdrawal
Stimulant-Induced Mental Disorders
Unspecified Stimulant-Related Disorder
Stimulant Use Disorder
Diagnostic Criteria
A. A pattern of amphetamine-type substance, cocaine, or other stimulant use
leading to clinically significant impairment or distress, as manifested by at least

two of the following, occurring within a 12-month period:
1. The stimulant is often taken in larger amounts or over a longer period than
was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control
stimulant use.
3. A great deal of time is spent in activities necessary to obtain the stimulant,
use the stimulant, or recover from its effects.
4. Craving, or a strong desire or urge to use the stimulant.
5. Recurrent stimulant use resulting in a failure to fulfill major role obligations at
work, school, or home.
6. Continued stimulant use despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of the stimulant.
7. Important social, occupational, or recreational activities are given up or
reduced because of stimulant use.
8. Recurrent stimulant use in situations in which it is physically hazardous.
9. Stimulant use is continued despite knowledge of having a persistent or
recurrent physical or psychological problem that is likely to have been caused
or exacerbated by the stimulant.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of the stimulant to achieve
intoxication or desired effect.
b. A markedly diminished effect with continued use of the same amount of
the stimulant.
Note: This criterion is not considered to be met for those taking stimulant
medications solely under appropriate medical supervision, such as
medications for attention-deficit/hyperactivity disorder or narcolepsy.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for the stimulant (refer to Criteria
A and B of the criteria set for stimulant withdrawal).
b. The stimulant (or a closely related substance) is taken to relieve or avoid
withdrawal symptoms.
Note: This criterion is not considered to be met for those taking stimulant
medications solely under appropriate medical supervision, such as
medications for attention-deficit/hyperactivity disorder or narcolepsy.
Specify if:
In early remission: After full criteria for stimulant use disorder were previously
met, none of the criteria for stimulant use disorder have been met for at least 3
months but for less than 12 months (with the exception that Criterion A4,

“Craving, or a strong desire or urge to use the stimulant,” may be met).
In sustained remission: After full criteria for stimulant use disorder were
previously met, none of the criteria for stimulant use disorder have been met at
any time during a period of 12 months or longer (with the exception that Criterion
A4, “Craving, or a strong desire or urge to use the stimulant,” may be met).
Specify if:
In a controlled environment: This additional specifier is used if the individual is
in an environment where access to stimulants is restricted.
Code based on current severity/remission: If an amphetamine-type substance
intoxication, amphetamine-type substance withdrawal, or amphetamine-type
substance-induced mental disorder is also present, do not use the codes below for
amphetamine-type substance use disorder. Instead, the comorbid amphetaminetype substance use disorder is indicated in the 4th character of the amphetaminetype substance-induced disorder code (see the coding note for amphetamine-type
substance intoxication, amphetamine-type substance withdrawal, or a specific
amphetamine-type substance-induced mental disorder). For example, if there is
comorbid amphetamine-induced depressive disorder and amphetamine use
disorder, only the amphetamine-induced depressive disorder code is given, with the
4th character indicating whether the comorbid amphetamine use disorder is mild,
moderate, or severe: F15.14 for mild amphetamine use disorder with amphetamineinduced depressive disorder or F15.24 for a moderate or severe amphetamine use
disorder with amphetamine-induced depressive disorder. (The instructions for
amphetamine-type substance also apply to other or unspecified stimulant
intoxication, other or unspecified stimulant withdrawal, and other or unspecified
stimulant-induced mental disorder.) Similarly, if there is comorbid cocaine-induced
depressive disorder and cocaine use disorder, only the cocaine-induced depressive
disorder code is given, with the 4th character indicating whether the comorbid
cocaine use disorder is mild, moderate,
or severe: F14.14 for a mild cocaine use disorder with cocaine-induced depressive
disorder or F14.24 for a moderate or severe cocaine use disorder with cocaineinduced depressive disorder.
Specify current severity/remission:
Mild: Presence of 2–3 symptoms.
F15.10 Amphetamine-type substance
F14.10 Cocaine
F15.10 Other or unspecified stimulant
Mild, In early remission
F15.11 Amphetamine-type substance
F14.11 Cocaine

F15.11 Other or unspecified stimulant
Mild, In sustained remission
F15.11 Amphetamine-type substance
F14.11 Cocaine
F15.11 Other or unspecified stimulant
Moderate: Presence of 4–5 symptoms.
F15.20 Amphetamine-type substance
F14.20 Cocaine
F15.20 Other or unspecified stimulant
Moderate, In early remission
F15.21 Amphetamine-type substance
F14.21 Cocaine
F15.21 Other or unspecified stimulant
Moderate, In sustained remission
F15.21 Amphetamine-type substance
F14.21 Cocaine
F15.21 Other or unspecified stimulant
Severe: Presence of 6 or more symptoms.
F15.20 Amphetamine-type substance
F14.20 Cocaine
F15.20 Other or unspecified stimulant
Severe, In early remission
F15.21 Amphetamine-type substance
F14.21 Cocaine
F15.21 Other or unspecified stimulant
Severe, In sustained remission
F15.21 Amphetamine-type substance
F14.21 Cocaine
F15.21 Other or unspecified stimulant
Specifiers
“In a controlled environment” applies as a further specifier of remission if the individual is both
in remission and in a controlled environment (i.e., in early remission in a controlled environment
or in sustained remission in a controlled environment). Examples of these environments are
closely supervised and substance-free jails, therapeutic communities, and locked hospital units.

Diagnostic Features
Stimulants are a type of psychoactive substance that increases activity in the brain and can
temporarily elevate alertness, mood, and awareness. Stimulants covered in this chapter include
amphetamine and prescription stimulants with similar effects (e.g., methylphenidate) and
cocaine. Substance-related disorders involving certain other substances with stimulant properties
are classified in other sections of this chapter. These include caffeine (in caffeine-related
disorders), 
nicotine 
(in 
tobacco-related 
disorders), 
and 
MDMA 
(3,4methylenedioxymethamphetamine; in other hallucinogen-related disorders), which has both
stimulant and hallucinogenic effects.
Given that the effects of amphetamine-type substances are similar to those of cocaine,
amphetamine-related disorders and cocaine-related disorders are grouped under the single rubric
“stimulant-related disorders.” Amphetamine-type substances (and other or unspecified
stimulants) and cocaine have different ICD-10-CM codes (e.g., F15.10 mild amphetamine-type
substance use disorder, F14.10 mild cocaine use disorder). The particular stimulant used by the
individual is recorded in the diagnosis (e.g., “methamphetamine withdrawal,” “methylphenidate
use disorder,” “cocaine intoxication”).
The amphetamine-type substances include stimulants with a substituted phenylethylamine
structure, such as amphetamine, dextroamphetamine, and methamphetamine. Also included are
substances that are structurally different but have similar effects, such as methylphenidate,
modafinil, and armodafinil. These amphetamine-type substances are usually taken orally or
intravenously, although methamphetamine is also taken by the nasal route. In addition to the
synthetic amphetamine-type compounds, there are naturally occurring, plant-derived stimulants
such as khât, as well as synthetic chemical khât analogs, called cathinones.
Amphetamines and other stimulants may be obtained by prescription for the treatment of
obesity, attention-deficit/hyperactivity disorder, and narcolepsy. Consequently, prescribed
stimulants may be diverted into the illegal market.
Cocaine, a naturally occurring substance produced by the coca plant, is consumed in several
preparations (e.g., coca leaves, coca paste, cocaine hydrochloride, and cocaine alkaloids such as
freebase and crack) that differ in potency because of varying levels of purity and speed of onset.
However, in all of the forms, cocaine is the active ingredient. Cocaine hydrochloride powder is
usually “snorted” through the nostrils or dissolved in water and injected intravenously. Crack and
other cocaine alkaloids are easily vaporized and inhaled, and thus their effects have an extremely
rapid onset.
Individuals exposed to amphetamine-type substances or cocaine can develop stimulant use
disorder as rapidly as 1 week, although the onset is not always this rapid. Regardless of the route
of administration, tolerance occurs with repeated use. Withdrawal symptoms, particularly
hypersomnia, increased appetite, and dysphoria, can occur and can enhance craving. Most
individuals with stimulant use disorder have experienced tolerance or withdrawal.
Use patterns and course are similar for disorders involving amphetamine-type substances and
cocaine, as both are potent central nervous system stimulants with similar psychoactive and
sympathomimetic effects. Amphetamine-type substances are longer acting than cocaine and thus
are used fewer times per day. Usage may be chronic or episodic, with binges punctuated by brief
non-use periods. Aggressive or violent behavior is common when high doses are smoked,
ingested, or administered intravenously. Intense temporary anxiety resembling panic disorder or

Stimulant use disorder: amphetamine-type substances.
generalized anxiety disorder, as well as paranoid ideation and psychotic episodes that resemble
schizophrenia, is seen with high-dose use.
Withdrawal states are associated with temporary but intense depressive symptoms that can
resemble a major depressive episode; the depressive symptoms usually resolve
within 1 week. Tolerance to amphetamine-type substances develops and leads to escalation
of the dose. Conversely, some users of amphetamine-type substances develop sensitization,
characterized by enhanced effects.
Associated Features
When injected or smoked, stimulants typically produce an instant feeling of well-being,
confidence, and euphoria. Dramatic behavioral changes can rapidly develop with stimulant use
disorder. Chaotic behavior, social isolation, aggressive behavior, and sexual dysfunction can
result from long-term stimulant use disorder.
Individuals with acute intoxication may present with rambling speech, headache, transient
ideas of reference, and tinnitus. There may be paranoid ideation, auditory hallucinations in a
clear sensorium, and tactile hallucinations, which the individual usually recognizes as drug
effects. Threats or acting out of aggressive behavior may occur. Depression, suicidal thoughts,
irritability, anhedonia, emotional lability, or disturbances in attention and concentration
commonly occur during withdrawal. Mental disturbances associated with cocaine use usually
resolve hours to days after cessation of use but can persist for 1 month. Physiological changes
during stimulant withdrawal are opposite to those of the intoxication phase, sometimes including
bradycardia. Temporary depressive symptoms may meet symptomatic and duration criteria for
major depressive episode. Histories consistent with repeated panic attacks, social anxiety
disorder–like behavior, and generalized anxiety–like syndromes are common, as are eating
disorders. One extreme instance of stimulant toxicity is stimulant-induced psychotic disorder, a
disorder that resembles schizophrenia, with delusions and hallucinations.
Individuals with stimulant use disorder often develop conditioned responses to drug-related
stimuli (e.g., craving on seeing any white powderlike substance). These responses contribute to
relapse, are difficult to extinguish, and persist after detoxification.
Depressive symptoms with suicidal thoughts or behavior can occur and are generally the
most serious problems seen during stimulant withdrawal.
Prevalence
Estimated 
12-month 
prevalence 
of
amphetamine-type substance use disorder in the United States is 0.4% among individuals 12
years and older. Twelve-month prevalence is 0.1% among individuals ages 12–17 years, 0.5%
among those ages 18–25, and 0.4% among those age 26 and older. Rates are 0.5% for men and
0.2% for women, overall. Rates are approximately 0.4% among Hispanics and non-Hispanic
Whites and 0.1% among African Americans and Asian Americans. Prevalence estimates for
American Indian/Alaskan Natives and Native Hawaiian/Pacific Islander populations are difficult
to determine, given small sample sizes, but there is some evidence for higher rates in American

Stimulant use disorder: cocaine.
Temperamental.
Indians/Alaskan Natives.
Among U.S. adults, 6.6% (annual average) used prescription stimulants overall; 4.5% used
without misuse, 1.9% misused without use disorders, and 0.2% had use disorders. While nonHispanic Whites are more likely to use prescription stimulants nonmedically, Hispanics tend to
use them more frequently and have higher rates of prescription stimulant use disorder.
Estimated 12-month prevalence of cocaine use disorder in the
United States is 0.4% among individuals 12 years and older. Rates are 0.1% among individuals
ages 12–17 years, 0.7% among those ages 18–25 years, and 0.3% among those age 26 and older.
Rates are 0.5% for men and 0.2% for women, overall. Rates are 0.4% among African Americans
and non-Hispanic Whites, 0.3% in Hispanics, and < 0.1% among Asian Americans.
Development and Course
In the United States, stimulant use disorder occurs throughout all levels of society and is more
common among individuals ages 18–25 years compared with individuals ages 12–17 or 26 years
and older. On average, first regular use among individuals in treatment occurs at approximately
age 23 years. For primary methamphetamine treatment admissions, the average age is 34 years,
and for primary cocaine treatment admissions, the average age is 44 years for smoked cocaine
and 37 years for other routes.
Some persons begin stimulant use to control weight or to improve performance in school,
work, or athletics. Initial use may include obtaining medications such as methylphenidate or
amphetamine salts prescribed to others for the treatment of attention-deficit/hyperactivity
disorder. Among primary treatment admissions for amphetamine-type substance use in the
United States, 61% reported smoking, 26% reported injecting, and 9% reported snorting,
suggesting that stimulant use disorder can develop from multiple modes of administration.
Patterns of stimulant administration include episodic or daily (or almost daily) use. Episodic
use (e.g., intense use over a weekend or on one or more weekdays) tends to be separated by 2 or
more days of nonuse. “Binges” involve continuous high-dose use over hours or days and are
often associated with physical dependence. Binges usually terminate only when stimulant
supplies are depleted or exhaustion ensues. Chronic daily use may involve high or low doses,
often with an increase in dose over time.
Stimulant smoking and intravenous use are associated with rapid progression to severe-level
stimulant use disorder, often occurring over weeks to months. Intranasal use of cocaine and oral
use of amphetamine-type substances result in more gradual progression occurring over months to
years. With continued use, there is a diminution of pleasurable effects because of tolerance and
an increase in dysphoric effects.
Risk and Prognostic Factors
Comorbid bipolar disorder, schizophrenia, antisocial personality disorder, and
other substance use disorders are risk factors for developing stimulant use disorder and for
relapse to cocaine use in treatment samples. Higher stress reactivity has been correlated with
frequency of cocaine use in some U.S. treatment samples. Conduct disorder in childhood and
antisocial personality disorder are associated with the development of stimulant-related

Environmental.
disorders. In the United States, previous use of another substance, being male, having a Cluster B
personality disorder, family history of substance use disorder, and being separated, divorced, or
widowed all result in increased risk of using cocaine. Men who have sex with men are also at
higher risk for methamphetamine use.
Predictors of cocaine use among a cohort of U.S. teenagers include prenatal
cocaine exposure, postnatal cocaine use by parents, and exposure to community violence during
childhood. Research in industrialized countries suggests that exposure to intimate partner
violence or childhood mistreatment often co-occurs with stimulant use, especially in women. In a
cohort of U.S. women followed up longitudinally, socioeconomic status, including food
insecurity, had a dose-dependent effect on risk of stimulant use. For youth, especially girls, risk
factors include living in an unstable home environment, having a psychiatric condition, criminal
behavior, and associating with dealers and users.
Culture-Related Diagnostic Issues
The prevalence of cocaine use in the United States increased between 2001–2002 and 2012–
2013 among non-Latinx Whites, African Americans, and Latinx, but the prevalence of cocaine
use disorder increased only among Whites. Despite small variations, cocaine and other stimulant
use disorder diagnostic criteria perform equally across gender and
ethnoracial groups. In limited data on prevalence estimates, it appears that American
Indian/Alaskan Native populations are at higher risk for methamphetamine use disorder, and, to
a lesser degree, cocaine use disorder, than are non-Hispanic Whites, while native
Hawaiian/Pacific Islanders appear to have similar risks to non-Hispanic Whites.
Approximately 64% of individuals admitted to publicly funded substance abuse treatment
programs for primary methamphetamine/amphetamine-related disorders are non-Hispanic White,
followed by 20% of Hispanic origin, 3% Asian and Pacific Islander, and 6% non-Hispanic
Black. Among individuals admitted for primary treatment related to smoked cocaine, 51% were
non-Hispanic Black, 35% non-Hispanic White, 8% Hispanic, and 1% Asian/Pacific Islander. For
admissions related to other routes of cocaine administration, 47% were non-Hispanic White,
31% were non-Hispanic Black, 17% were of Hispanic origin, and 1% were Asian/Pacific
Islander. Rates of disorders in clinical samples should be interpreted with caution because they
may be affected by differential access to and utilization of services, pathways to care,
criminalization, stigma, and racial bias in diagnosis and referral for treatment.
Sex- and Gender-Related Diagnostic Issues
In the United States, women with cocaine use disorder more frequently have comorbid
psychiatric disorders, such as depression and posttraumatic stress disorder (PTSD), compared
with men. Gonadal hormones affect a male’s responses to cocaine. Females with cocaine use
disorder and higher levels of progesterone have lower stress-induced and cue-induced cocaine
craving and lower cue-induced changes in blood pressure than females with cocaine use disorder
and lower levels of progesterone. This may explain why use of cocaine in pregnant females is
lower than in nonpregnant females.

Diagnostic Markers
Benzoylecgonine, a metabolite of cocaine, typically remains in the urine for 1–3 days after a
single dose and may be present for 7–12 days in individuals using repeated high doses. Mildly
elevated liver function tests can be present in cocaine injectors or users with concomitant alcohol
use. There are no neurobiological markers of diagnostic utility. Discontinuation of chronic
cocaine use may be associated with electroencephalographic changes, suggesting persistent
abnormalities; alterations in secretion patterns of prolactin; and downregulation of dopamine
receptors.
Short-half-life amphetamine-type substances (e.g., methamphetamine) can be detected for 1–
3 days, and possibly up to 4 days depending on dosage and metabolism. Hair samples can be
used to detect presence of amphetamine-type substances for up to 90 days. Other laboratory
findings, as well as physical findings and other medical conditions (e.g., weight loss,
malnutrition; poor hygiene), are similar for both cocaine and amphetamine-type substance use
disorder.
Association With Suicidal Thoughts or Behavior
Few data on the association of stimulant use disorders and suicide are available because most
studies examining suicidal thoughts and behavior examine use of stimulants rather than stimulant
use disorders. One systematic review found that regular or problem amphetamine use (examining
primarily individuals who inject amphetamines and/or individuals admitted to treatment for use
of amphetamines) is associated with increased suicide mortality. A general population study of
adults in the United States found an association of prescription stimulant use disorder with
suicidal thoughts. In a study of individuals admitted to substance use treatment, those with
cocaine use disorder were much more likely to report suicidal thoughts than those with other
substance use disorders. In a study of both men and women in the U.S. Veterans Administration
health care system,
cocaine and amphetamine use disorders were each associated with increased rates of suicide
deaths.
Functional Consequences of Stimulant Use Disorder
Various medical conditions may occur depending on the route of administration. Intranasal users
often develop sinusitis, irritation, bleeding of the nasal mucosa, and a perforated nasal septum.
Individuals who smoke stimulants are at increased risk for respiratory problems (e.g., coughing,
bronchitis, and pneumonitis). Injectors have puncture marks and “tracks,” most commonly on
their forearms. Risk of HIV and hepatitis C infection increases with frequent intravenous
injections and unsafe sexual activity. Other sexually transmitted diseases, hepatitis B, and
tuberculosis and other lung infections are also seen. Weight loss and malnutrition are common.
Chest pain may be a common symptom during stimulant intoxication. Myocardial infarction,
palpitations and arrhythmias, sudden death from respiratory or cardiac arrest, and stroke have
been associated with stimulant use among young and otherwise healthy individuals.
Pneumothorax can result from performing Valsalva-like maneuvers done to better absorb inhaled

Phencyclidine intoxication.
Stimulant intoxication, stimulant withdrawal, and stimulant-induced mental disorders.
Independent mental disorders.
smoke. Cocaine use is associated with irregularities in placental blood flow, abruptio placentae,
premature labor and delivery, and an increased prevalence of infants with very low birth weights.
Individuals with stimulant use disorder may become involved in theft, prostitution, or drug
dealing in order to acquire drugs or money for drugs. Traumatic injuries due to violent behavior
are common among individuals trafficking drugs.
Neurocognitive impairment is common among both methamphetamine and cocaine users,
including deficits related to attention, impulsivity, verbal learning/memory, working memory,
and executive functioning. Transient psychosis and seizure have also been reported with chronic
use of either cocaine or methamphetamine, possibly related to patterns of use or the exacerbation
of preexisting vulnerabilities. Amphetamine use can cause toxic effects related to elevated body
temperature, and there is some evidence that chronic use causes neuroinflammation and
neurotoxicity in dopaminergic neurons. Oral health problems include “meth mouth” with gum
disease, tooth decay, and mouth sores related to the toxic effects of smoking the drug and to
bruxism while intoxicated. Adverse pulmonary effects appear to be less common for
amphetamine-type substances because they are smoked fewer times per day, although
methamphetamine use is still associated with a risk of pulmonary arterial hypertension.
Emergency department visits are common for stimulant-related mental disorder symptoms,
injury, skin infections, and dental pathology. In the United States, diagnosis of a stimulant use
disorder is associated with a 20% increase in 30-day readmission rates in assessment of followup after hospitalization for “any cause” (a standard measure of overall hospital quality of care).
Differential Diagnosis
Intoxication with phencyclidine (PCP or “angel dust”) or synthetic
“designer drugs” such as mephedrone (known by different names, including “bath salts”) may
cause a similar clinical picture and can only be distinguished from stimulant intoxication by the
presence of cocaine or amphetamine-type substance metabolites in a urine or plasma sample.
Stimulant 
use
disorder is differentiated from stimulant intoxication, stimulant withdrawal, and stimulantinduced mental disorders (e.g., stimulant-induced depressive disorder) in that stimulant use
disorder describes a problematic pattern of stimulant use that involves impaired control over
stimulant use, social impairment attributable to stimulant use, risky stimulant use (e.g., continued
stimulant use despite medical complications), and pharmacological symptoms (the development
of tolerance or withdrawal), whereas stimulant
intoxication, stimulant withdrawal, and stimulant-induced mental disorders describe psychiatric
syndromes that occur in the context of heavy use. Stimulant intoxication, stimulant withdrawal,
and stimulant-induced mental disorders occur frequently in individuals with stimulant use
disorder. In such cases, a diagnosis of stimulant intoxication, stimulant withdrawal, or a
stimulant-induced mental disorder should be given in addition to a diagnosis of stimulant use
disorder, the presence of which is indicated in the diagnostic code.
Some of the effects of stimulant use may resemble symptoms of
independent mental disorders, such as psychosis (schizophrenia) and low mood (major

depressive disorder). Discerning whether these behaviors occurred before the intake of the drug
is important in the differentiation of acute drug effects from a preexisting mental disorder.
Comorbidity
Stimulant-related disorders often co-occur with other substance use disorders, especially those
involving substances with sedative properties, which are often taken to reduce insomnia,
nervousness, and other unpleasant side effects. Individuals admitted to treatment for cocaine use
are likely to also use heroin, PCP, or alcohol, and individuals admitted for amphetamine-type
substance use disorder are likely to use marijuana, heroin, or alcohol. Stimulant use disorder may
be associated with posttraumatic stress disorder, antisocial personality disorder, attentiondeficit/hyperactivity disorder, and gambling disorder. Cardiopulmonary problems are often
present in individuals seeking treatment for cocaine-related problems, with chest pain being the
most common. Medical problems occur in response to adulterants used as “cutting” agents.
Cocaine users who ingest cocaine cut with levamisole, an antimicrobial and veterinary
medication, may experience agranulocytosis and febrile neutropenia.
Stimulant Intoxication
Diagnostic Criteria
A. Recent use of an amphetamine-type substance, cocaine, or other stimulant.
B. Clinically significant problematic behavioral or psychological changes (e.g.,
euphoria 
or 
affective 
blunting; 
changes 
in 
sociability; 
hypervigilance;
interpersonal sensitivity; anxiety, tension, or anger; stereotyped behaviors;
impaired judgment) that developed during, or shortly after, use of a stimulant.
C. Two (or more) of the following signs or symptoms, developing during, or shortly
after, stimulant use:
1. Tachycardia or bradycardia.
2. Pupillary dilation.
3. Elevated or lowered blood pressure.
4. Perspiration or chills.
5. Nausea or vomiting.
6. Evidence of weight loss.
7. Psychomotor agitation or retardation.
8. Muscular weakness, respiratory depression, chest pain, or cardiac
arrhythmias.
9. Confusion, seizures, dyskinesias, dystonias, or coma.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication with
another substance.

641
Specify the particular intoxicant (i.e., amphetamine-type substance, cocaine, or
other stimulant).
Specify if:
With perceptual disturbances: This specifier may be noted when
hallucinations with intact reality testing or auditory, visual, or tactile illusions
occur in the absence of a delirium.
Coding note: The ICD-10-CM code depends on whether the stimulant is an
amphetamine-type substance, cocaine, or other stimulant; whether there is a
comorbid amphetamine-type substance, cocaine, or other stimulant use disorder;
and whether or not there are perceptual disturbances.
For amphetamine-type substance, cocaine, or other stimulant intoxication,
without perceptual disturbances: If a mild amphetamine-type substance or
other stimulant use disorder is comorbid, the ICD-10-CM code is F15.120, and if
a moderate or severe amphetamine-type substance or other stimulant use
disorder is comorbid, the ICD-10-CM code is F15.220. If there is no comorbid
amphetamine-type substance or other stimulant use disorder, then the ICD-10CM code is F15.920. Similarly, if a mild cocaine use disorder is comorbid, the
ICD-10-CM code is F14.120, and if a moderate or severe cocaine use disorder is
comorbid, the ICD-10-CM code is F14.220. If there is no comorbid cocaine use
disorder, then the ICD-10-CM code is F14.920.
For amphetamine-type substance, cocaine, or other stimulant intoxication,
with perceptual disturbances: If a mild amphetamine-type substance or other
stimulant use disorder is comorbid, the ICD-10-CM code is F15.122, and if a
moderate or severe amphetamine-type substance or other stimulant use
disorder is comorbid, the ICD-10-CM code is F15.222. If there is no comorbid
amphetamine-type substance or other stimulant use disorder, then the ICD-10CM code is F15.922. Similarly, if a mild cocaine use disorder is comorbid, the
ICD-10-CM code is F14.122, and if a moderate or severe cocaine use disorder is
comorbid, the ICD-10-CM code is F14.222. If there is no comorbid cocaine use
disorder, then the ICD-10-CM code is F14.922.
Diagnostic Features
The essential feature of stimulant intoxication, related to amphetamine-type substances and
cocaine, is the presence of clinically significant behavioral or psychological changes that develop
during, or shortly after, use of stimulants (Criteria A and B). Auditory hallucinations may be
prominent, as may paranoid ideation, and these symptoms must be distinguished from an
independent psychotic disorder such as schizophrenia. Stimulant intoxication usually begins with
a “high” feeling and includes one or more of the following: euphoria with enhanced vigor,
gregariousness, 
hyperactivity, 
restlessness, 
hypervigilance, 
interpersonal 
sensitivity,
talkativeness, anxiety, tension, alertness, grandiosity, stereotyped and repetitive behavior, anger,
impaired judgment, and, in the case of chronic intoxication, affective blunting with fatigue or

sadness and social withdrawal. These behavioral and psychological changes are accompanied by
two or more of the following signs and symptoms that develop during or shortly after stimulant
use: tachycardia or bradycardia; pupillary dilation; elevated or lowered blood pressure;
perspiration or chills; nausea or vomiting; evidence of weight loss; psychomotor agitation or
retardation; muscular weakness, respiratory depression, chest pain, or cardiac arrhythmias; and
confusion, seizures, dyskinesias, dystonias, or coma (Criterion C). Intoxication, either acute or
chronic, is often associated with impaired social or occupational functioning. Severe intoxication
can lead to convulsions, cardiac arrhythmias, hyperpyrexia, and death. For the diagnosis of
stimulant intoxication to be made, the symptoms must not be attributable to another medical
condition and are not better explained by another mental disorder
(Criterion D). While stimulant intoxication occurs in individuals with stimulant use disorders,
intoxication is not a criterion for stimulant use disorder, which is confirmed by the presence of 2
of the 11 diagnostic criteria for use disorder.
Associated Features
The magnitude and direction of the behavioral and physiological changes depend on many
variables, including the dose used and the characteristics of the individual using the substance or
the context (e.g., tolerance, rate of absorption, chronicity of use, context in which taken).
Stimulant effects such as euphoria, increased pulse and blood pressure, and psychomotor activity
are most commonly seen. Depressant effects such as sadness, bradycardia, decreased blood
pressure, and decreased psychomotor activity are less common and generally emerge only with
chronic high-dose use.
Prevalence
Although prevalence of stimulant intoxication is not known, prevalence of stimulant use can be
used as a proxy. Many individuals who use stimulants may not have symptoms that fully meet
the criteria for stimulant intoxication, which requires “clinically significant problematic
behavioral or psychological changes.” Thus, rates of stimulant use can be considered the upper
bounds of the likely prevalence of stimulant intoxication.
Estimated 12-month prevalence of cocaine use in the United States is 2.2% for individuals
age 12 and older (0.5% among individuals ages 12–17-years, 6.2% among individuals ages 18–
25 years, and 1.7% among individuals age 26 and older); 3% of men/boys and 1.4% of
women/girls used cocaine in the last 12 months. Twelve-month prevalence of cocaine use is
2.3% among Whites, 2.2% among Hispanics, 1.7% among African Americans, and 1% among
Asian Americans.
Estimated 12-month prevalence of methamphetamine use in the United States is 0.6% for
individuals age 12 and older (0.2% among individuals ages 12–17 years, 1.1% among
individuals ages 18–25 years, and 0.6% among individuals age 26 and older). Twelve-month
prevalence of methamphetamine use is 0.8% among men/boys and 0.4% among women/girls.
Twelve-month prevalence of methamphetamine use is 0.7% among Whites, 0.6% among
Hispanics, 0.2% among African Americans, and 0.1% among Asian Americans. Small sample

Stimulant-induced mental disorders.
Independent mental disorders.
sizes make estimating rates among American Indians/Alaskan Natives difficult.
Differential Diagnosis
Stimulant intoxication is distinguished from stimulant-induced
mental disorders (e.g., stimulant-induced anxiety disorder, with onset during intoxication)
because the symptoms (e.g., anxiety) in the latter disorders are in excess of those usually seen in
stimulant intoxication, predominate in the clinical presentation, and meet full criteria for the
relevant disorder.
Salient mental disturbances associated with stimulant intoxication
should be distinguished from the symptoms of schizophrenia, bipolar and depressive disorders,
generalized anxiety disorder, and panic disorder as described in this manual.
Comorbidity
Given the typical overlap of stimulant intoxication with stimulant use disorder, see
“Comorbidity” under Stimulant Use Disorder for more details about co-occurring conditions that
are likely to be encountered.
Stimulant Withdrawal
Diagnostic Criteria
A. Cessation of (or reduction in) prolonged amphetamine-type substance, cocaine,
or other stimulant use.
B. Dysphoric mood and two (or more) of the following physiological changes,
developing within a few hours to several days after Criterion A:
1. Fatigue.
2. Vivid, unpleasant dreams.
3. Insomnia or hypersomnia.
4. Increased appetite.
5. Psychomotor retardation or agitation.
C. The signs or symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication or
withdrawal from another substance.
Specify the particular substance that causes the withdrawal syndrome (i.e.,
amphetamine-type substance, cocaine, or other stimulant).
Coding note: The ICD-10-CM code depends on whether the stimulant is an

Stimulant-induced mental disorders.
amphetamine-type substance, cocaine, or other stimulant and on whether or not
there is a comorbid amphetamine-type substance, cocaine, or other stimulant use
disorder. If mild amphetamine-type substance or other stimulant use disorder is
comorbid, the ICD-10-CM code is F15.13. If moderate or severe amphetamine-type
substance or other stimulant use disorder is comorbid, the ICD-10-CM code is
F15.23. For amphetamine-type substance or other stimulant withdrawal occurring in
the absence of amphetamine-type substance or other stimulant use disorder (e.g., in
a patient taking amphetamine solely under appropriate medical supervision), the
ICD-10-CM code is F15.93. If mild cocaine use disorder is comorbid, the ICD-10-CM
code is F14.13. If moderate or severe cocaine use disorder is comorbid, the ICD-10CM code is F14.23. For cocaine withdrawal occurring in the absence of a cocaine
use disorder, the ICD-10-CM code is F14.93.
Diagnostic Features
The essential feature of stimulant withdrawal is the presence of a characteristic withdrawal
syndrome that develops within a few hours to several days after the cessation of (or marked
reduction in) stimulant use (generally high dose) that has been prolonged (Criterion A). The
withdrawal syndrome is characterized by the development of dysphoric mood accompanied by
two or more of the following physiological changes: fatigue, vivid and unpleasant dreams,
insomnia or hypersomnia, increased appetite, and psychomotor retardation or agitation (Criterion
B). Bradycardia is often present and is a reliable measure of stimulant withdrawal.
Anhedonia and drug craving can often be present but are not part of the diagnostic criteria.
These symptoms cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning (Criterion C). The symptoms must not be attributable to
another medical condition and are not better explained by another mental disorder (Criterion D).
Associated Features
Acute withdrawal symptoms (“a crash”) are often seen after periods of repetitive high-dose use
(“runs” or “binges”). These symptoms are characterized by intense and unpleasant feelings of
lassitude and depression and increased appetite, generally requiring several days of rest and
recuperation. Depressive symptoms with suicidal thoughts or behavior can occur and are
generally the most serious problems seen during “crashing” or other forms of stimulant
withdrawal. Many individuals with stimulant use disorder may experience a withdrawal
syndrome at some point.
Differential Diagnosis
Stimulant withdrawal is distinguished from stimulant-induced
mental disorders (e.g., stimulant-induced depressive disorder, with onset during withdrawal)
because the symptoms (e.g., depressed mood) in these latter disorders are in excess of those
usually associated with stimulant withdrawal, predominate in the clinical presentation, and are
severe enough to warrant clinical attention.

Comorbidity
Given the typical overlap of stimulant withdrawal with stimulant use disorder, see
“Comorbidity” under Stimulant Use Disorder for more details about co-occurring conditions that
are likely to be encountered.
Stimulant-Induced Mental Disorders
The following stimulant-induced mental disorders (which include amphetamine-type substance–,
cocaine-, and other stimulant–induced mental disorders) are described in other chapters of the
manual with disorders with which they share phenomenology (see the substance/medicationinduced mental disorders in these chapters): stimulant-induced psychotic disorder
(“Schizophrenia Spectrum and Other Psychotic Disorders”); stimulant-induced bipolar and
related disorder (“Bipolar and Related Disorders”); stimulant-induced depressive disorder
(“Depressive Disorders”); stimulant-induced anxiety disorder (“Anxiety Disorders”); stimulantinduced obsessive-compulsive disorder (“Obsessive-Compulsive and Related Disorders”);
stimulant-induced sleep disorder (“Sleep-Wake Disorders”); stimulant-induced sexual
dysfunction (“Sexual Dysfunctions”); and stimulant-induced mild neurocognitive disorder
(“Neurocognitive Disorders”). For stimulant intoxication delirium and delirium induced by
stimulants taken as prescribed, see the criteria and discussion of delirium in the chapter
“Neurocognitive Disorders.” These stimulant-induced mental disorders are diagnosed instead of
stimulant intoxication or stimulant withdrawal only when the symptoms are sufficiently severe to
warrant independent clinical attention.
Unspecified Stimulant-Related Disorder
This category applies to presentations in which symptoms characteristic of a
stimulant-related disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for any specific stimulant-related disorder or any of the disorders
in the substance-related and addictive disorders diagnostic class.
Coding note: The ICD-10-CM code depends on whether the stimulant is an
amphetamine-type substance, cocaine, or other stimulant. The ICD-10-CM code for
an unspecified amphetamine-type substance or other stimulant–related disorder is
F15.99. The ICD-10-CM code for an unspecified cocaine-related disorder is F14.99.
Tobacco-Related Disorders
Tobacco Use Disorder
Tobacco Withdrawal

Tobacco-Induced Mental Disorders
Unspecified Tobacco-Related Disorder
Tobacco Use Disorder
Diagnostic Criteria
A. A problematic pattern of tobacco use leading to clinically significant impairment
or distress, as manifested by at least two of the following, occurring within a 12month period:
1. Tobacco is often taken in larger amounts or over a longer period than was
intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control
tobacco use.
3. A great deal of time is spent in activities necessary to obtain or use tobacco.
4. Craving, or a strong desire or urge to use tobacco.
5. Recurrent tobacco use resulting in a failure to fulfill major role obligations at
work, school, or home (e.g., interference with work).
6. Continued tobacco use despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of tobacco (e.g.,
arguments with others about tobacco use).
7. Important social, occupational, or recreational activities are given up or
reduced because of tobacco use.
8. Recurrent tobacco use in situations in which it is physically hazardous (e.g.,
smoking in bed).
9. Tobacco use is continued despite knowledge of having a persistent or
recurrent physical or psychological problem that is likely to have been caused
or exacerbated by tobacco.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of tobacco to achieve the desired
effect.
b. A markedly diminished effect with continued use of the same amount of
tobacco.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for tobacco (refer to Criteria A
and B of the criteria set for tobacco withdrawal).
b. Tobacco (or a closely related substance, such as nicotine) is taken to
relieve or avoid withdrawal symptoms.
Specify if:

646
In early remission: After full criteria for tobacco use disorder were previously
met, none of the criteria for tobacco use disorder have been met for at least 3
months but for less than 12 months (with the exception that Criterion A4,
“Craving, or a strong desire or urge to use tobacco,” may be met).
In sustained remission: After full criteria for tobacco use disorder were
previously met, none of the criteria for tobacco use disorder have been met at
any time during a period of 12 months or longer (with the exception that Criterion
A4, “Craving, or a strong desire or urge to use tobacco,” may be met).
Specify if:
On maintenance therapy: The individual is taking a long-term maintenance
medication, such as nicotine replacement medication, and no criteria for tobacco
use disorder have been met for that class of medication (except tolerance to, or
withdrawal from, the nicotine replacement medication).
In a controlled environment: This additional specifier is used if the individual is
in an environment where access to tobacco is restricted.
Code based on current severity/remission: If a tobacco withdrawal or tobaccoinduced sleep disorder is also present, do not use the codes below for tobacco use
disorder. Instead, the comorbid tobacco use disorder is indicated in the 4th character
of the tobacco-induced disorder code (see the coding note for tobacco withdrawal or
tobacco-induced sleep disorder). For example, if there is comorbid tobacco-induced
sleep disorder and tobacco use disorder, only the tobacco-induced sleep disorder
code is given, with the 4th character indicating whether the comorbid tobacco use
disorder is moderate or severe: F17.208 for moderate or severe tobacco use
disorder with tobacco-induced sleep disorder. It is not permissible to code a
comorbid mild tobacco use disorder with a tobacco-induced sleep disorder.
Specify current severity/remission:
Z72.0 Mild: Presence of 2–3 symptoms.
F17.200 Moderate: Presence of 4–5 symptoms.
F17.201 Moderate, In early remission
F17.201 Moderate, In sustained remission
F17.200 Severe: Presence of 6 or more symptoms.
F17.201 Severe, In early remission
F17.201 Severe, In sustained remission
Specifiers
“On maintenance therapy” applies as a specifier to be added to “in remission” if the individual is
both in remission and on maintenance therapy. “In a controlled environment” applies as a further
specifier of remission if the individual is both in remission and in a controlled environment (i.e.,
in early remission in a controlled environment or in sustained remission in a controlled

environment). Examples of these environments are closely supervised and substance-free jails,
therapeutic communities, and locked hospital units.
Diagnostic Features
Tobacco use disorder can develop with use of all forms of tobacco (e.g., cigarettes, chewing
tobacco, snuff, pipes, cigars, electronic nicotine delivery devices such as electronic cigarettes [ecigarettes]) and with prescription nicotine-containing medications (nicotine gum and patch). The
relative ability of these products to produce tobacco use disorder or to induce withdrawal is
associated with the rapidity of the route of administration (smoked over oral over transdermal)
and the nicotine content of the product. The name of this substance category was changed from
“nicotine” in prior editions of DSM to “tobacco” in DSM-5 on the basis of harms from addiction
being associated mostly with tobacco and much less with nicotine.
Tobacco use disorder is common among individuals who use cigarettes and smokeless
tobacco daily, is less common among individuals who use e-cigarettes, and is uncommon
among those who do not use tobacco daily or use nicotine medications. Tolerance to tobacco
is exemplified by the disappearance of nausea and dizziness after intake and by a more intense
effect of tobacco the first time it is used during the day. Cessation of tobacco use can produce a
well-defined withdrawal syndrome. Many individuals with tobacco use disorder use tobacco to
relieve or to avoid withdrawal symptoms (e.g., after being in a situation where use is restricted).
Many individuals with tobacco use disorder have tobacco-related physical symptoms or diseases
and continue to smoke. The large majority report craving when they do not smoke for several
hours. Spending excessive time using tobacco can be exemplified by chain-smoking (i.e.,
smoking one cigarette after another with no time between cigarettes). Because tobacco sources
are readily and legally available, and because tobacco intoxication is very rare, spending a great
deal of time attempting to procure tobacco or recovering from its effects is uncommon. Giving
up important social, occupational, or recreational activities can occur when an individual forgoes
an activity because it occurs in tobacco use–restricted areas. Use of tobacco rarely results in
failure to fulfill major role obligations (e.g., interference with work or home responsibilities), but
persistent social or interpersonal problems (e.g., having arguments with others about tobacco use,
avoiding social situations because of others’ disapproval of tobacco use) or use that is physically
hazardous (e.g., smoking in bed, smoking around flammable chemicals) occur at an intermediate
prevalence. Although these criteria are less often endorsed by tobacco users, if endorsed, they
can indicate a more severe disorder.
Associated Features
Smoking within 30 minutes of waking, smoking daily, smoking more cigarettes per day, and
waking at night to smoke are associated with tobacco use disorder. Environmental cues can
evoke craving and withdrawal. Serious medical conditions often occur, including lung and other
cancers, cardiac and pulmonary disease, perinatal problems, cough, shortness of breath, and
accelerated skin aging.

Temperamental.
Environmental.
Genetic and physiological.
Prevalence
Although cigarettes are the most commonly used tobacco product, use of other tobacco products
(especially e-cigarettes) has become more common. In the United States, 19% of adults used a
tobacco product in the last year, 19% used more than one product, 14% used cigarettes, 4% used
cigars, 3% used e-cigarettes, and 2% used smokeless tobacco. One fourth (24%) of current U.S.
smokers are nondaily smokers.
The 12-month prevalence of DSM-5 tobacco use disorder in the United States in 2012–2013
was 20% among adults age 18 years and older and 29.6% among Native Americans, 22.3%
among non-Latinx Whites, 20.1% among African Americans, 12.2% among Latinx, and 11.2%
among Asian Americans and Pacific Islanders. Prevalence was higher among men; those who
were young, unmarried, less educated, poor, or residing in the southern United States; and those
with almost any psychiatric disorder. The prevalence among current daily smokers is
approximately 50%.
Global comparisons show that in all geographic regions of the world, the age-standardized
prevalence of daily tobacco smoking is higher in men than in women, but the gender ratio varies
greatly, from 16.9:1 in East Asia to 1.2:1 in Australasia.
Development and Course
About 20% of U.S. high school seniors report having ever smoked cigarettes, and about 5% have
used in the past 30 days. Among adolescents who smoke cigarettes at least monthly, most of
these individuals will become daily tobacco users in the future. Initiation of smoking after age 21
years is rare. Some of the tobacco use disorder criteria symptoms (e.g., craving) occur soon after
beginning tobacco use, suggesting the addiction process begins with initial use; however,
fulfilling DSM criteria usually occurs over several years.
Nondaily smoking has become more prevalent since the late 1990s in the United States,
especially among individuals ages 18–34 years, Blacks, Hispanics, and individuals with at least a
college education.
Risk and Prognostic Factors
Individuals with externalizing personality traits are more likely to initiate
tobacco use. Children with attention-deficit/hyperactivity disorder or conduct disorder, and
adults with depressive, bipolar, anxiety, personality, psychotic, or other substance use disorders,
are at higher risk for starting and continuing tobacco use and of tobacco use disorder.
Persons with low incomes and low educational levels are more likely to initiate
tobacco use and are less likely to stop.
Genetic factors contribute to the onset of tobacco use, the continuation
of tobacco use, and the development of tobacco use disorder, with a degree of heritability
equivalent to that observed with other substance use disorders (i.e., about 50%). Some of this
risk is specific to tobacco, and some is common with the vulnerability to developing any
substance use disorder.

Culture-Related Diagnostic Issues
Acceptance of tobacco use varies across cultural contexts. Age-standardized prevalence of daily
tobacco smoking varies greatly by geographic region, ranging from 4.7% in Western SubSaharan Africa to 24.2% in Eastern Europe. The degree to which these geographic differences
are the result of income, education, and tobacco control activities in a country is unclear.
Prevalence of tobacco use in the United States varies by age, gender, and ethnoracial
background, with lower rates of smoking onset and progression to daily smoking among Black
youth, especially young women. Liver enzyme polymorphisms that vary across ethnoracial
groups can affect nicotine metabolism, contributing to variation in smoking behavior. Higher
tobacco use disorder prevalence is also associated with exposure to racism and ethnic
discrimination. Prevalence of DSM-IV nicotine dependence is higher among adult lesbian, gay,
and bisexual individuals than among heterosexuals, possibly also due to an association with
exposure to sexual orientation–related discrimination. Among individuals with DSM-IV nicotine
dependence, lower income and education are associated with disorder persistence.
Sex- and Gender-Related Diagnostic Issues
The ratio of men to women among U.S. smokers is approximately 1.4:1 and has been stable
between 2004 and 2014. This ratio is generally consistent across various income and educational
levels. The ratio diminishes in older age groups as fewer men are smoking as age increases. The
literature from several U.S. settings suggests that negative reinforcement (i.e., that smoking
relieves negative affect) is a greater motivator in women than in men. Menstrual cycle effects on
smoking are found inconsistently, but tobacco withdrawal appears worse in the luteal than the
follicular phase of the cycle. Pregnant females smoke at a lower rate than nonpregnant females
but relapse back to smoking rapidly after delivery.
Diagnostic Markers
The following biomarkers can be used to measure the extent of tobacco or nicotine use: carbon
monoxide in the breath and nicotine and its metabolite cotinine in blood, saliva, or urine;
however, these are only weakly associated with tobacco use disorder.
Association With Suicidal Thoughts or Behavior
National U.S. survey data show that past-year cigarette use is associated with a two- to threefold
increased risk of suicidal thoughts and behavior, with earlier age at first tobacco use increasing
risk. Evidence from the U.S. Veterans Health Administration shows that even after adjustment
for covariates, tobacco use disorder is associated with an increased risk of suicide. A large study
of twins in Finland found that the relationship between tobacco use and suicide increased in a
dose-response manner, and that for identical twins discordant for tobacco use, tobacco use was
associated with a sixfold increased risk for suicide.
Functional Consequences of Tobacco Use Disorder
Medical consequences of tobacco use often begin when tobacco users are in their 40s and usually

F17.203
become progressively more debilitating over time. One-half of smokers who do not stop using
tobacco will die early from a tobacco-related illness, and smoking-related morbidity occurs in
more than one-half of tobacco users. Most medical conditions result from exposure to carbon
monoxide, tars, and other non-nicotine components of tobacco. The major predictor of
reversibility is duration of smoking. Secondhand smoke increases the risk of heart disease and
cancer by 30%. Long-term use of nicotine medications does not appear to cause medical harm.
Comorbidity
The most common medical conditions from smoking are cardiovascular illnesses, chronic
obstructive pulmonary disease, and cancers. Smoking also increases perinatal problems, such as
low birth weight and miscarriage. Prevalence of smoking is almost twice as high in individuals
with major depressive disorder; although the prevalence of smoking in the United States is
higher among individuals with low socioeconomic status, the increased prevalence of smoking
among those with depression is independent of socioeconomic status. The most common
psychiatric comorbidities associated with smoking are alcohol and other substance, depressive,
bipolar, anxiety, personality, and attention-deficit/hyperactivity disorders. In the United States,
individuals with a psychiatric disorder are three times more likely than others to have tobacco
use disorder. Adults with DSM-5 tobacco use disorder are significantly more likely than other
adults to have comorbid psychiatric disorders, including other DSM-5 substance use disorders,
major depressive disorder, bipolar I disorder, panic disorder, generalized anxiety disorder,
posttraumatic stress disorder, and borderline and antisocial personality disorders.
Tobacco Withdrawal
Diagnostic Criteria
A. Daily use of tobacco for at least several weeks.
B. Abrupt cessation of tobacco use, or reduction in the amount of tobacco used,
followed within 24 hours by four (or more) of the following signs or symptoms:
1. Irritability, frustration, or anger.
2. Anxiety.
3. Difficulty concentrating.
4. Increased appetite.
5. Restlessness.
6. Depressed mood.
7. Insomnia.
C. The signs or symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.

D. The signs or symptoms are not attributed to another medical condition and are
not better explained by another mental disorder, including intoxication or
withdrawal from another substance.
Coding note: The ICD-10-CM code for tobacco withdrawal is F17.203. Note that the
ICD-10-CM code indicates the comorbid presence of a moderate or severe tobacco
use disorder, reflecting the fact that tobacco withdrawal can only occur in the
presence of a moderate or severe tobacco use disorder.
Diagnostic Features
Withdrawal symptoms impair the ability to stop tobacco use. The symptoms after abstinence
from tobacco are in large part due to nicotine deprivation. Tobacco withdrawal is common
among daily tobacco users who stop or reduce their use of tobacco. Symptoms are more intense
among individuals who smoke cigarettes and also use smokeless tobacco or electronic cigarettes
daily. This symptom intensity is likely attributable to the more rapid onset and higher levels of
nicotine with cigarette smoking. Significant withdrawal among those who are nondaily cigarette
users or use only nicotine medications is uncommon.
Typically, heart rate decreases by 5–12 bpm in the first few days after stopping smoking, and
weight increases an average of 4–7 lb (2–3 kg) over the first year after stopping smoking.
Tobacco withdrawal can produce clinically significant mood changes and functional impairment.
Because of conditioning effects, withdrawal can be prompted by environmental cues such as
seeing others smoking. Gradual reduction of tobacco decreases the severity of withdrawal.
Associated Features
Craving for tobacco or nicotine is very common during abstinence and has a large effect on the
ability to remain abstinent. Abstinence can increase impulsivity and anhedonia and can decrease
positive affect. Abstinence from tobacco or nicotine also appears to increase craving for sweet or
sugary foods and impairs performance on tasks requiring vigilance. Smoking increases the
metabolism of many medications used to treat mental disorders; thus, cessation of smoking can
increase the blood levels of these medications, and this can produce clinically significant
outcomes. This effect appears to be due not to nicotine but rather to other compounds in tobacco.
Prevalence
Approximately 50% of daily smokers who quit for 2 or more days will have four or more
symptoms of tobacco withdrawal. The most commonly endorsed signs and symptoms are
anxiety, irritability, and difficulty concentrating. The least commonly endorsed symptoms are
depression and insomnia.
Development and Course
Tobacco withdrawal usually begins within 24 hours of stopping or cutting down tobacco use,
peaks at 2–3 days after abstinence, and usually lasts 2–3 weeks. Tobacco withdrawal symptoms
can occur among adolescent tobacco users, even prior to daily tobacco use. Prolonged symptoms
beyond 1 month can occur but are uncommon.

Temperamental.
Genetic and physiological.
Risk and Prognostic Factors
Smokers with depressive disorders, bipolar disorders, anxiety disorders,
attention-deficit/hyperactivity disorder, and other substance use disorders have more severe
withdrawal.
Genotype can influence the probability of withdrawal upon abstinence.
Diagnostic Markers
The following biomarkers can be used to measure the extent of tobacco or nicotine use but are
only weakly associated with tobacco withdrawal: carbon monoxide in the breath and nicotine
and its metabolite cotinine in blood, saliva, or urine.
Functional Consequences of Tobacco Withdrawal
Tobacco withdrawal can cause significant distress and difficulty functioning in a minority of
smokers, but this may be uncommon. Withdrawal impairs the ability to stop or control tobacco
use. Whether tobacco withdrawal can prompt the development of a new mental disorder or
recurrence of a mental disorder is debatable, but if this occurs, it would be in a small minority of
tobacco users.
Differential Diagnosis
The symptoms of tobacco withdrawal overlap with those of other substance withdrawal
syndromes (e.g., alcohol withdrawal; sedative, hypnotic, or anxiolytic withdrawal; stimulant
withdrawal; caffeine withdrawal; opioid withdrawal); caffeine intoxication; anxiety, depressive,
bipolar, and sleep disorders; and medication-induced akathisia. Admission to smoke-free
inpatient units or voluntary smoking cessation can induce withdrawal symptoms that mimic,
intensify, or disguise other disorders or adverse effects of medications used to treat mental
disorders (e.g., irritability thought to be due to alcohol withdrawal could be due to tobacco
withdrawal). Reduction in symptoms with the use of nicotine confirms the diagnosis.
Comorbidity
Given the typical overlap of tobacco withdrawal with tobacco use disorder, see “Comorbidity”
under Tobacco Use Disorder for more details about co-occurring conditions that are likely to be
encountered.
Tobacco-Induced Mental Disorders
Tobacco-induced sleep disorder is discussed in the chapter “Sleep-Wake Disorders” (see
“Substance/Medication-Induced Sleep Disorder”).
Unspecified Tobacco-Related Disorder

F17.209
This category applies to presentations in which symptoms characteristic of a
tobacco-related disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for any specific tobacco-related disorder or any of the disorders
in the substance-related and addictive disorders diagnostic class.
Other (or Unknown) Substance–Related
Disorders
Other (or Unknown) Substance Use Disorder
Other (or Unknown) Substance Intoxication
Other (or Unknown) Substance Withdrawal
Other (or Unknown) Substance–Induced Mental Disorders
Unspecified Other (or Unknown) Substance–Related Disorder
Other (or Unknown) Substance Use Disorder
Diagnostic Criteria
A. A problematic pattern of use of an intoxicating substance not able to be
classified within the alcohol; caffeine; cannabis; hallucinogen (phencyclidine and
others); inhalant; opioid; sedative, hypnotic, or anxiolytic; stimulant; or tobacco
categories and leading to clinically significant impairment or distress, as
manifested by at least two of the following, occurring within a 12-month period:
1. The substance is often taken in larger amounts or over a longer period than
was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control use
of the substance.
3. A great deal of time is spent in activities necessary to obtain the substance,
use the substance, or recover from its effects.
4. Craving, or a strong desire or urge to use the substance.
5. Recurrent use of the substance resulting in a failure to fulfill major role
obligations at work, school, or home.

6. Continued use of the substance despite having persistent or recurrent social
or interpersonal problems caused or exacerbated by the effects of its use.
7. Important social, occupational, or recreational activities are given up or
reduced because of use of the substance.
8. Recurrent use of the substance in situations in which it is physically
hazardous.
9. Use of the substance is continued despite knowledge of having a persistent
or recurrent physical or psychological problem that is likely to have been
caused or exacerbated by the substance.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of the substance to achieve
intoxication or desired effect.
b. A markedly diminished effect with continued use of the same amount of
the substance.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for other (or unknown) substance
(refer to Criteria A and B of the criteria sets for other [or unknown]
substance withdrawal).
b. The substance (or a closely related substance) is taken to relieve or avoid
withdrawal symptoms.
Specify if:
In early remission: After full criteria for other (or unknown) substance use
disorder were previously met, none of the criteria for other (or unknown)
substance use disorder have been met for at least 3 months but for less than 12
months (with the exception that Criterion A4, “Craving, or a strong desire or urge
to use the substance,” may be met).
In sustained remission: After full criteria for other (or unknown) substance use
disorder were previously met, none of the criteria for other (or unknown)
substance use disorder have been met at any time during a period of 12 months
or longer (with the exception that Criterion A4, “Craving, or a strong desire or
urge to use the substance,” may be met).
Specify if:
In a controlled environment: This additional specifier is used if the individual is
in an environment where access to the substance is restricted.
Code based on current severity/remission: If an other (or unknown) substance
intoxication, other (or unknown) substance withdrawal, or other (or unknown)
substance–induced mental disorder is present, do not use the codes below for other
(or unknown) substance use disorder. Instead, the comorbid other (or unknown)
substance use disorder is indicated in the 4th character of the other (or unknown)

substance–induced disorder code (see the coding note for other [or unknown]
substance intoxication, other [or unknown] substance withdrawal, or specific other
[or unknown] substance–induced mental disorder). For example, if there is comorbid
other (or unknown) substance–induced depressive disorder and other (or unknown)
substance use disorder, only the other (or unknown) substance–induced depressive
disorder code is given, with the 4th character indicating whether the comorbid other
(or unknown) substance use disorder is mild, moderate, or severe: F19.14 for other
(or unknown) substance use disorder with other (or unknown) substance–induced
depressive disorder or F19.24 for a moderate or severe other (or unknown)
substance use disorder with other (or unknown) substance–induced depressive
disorder.
Specify current severity/remission:
F19.10 Mild: Presence of 2–3 symptoms.
F19.11 Mild, In early remission
F19.11 Mild, In sustained remission
F19.20 Moderate: Presence of 4–5 symptoms.
F19.21 Moderate, In early remission
F19.21 Moderate, In sustained remission
F19.20 Severe: Presence of 6 or more symptoms.
F19.21 Severe, In early remission
F19.21 Severe, In sustained remission
Specifiers
“In a controlled environment” applies as a further specifier of remission if the individual is both
in remission and in a controlled environment (i.e., in early remission in a controlled environment
or in sustained remission in a controlled environment). Examples of these environments are
closely supervised and substance-free jails, therapeutic communities, and locked hospital units.
Diagnostic Features
The diagnostic class other (or unknown) substance–related disorders applies to substances that
are not included within any of the nine substance classes presented earlier in this chapter (i.e., to
alcohol; caffeine; cannabis; hallucinogens [phencyclidine and others]; inhalants; opioids;
sedatives, hypnotics, or anxiolytics; stimulants; or tobacco). Such substances include anabolic
steroids; nonsteroidal anti-inflammatory drugs; corticosteroids; antiparkinsonian medications;
antihistamines; nitrous oxide; amyl-, butyl-, or isobutyl-nitrites; betel nut, which is chewed in
many geographic regions to produce mild euphoria and a floating sensation; and kava (from a
South Pacific pepper plant), which produces mild euphoria, sedation, incoordination, and weight
loss, as well as health effects (e.g., mild hepatitis, lung abnormalities). Note that gaseous
substances are included with the inhalant category only if they are hydrocarbon agents; other

gaseous substances (including nitrous oxide mentioned above) are included in the other (or
unknown) substance category. Unknown substance–related disorders are associated with
unidentified substances, such as intoxications in which the individual cannot identify the
ingested drug, or substance use disorders involving either new, black market drugs not yet
identified or familiar drugs illegally sold under false names.
Note that substances included within the scope of one of the substance classes should be
coded within that respective substance class and are inappropriate to include in the “other
substance” category. For example, the following substances are explicitly included in specific
substance classes and should not be included in the “other substance” category: synthetic
cannabinoids are included in the cannabis category; propofol is included in the sedative,
hypnotic, or anxiolytic category; and cathinones (including khât plant agents and synthetic
chemical derivatives) are included in the stimulant category.
Other (or unknown) substance use disorder is a mental disorder in which repeated use of an
other or unknown substance typically continues, despite the individual’s knowing that the
substance is causing serious problems for the individual. Those problems are reflected in the
diagnostic criteria. When the substance is known but does not fit within any of the other nine
substance classes, it should be reflected when recording and coding the name of the disorder
(e.g., “nitrous oxide use disorder,” using the applicable code for other [or unknown] substance
use disorder).
Associated Features
A diagnosis of other (or unknown) substance use disorder is supported by any of the following:
the individual’s reported use of a substance that is not among the nine classes listed in this
chapter; recurring episodes of intoxication with negative results in standard drug screens, which
may not detect new or rarely used substances; and the presence of symptoms characteristic of an
unidentified substance that has newly appeared in the individual’s community.
Because of access to nitrous oxide (“laughing gas”), membership in certain populations may
be associated with frequent use of the substance and possibly with a diagnosis of nitrous oxide
use disorder. The role of this gas as an anesthetic agent leads to misuse by some medical and
dental professionals, and its use as a propellant for commercial products (e.g., whipped cream
dispensers) contributes to misuse by food service workers. Nitrous oxide misuse by adolescents
and young adults is significant, and some individuals with very frequent use may present with
serious medical complications and mental conditions, including myeloneuropathy, spinal cord
subacute combined degeneration, peripheral neuropathy, and psychosis.
Use of amyl-, butyl-, and isobutyl (and similar) nitrite gases is prevalent among homosexual
men and some adolescents, especially those with conduct disorder.
Substance use disorders generally are associated with elevated risks of suicide, but there is no
evidence of unique risk factors for suicide with other (or unknown) substance use disorder.
Prevalence
Based on extremely limited data, the prevalence of most other (or unknown) substance use
disorders is likely lower than that of use disorders involving the nine substance classes in this

Use of other or unknown substances without meeting criteria for other (or unknown) substance
use disorder.
Substance use disorders.
Other (or unknown) substance intoxication, other (or unknown) substance withdrawal, and
other (or unknown) substance–induced mental disorders.
chapter. For certain gaseous substances, prevalence of use is not rare (lifetime prevalence in the
U.S. household population for individuals age 12 and older is estimated at 4.6% for nitrous oxide
and 2.5% for nitrites), but how often the patterns of use qualify for a use disorder is unknown.
Development and Course
No single pattern of development or course characterizes the pharmacologically varied other (or
unknown) substance use disorders. Often unknown substance use disorders will be reclassified
when the unknown substance eventually is identified.
Risk and Prognostic Factors
Risk and prognostic factors for other (or unknown) substance use disorders are thought to be
similar to those for most substance use disorders and include the presence of any other substance
use disorders, conduct disorder, or antisocial personality disorder in the individual or the
individual’s family; early onset of substance problems; easy availability of the substance in the
individual’s environment; childhood maltreatment or trauma; and evidence of limited early selfcontrol and behavioral disinhibition.
Culture-Related Diagnostic Issues
Certain cultures may be associated with other (or unknown) substance use disorders involving
specific indigenous substances within the cultural region, such as betel nut.
Diagnostic Markers
Urine, breath, or saliva tests may correctly identify a commonly used substance falsely sold as a
novel product. However, routine clinical tests usually cannot identify truly unusual or new
substances, which may require testing in specialized laboratories.
Differential Diagnosis
Use of unknown substances is not rare among adolescents, but most use does not meet the
diagnostic standard of two or more criteria for other (or unknown) substance use disorder in a
12-month period.
Other (or unknown) substance use disorder may co-occur with various
substance use disorders that involve any of the nine substance classes presented earlier in this
chapter, and the symptoms of the disorders may be similar and overlapping. To disentangle
symptom patterns, it is helpful to inquire about which symptoms persisted during periods when
some of the substances were not being used.
Other (or unknown) substance use disorder is differentiated from other (or unknown) substance
intoxication, other (or unknown) substance withdrawal, and other-(or unknown) substanceinduced mental disorders (e.g., corticosteroid-induced bipolar and related disorder) in that other
(or unknown) substance use disorder describes a problematic pattern of use of the other (or
unknown) substance that involves impaired control over the use of the substance, social

impairment attributable to use of the substance, risky use of the substance (e.g., continued use
despite medical complications), and pharmacological symptoms (the development of
tolerance or withdrawal), whereas other (or unknown) substance intoxication, other (or
unknown) substance withdrawal, and other (or unknown) substance-induced mental disorders
describe psychiatric syndromes that occur in the context of heavy use. Other (or unknown)
substance intoxication, other (or unknown) substance withdrawal, and other (or unknown)
substance–induced mental disorders may occur in individuals with other (or unknown) substance
use disorder. In such cases, a diagnosis of other (or unknown) substance intoxication, other (or
unknown) substance withdrawal, or other (or unknown) substance–induced mental disorder
should be given in addition to a diagnosis of other (or unknown) substance use disorder, the
presence of which is indicated in the diagnostic code.
Comorbidity
Substance use disorders, including other (or unknown) substance use disorder, are commonly
comorbid with one another, with conduct disorder in adolescence, and with antisocial personality
disorder.
Other (or Unknown) Substance Intoxication
Diagnostic Criteria
A. The development of a reversible substance-specific syndrome attributable to
recent ingestion of (or exposure to) a substance that is not listed elsewhere or is
unknown.
B. Clinically significant problematic behavioral or psychological changes that are
attributable to the effect of the substance on the central nervous system (e.g.,
impaired motor coordination, psychomotor agitation or retardation, euphoria,
anxiety, belligerence, mood lability, cognitive impairment, impaired judgment,
social withdrawal) and develop during, or shortly after, use of the substance.
C. The signs or symptoms are not attributable to another medical condition and are
not better explained by another mental disorder, including intoxication with
another substance.
Specify if:
With perceptual disturbances: This specifier may be noted when
hallucinations with intact reality testing or auditory, visual, or tactile illusions
occur in the absence of a delirium.
Coding note: The ICD-10-CM code depends on whether there is a comorbid other
(or unknown) substance use disorder involving the same substance and whether or
not there are perceptual disturbances.

For other (or unknown) substance intoxication, without perceptual
disturbances: If a mild other (or unknown) substance use disorder is comorbid,
the ICD-10-CM code is F19.120, and if a moderate or severe other (or unknown)
substance use disorder is comorbid, the ICD-10-CM code is F19.220. If there is
no comorbid other (or unknown) substance use disorder, then the ICD-10-CM
code is F19.920.
For 
other 
(or 
unknown) 
substance 
intoxication, 
with 
perceptual
disturbances: If a mild other (or unknown) substance use disorder is comorbid,
the ICD-10-CM code is F19.122, and if a moderate or severe other (or unknown)
substance use disorder is comorbid, the ICD-10-CM code is F19.222. If there is
no comorbid other (or unknown) substance use disorder, then the ICD-10-CM
code is F19.922.
Note: For information on Risk and Prognostic Factors, Culture-Related Diagnostic
Issues, and Diagnostic Markers, see the corresponding sections in Other (or Unknown)
Substance Use Disorder.
Diagnostic Features
The essential feature of other (or unknown) substance intoxication is the presence of clinically
significant behavioral or psychological changes that develop during, or immediately after, use of
either a) a substance not included within one of the nine substance classes presented in this
chapter (i.e., alcohol; caffeine; cannabis; phencyclidine and other hallucinogens; inhalants;
opioids; sedatives, hypnotics, or anxiolytics; stimulants; or tobacco) or b) an unknown substance.
If the substance is known, it should be reflected in the name of the disorder upon coding (e.g.,
“kava intoxication”).
Application of the diagnostic criteria for other (or unknown) substance intoxication is very
challenging. Criterion A requires development of a reversible “substance-specific syndrome,”
but if the substance is unknown, that syndrome usually will be unknown. To resolve this conflict,
clinicians may ask the individual or obtain collateral history as to whether the individual has
experienced a similar episode after using substances with the same “street” name or from the
same source. Similarly, hospital emergency departments sometimes recognize over a few days
numerous presentations of a severe, unfamiliar intoxication syndrome from a newly available,
previously unknown substance. Because of the great variety of intoxicating substances, Criterion
B can provide only broad examples of signs and symptoms from some intoxications, with no
threshold for the number of symptoms required for a diagnosis; clinical judgment guides those
decisions. Criterion C requires ruling out other medical conditions, mental disorders, or
intoxications.
Prevalence
The prevalence of other (or unknown) substance intoxication is unknown.
Development and Course

Use of other or unknown substance, without meeting criteria for other (or unknown) substance
intoxication.
Substance intoxication or other substance/medication-induced mental disorders.
Other toxic, metabolic, traumatic, neoplastic, vascular, or infectious disorders that impair brain
function and cognition.
Intoxications usually appear and then peak minutes to hours after use of the substance, but the
onset and course vary with the substance and the route of administration. Generally, substances
used by pulmonary inhalation and intravenous injection have the most rapid onset of action,
whereas those ingested by mouth and requiring metabolism to an active product are much
slower. (For example, after ingestion of certain mushrooms, the first signs of an eventually fatal
intoxication may not appear for a few days.) Intoxication effects usually resolve within hours to a
very few days. However, the body may completely eliminate an anesthetic gas such as nitrous
oxide just minutes after use ends. At the other extreme, some “hit-and-run” intoxicating
substances poison systems, leaving permanent impairments. For example, MPTP (1-methyl-4phenyl-1,2,3,6-tetrahydropyridine), a contaminating by-product in the synthesis of a certain
opioid, kills dopaminergic cells and induces permanent parkinsonism in individuals who had
sought opioid intoxication.
Functional Consequences of Other (or Unknown) Substance
Intoxication
Impairment from intoxication with any substance may have serious consequences, including
dysfunction at work, social indiscretions, problems in interpersonal relationships, failure to fulfill
role obligations, traffic accidents, fighting, high-risk behaviors (i.e., having unprotected sex), and
substance or medication overdose. The pattern of consequences will vary with the particular
substance.
Differential Diagnosis
The individual used an other or unknown substance(s), but the dose was insufficient to produce
symptoms that meet the diagnostic criteria required for the diagnosis.
Familiar 
substances
may be sold in the black market as novel products, and individuals may experience intoxication
from those substances. History, toxicology screens, or chemical testing of the substance itself
may help to identify it. Other substance intoxication is distinguished from other
substance/medication-induced mental disorders (e.g., corticosteroid-induced anxiety disorder)
because the symptoms (e.g., anxiety) in these latter disorders are in excess of those (if known)
usually associated with the specific substance intoxication, predominate in the clinical
presentation, and are severe enough to warrant clinical attention.
Numerous neurological and other medical conditions may produce rapid onset of signs and
symptoms mimicking those of intoxications, including the examples in Criterion B.
Paradoxically, drug withdrawals also must be ruled out; for example, lethargy may indicate
withdrawal from one drug or intoxication with another substance.
Comorbidity

As with all substance-related disorders, conduct disorder in adolescence, antisocial personality
disorder, and other substance use disorders tend to co-occur with other (or unknown) substance
intoxication.
Other (or Unknown) Substance Withdrawal
Diagnostic Criteria
A. Cessation of (or reduction in) use of a substance that has been heavy and
prolonged.
B. The development of a substance-specific syndrome shortly after the cessation of
(or reduction in) substance use.
C. The substance-specific syndrome causes clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
D. The symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including withdrawal from another
substance.
E. The substance involved cannot be classified under any of the other substance
categories (alcohol; caffeine; cannabis; opioids; sedatives, hypnotics, or
anxiolytics; stimulants; or tobacco) or is unknown.
Specify if:
With perceptual disturbances: This specifier may be noted when
hallucinations with intact reality testing or auditory, visual, or tactile illusions
occur in the absence of a delirium.
Coding note: The ICD-10-CM code depends on whether or not there is a comorbid
other (or unknown) substance use disorder and whether or not there are perceptual
disturbances.
For other (or unknown) substance withdrawal, without perceptual
disturbances: If a mild other (or unknown) substance use disorder is comorbid,
the ICD-10-CM code is F19.130, and if a moderate or severe other (or unknown)
substance use disorder is comorbid, the ICD-10-CM code is F19.230. If there is
no comorbid other (or unknown) substance use disorder (e.g., in a patient taking
an other [or unknown] substance solely under appropriate medical supervision),
then the ICD-10-CM code is F19.930.
For 
other 
(or 
unknown) 
substance 
withdrawal, 
with 
perceptual
disturbances: If a mild other (or unknown) substance use disorder is comorbid,
the ICD-10-CM code is
F19.132, and if a moderate or severe other (or unknown) substance use disorder

is comorbid, the ICD-10-CM code is F19.232. If there is no comorbid other (or
unknown) substance use disorder (e.g., in a patient taking an other [or unknown]
substance solely under appropriate medical supervision), then the ICD-10-CM
code is F19.932.
Note: For information on Risk and Prognostic Factors and Diagnostic Markers, see the
corresponding sections in Other (or Unknown) Substance Use Disorder.
Diagnostic Features
Other (or unknown) substance withdrawal is a clinically significant syndrome that develops
during or within a few hours to days after reducing or terminating dosing with a substance
(Criteria A and B). Although recent dose reduction or termination usually is clear in the history,
other diagnostic procedures are very challenging if the drug is unknown. Criterion B requires
development of a “substance-specific syndrome” (i.e., the individual’s signs and symptoms must
correspond with the known withdrawal syndrome for the recently stopped drug)—a requirement
that rarely can be met with an unknown substance. Consequently, clinical judgment must guide
such decisions when this information is limited. Criterion D requires ruling out other medical
conditions, mental disorders, or withdrawals from familiar substances. When the substance is
known, it should be reflected in the name of the disorder upon coding (e.g., “betel nut
withdrawal”).
Prevalence
The prevalence of other (or unknown) substance withdrawal is unknown.
Development and Course
Withdrawal signs commonly appear some hours after use of the substance is terminated, but the
onset and course vary greatly, depending on the dose typically used and the rate of elimination of
the specific substance from the body. At peak severity, withdrawal symptoms from some
substances involve only moderate levels of discomfort, whereas withdrawal from other
substances may be fatal. Withdrawal-associated dysphoria often motivates relapse to substance
use. Withdrawal symptoms slowly abate over days, weeks, or months, depending on the
particular drug and doses to which the individual became tolerant.
Functional Consequences of Other (or Unknown) Substance
Withdrawal
Withdrawal from any substance may have serious consequences, including physical signs and
symptoms (e.g., malaise, vital sign changes, abdominal distress, headache), intense drug craving,
anxiety, depression, agitation, psychotic symptoms, or cognitive impairments. These
consequences may lead to problems such as dysfunction at work, problems in interpersonal
relationships, failure to fulfill role obligations, traffic accidents, fighting, high-risk behavior (e.g.,
having unprotected sex), suicide attempts, and substance or medication overdose. The pattern of
consequences will vary with the particular substance.

Dose reduction after extended dosing, but not meeting the criteria for other (or unknown)
substance withdrawal.
Substance withdrawal or other substance/medication-induced mental disorders.
Other toxic, metabolic, traumatic, neoplastic, vascular, or infectious disorders that impair brain
function and cognition.
Differential Diagnosis
The individual used other (or unknown) substances, but the dose that was used was insufficient
to produce symptoms that meet the criteria required for the withdrawal diagnosis.
Familiar 
substances
may be sold in the black market as novel products, and individuals may experience withdrawal
when discontinuing those substances. History, toxicology screens, or
chemical testing of the substance itself may help to identify it. Other substance withdrawal is
distinguished from other substance/medication-induced mental disorders (e.g., venlafaxineinduced anxiety disorder, with onset during withdrawal) because the symptoms (e.g., anxiety) in
these latter disorders are in excess of symptoms (if known) usually associated with the specific
substance withdrawal, predominate in the clinical presentation, and are severe enough to warrant
clinical attention.
Numerous neurological and other medical conditions may produce rapid onset of signs and
symptoms mimicking those of withdrawals. Paradoxically, drug intoxications also must be ruled
out; for example, lethargy may indicate withdrawal from one drug or intoxication with another
substance.
Comorbidity
As with all substance-related disorders, conduct disorder in adolescence, antisocial personality
disorder, and other substance use disorders are likely to co-occur with other (or unknown)
substance withdrawal.
Other (or Unknown) Substance–Induced Mental
Disorders
Because the category of other or unknown substances is inherently ill-defined, the extent and
range of these substance-induced mental disorders are uncertain. Nevertheless, other (or
unknown) substance–induced mental disorders are possible and are described in other chapters of
the manual with disorders with which they share phenomenology (see the substance/medicationinduced mental disorders in these chapters): other (or unknown) substance–induced psychotic
disorder (“Schizophrenia Spectrum and Other Psychotic Disorders”); other (or unknown)
substance–induced bipolar and related disorder (“Bipolar and Related Disorders”); other (or
unknown) substance–induced depressive disorder (“Depressive Disorders”); other (or unknown)
substance–induced anxiety disorders (“Anxiety Disorders”); other (or unknown) substance–
induced obsessive-compulsive disorder (“Obsessive-Compulsive and Related Disorders”); other
(or unknown) substance–induced sleep disorder (“Sleep-Wake Disorders”); other (or unknown)
substance–induced sexual dysfunction (“Sexual Dysfunctions”); and other (or unknown)

F63.0
substance/medication–induced major or mild neurocognitive disorder (“Neurocognitive
Disorders”). For other (or unknown) substance–induced intoxication delirium, other (or
unknown) substance–induced withdrawal delirium, and delirium induced by other (or unknown)
substance taken as prescribed, see the criteria and discussion of delirium in the chapter
“Neurocognitive Disorders.” These other (or unknown) substance–induced mental disorders are
diagnosed instead of other (or unknown) substance intoxication or other (or unknown) substance
withdrawal only when the symptoms are sufficiently severe to warrant independent clinical
attention.
Unspecified Other (or Unknown) Substance–Related
Disorder
F19.99
This category applies to presentations in which symptoms characteristic of an other
(or unknown) substance–related disorder that cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning
predominate but do not meet the full criteria for any specific other (or unknown)
substance–related disorder or any of the disorders in the substance-related
disorders diagnostic class.
Non-Substance-Related Disorders
Gambling Disorder
Diagnostic Criteria
A. Persistent and recurrent problematic gambling behavior leading to clinically
significant impairment or distress, as indicated by the individual exhibiting four
(or more) of the following in a 12-month period:
1. Needs to gamble with increasing amounts of money in order to achieve the
desired excitement.
2. Is restless or irritable when attempting to cut down or stop gambling.
3. Has made repeated unsuccessful efforts to control, cut back, or stop
gambling.
4. Is often preoccupied with gambling (e.g., having persistent thoughts of

reliving past gambling experiences, handicapping or planning the next
venture, thinking of ways to get money with which to gamble).
5. Often gambles when feeling distressed (e.g., helpless, guilty, anxious,
depressed).
6. After losing money gambling, often returns another day to get even (“chasing”
one’s losses).
7. Lies to conceal the extent of involvement with gambling.
8. Has jeopardized or lost a significant relationship, job, or educational or career
opportunity because of gambling.
9. Relies on others to provide money to relieve desperate financial situations
caused by gambling.
B. The gambling behavior is not better explained by a manic episode.
Specify if:
Episodic: Meeting diagnostic criteria at more than one time point, with
symptoms subsiding between periods of gambling disorder for at least several
months.
Persistent: Experiencing continuous symptoms, to meet diagnostic criteria for
multiple years.
Specify if:
In early remission: After full criteria for gambling disorder were previously met,
none of the criteria for gambling disorder have been met for at least 3 months
but for less than 12 months.
In sustained remission: After full criteria for gambling disorder were previously
met, none of the criteria for gambling disorder have been met during a period of
12 months or longer.
Specify current severity:
Mild: 4–5 criteria met.
Moderate: 6–7 criteria met.
Severe: 8–9 criteria met.
Note: Although some behavioral conditions that do not involve ingestion of substances
have similarities to substance-related disorders, only one disorder—gambling disorder—
has sufficient data to be included in this section.
Specifiers
Severity is based on the number of criteria endorsed. Individuals with mild gambling disorder
may exhibit only 4–5 of the criteria, with the most frequently endorsed criteria usually related to
preoccupation with gambling and “chasing” losses. Individuals with moderately severe gambling
disorder exhibit more of the criteria (i.e., 6–7). Individuals with the most severe form will exhibit

all or most of the nine criteria (i.e., 8–9). Jeopardizing relationships or career opportunities
because of gambling and relying on others to provide money for gambling losses are typically
the least often endorsed criteria and most often occur among those with more severe gambling
disorder. Furthermore, individuals presenting for treatment of gambling disorder typically have
moderate to severe forms of the disorder.
Diagnostic Features
Gambling involves risking something of value in the hopes of obtaining something of greater
value. In many cultures, individuals gamble on games and events, and most do so without
experiencing problems. However, some individuals develop substantial impairment related to
their gambling behaviors. The essential feature of gambling disorder is persistent and recurrent
maladaptive gambling behavior that disrupts personal, family, and/or vocational pursuits
(Criterion A). Gambling disorder is defined as a cluster of four or more of the symptoms listed in
Criterion A occurring at any time in the same 12-month period.
A pattern of “chasing one’s losses” may develop, with an urgent need to continue gambling
(often with placing larger bets or taking greater risks) to undo a loss or series of losses. The
individual may abandon a gambling strategy and try to win back losses all at once. Although
many gamblers may “chase” for short periods of time, it is the frequent, and often long-term,
“chase” that is characteristic of gambling disorder (Criterion A6). Individuals may lie to family
members, therapists, or others to conceal the extent of involvement with gambling; these
instances of deceit may also include, but are not limited to, covering up illegal behaviors such as
forgery, fraud, theft, or embezzlement to obtain money with which to gamble (Criterion A7).
Individuals may also engage in “bailout” behavior, turning to family or others for help with a
desperate financial situation that was caused by gambling (Criterion A9).
In some cases, symptoms meeting diagnostic criteria for gambling disorder may occur as a
direct physiological consequence of taking dopaminergic medications, such as those used to treat
Parkinson’s disease. When such symptoms are induced by a medication, these cases would be
diagnosed as gambling disorder.
Associated Features
Distortions in thinking (e.g., denial, superstitions, a sense of power and control over the outcome
of chance events, overconfidence) may be present in individuals with gambling disorder. Many
individuals with gambling disorder believe that money is both the cause of and the solution to
their problems. Some individuals with gambling disorder are impulsive, competitive, energetic,
restless, and easily bored; they may be overly concerned with the approval of others and may be
generous to the point of extravagance when winning. Other individuals with gambling disorder
are depressed and lonely, and they may gamble when feeling helpless, guilty, or depressed.
Prevalence
The past-year prevalence rate of gambling disorder is about 0.2%–0.3% in the general U.S.
population, with a range of 0.1%–0.7% observed across international studies. In the

general U.S. population, the lifetime prevalence rate is about 0.4%–1.0%. For women, the
lifetime prevalence rate of gambling disorder is about 0.2%, and for men it is about 0.6%. The
12-month prevalence of DSM-5 gambling disorder varies among ethnoracial groups in the
United States: it is 0.52% in African Americans, 0.25% in Latinx, and 0.23% in non-Latinx
Whites.
Development and Course
The onset of gambling disorder can occur during adolescence or young adulthood, but in other
individuals it manifests during middle or even older adulthood. Generally, gambling disorder
develops over the course of years, although the progression appears to be more rapid in women
than in men. National data from the United States and Canada show that most individuals who
develop a gambling disorder evidence a pattern of gambling that gradually increases in both
frequency and amount of wagering. Certainly, milder forms can develop into more severe cases.
Most individuals with gambling disorder report that one or two types of gambling are most
problematic for them, although some individuals participate in many forms of gambling.
Individuals are likely to engage in certain types of gambling (e.g., buying scratch tickets daily)
more frequently than others (e.g., playing slot machines or blackjack at the casino weekly).
Frequency of gambling can be related more to the type of gambling than to the severity of the
overall gambling disorder. For example, purchasing a single scratch ticket each day may not be
problematic, while less frequent casino, sports, or card gambling may be part of a gambling
disorder. Similarly, amounts of money spent wagering are not in themselves indicative of
gambling disorder. Some individuals can wager thousands of dollars per month and not have a
problem with gambling, while others may wager much smaller amounts but experience
substantial gambling-related difficulties.
Gambling patterns may be regular or episodic, and gambling disorder can be persistent or in
remission. Gambling can increase during periods of stress or depression and during periods of
substance use or abstinence. There may be periods of heavy gambling and severe problems,
times of total abstinence, and periods of nonproblematic gambling. Gambling disorder is
sometimes associated with spontaneous, long-term remissions. Nevertheless, some individuals
underestimate their vulnerability to develop gambling disorder or to relapse following remission.
When in a period of remission, they may incorrectly assume that they will have no problem
regulating gambling and that they can engage in some forms of gambling nonproblematically,
only to experience a relapse of gambling disorder.
Early expression of gambling disorder is more common among young men (ages 18–21
years) than among young women. Individuals who begin gambling in youth often do so with
family members or friends. Development of early-life gambling disorder appears to be associated
with impulsivity and substance abuse. Internet gambling has been linked to risky and
problematic gambling among youth and may be conducted in a more isolative (i.e., nonpeer)
fashion. Some video gaming characteristics (e.g., loot boxes or loot crates containing prizes
determined by chance that may be of higher or lower value or desirability) overlap with
gambling behavior and may influence the course of gambling disorder. Many high school and
college students who develop gambling disorder grow out of the disorder over time, although it
remains a lifelong problem for some. Mid- and later-life onset of gambling disorder is more
common among women than among men.

Temperamental.
Genetic and physiological.
Course modifiers.
There are age and gender variations in the type of gambling activities and the prevalence
rates of gambling disorder. Gambling disorder in the United States is more common among
younger and middle-age individuals than among older adults. Among U.S. young adults (ages
18–21 years), the disorder is more prevalent in young men than in young women. Younger
individuals prefer different forms of gambling (e.g., sports betting), whereas older adults are
more likely to develop problems with slot machine and bingo gambling. Although the
proportions of individuals who seek treatment for gambling disorder are low across all age
groups in the United States, younger individuals are especially unlikely to present for treatment.
Risk and Prognostic Factors
Gambling that begins in childhood or early adolescence is associated with
increased rates of gambling disorder. Gambling disorder also appears to aggregate with
antisocial personality disorder, depressive and bipolar disorders, and other substance use
disorders, particularly alcohol use disorder.
Gambling disorder can aggregate in families, and this effect appears to
relate to both environmental and genetic factors. Gambling problems are more frequent in
monozygotic than in dizygotic twins. Gambling disorder is also more prevalent among firstdegree relatives of individuals with moderate to severe alcohol use disorder than among the
general population.
Many individuals, including adolescents and young adults, are likely to resolve
their problems with gambling disorder over time, although a strong predictor of future gambling
problems 
is 
previous 
gambling 
problems. 
Psychopathology, 
including 
attentiondeficit/hyperactivity and anxiety disorders, has been found to be associated with increased risk of
onset of gambling disorder among those who gamble and with persistence of gambling disorder
symptoms over time.
Culture-Related Diagnostic Issues
Types of gambling activities vary across cultural contexts and ethnoracial groups (e.g., pai gow,
cockfights, blackjack, horse racing). Some Indigenous populations in Canada, New Zealand, and
the United States have high prevalence rates of gambling problems, possibly related to limited
economic opportunities, the expectation that gambling may help advance social goals, and the
location of casinos on some U.S. tribal lands. U.S.-born individuals have higher rates of
gambling problems than first-generation immigrants to the United States. Endorsement of
specific disorder criteria may vary across ethnoracial groups. For example, among individuals
with gambling problems, Asian Americans may be less likely than other groups to endorse being
preoccupied with gambling (Criterion A4), while African Americans and Latinx may be more
likely to endorse repeated unsuccessful efforts to control gambling (Criterion A3).
Sex- and Gender-Related Diagnostic Issues
Men develop gambling disorder at higher rates than women, although this gender gap may be
narrowing. Data from treatment-seeking populations have suggested that women may develop

Nondisordered gambling.
Manic episode.
gambling problems more rapidly after the onset of gambling (so-called telescoping), although
general population data suggest that men progress more rapidly to disordered gambling than
women do. Although women seek treatment sooner than men do, rates of treatment seeking in
U.S. national surveys are low (< 10%) among individuals with gambling disorder regardless of
gender.
Women may gamble as a maladaptive approach to negative affect, whereas men may gamble
more for the thrill of it. Compared with men, women may also experience more shame related to
gambling. Men tend to wager on different forms of gambling than women, with cards, sports,
and horse race gambling more prevalent among men, and slot machine and bingo gambling more
common among women. Women with gambling disorder are more likely than men with
gambling disorder to have depressive, bipolar, and anxiety disorders.
Association With Suicidal Thoughts or Behavior
In a U.S. study, up to half of individuals in treatment for gambling disorder in Connecticut
reported suicidal thoughts, and about 17% reported attempted suicide. A nationwide register
study in Sweden showed that compared with individuals without gambling disorder, individuals
ages 20–74 years with gambling disorder have a 15-fold increased suicide mortality rate.
Functional Consequences of Gambling Disorder
Areas of psychosocial, health, and mental health functioning may be adversely affected by
gambling disorder. Specifically, individuals with gambling disorder may, because of their
involvement with gambling, jeopardize or lose important relationships with family members or
friends. Such problems may occur from repeatedly lying to others to cover up the extent of
gambling or from requesting money that is used for gambling or to pay off gambling debts.
Employment or educational activities may likewise be adversely impacted by gambling disorder;
absenteeism or poor work or school performance can occur with gambling disorder, as
individuals may gamble during work or school hours or be preoccupied with gambling or its
adverse consequences when they should be working or studying. Individuals with gambling
disorder in a U.S. national sample had poor general health and utilized medical services at high
rates.
Differential Diagnosis
Gambling disorder must be distinguished from professional and social
gambling. In professional gambling, risks are limited and discipline is central. Social gambling
typically occurs with friends or colleagues and lasts for a limited period of time, with acceptable
losses. Some persons can experience problems associated with gambling (e.g., short-term
chasing behavior and loss of control) that do not meet the full criteria for gambling disorder.
Loss of judgment and excessive gambling may occur during a manic episode. An
additional diagnosis of gambling disorder should be given only if the gambling behavior is not
better explained by manic episodes (e.g., a history of maladaptive gambling behavior at times
other than during a manic episode). Alternatively, an individual with gambling disorder may,

Personality disorders.
Gambling symptoms due to dopaminergic medications.
during a period of gambling, exhibit behavior that resembles a manic episode, but once the
individual is away from the gambling, these manic-like features dissipate.
Problems with gambling may occur in individuals with antisocial
personality disorder and other personality disorders. If the criteria are met for both disorders,
both can be diagnosed.
Some 
individuals 
taking 
dopaminergic
medications (e.g., for Parkinson‘s disease) may experience urges to gamble that might be
distressing or impairing enough to meet criteria for gambling disorder. In such cases, a diagnosis
of gambling disorder would be warranted.
Comorbidity
Gambling disorder is associated with poor general health. In addition, some specific medical
conditions, such as tachycardia and angina, are more common among individuals with gambling
disorder than in the general population, even when other substance use disorders, including
tobacco use disorder, are controlled for. In U.S. national surveys, individuals with gambling
disorder have high rates of comorbidity with other mental disorders, such as substance use
disorders, depressive disorders, anxiety disorders, and personality disorders. In some individuals,
other mental disorders may precede gambling disorder and be either absent or present during the
manifestation of gambling disorder. Gambling disorder may also occur prior to the onset of other
mental disorders, especially bipolar and related disorders, anxiety disorders, and substance use
disorders. In a U.S. national survey, in approximately three-quarters of cases of individuals with
gambling disorder and another mental disorder, other psychopathology preceded the gambling
disorder.

# 17 - Neurocognitive Disorders

# Neurocognitive Disorders

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Neurocognitive Disorders
The neurocognitive disorders (NCDs) begin with delirium, followed by the
syndromes of major NCD, mild NCD, and their etiological subtypes. The major or mild NCD
subtypes are NCD due to Alzheimer’s disease; vascular NCD; NCD with Lewy bodies; NCD due
to Parkinson’s disease; frontotemporal NCD; NCD due to traumatic brain injury; NCD due to
HIV infection; substance/medication-induced NCD; NCD due to Huntington’s disease; NCD due
to prion disease; NCD due to another medical condition; NCD due to multiple etiologies; and
unspecified NCD. The NCD category encompasses the group of disorders in which the primary
clinical deficit is in cognitive function, and that are acquired rather than developmental.
Although cognitive deficits are present in many if not all mental disorders (e.g., schizophrenia,
bipolar disorders), only disorders whose core features are cognitive are included in the NCD
category. The NCDs are those in which impaired cognition has not been present since birth or
very early life, and thus represents a decline from a previously attained level of functioning.
The NCDs are unique among DSM-5 categories in that these are syndromes for which the
underlying pathology, and frequently the etiology as well, can potentially be determined. The
various underlying disease entities have all been the subject of extensive research, clinical
experience, and expert consensus on diagnostic criteria. The DSM-5 criteria for these disorders
have been developed in close consultation with the expert groups for each of the disease entities
and align as closely as possible with the current consensus criteria for each of them. The
potential utility of biomarkers is also discussed in relation to diagnosis. Dementia is subsumed
under the newly named entity major neurocognitive disorder, although the term dementia is not
precluded from use in the etiological subtypes in which that term is standard. Furthermore,
DSM-5 recognizes a less severe level of cognitive impairment, mild neurocognitive disorder,
which can also be a focus of care. Diagnostic criteria are provided for both these syndromic
entities, followed by diagnostic criteria for the different etiological subtypes. Several of the
NCDs frequently coexist with one another, and their relationships may be multiply characterized
under different chapter subheadings, including “Differential Diagnosis” (e.g., NCD due to
Alzheimer’s disease vs. vascular NCD), “Risk and Prognostic Factors” (e.g., vascular pathology
increasing the clinical expression of Alzheimer’s disease), or “Comorbidity” (e.g., mixed
Alzheimer’s disease–vascular pathology).
The term dementia is retained in DSM-5 for continuity and may be used in settings where
physicians and patients are accustomed to this term. Although dementia is the customary term
for disorders like the degenerative dementias that usually affect older adults, the term
neurocognitive disorder is widely used and often preferred for conditions affecting younger
individuals, such as impairment secondary to traumatic brain injury or HIV infection.
Furthermore, the major NCD definition is somewhat broader than the term dementia, in that a
diagnosis of major NCD can be made if there is a significant cognitive decline in only one
cognitive domain, whereas a diagnosis of dementia in ICD-10 and ICD-11 (and formerly in

DSM-IV) requires multiple cognitive deficits. Thus, cases that would qualify in ICD-10 and
ICD-11 (and formerly DSM-IV) for a diagnosis of amnestic disorder (memory impairment in the
absence of other cognitive deficits) are diagnosed as major NCD in DSM-5.
Neurocognitive Domains
The criteria for the various NCDs are based on defined cognitive domains. Table 1 provides for
each of the key domains a working definition, examples of symptoms or observations regarding
impairments in everyday activities, and examples of assessments. The domains thus defined,
along with guidelines for clinical thresholds, form the basis on which the NCDs, their levels, and
their subtypes may be diagnosed.
TABLE 1 Neurocognitive domains
Cognitive domain
Examples of symptoms or observations
Examples of assessments
Complex attention
(sustained attention,
divided attention,
selective attention,
processing speed)
Major: Has increased difficulty in environments
with multiple stimuli (TV, radio, conversation);
is easily distracted by competing events in the
environment. Is unable to attend unless input is
restricted and simplified. Has difficulty holding
new information in mind, such as recalling
phone numbers or addresses just given, or
reporting what was just said. Is unable to
perform mental calculations. All thinking takes
longer than usual, and components to be
processed must be simplified to one or a few.
Mild: Normal tasks take longer than previously.
Begins to find errors in routine tasks; finds
work needs more double-checking than
previously. Thinking is easier when not
competing with other things (radio, TV, other
conversations, cell phone, driving).
Sustained attention: Maintenance of attention
over time (e.g., pressing a button every time a
tone is heard, and over a period of time).
Selective attention: Maintenance of attention
despite competing stimuli or distractors:
hearing numbers and letters read and asked to
count only letters.
Divided attention: Attending to two tasks within
the same time period: rapidly tapping while
learning a story being read. Processing speed
can be quantified on any task by timing it (e.g.,
time to put together a design of blocks; time to
match symbols with numbers; speed in
responding, such as counting speed or serial 3
speed).
Executive function
(planning, decisionmaking, working
memory, responding
to feedback/error
correction, overriding
habits/inhibition,
mental flexibility)
Major: Abandons complex projects. Needs to
focus on one task at a time. Needs to rely on
others to plan instrumental activities of daily
living or make decisions.
Mild: Increased effort required to complete
multistage projects. Has increased difficulty
multitasking or difficulty resuming a task
interrupted by a visitor or phone call. May
complain of increased fatigue from the extra
effort required to organize, plan, and make
decisions. May report that large social
gatherings are more taxing or less enjoyable
because of increased effort required to follow
shifting conversations.
Planning: Ability to find the exit to a maze;
interpret a sequential picture or object
arrangement.
Decision-making: Performance of tasks that
assess process of deciding in the face of
competing alternatives (e.g., simulated
gambling).
Working memory: Ability to hold information for
a brief period and to manipulate it (e.g., adding
up a list of numbers or repeating a series of
numbers or words backward).
Feedback/error utilization: Ability to benefit
from feedback to infer the rules for solving a
problem.
Overriding habits/inhibition: Ability to choose a
more complex and effortful solution to be
correct (e.g., looking away from the direction
indicated by an arrow; naming the color of a
word’s font rather than naming the word)

670
Major: Repeats self in conversation, often within
the same conversation. Cannot keep track of
short list of items when shopping or of plans
for the day. Requires frequent reminders to
orient to task at hand.
Mild: Has difficulty recalling recent events, and
Learning and memory
(immediate memory,
recent memory
[including free recall,
cued recall, and
recognition memory],
very-long-term
memory [semantic;
autobiographical],
implicit learning)
relies increasingly on list making or calendar.
Needs occasional reminders or re-reading to
keep track of characters in a movie or novel.
Occasionally may repeat self over a few weeks
to the same person. Loses track of whether bills
have already been paid.
Note: Except in severe forms of major
neurocognitive disorder, semantic,
autobiographical, and implicit learning are
relatively preserved, compared with recent
memory.
Major: Has significant difficulties with
Language (expressive
language [including
naming, word
finding, fluency, and
grammar, and syntax]
and receptive
language)
expressive or receptive language. Often uses
general-use phrases such as “that thing” and
“you know what I mean,” and prefers general
pronouns rather than names. With severe
impairment, may not even recall names of
closer friends and family. Idiosyncratic word
usage, grammatical errors, and spontaneity of
output and economy of utterances occur.
Stereotypy of speech occurs; echolalia and
automatic speech typically precede mutism.
Mild: Has noticeable word-finding difficulty.
May substitute general for specific terms. May
avoid use of specific names of acquaintances.
Grammatical errors involve subtle omission or
incorrect use of articles, prepositions, auxiliary
verbs, etc.
Major: Has significant difficulties with
previously familiar activities (using tools,
driving motor vehicle), navigating in familiar
environments; is often more confused at dusk,
when shadows and lowering levels of light
change perceptions.
Mild: May need to rely more on maps or others
Perceptual-motor
(includes abilities
subsumed under the
terms visual
perception,
visuoconstructional,
perceptual-motor,
praxis, and gnosis)
for directions. Uses notes and follows others to
get to a new place. May find self lost or turned
around when not concentrating on task. Is less
precise in parking. Needs to expend greater
effort for spatial tasks such as carpentry,
assembly sewing or knitting
word s font rather than naming the word).
Mental/cognitive flexibility: Ability to shift
between two concepts, tasks, or response rules
(e.g., from number to letter, from verbal to keypress response, from adding numbers to
ordering numbers, from ordering objects by size
to ordering by color).
Immediate memory span: Ability to repeat a list
of words or digits. Note: Immediate memory
sometimes subsumed under “working memory”
(see “Executive Function”).
Recent memory: Assesses the process of encoding
new information (e.g., word lists, a short story,
or diagrams). The aspects of recent memory
that can be tested include 1) free recall (the
individual is asked to recall as many words,
diagrams, or elements of a story as possible);
2) cued recall (examiner aids recall by
providing semantic cues such as “List all the
food items on the list” or “Name all of the
children from the story”); and 3) recognition
memory (examiner asks about specific items—
e.g., “Was ’apple’ on the list?” or “Did you see
this diagram or figure?”). Other aspects of
memory that can be assessed include semantic
memory (memory for facts), autobiographical
memory (memory for personal events or
people), and implicit (procedural) learning
(unconscious learning of skills).
Expressive language: Confrontational naming
(identification of objects or pictures); fluency
(e.g., name as many items as possible in a
semantic [e.g., animals] or phonemic [e.g.,
words starting with “f”] category in 1 minute).
Grammar and syntax (e.g., omission or incorrect
use of articles, prepositions, auxiliary verbs):
Errors observed during naming and fluency
tests are compared with norms to assess
frequency of errors and compare with normal
slips of the tongue.
Receptive language: Comprehension (word
definition and object-pointing tasks involving
animate and inanimate stimuli): performance of
actions/activities according to verbal command.
Visual perception: Line bisection tasks can be
used to detect basic visual defect or attentional
neglect. Motor-free perceptual tasks (including
facial recognition) require the identification
and/or matching of figures—best when tasks
cannot be verbally mediated (e.g., figures are
not objects); some require the decision of
whether a figure can be “real” or not based on
dimensionality.
Visuoconstructional: Assembly of items requiring
hand-eye coordination, such as drawing,
copying, and block assembly.

assembly, sewing, or knitting.
Perceptual-motor: Integrating perception with
purposeful movement (e.g., inserting blocks
into a form board without visual cues; rapidly
inserting pegs into a slotted board).
Praxis: Integrity of learned movements, such as
ability to imitate gestures (wave goodbye) or
pantomime use of objects to command (“Show
me how you would use a hammer”).
Gnosis: Perceptual integrity of awareness and
recognition, such as recognition of faces and
colors.
Social cognition
(recognition of
emotions, theory of
mind)
Major: Behavior clearly out of acceptable social
range; shows insensitivity to social standards of
modesty in dress or of political, religious, or
sexual topics of conversation. Focuses
excessively on a topic despite group’s
disinterest or direct feedback. Behavioral
intention without regard to family or friends.
Makes decisions without regard to safety (e.g.,
inappropriate clothing for weather or social
setting). Typically, has little insight into these
changes.
Mild: Has subtle changes in behavior or attitude,
often described as a change in personality, such
as less ability to recognize social cues or read
facial expressions, decreased empathy,
increased extraversion or introversion,
decreased inhibition, or subtle or episodic
apathy or restlessness.
Recognition of emotions: Identification of
emotion in images of faces representing a
variety of both positive and negative emotions.
Theory of mind: Ability to consider another
person’s mental state (thoughts, desires,
intentions) or experience—story cards with
questions to elicit information about the mental
state of the individuals portrayed, such as
“Where will the girl look for the lost bag?” or
“Why is the boy sad?”
Delirium
Diagnostic Criteria
A. A disturbance in attention (i.e., reduced ability to direct, focus, sustain, and shift
attention) accompanied by reduced awareness of the environment.
B. The disturbance develops over a short period of time (usually hours to a few
days), represents a change from baseline attention and awareness, and tends to
fluctuate in severity during the course of a day.
C. An additional disturbance in cognition (e.g., memory deficit, disorientation,
language, visuospatial ability, or perception).
D. The disturbances in Criteria A and C are not better explained by another
preexisting, established, or evolving neurocognitive disorder and do not occur in
the context of a severely reduced level of arousal, such as coma.
E. There is evidence from the history, physical examination, or laboratory findings
that the disturbance is a direct physiological consequence of another medical
condition, substance intoxication or withdrawal (i.e., due to a drug of abuse or to
a medication), or exposure to a toxin, or is due to multiple etiologies.

Specify if:
Acute: Lasting a few hours or days.
Persistent: Lasting weeks or months.
Specify if:
Hyperactive: The individual has a hyperactive level of psychomotor activity that
may be accompanied by mood lability, agitation, and/or refusal to cooperate with
medical care.
Hypoactive: The individual has a hypoactive level of psychomotor activity that
may be accompanied by sluggishness and lethargy that approaches stupor.
Mixed level of activity: The individual has a normal level of psychomotor
activity even though attention and awareness are disturbed. Also includes
individuals whose activity level rapidly fluctuates.
Specify whether:
Substance intoxication delirium: This diagnosis should be made instead of
substance intoxication when the symptoms in Criteria A and C predominate in
the clinical picture and when they are sufficiently severe to warrant clinical
attention.
Coding note: The ICD-10-CM codes for the [specific substance] intoxication
delirium are indicated in the table below. Note that the ICD-10-CM code
depends on whether or not there is a comorbid substance use disorder
present for the same class of substance. If a mild substance use disorder is
comorbid with the substance intoxication delirium, the 4th position character is
“1,” and the clinician should record “mild [substance] use disorder” before the
substance intoxication delirium (e.g., “mild cocaine use disorder with cocaine
intoxication delirium”). If a moderate or severe substance use disorder is
comorbid with the substance intoxication delirium, the 4th position character is
“2,” and the clinician should record “moderate [substance] use disorder” or
“severe [substance] use disorder,” depending on the severity of the comorbid
substance use disorder. If there is no comorbid substance use disorder (e.g.,
after a one-time heavy use of the substance), then the 4th position character is
“9,” and the clinician should record only the substance intoxication delirium.
ICD-10-CM
Substance intoxication delirium
With mild use
disorder
With moderate or
severe use
disorder
Without use
disorder
Alcohol
F10.121
F10.221
F10.921
Cannabis
F12.121
F12.221
F12.921
Phencyclidine
F16.121
F16.221
F16.921
Other hallucinogen
F16.121
F16.221
F16.921

Inhalant
F18.121
F18.221
F18.921
Opioid
F11.121
F11.221
F11.921
Sedative, hypnotic, or anxiolytic
F13.121
F13.221
F13.921
Amphetamine-type substance (or other
stimulant)
F15.121
F15.221
F15.921
Cocaine
F14.121
F14.221
F14.921
Other (or unknown) substance
F19.121
F19.221
F19.921
Substance withdrawal delirium: This diagnosis should be made instead of
substance withdrawal when the symptoms in Criteria A and C predominate in the
clinical picture and when they are sufficiently severe to warrant clinical attention.
Coding note: The ICD-10-CM codes for the [specific substance] withdrawal
delirium are indicated in the table below. Note that the ICD-10-CM code
depends on whether or not there is a comorbid substance use disorder
present for the same class of substance. If a mild substance use disorder is
comorbid with the substance withdrawal delirium, the 4th position character is
“1,” and the clinician should record “mild [substance] use disorder” before the
substance withdrawal delirium (e.g., “mild alcohol use disorder with alcohol
withdrawal delirium”). If a moderate or severe substance use disorder is
comorbid with the substance withdrawal delirium, the 4th position character is
“2,” and the clinician should record “moderate [substance] use disorder” or
“severe [substance] use disorder,” depending on the severity of the comorbid
substance use disorder. If there is no comorbid substance use disorder (e.g.,
after regular use of an anxiolytic substance taken as prescribed), then the 4th
position character is “9,” and the clinician should record only the substance
withdrawal delirium.
ICD-10-CM
Substance withdrawal delirium
With mild use
disorder
With moderate or
severe use
disorder
Without use
disorder
Alcohol
F10.131
F10.231
F10.931
Opioid
F11.188
F11.288
F11.988
Sedative, hypnotic, or anxiolytic
F13.131
F13.231
F13.931
Other (or unknown) substance
F19.131
F19.231
F19.931
Medication-induced delirium: This diagnosis applies when the symptoms in
Criteria A and C arise as a side effect of a medication taken as prescribed.
Code [specific medication]–induced delirium: F11.921 opioid taken as
prescribed (or F11.988 if during withdrawal from opioid taken as prescribed);
F12.921 pharmaceutical cannabis receptor agonist taken as prescribed;
F13.921 sedative, hypnotic, or anxiolytic taken as prescribed (or F13.931 if

Substance intoxication delirium.
during withdrawal from sedative, hypnotic, or anxiolytic taken as prescribed);
F15.921 amphetamine-type substance or other stimulant taken as prescribed;
F16.921 ketamine or other hallucinogen taken as prescribed or for medical
reasons; F19.921 for medications that do not fit into any of the classes (e.g.,
dexamethasone) and in cases in which a substance is judged to be an
etiological factor but the specific class of substance is unknown (or F19.931 if
during withdrawal from medications that do not fit into any of the classes,
taken as prescribed).
F05 Delirium due to another medical condition: There is evidence from the
history, physical examination, or laboratory findings that the disturbance is
attributable to the physiological consequences of another medical condition.
Coding note: Include the name of the other medical condition in the name of
the delirium (e.g., F05 delirium due to hepatic encephalopathy). The other
medical condition should also be coded and listed separately immediately
before the delirium due to another medical condition (e.g., K72.90 hepatic
encephalopathy; F05 delirium due to hepatic encephalopathy).
F05 Delirium due to multiple etiologies: There is evidence from the history,
physical examination, or laboratory findings that the delirium has more than one
etiology (e.g., more than one etiological medical condition; another medical
condition plus substance intoxication or medication side effect).
Coding note: Use multiple separate codes reflecting specific delirium
etiologies (e.g., K72.90 hepatic encephalopathy; F05 delirium due to hepatic
failure; F10.231 alcohol withdrawal delirium). Note that the etiological medical
condition both appears as a separate code that precedes the delirium code
and is substituted into the delirium due to another medical condition rubric.
Recording Procedures
The name of the substance intoxication delirium begins with the
specific substance (e.g., cocaine) that is presumed to be causing the delirium. The diagnostic
code is selected from the table included in the criteria set, which is based on the drug class and
presence or absence of a comorbid substance use disorder. For substances that do not fit into any
of the classes (e.g., dexamethasone), the code for “other substance” should be used; and in cases
in which a substance is judged to be an etiological factor but the specific class of substance is
unknown, the category “unknown substance” should be used.
When recording the name of the disorder, the comorbid substance use disorder (if any) is
listed first, followed by the word “with,” followed by the name of the substance intoxication
delirium, followed by the course (i.e., acute, persistent), followed by the specifier indicating level
of psychomotor activity (i.e., hyperactive, hypoactive, mixed level of activity). For example, in
the case of acute hyperactive intoxication delirium occurring in a man with a severe cocaine use
disorder, the diagnosis is F14.221 severe cocaine use disorder with cocaine intoxication delirium,
acute, hyperactive. A separate diagnosis of the comorbid severe cocaine use disorder is not
given. If the intoxication delirium occurs without a comorbid substance use disorder (e.g., after a
one-time heavy use of the substance), no accompanying substance use disorder is noted (e.g.,

Substance withdrawal delirium.
Medication-induced delirium.
F16.921 phencyclidine intoxication delirium, acute, hypoactive).
The name of the substance withdrawal delirium begins with the
specific substance (e.g., alcohol) that is presumed to be causing the withdrawal delirium. The
diagnostic code is selected from substance-specific codes in the coding note included in the
criteria set. When recording the name of the disorder, the comorbid substance use disorder (if
any) is listed first, followed by the word “with,” followed by the substance withdrawal delirium,
followed by the course (i.e., acute, persistent), followed by the specifier indicating level of
psychomotor activity (i.e., hyperactive, hypoactive, mixed level of activity). For example, in the
case of acute hyperactive withdrawal delirium occurring in a man with a severe alcohol use
disorder, the diagnosis is F10.231 severe alcohol use disorder with alcohol withdrawal delirium,
acute, hyperactive. A separate diagnosis of the comorbid severe alcohol use disorder is not given.
The name of the medication-induced delirium begins with the
specific substance (e.g., dexamethasone) that is presumed to be causing the delirium. The name
of the disorder is followed by the course (i.e., acute, persistent), followed by the specifier
indicating level of psychomotor activity (i.e., hyperactive, hypoactive, mixed level of activity).
For example, in the case of acute hyperactive medication-induced delirium occurring in a man
using dexamethasone as prescribed, the diagnosis is F19.921 dexamethasone-induced delirium,
acute, hyperactive.
Specifiers
Regarding course, in hospital settings, delirium usually lasts about 1 week, but some symptoms
often persist even after individuals are discharged from the hospital.
Individuals with delirium may rapidly switch between hyperactive and hypoactive states. The
hyperactive state may be more common or more frequently recognized and often is associated
with medication side effects and drug withdrawal. The hypoactive state may be more frequent in
older adults and is often unrecognized among older individuals in emergency departments and
hospitals.
Diagnostic Features
The essential feature of delirium is an acute impairment of consciousness characterized by a
disturbance in attention accompanied by reduced awareness of the environment, both core
features of normal consciousness. Because these deficits reflect an altered state of consciousness
affecting many higher cerebral cortical functions of the cerebral cortex, they are accompanied by
a change from baseline in other cognitive functions that cannot be better explained by a
preexisting or evolving neurocognitive disorder (NCD). The disturbance in attention (Criterion
A) is manifested by reduced ability to direct, focus, sustain, and shift attention. Questions must
be repeated because the individual’s attention wanders, or the individual may perseverate with an
answer to a previous question rather than appropriately shift attention. The individual is easily
distracted by irrelevant stimuli. The disturbance in awareness affects both internal thinking and
insight as well as difficulty making sense of what is happening in the external environment.
The disturbance develops over a short period of time, usually hours to a few days, and tends

to fluctuate during the course of the day, often with worsening in the evening and night when
external orienting stimuli decrease (Criterion B). There is evidence from the history, physical
examination, or laboratory findings that the disturbance is a physiological consequence of an
underlying medical condition, substance intoxication or withdrawal, use of a medication, or a
toxin exposure, or a combination of these factors (Criterion E). The etiology should be coded
according to the etiologically appropriate subtype (i.e., substance or medication intoxication,
substance withdrawal, another medical condition, or multiple etiologies). Delirium often occurs
in the context of an underlying NCD. The impaired brain function of individuals with mild and
major NCD renders them more vulnerable to developing a delirium.
There is an accompanying change in at least one other area that may include memory and
learning (particularly recent memory), disorientation (particularly to time and place), alteration in
language (particularly semantic comprehension), or perceptual distortion or a perceptual-motor
disturbance (Criterion C). The perceptual disturbances accompanying delirium include
misinterpretations, illusions, or hallucinations; these disturbances are typically visual, but may
occur in other modalities as well, and range from simple and uniform to highly complex.
Normal attention/arousal, delirium, and coma lie on a continuum. Coma is defined as a state
of unconsciousness with an absence of cognition or sleep-wake cycle, along with the lack of any
meaningful response to verbal or physical stimuli. Delirium is an impaired state of consciousness
in the setting of an aroused cortex. The ability to evaluate cognition to diagnose delirium
depends on there being a level of cortical arousal and wakefulness sufficient for response to
verbal stimulation; hence, delirium should not be diagnosed in the context of coma (Criterion D).
Stuporous individuals also have a reduced level of brain arousal, but not to the extent of the
complete unconsciousness of coma. Coma and stupor can be due to neurological conditions or
drug-induced as with iatrogenic deep sedation in intensive care unit (ICU) settings or general
anesthesia. Those individuals who show only minimal responses to verbal or physical
stimulation are incapable of engaging with attempts at standardized testing or even interview.
This inability to engage should be classified as a disorder of arousal such as coma or stupor, and
not as delirium. However, delirium can be a stage that follows emergence from coma or stupor,
especially when coma is the result of a neurological condition. Further, the sleep-wake cycle
disturbance characteristic of the circadian rhythm disturbance in delirium can interfere with full
assessment of the individual if in a sleep phase, which should be distinguished from a disorder of
brain arousal.
Associated Features
Delirium is often associated with a disturbance in the sleep-wake cycle. This disturbance can
include daytime sleepiness, nighttime agitation, difficulty falling asleep, excessive sleepiness
throughout the day, or wakefulness throughout the night. In some cases, complete reversal of the
night-day sleep-wake cycle can occur. Sleep-wake cycle disturbances are very common in
delirium and have been proposed as a core criterion for the diagnosis.
The individual with delirium may exhibit emotional disturbances, such as anxiety, fear,
depression, irritability, anger, euphoria, and apathy. There may be rapid and unpredictable shifts

from one emotional state to another. The disturbed emotional state may also be evident in calling
out, screaming, cursing, muttering, moaning, or making other sounds. These behaviors are
especially prevalent at night and under conditions in which stimulation and environmental cues
are lacking.
Prevalence
The prevalence of delirium is highest among hospitalized older individuals and varies depending
on the individuals’ characteristics, setting of care, and sensitivity of the detection method. Data
from the United States and Finland indicate that the prevalence of delirium in the community
overall is low (1%–2%). The prevalence is 8%–17% in older individuals presenting to North
American emergency departments, where the delirium often indicates a medical illness.
Based on data from various countries, the prevalence of delirium when individuals are
admitted to the hospital ranges from 18% to 35%, and estimates of the occurrence of delirium
arising during hospitalization range from 29% to 64% in general hospital populations.
Internationally, delirium occurs in 11%–51% of older individuals postoperatively and in up to
81% of those in intensive care. The prevalence of delirium ranges from 20% to 22% in
individuals in nursing homes or post–acute care settings and occurs in up to 88% of individuals
with terminal illness at the end of life. Despite having higher risk factors for delirium, such as
cardiovascular disease, sepsis, and respiratory failure, younger African Americans
tended to have lower rates of the occurrence of delirium compared with White individuals of
similar age in a large case series of ICU patients in the United States.
Development and Course
The majority of individuals with delirium have a full recovery with or without treatment,
especially those who are not elderly. Delirium may progress to stupor, coma, seizures, or death,
particularly if undetected and the underlying cause(s) remains untreated.
There is increasing evidence that delirium may be associated in long-term follow-up with
cognitive decline or major NCD in the elderly, particularly in those with preexisting underlying
cognitive impairment. Mortality among hospitalized individuals with delirium is high; as many
as 38%–41% of individuals with delirium die within 1 year after diagnosis; the risk of death is
particularly great among those with malignancies and other significant underlying medical
illness.
Risk and Prognostic Factors
Delirium may be increased in the context of functional impairment, preexisting cognitive
impairment, sensory impairment (e.g., vision/hearing), increasing age, illness severity or
comorbidity, infection, depression, history of stroke, and history of alcohol use. Both major and
mild NCDs can increase the risk for delirium and complicate the course. Falls may be an
outcome of delirium but are not found to be a risk factor. In a meta-analysis of studies from 1990
through 2016, anticholinergic use was not a validated predictor of delirium.
Older individuals are especially susceptible to delirium compared with younger adults.

Psychotic disorders and bipolar and depressive disorders with psychotic features.
Acute stress disorder.
Malingering and factitious disorder.
Other neurocognitive disorders.
Among children, susceptibility to delirium in infancy and through childhood may be associated
with significant childhood morbidity and mortality, whereas individuals in early adulthood
through mid-adulthood may have less susceptibility to delirium and lower mortality risk.
Sex- and Gender-Related Diagnostic Issues
The symptoms associated with delirium may vary in men and women. Men more commonly
manifest motor agitation and affective lability, whereas women more commonly manifest
hypoactive delirium. Male sex is a risk factor for delirium, and sex- or gender-related factors
may interact with other risk factors.
Diagnostic Markers
In addition to laboratory findings characteristic of underlying medical conditions (or intoxication
or 
withdrawal 
states), 
there 
is 
often 
generalized 
irregular 
theta 
slowing 
on
electroencephalography, and fast activity is occasionally found (e.g., in some cases of alcohol
withdrawal delirium). However, electroencephalography is unable to detect slowing associated
with delirium without comparison to premorbid baseline alpha rhythms unless the slowing is in
the abnormal theta or delta frequency range.
Functional Consequences of Delirium
Delirium itself is associated with increased functional decline and risk of institutional placement.
Hospitalized individuals 65 years or older with delirium are at greater risk for poor outcomes
following discharge, including mortality, institutionalization, and dementia.
Differential Diagnosis
Delirium 
that 
is
characterized by vivid hallucinations, delusions, language disturbances, and agitation must be
distinguished from brief psychotic disorder, schizophrenia,
schizophreniform disorder, and other psychotic disorders, as well as from manic or major
depressive episodes, with psychotic features.
Delirium associated with fear, anxiety, and dissociative symptoms, such as
depersonalization, must be distinguished from acute stress disorder, which is precipitated by
exposure to a severely traumatic event.
Delirium can be distinguished from these disorders on the basis
of the often atypical symptomatic presentation in malingering and factitious disorder and the
absence of another medical condition or substance that is etiologically related to the apparent
cognitive disturbance.
The most common differential diagnostic issue when evaluating
confusion in older adults is disentangling symptoms of delirium and major NCD. The clinician
must determine whether the individual has delirium; a delirium superimposed on a preexisting
NCD, such as that due to Alzheimer’s disease; or an NCD without delirium. The traditional

distinction between delirium and major NCD according to acuteness of onset and temporal
course is particularly difficult in those elderly individuals who had a prior NCD that may not
have been recognized, or who developed persistent cognitive impairment following an episode of
delirium. When delirium and major NCD are comorbid, the management of the delirium should
generally be given priority.
Other Specified Delirium
R41.0
This category applies to presentations in which symptoms characteristic of delirium
that cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning predominate but do not meet the full criteria for
delirium or any of the disorders in the neurocognitive disorders diagnostic class. The
other specified delirium category is used in situations in which the clinician chooses
to communicate the specific reason that the presentation does not meet the criteria
for delirium or any specific neurocognitive disorder. This is done by recording “other
specified delirium” followed by the specific reason (e.g., “subsyndromal delirium”).
An example of a presentation that can be specified using the “other specified”
designation is the following:
Subsyndromal delirium: A delirium-like presentation involving disturbances in
attention, higher-level thought, and circadian rhythm, in which the severity of
cognitive impairment falls short of that required for the diagnosis of delirium.
Unspecified Delirium
R41.0
This category applies to presentations in which symptoms characteristic of delirium
that cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning predominate but do not meet the full criteria for
delirium or any of the disorders in the neurocognitive disorders diagnostic class. The
unspecified delirium category is used in situations in which the clinician chooses not
to specify the reason that the criteria are not met for delirium, and includes
presentations for which there is insufficient information to make a more specific
diagnosis (e.g., in emergency room settings).
Major and Mild Neurocognitive Disorders

Major Neurocognitive Disorder
Diagnostic Criteria
A. Evidence of significant cognitive decline from a previous level of performance in
one or more cognitive domains (complex attention, executive function, learning
and memory, language, perceptual-motor, or social cognition) based on:
1. Concern of the individual, a knowledgeable informant, or the clinician that
there has been a significant decline in cognitive function; and
2. A substantial impairment in cognitive performance, preferably documented by
standardized neuropsychological testing or, in its absence, another quantified
clinical assessment.
B. The cognitive deficits interfere with independence in everyday activities (i.e., at a
minimum, requiring assistance with complex instrumental activities of daily living
such as paying bills or managing medications).
C. The cognitive deficits do not occur exclusively in the context of a delirium.
D. The cognitive deficits are not better explained by another mental disorder (e.g.,
major depressive disorder, schizophrenia).
Specify whether due to:
Note: Each subtype listed has specific diagnostic criteria and corresponding text,
which follow the general discussion of major and mild neurocognitive disorders.
Alzheimer’s disease
Frontotemporal degeneration
Lewy body disease
Vascular disease
Traumatic brain injury
Substance/medication use
HIV infection
Prion disease
Parkinson’s disease
Huntington’s disease
Another medical condition
Multiple etiologies
Unspecified etiology
Coding note: Code based on medical or substance etiology. In most cases of major
neurocognitive disorder, there is need for an additional code for the etiological
medical condition, which must immediately precede the diagnostic code for major
neurocognitive disorder, as noted in the coding table on pp. 682–683.

Specify (see coding table for details):
Without behavioral disturbance: If the cognitive disturbance is not
accompanied by any clinically significant behavioral disturbance.
With behavioral disturbance (specify disturbance): If the cognitive disturbance
is accompanied by a clinically significant behavioral disturbance (e.g., psychotic
symptoms, mood disturbance, agitation, apathy, or other behavioral symptoms).
Coding note: Use additional code(s) to indicate clinically significant psychiatric
symptoms due to the same medical condition causing the major neurocognitive
disorder (e.g., F06.2 psychotic disorder due to Alzheimer’s disease, with
delusions; F06.32 depressive disorder due to Parkinson’s disease, with major
depressive–like episode). Note: Mental disorders due to another medical
condition are included with disorders with which they share phenomenology
(e.g., for depressive disorders due to another medical condition, see the chapter
“Depressive Disorders”).
Specify current severity:
Mild: Difficulties with instrumental activities of daily living (e.g., housework,
managing money).
Moderate: Difficulties with basic activities of daily living (e.g., feeding, dressing).
Severe: Fully dependent.
Coding and Recording Procedures
The following are examples of coding and recording major neurocognitive disorders
due to an etiological subtype (for more information, see coding table on pp. 682–683
and coding notes in the specific diagnostic criteria for each major and mild
neurocognitive disorder subtype):
Major neurocognitive disorder due to probable Alzheimer’s disease,
without behavioral disturbance, mild: G30.9 Alzheimer’s disease, F02.80
major neurocognitive disorder due to probable Alzheimer’s disease, without
behavioral disturbance, mild.
Major neurocognitive disorder due to traumatic brain injury, with
behavioral disturbance, moderate: S06.2X9S diffuse traumatic brain injury
with loss of consciousness of unspecified duration, sequela; F02.81 major
neurocognitive disorder due to traumatic brain injury, with behavioral
disturbance, moderate; F06.34 bipolar and related disorder due to traumatic
brain injury, with mixed features.
Mild Neurocognitive Disorder
Diagnostic Criteria

A. Evidence of modest cognitive decline from a previous level of performance in
one or more cognitive domains (complex attention, executive function, learning
and memory, language, perceptual-motor, or social cognition) based on:
1. Concern of the individual, a knowledgeable informant, or the clinician that
there has been a mild decline in cognitive function; and
2. A modest impairment in cognitive performance, preferably documented by
standardized neuropsychological testing or, in its absence, another quantified
clinical assessment.
B. The cognitive deficits do not interfere with capacity for independence in everyday
activities (i.e., complex instrumental activities of daily living such as paying bills
or managing medications are preserved, but greater effort, compensatory
strategies, or accommodation may be required).
C. The cognitive deficits do not occur exclusively in the context of a delirium.
D. The cognitive deficits are not better explained by another mental disorder (e.g.,
major depressive disorder, schizophrenia).
Specify whether due to:
Note: Each subtype listed has specific diagnostic criteria and corresponding text,
which follow the general discussion of major and mild neurocognitive disorders.
Alzheimer’s disease
Frontotemporal degeneration
Lewy body disease
Vascular disease
Traumatic brain injury
Substance/medication use
HIV infection
Prion disease
Parkinson’s disease
Huntington’s disease
Another medical condition
Multiple etiologies
Unspecified etiology
Coding note: For mild neurocognitive disorder due to any of the medical etiologies
listed above, code G31.84. Do not use additional codes for the presumed etiological
medical conditions. For substance/medication-induced mild neurocognitive disorder,
code based on type of substance; see “Substance/Medication-Induced Major or Mild
Neurocognitive Disorder.” For unspecified mild neurocognitive disorder, code R41.9.

Specify (behavioral disturbance cannot be coded but should still be recorded):
Without behavioral disturbance: If the cognitive disturbance is not
accompanied by any clinically significant behavioral disturbance.
With behavioral disturbance (specify disturbance): If the cognitive disturbance
is accompanied by a clinically significant behavioral disturbance (e.g., psychotic
symptoms, mood disturbance, agitation, apathy, or other behavioral symptoms).
Coding note: Use additional code(s) to indicate clinically significant psychiatric
symptoms due to the same medical condition causing the mild neurocognitive
disorder (e.g., F06.2 psychotic disorder due to traumatic brain injury, with
delusions; F06.32 depressive disorder due to HIV disease, with major
depressive–like episode). Note: Mental disorders due to another medical
condition are included with disorders with which they share phenomenology
(e.g., for depressive disorders due to another medical condition, see the chapter
“Depressive Disorders”).
Coding and Recording Procedures
The following are examples of coding and recording mild neurocognitive disorders
due to an etiological subtype (for more information, see coding table on pp. 682–683
and coding notes in the specific diagnostic criteria for each major and mild
neurocognitive disorder subtype):
G31.84 Mild neurocognitive disorder due to Alzheimer’s disease, without
behavioral disturbance.
G31.84 Mild neurocognitive disorder due to traumatic brain injury, with
behavioral disturbance; F06.34 bipolar and related disorder due to traumatic
brain injury, with mixed features.
Etiological subtype
Associated
etiological medical
code for major
neurocognitive
disordera
Major
neurocognitive
disorder code
Mild neurocognitive disorder code
Alzheimer’s disease
G30.9
F02.8xb
G31.84c Do not use additional code for
Alzheimer’s disease.
Frontotemporal
degeneration
G31.09
F02.8xb
G31.84c Do not use additional code for
frontotemporal degeneration.
Lewy body disease
G31.83
F02.8xb
G31.84c Do not use additional code for
Lewy body disease.
Vascular disease
No additional
medical code.
F01.5xb Do not use
additional code for the
vascular disease.
G31.84c Do not use additional code for the
vascular disease.
Traumatic brain injury
S06.2X9S
F02.8xb
G31.84c Do not use additional code for the
traumatic brain injury.
Substance/medicationinduced
No additional
medical code.
Code based on the
type of substance
causing the major
Code based on the type of substance
causing the mild neurocognitive disorder.d

causing the major
neurocognitive
disorder.d
HIV infection
B20
F02.8xb
G31.84c Do not use additional code for
HIV infection.
Prion disease
A81.9
F02.8xb
G31.84c Do not use additional code for
prion disease.
Parkinson’s disease
G20
F02.8xb
G31.84c Do not use additional code for
Parkinson’s disease.
Huntington’s disease
G10
F02.8xb
G31.84c Do not use additional code for
Huntington’s disease.
Due to another
medical condition
Code the other
medical condition
first (e.g., G35
multiple sclerosis).
F02.8xb
G31.84c Do not use additional codes for
the presumed etiological medical
conditions.
Due to multiple
etiologies
Code all of the
etiological medical
conditions first (with
the exception of
vascular disease).
F02.8xb (code once
for major
neurocognitive
disorder due to all
etiologies that apply)
Code also major
vascular NCD
(F01.5x), if present.
Code also the relevant
substance/medicationinduced major
neurocognitive
disorders if
substances or
medications play a
role in the etiology.
G31.84c Do not use additional codes for
the presumed etiological medical
conditions. Code also the relevant
substance/medication-induced mild
neurocognitive disorders if substances or
medications play a role in the etiology.
Unspecified
neurocognitive
disorder
No additional
medical code.
R41.9c
R41.9c
aCode first, before code for major neurocognitive disorder.
bCode fifth character based on symptom specifier: .x0 without behavioral disturbance; .x1 with behavioral disturbance
(e.g., psychotic symptoms, mood disturbance, agitation, apathy, or other behavioral symptoms). Note: The severity
specifiers “mild,” “moderate,” and “severe” cannot be coded for major neurocognitive disorder but should still be recorded.
cNote: “With behavioral disturbance” and “without behavioral disturbance” cannot be coded but should still be recorded.
dSee coding table in “Substance/Medication-Induced Major or Mild Neurocognitive Disorder” for ICD-10-CM code. Note:
The severity specifiers “mild,” “moderate,” and “severe” (for substance/medication-induced major neurocognitive
disorder) and the accompanying symptom specifiers “with behavioral disturbance” and “without behavioral disturbance”
(for substance/medication-induced major or mild neurocognitive disorder) cannot be coded but should still be recorded.
Subtypes
Major and mild neurocognitive disorders (NCDs) are primarily subtyped according to the known
or presumed etiological/pathological entity or entities underlying the cognitive decline. These
subtypes are distinguished on the basis of a combination of time course, characteristic domains
affected, and associated symptoms. For certain etiological subtypes, the diagnosis depends
substantially on the presence of a potentially causative entity, such as Parkinson’s or

Huntington’s disease, or a traumatic brain injury or stroke in the appropriate time period. For
other etiological subtypes (generally the neurodegenerative diseases like Alzheimer’s disease,
frontotemporal degeneration, and Lewy body disease), the diagnosis is based primarily on the
cognitive, behavioral, and functional symptoms. Typically, the differentiation among these
syndromes that lack an independently recognized etiological entity is clearer at the level of major
NCD than at the level of mild NCD, but sometimes characteristic symptoms and associated
features are present at the mild level as well.
NCDs are frequently managed by clinicians in multiple disciplines. For many subtypes,
multidisciplinary international expert groups have developed specialized consensus criteria based
on clinicopathological correlation with underlying brain pathology. The subtype criteria here
have been harmonized with those expert criteria.
Specifiers
Evidence for distinct behavioral features in NCDs has been recognized, particularly in the areas
of psychotic symptoms and depression. Psychotic features are common in many NCDs,
particularly at the mild-to-moderate stage of major NCDs due to Alzheimer’s disease, Lewy
body disease, and frontotemporal degeneration. If the psychotic symptoms are judged to be due
to the Alzheimer’s disease, Lewy body disease, or frontotemporal degeneration, an additional
diagnosis of psychotic disorder due to Alzheimer’s disease, psychotic disorder due to Lewy body
disease, or psychotic disorder due to frontotemporal degeneration may be given. Paranoia and
other delusions are common features, and often a persecutory theme may be a prominent aspect
of delusional ideation. In contrast to psychotic disorders with onset in earlier life (e.g.,
schizophrenia), disorganized speech and disorganized behavior are not characteristic of
psychosis in NCDs. Hallucinations may occur in any modality, although visual hallucinations are
more common in NCDs than in depressive, bipolar, or psychotic disorders.
Mood disturbances, including depression, anxiety, and elation, may occur. Depression is
common early in the course (including at the mild NCD level) of NCD due to Alzheimer’s
disease and Parkinson’s disease, while elation may occur more commonly in frontotemporal
degeneration. If the mood disturbance is judged to be due to the Alzheimer’s disease,
Parkinson’s disease, or frontotemporal degeneration, an additional diagnosis of depressive
disorder due to Alzheimer’s disease, depressive disorder due to Parkinson’s disease, or bipolar
and related disorder due to frontotemporal degeneration may be given. Mood symptoms are
increasingly recognized to be a significant feature in the earliest stages of mild NCDs such that
clinical recognition and intervention may be important.
Agitation is common in a wide variety of NCDs, particularly in major NCD of moderate to
severe severity, and often occurs in the setting of confusion or frustration. It may arise as
combative behaviors, particularly in the context of resisting caregiving duties such as bathing
and dressing. Agitation is characterized as disruptive motor or vocal activity and tends to occur
with advanced stages of cognitive impairment across all of the NCDs.
Individuals with NCD can present with a wide variety of behavioral symptoms that are the
focus of treatment. Sleep disturbance is a common symptom that can create a need for clinical
attention and may include symptoms of insomnia, hypersomnia, and circadian rhythm
disturbances.

685
Apathy is common in mild and major NCD. It is observed particularly in NCD due to
Alzheimer’s disease and may be a prominent feature of NCD due to frontotemporal
degeneration. Apathy is typically characterized by diminished motivation and reduced goaldirected behavior accompanied by decreased emotional responsiveness. Symptoms of apathy
may manifest early in the course of NCDs when a loss of motivation to pursue daily activities or
hobbies may be observed.
Other important behavioral symptoms include wandering, disinhibition, hyperphagia, and
hoarding. Some of these symptoms are characteristic of specific disorders, as discussed in the
relevant sections. When more than one behavioral disturbance is observed, each type should be
noted in writing with the specifier “with behavioral disturbance.”
Diagnostic Features
Major and mild NCDs exist on a spectrum of cognitive and functional impairment. Major NCD
roughly corresponds to the condition labeled in ICD-10 and ICD-11 (as well as in DSM-IV) as
dementia. The core feature of NCDs is acquired cognitive decline in one or more cognitive
domains (Criterion A) based on both 1) a concern about cognition on the part of the individual, a
knowledgeable informant, or the clinician, and 2) performance on an objective assessment that
falls below the expected level or that has been observed to decline over time. Both a concern and
objective evidence are required because they are complementary. When there is an exclusive
focus on objective testing, a disorder may go undiagnosed in high-functioning individuals whose
currently “normal” performance actually represents a substantial decline in abilities, or an illness
may be incorrectly diagnosed in individuals whose currently “low” performance does not
represent a change from their own baseline or is a result of extraneous factors like test conditions
or a passing illness. Alternatively, excessive focus on subjective symptoms may fail to diagnose
illness in individuals with poor insight, or whose informants deny or fail to notice their
symptoms, or it may be overly sensitive in the so-called worried well.
A cognitive concern differs from a complaint in that it may or may not be voiced
spontaneously. Rather, it may need to be elicited by careful questioning about specific symptoms
that commonly occur in individuals with cognitive deficits (see Table 1 in the introduction to this
chapter). For example, memory concerns include difficulty remembering a short grocery list or
keeping track of the plot of a television program; executive concerns include difficulty resuming
a task when interrupted, organizing tax records, or planning a holiday meal. At the mild NCD
level, the individual is likely to describe these tasks as being more difficult or as requiring extra
time or effort or compensatory strategies. At the major NCD level, such tasks may only be
completed with assistance or may be abandoned altogether. At the mild NCD level, individuals
and their families may not notice such symptoms or may view them as normal, particularly in the
elderly; thus, careful history taking is of paramount importance. The difficulties must represent
changes rather than lifelong patterns: the individual or informant may clarify this issue, or the
clinician can infer change from prior experience with the individual or from occupational or
other clues. It is also critical to determine that the difficulties are related to cognitive loss rather
than to motor or sensory limitations.
Neuropsychological testing, with performance compared with norms appropriate to the

individual’s age, sex, educational attainment, and cultural background, is part of the standard
evaluation of NCDs and is particularly critical in the evaluation of mild NCD. The use of
culturally validated assessment instruments is preferred, which are available for many
racial/ethnic and linguistic populations. For major NCD, performance is typically 2 or more
standard deviations below appropriate norms (3rd percentile or below). For mild NCD,
performance typically lies in the 1–2 standard deviation range (between the 3rd and 16th
percentiles). However, neuropsychological testing is not available in all settings, and
neuropsychological thresholds are sensitive to the specific test(s) and norms employed, as well as
to test conditions, sensory limitations, and intercurrent illness. A variety of brief
office-based or “bedside” assessments, as described in Table 1, can also supply objective
data in settings where such testing is unavailable or infeasible. In any case, as with cognitive
concerns, objective performance must be interpreted in light of the individual’s prior
performance. Optimally, this information would be available from a prior administration of the
same test, but often it must be inferred based on appropriate norms, along with the individual’s
educational history, occupation, and other factors. Norms are more challenging to interpret in
individuals with very high or very low levels of education and in individuals being tested outside
their own language or cultural background.
Criterion B relates to the individual’s level of independence in everyday functioning.
Individuals with major NCD will have impairment of sufficient severity so as to interfere with
independence, such that others will have to take over tasks that the individuals were previously
able to complete on their own. Individuals with mild NCD will have preserved independence,
although there may be subtle interference with function or a report that tasks require more effort
or take more time than previously.
The distinction between major and mild NCD is inherently arbitrary, and the disorders exist
along a continuum. Precise thresholds are therefore difficult to determine. Careful history taking,
observation, and integration with other findings are required, and the implications of making a
diagnosis should be considered when an individual’s clinical manifestations lie at a boundary.
Associated Features
Typically the associated features that support a diagnosis of major or mild NCD will be specific
to the etiological subtype (e.g., neuroleptic sensitivity and visual hallucinations in NCD due to
Lewy body disease). Diagnostic features specific to each of the subtypes are found in the
relevant sections.
Prevalence
The prevalence of NCD varies widely by age and by etiological subtype. Overall prevalence
estimates are generally only available for older populations. Among individuals older than 60
years, prevalence increases steeply with age, so prevalence estimates are more accurate for
narrow age bands than for broad categories such as “over 65” (where the mean age can vary
greatly with the life expectancy of the given population). For those etiological subtypes
occurring across the life span, prevalence estimates for NCD are likely to be available, if at all,

only as the fraction of individuals who develop NCD among those with the relevant condition
(e.g., traumatic brain injury, HIV infection).
Female gender is associated with higher prevalence of dementia overall, and especially
Alzheimer’s disease, but this difference is largely, if not wholly, attributable to greater longevity
in females.
Overall, international prevalence estimates for dementia (which is largely congruent with
major NCD) are approximately 1%–2% at age 65 years and as high as 30% by age 85 years. The
prevalence of mild NCD is very sensitive to the definition of the disorder, particularly in
community settings, where evaluations are less detailed. In addition, in contrast with clinical
settings, where cognitive concern must be high to seek and locate care, there may be a less clear
decline from baseline functioning. Estimates of the prevalence of mild cognitive impairment
(which is substantially congruent with mild NCD) among older individuals are fairly variable,
ranging from 2% to 10% at age 65 and 5% to 25% by age 85.
Prevalence and incidence of dementia vary cross-nationally and among ethnic and racialized
populations in the United States, although methodological differences complicate rate
comparisons. Some U.S. studies found that incidence is highest in African Americans followed,
in decreasing order, by American Indians/Alaska Natives, Latinx, Pacific Islanders, non-Latinx
Whites, and Asian Americans. Among four Asian American populations, Filipino Americans had
the highest incidence, followed by Japanese Americans, Chinese
Americans, and Asian-Indian Americans. Latinx subpopulations in the United States have
been found to vary considerably in prevalence and incidence of dementia; Caribbean Hispanics
have much higher rates than Mexican Americans in some U.S. studies.
Development and Course
The course of NCD varies across etiological subtypes, and this variation can be useful in
differential diagnosis. Some subtypes (e.g., those related to traumatic brain injury or stroke)
typically begin at a specific time and (at least after initial symptoms related to inflammation or
swelling subside) remain static. Others may fluctuate over time (although if this occurs, the
possibility of delirium superimposed on NCD should be considered). NCDs due to
neurodegenerative diseases like Alzheimer’s disease or frontotemporal degeneration typically are
marked by insidious onset and gradual progression, and the pattern of onset of cognitive deficits
and associated features helps to distinguish among them.
NCDs with onset in childhood and adolescence may have broad repercussions for social and
intellectual development, and in this setting intellectual developmental disorder (intellectual
disability) or other neurodevelopmental disorders may also be diagnosed to capture the full
diagnostic picture and ensure the provision of a broad range of services. In older individuals,
NCDs often occur in the setting of medical illnesses, frailty, and sensory loss, which complicate
the clinical picture for diagnosis and treatment.
When cognitive loss occurs in youth to midlife, individuals and families are likely to seek
care. NCDs are typically easiest to identify at younger ages, although in some settings
malingering or factitious disorder may be a concern. Very late in life, cognitive symptoms may

not cause concern or may go unnoticed. In late life, mild NCD must also be distinguished from
the more modest deficits associated with “normal aging,” although a substantial fraction of what
has been ascribed to normal aging likely represents prodromal phases of various NCDs. In
addition, it becomes harder to recognize mild NCD with age because of the increasing
prevalence of medical illness and sensory deficits. It becomes harder to differentiate among
subtypes with age because there are multiple potential sources of neurocognitive decline.
Risk and Prognostic Factors
Risk factors vary not only by etiological subtype but also by age at onset within etiological
subtypes. Some subtypes are distributed throughout the life span, whereas others occur
exclusively or primarily in late life. Even within the NCDs of aging, the relative prevalence
varies with age: Alzheimer’s disease is uncommon before age 60 years, and the prevalence
increases steeply thereafter, while the overall less common frontotemporal degeneration has
earlier onset and represents a progressively smaller fraction of NCDs with age. The strongest risk
factor for major and mild NCDs is age, primarily because age increases the risk of
neurodegenerative and cerebrovascular disease.
Risk of NCDs varies by ethnic and racialized background and is associated with variation in
risk of underlying diseases (e.g., hypertension, diabetes), predisposing conditions (e.g., head
injury), environment (e.g., access to nutritious food, safe spaces for exercise), and other factors.
For example, in the United States, African Americans and Latinx tend to be at higher risk for
vascular dementia than Whites. Lower education and literacy are risk factors for NCDs that also
can vary by ethnoracial group because of differential exposure to adverse social determinants of
health.
Culture-Related Diagnostic Issues
Individuals’ and families’ level of awareness and concern about neurocognitive symptoms may
vary across ethnic, racialized, and occupational groups. Cultural differences regarding whether
decreased cognitive ability is seen as a normal part of aging (“normalization”) and in dementiarelated stigma can delay families’ recognition of a problem and
decrease help seeking for individuals in the early stages of cognitive loss. For example, social
stigma appears to be associated with underutilization of services for cognitive impairment among
some underserved ethnic and racialized groups (e.g., Chinese Americans, Korean Americans).
Neurocognitive symptoms are more likely to be noticed, particularly at the mild level, in
individuals who engage in complex occupational, domestic, or recreational activities. In addition,
norms for neuropsychological testing tend to be available only for broad populations, and thus
they may not be easily applicable to individuals with less than high school education or those
being evaluated outside their primary language or culture. Culturally related diagnostic
challenges include accounting for intraethnic variation in the interpretation of assessments;
evaluating the effect on neuropsychological testing of a) the test taker’s stereotype threat (i.e.,
anxiety from concerns that he or she will confirm the negative stereotype of the ethnic or
racialized group by underperforming) and/or b) the clinician’s implicit (unconscious) bias on test

interpretation; and selecting the appropriate language when assessing bilingual individuals.
Bilingual individuals with dementia may lose their facility with acquired nonnative
languages, which might affect their ability to communicate with caregivers. The caregiving
environment may be influenced by cultural norms of family responsibility to care for the elderly,
for example, by affecting the decision whether to care for the elder with NCD at home or in a
care facility. In some cultures, adult children are expected to provide care for their older parents
(e.g., filial piety) so that a functional limitation may not be as obvious to the dependent elder or
the family.
Sex- and Gender-Related Diagnostic Issues
Some studies show that men and women experience major and mild NCD differently. Sex- and
gender-related factors may influence incidence and prevalence, the etiology (risk and protective
factors), and the clinical manifestations of major and mild NCD. More women than men
experience major NCD because of their longer life span. Thus, a woman of a given age has a
higher cumulative risk of developing major NCD before death than a man of the same age. The
difference in incidence rates is less clear and may vary across populations and over time because
of gender-related factors (e.g., education, occupation, family role, stress). For example, the
incidence of dementia in several higher-income countries has declined in the past 30 years, and
the decline was different in men and women across countries. Women tend to express a broader
range of symptoms. In particular, women tend to manifest more psychiatric symptoms such as
depression, anxiety, and delusions. Men tend to manifest more aggression, apathy, and
vegetative symptoms.
Like age, culture, and occupation, sex and gender issues may affect the level of concern and
awareness of cognitive symptoms. In addition, for late-life NCDs, women are likely to be older,
to have more medical comorbidity, and to live alone, which can complicate evaluation and
treatment. In addition, there are sex and gender differences in the frequency of some of the
etiological subtypes.
Diagnostic Markers
In addition to a careful history, neuropsychological assessments are the key measures for
diagnosis of NCDs, particularly at the mild level, where functional changes are minimal and
symptoms more subtle. Ideally, individuals will be referred for formal neuropsychological
testing, which will provide a quantitative assessment of all relevant domains and thus help with
diagnosis; provide guidance to the family on areas where the individual may require more
support; and serve as a benchmark for further decline or response to therapies. When such testing
is unavailable or not feasible, the brief assessments in Table 1 can provide insight into each
domain. More global brief mental status tests may be helpful but may be
insensitive, particularly to modest changes in a single domain or in those with high premorbid
abilities, and may be overly sensitive in those with low premorbid abilities.
In distinguishing among etiological subtypes, additional diagnostic markers may come into
play, particularly neuroimaging studies such as magnetic resonance imaging scans and positron

Normal cognition.
Delirium.
Major depressive disorder.
Specific learning disorder and other neurodevelopmental disorders.
emission tomography scans. In addition, specific markers may be involved in the assessment of
specific subtypes and may become more important as additional research findings accumulate
over time, as discussed in the relevant sections.
Association With Suicidal Thoughts or Behavior
Large-scale studies indicate elevated rates of suicidal behavior in individuals with NCD due to a
variety of etiologies compared with persons without an NCD. A nationwide study in Taiwan
reported that attempted suicide in late life is associated with subsequent dementia.
Functional Consequences of Major and Mild Neurocognitive Disorders
By definition, major and mild NCDs affect functioning, given the central role of cognition in
human life. Thus, the criteria for the disorders, and the threshold for differentiating mild from
major NCD, are based in part on functional assessment. Within major NCD there is a broad
range of functional impairment, as implemented in the severity specifiers. In addition, the
specific functions that are compromised can help identify the cognitive domains affected,
particularly when neuropsychological testing is not available or is difficult to interpret.
Differential Diagnosis
The differential diagnosis between normal cognition and mild NCD, as
between mild and major NCD, is challenging because the boundaries are inherently arbitrary.
Careful history taking and objective assessment are critical to these distinctions. A longitudinal
evaluation using quantified assessments may be key in detecting mild NCD.
Both mild and major NCD may be difficult to distinguish from a persistent delirium,
which can co-occur. Careful assessment of attention and arousal will help to make the
distinction.
The distinction between mild NCD and major depressive disorder,
which may co-occur with NCD, can also be challenging. Specific patterns of cognitive deficits
may be helpful. For example, consistent memory and executive function deficits are typical of
Alzheimer’s disease, whereas nonspecific or more variable performance is seen in major
depression. Alternatively, treatment of the depressive disorder with repeated observation over
time may be required to make the diagnosis.
A careful clarification of the
individual’s baseline status will help distinguish an NCD from a specific learning disorder or
other neurodevelopmental disorders. Additional issues may enter the differential for specific
etiological subtypes, as described in the relevant sections.
Comorbidity
NCDs are common in older individuals and thus often co-occur with a wide variety of agerelated diseases that may complicate diagnosis or treatment. Most notable of these is delirium,
for which NCD increases the risk. In older individuals, a delirium during hospitalization is, in
many cases, the first time that an NCD is noticed, although a careful history will often reveal
evidence of earlier decline. Mixed NCDs are also common in older

690
individuals, as many etiological entities increase in prevalence with age. In younger individuals,
NCD often co-occurs with neurodevelopmental disorders; for example, a head injury in a
preschool child may also lead to significant developmental and learning issues. Additional
comorbidity of NCD is often related to the etiological subtype, as discussed in the relevant
sections.
Major or Mild Neurocognitive Disorder Due to Alzheimer’s
Disease
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. There is insidious onset and gradual progression of impairment in one or more
cognitive domains (for major neurocognitive disorder, at least two domains must
be impaired).
C. Criteria are met for either probable or possible Alzheimer’s disease as follows:
For major neurocognitive disorder:
Probable Alzheimer’s disease is diagnosed if either of the following is present;
otherwise, possible Alzheimer’s disease should be diagnosed.
1. Evidence of a causative Alzheimer’s disease genetic mutation from family
history or genetic testing.
2. All three of the following are present:
a. Clear evidence of decline in memory and learning and at least one other
cognitive domain (based on detailed history or serial neuropsychological
testing).
b. Steadily progressive, gradual decline in cognition, without extended
plateaus.
c. No evidence of mixed etiology (i.e., absence of other neurodegenerative
or cerebrovascular disease, or another neurological, mental, or systemic
disease or condition likely contributing to cognitive decline).
For mild neurocognitive disorder:
Probable Alzheimer’s disease is diagnosed if there is evidence of a causative
Alzheimer’s disease genetic mutation from either genetic testing or family history.
Possible Alzheimer’s disease is diagnosed if there is no evidence of a
causative Alzheimer’s disease genetic mutation from either genetic testing or
family history, and all three of the following are present:
1. Clear evidence of decline in memory and learning.
2. Steadily progressive, gradual decline in cognition, without extended plateaus.

3. No evidence of mixed etiology (i.e., absence of other neurodegenerative or
cerebrovascular disease, or another neurological or systemic disease or
condition likely contributing to cognitive decline).
D. The disturbance is not better explained by cerebrovascular disease, another
neurodegenerative disease, the effects of a substance, or another mental,
neurological, or systemic disorder.
Coding note (see coding table on pp. 682–683):
For major neurocognitive disorder due to probable or possible Alzheimer’s disease,
with behavioral disturbance, code first G30.9 Alzheimer’s disease, followed by
F02.81. For major neurocognitive disorder due to probable or possible Alzheimer’s
disease, without behavioral disturbance, code first G30.9 Alzheimer’s disease,
followed by F02.80.
Note: The severity specifiers “mild,” “moderate,” and “severe” cannot be coded for
major neurocognitive disorder but should still be recorded.
For mild neurocognitive disorder due to Alzheimer’s disease, code G31.84. (Note:
Do not use the additional code for Alzheimer’s disease. “With behavioral
disturbance” and “without behavioral disturbance” cannot be coded but should still
be recorded.)
For major or mild neurocognitive disorder due to Alzheimer’s disease: Use additional
code(s) to indicate clinically significant psychiatric symptoms due to Alzheimer’s
disease (e.g., F06.2 psychotic disorder due to Alzheimer’s disease, with delusions;
F06.32 depressive disorder due to Alzheimer’s disease, with major depressive–like
episode).
Diagnostic Features
Beyond the neurocognitive disorder (NCD) syndrome (Criterion A), the core features of major or
mild NCD due to Alzheimer’s disease include an insidious onset and gradual progression of
cognitive and behavioral symptoms (Criterion B). The typical presentation is amnestic (i.e., with
impairment in memory and learning). Unusual nonamnestic presentations, particularly
visuospatial and logopenic aphasic variants, also exist. A significant proportion of individuals,
likely more than half, first present with behavioral symptoms before the onset of cognitive
symptoms; the presence of behavioral disturbance should be noted using the appropriate specifier
codes. At the mild NCD phase, Alzheimer’s disease manifests typically with impairment in
memory and learning, sometimes accompanied by deficits in executive function. At the major
NCD phase, visuoconstructional/perceptual-motor ability and language (e.g., word retrieval) will
also be impaired, particularly when the NCD is moderate to severe. Social cognition tends to be
preserved until late in the course of the disease with the exception of individuals who have the
less common variants with significant dysexecutive and behavioral disturbance.
A level of diagnostic certainty must be specified denoting Alzheimer’s disease as the
“probable” or “possible” etiology (Criterion C). Probable Alzheimer’s disease is diagnosed in

both major and mild NCD if there is evidence of a causative Alzheimer’s disease gene, either
from genetic testing or from an autosomal dominant family history coupled with autopsy
confirmation or a genetic test in an affected family member. At present, the designation of
“probable” represents the highest level of diagnostic certainty within the current criteria
framework. However, current developments in biomarkers continue to increase diagnostic
certainty (e.g., when brain positron emission tomography [PET] scans may indicate the presence
of Alzheimer’s pathology, such as evidence of amyloid and/or tau deposition by imaging or
cerebrospinal [CSF] analysis). For major NCD, a typical clinical picture, without extended
plateaus or evidence of mixed etiology, can also be diagnosed as due to probable Alzheimer’s
disease. However, in some individuals there may be prolonged periods of very slow or minimal
progression. For mild NCD, given the lesser degree of certainty that the deficits will progress,
these features are only sufficient for a possible Alzheimer’s etiology. As stated above, however,
new biomarker methods may affect the use of “probable” and “possible” in mild NCD. If the
etiology appears mixed, mild NCD due to multiple etiologies should be diagnosed. In any case,
for both mild and major NCD due to Alzheimer’s disease, the clinical features must not suggest
another primary etiology for the NCD (Criterion D). As biomarker data continue to inform the
nature of underlying pathologies, it is likely that the existence of multiple etiologies will be more
systematically mapped in the future to better identify diagnostic variations in NCD due to
multiple etiologies.
Associated Features
For individuals with NCD due to Alzheimer's disease, symptoms extend beyond cognitive
deficits to include neuropsychiatric symptoms such as agitation, apathy, depression, delusions,
and sleep disorders. Neuropsychiatric symptoms may also be described as
behavioral and psychological symptoms of dementia and have been observed in neurocognitive
disorders of all etiologies. These symptoms are nearly universal in Alzheimer's disease as
confirmed in two U.S. population samples, with 5-year follow-up in one reporting that 98% of
individuals with NCD due to Alzheimer's disease develop neuropsychiatric symptoms.
Neuropsychiatric symptoms lead to disability, worsening quality of life, greater impairment in
activities of daily living, faster cognitive and functional decline, greater caregiver burden, earlier
institutionalization, and accelerated mortality. Neuropsychiatric symptoms are often more
distressing than cognitive manifestations and are frequently the reason that health care assistance
is sought. These symptoms are also frequently present at the mild NCD stage, with evidence
suggesting that more than half of individuals who develop dementia begin with neuropsychiatric
symptoms. At the mild NCD stage or the mildest level of major NCD, depression, irritability,
and/or apathy are most often seen. With moderately severe major NCD, delusions, agitation,
combativeness, and wandering are common. Late in the illness, gait disturbance, dysphagia,
incontinence, myoclonus, and seizures are observed.
Prevalence
The prevalence of overall NCD due to Alzheimer’s disease rises steeply with age. In high-

income countries, it ranges from 5% to 10% in individuals ages 60–69 years to at least 25%
thereafter. An estimated 5.4 million Americans of all ages had dementia due to Alzheimer’s
disease in 2016, including about 200,000 individuals with disease onset before age 65. Dementia
due to Alzheimer’s disease is found in 11% of individuals age 65 and older and 32% of those age
85 and older. Estimates applying incidence rates of dementia due to Alzheimer’s disease to U.S.
census data indicate that 81% of those with the disease are age 75 or older. The percentage of
dementias attributable to Alzheimer’s disease ranges from about 60% to over 90%, depending on
the setting and diagnostic criteria. Mild NCD due to Alzheimer’s disease is likely to represent a
substantial fraction of mild cognitive impairment (MCI) as well.
Studies show that prevalence of dementia due to Alzheimer’s disease tends to vary by
ethnoracial background; for example, in the United States, prevalence in individuals age 65 years
and older ranges from 3.5% to 14.4%, depending on ethnoracial group, age, and assessment
methodology. Higher prevalence has been found among African Americans and U.S. Latinx of
Caribbean origin, after adjustment for gender and clinical comorbidities.
Development and Course
Major or mild NCD due to Alzheimer’s disease progresses gradually, at times with plateaus,
through severe dementia to death. The mean duration of survival after diagnosis is approximately
10 years, reflecting the advanced age of the majority of individuals rather than the course of the
disease; some individuals can live with the disease for as long as 20 years. Late-stage individuals
are eventually mute and bedbound. Death most commonly results from aspiration in those who
survive through the full course. In mild NCD due to Alzheimer’s disease, impairments increase
over time, and functional status gradually declines until symptoms reach the threshold for the
diagnosis of major NCD.
The onset of symptoms is usually at ages 70 through 89; early-onset forms seen in
individuals ages 40–59 are often, but not always, related to known causative mutations.
Symptoms and pathology do not differ much by onset ages. However, younger individuals are
more likely to survive the full course of the disease, while older individuals are more likely to
have numerous medical comorbidities that affect the course and management of the illness.
Diagnostic complexity is higher in older adults because of the increased likelihood of comorbid
medical illness and mixed pathology. Age at symptom onset, rate of cognitive decline, and
survival rates appear to vary by ethnoracial background. For example, compared
with non-Latinx Whites, U.S. Latinx can develop Alzheimer’s disease symptoms up to 4
years earlier, African Americans tend to show slower cognitive decline, and both underserved
groups may have longer survival periods.
Risk and Prognostic Factors
A number of risk factors have been identified, including low educational status, midlife
hypertension, obesity, and hearing loss, as well as late-life smoking, depression, physical
inactivity, social isolation, and diabetes. The co-occurrence of multiple vascular risk factors also
increases risk for Alzheimer’s disease and may act by increasing cerebrovascular pathology or

Genetic and physiological.
also through direct effects on Alzheimer’s pathology. Traumatic brain injury, especially in men,
may increase risk for major or mild NCD due to Alzheimer’s disease, although this relationship
remains controversial.
Age is definitively the strongest risk factor for Alzheimer’s disease, as
the prevalence estimates demonstrate. A strong genetic predisposition (60%–80% of attributable
risk) has been demonstrated. Rare mutations on chromosomes 1, 14, and 21 follow Mendelian
inheritance, leading to autosomal dominant forms. Individuals with Down syndrome (trisomy
21) may develop Alzheimer’s disease if they survive to midlife. The most common risk factors
are polygenic, with more than 45 risk genes/loci having been identified, typically with small
effects on risk. The strongest genetic susceptibility polymorphism, apolipoprotein E4
(APOE*E4), increases risk and decreases age at onset, particularly in homozygous individuals,
although some homozygous individuals survive to advanced ages without developing symptoms.
Ethnoracial and national origin are related to the genetic susceptibility profile for
Alzheimer’s disease. While APOE*E4 is associated with Alzheimer’s disease risk, this
association has not been consistently found across all ethnic and racialized groups. For example,
some studies have identified a unique mutation in the Gly206Ala presenilin 1 gene among
individuals of Puerto Rican descent with Alzheimer’s disease, which is also related to early
onset. Moreover, some studies have found a stronger association with ABCA7, a protein
transporter gene, among individuals who identify as African American than among U.S. Whites.
Culture-Related Diagnostic Issues
Detection of an NCD may be more difficult in cultural and socioeconomic settings where
memory loss is considered normal in old age, where older adults face fewer cognitive demands
in everyday life, or where very low educational levels pose greater challenges to objective
cognitive assessment.
Sex- and Gender-Related Diagnostic Issues
Women were found to have a higher incidence of Alzheimer’s disease than men in several
European studies, but the incidence was similar in men and women in most North American
studies. Some studies suggested that the symptoms of dementia progress faster in women than in
men. However, because women perform better than men of the same age on some verbal
memory tests, it is also possible that gender differences reflect the cut-off scores of tests used to
support a diagnosis. Different cut-off scores may be useful in men and women when assessing
for mild cognitive impairment.
Diagnostic Markers
Amyloid-predominant neuritic plaques, tau-predominant neurofibrillary tangles, and neuronal
loss observed microscopically or manifested in regional cortical atrophy (e.g., hippocampal,
parietal, frontal) are hallmarks of the pathological diagnosis of Alzheimer’s disease and may be
confirmed via postmortem histopathological examination. For
early-onset cases with apparent autosomal dominant inheritance, a mutation in one of the known

Other neurocognitive disorders.
causative Alzheimer’s disease genes—amyloid precursor protein (APP), presenilin 1 (PSEN1),
or presenilin 2 (PSEN2)—may be involved, and genetic testing for such mutations is
commercially available, although usually without clinical utility. While APOE E*4 cannot serve
as a diagnostic marker because it is a risk factor (i.e., neither necessary nor sufficient for disease
occurrence), in rare instances genetic testing at this locus may have utility in clinical settings.
Since amyloid beta-42 deposition in the brain occurs early in the pathophysiological cascade,
amyloid-based diagnostic tests such as amyloid imaging on brain PET scans and reduced levels
of amyloid beta-42 in the CSF may have diagnostic value. Similarly, tau PET imaging or CSF
analyses for elevated total tau or phospho-tau levels are available for clinical use. Signs of
neuronal injury, such as hippocampal and temporoparietal cortical atrophy on a magnetic
resonance image scan and temporoparietal hypometabolism on a fluorodeoxyglucose PET scan,
provide evidence of neuronal damage but are less specific for Alzheimer’s disease. Most of these
biomarkers have been validated and are widely available in tertiary care settings. Blood-derived
biomarkers for Alzheimer’s disease are being developed and are likely to become clinically
available as diagnostic, prognostic, and theranostic indicators.
Association With Suicidal Thoughts or Behavior
Alzheimer’s disease is associated with a moderate risk of suicide even many years after the
diagnosis; thus, ongoing assessment of mood and suicidality is appropriate. A large population
study in Denmark found that the risk of suicide in individuals with a hospital-determined
diagnosis of dementia was three- to eightfold greater compared with persons without dementia.
In contrast, several other studies found mixed results regarding suicide risk in individuals with
Alzheimer’s disease. A review of the neurobiology of suicide in the elderly found preliminary
evidence of an association with cognitive deficits and elderly suicidal behavior, especially
regarding impaired decision-making and reduced cognitive inhibition.
Functional Consequences of Major or Mild Neurocognitive Disorder
Due to Alzheimer’s Disease
Because of the effect on cognition, behavior, and functioning, NCD due to Alzheimer’s disease
has a serious and substantial impact on individuals, their caregivers, and families. Early in the
disease course, memory loss, disorientation, and mood symptoms adversely impact
independence, and create safety concerns (e.g., around driving). For individuals with onset at
younger ages, NCD due to Alzheimer’s disease can lead to early retirement. As the disease
advances, individuals become increasingly disabled in instrumental and basic daily living
activities, slowly becoming fully dependent on others. Caregivers for individuals with NCD due
to Alzheimer’s disease often see their social network deteriorate and develop a series of health
and mental health problems that can adversely affect outcomes for both the caregiver and the
individual with the NCD.
Differential Diagnosis
Major and mild NCDs due to other neurodegenerative processes
(e.g., Lewy body disease, frontotemporal degeneration) share the insidious onset and gradual
decline caused by Alzheimer’s disease but have distinctive core features of their own (which are

Other concurrent, active neurological or systemic illness.
Major depressive disorder.
not always present). For example, NCD with Lewy bodies is typically characterized by frequent
fluctuations in cognition early in the disease, parkinsonian features, gait imbalances, and visual
hallucinations. Individuals with frontotemporal NCD may present with a distinct behavioral or
language variant. The behavioral variant typically
first manifests with prominent changes in social behavior, such as disinhibition, apathy, or
perseverative behavior, that may not infrequently lead to a primary psychiatric diagnosis. In
contrast, the language variant of frontotemporal NCD may manifest with impairments in
expressive language or word comprehension.
In major or mild vascular NCD, there is typically a history of stroke temporally related to the
onset of cognitive impairment, and infarcts or hemosiderin deposits observed on brain imaging
can be judged sufficient to account for the clinical picture. However, major or mild vascular
NCD shares many clinical features with Alzheimer’s disease; frequently Alzheimer’s pathology
is present alone or in combination with vascular pathologies. It should be noted that white matter
change alone does not constitute enough evidence of cerebrovascular disease to propose a mixed
etiology if the other diagnostic considerations support the diagnosis of NCD due to Alzheimer’s
disease. The presence of subcortical ischemic changes on neuroimaging must be interpreted
carefully in view of whether concurrent Alzheimer’s pathology is present.
Other neurological or systemic illness
should be considered if there is an appropriate temporal relationship and severity to account for
the clinical picture. At the mild NCD level, it may be difficult to distinguish an Alzheimer’s
disease etiology from that of another medical condition (e.g., thyroid disorders, vitamin B12
deficiency).
Particularly at the mild NCD level, the differential diagnosis also
includes major depression. The presence of depression may be associated with reduced daily
functioning and poor concentration that may resemble an NCD, but improvement with treatment
of depression may be useful in making the distinction. If the symptoms meeting criteria for a
major depressive episode are judged to be due to the physiological effects of Alzheimer’s
disease, a diagnosis of depressive disorder due to Alzheimer’s disease, with major depressive–
like episode, should be given instead of major depressive disorder.
Comorbidity
Most individuals with Alzheimer’s disease are elderly and have multiple medical conditions that
can complicate diagnosis and influence the clinical course. Major or mild NCD due to
Alzheimer’s disease commonly co-occurs with cerebrovascular disease, which contributes to the
clinical picture. When a comorbid condition contributes to the NCD in an individual with
Alzheimer’s disease, then NCD due to multiple etiologies should be diagnosed.
Major or Mild Frontotemporal Neurocognitive Disorder

Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. The disturbance has insidious onset and gradual progression.
C. Either (1) or (2):
1. Behavioral variant:
a. Three or more of the following behavioral symptoms:
i. Behavioral disinhibition.
ii. Apathy or inertia.
iii. Loss of sympathy or empathy.
iv. Perseverative, stereotyped or compulsive/ritualistic behavior.
v. Hyperorality and dietary changes.
b. Prominent decline in social cognition and/or executive abilities.
2. Language variant:
a. Prominent decline in language ability, in the form of speech production,
word finding, object naming, grammar, or word comprehension.
D. Relative sparing of learning and memory and perceptual-motor function.
E. The disturbance is not better explained by cerebrovascular disease, another
neurodegenerative disease, the effects of a substance, or another mental,
neurological, or systemic disorder.
Probable frontotemporal neurocognitive disorder is diagnosed if either of the
following is present; otherwise, possible frontotemporal neurocognitive disorder
should be diagnosed:
1. Evidence of a causative frontotemporal neurocognitive disorder genetic mutation,
from either family history or genetic testing.
2. Evidence of disproportionate frontal and/or temporal lobe involvement from
neuroimaging.
Possible frontotemporal neurocognitive disorder is diagnosed if there is no
evidence of a genetic mutation, and neuroimaging has not been performed.
Coding note (see coding table on pp. 682–683):
For major neurocognitive disorder due to probable or possible frontotemporal
degeneration, with behavioral disturbance, code first G31.09 frontotemporal
degeneration, followed by F02.81. For major neurocognitive disorder due to probable
or possible frontotemporal degeneration, without behavioral disturbance, code first
G31.09 frontotemporal degeneration, followed by F02.80.
Note: The severity specifiers “mild,” “moderate,” and “severe” cannot be coded for
major neurocognitive disorder but should still be recorded.

For mild neurocognitive disorder due to frontotemporal degeneration, code G31.84.
(Note: Do not use the additional code for frontotemporal degeneration. “With
behavioral disturbance” and “without behavioral disturbance” cannot be coded but
should still be recorded.)
For major or mild frontotemporal neurocognitive disorder: Use additional code(s) to
indicate 
clinically 
significant 
psychiatric 
symptoms 
due 
to 
frontotemporal
degeneration (e.g., F06.33 bipolar and related disorder due to frontotemporal
degeneration, with manic features; F07.0 personality change due to frontotemporal
degeneration, disinhibited type).
Diagnostic Features
Major or mild frontotemporal neurocognitive disorder (NCD) comprises a number of syndromic
variants characterized by the progressive development of behavioral and personality change
and/or language impairment. The behavioral variant and two language variants (semantic and
agrammatic/nonfluent) exhibit distinct patterns of brain atrophy and some distinctive
neuropathology. The criteria must be met for either the behavioral or the language variant to
make the diagnosis, but many individuals present with features of both.
Individuals with behavioral-variant major or mild frontotemporal NCD present with varying
degrees of apathy or disinhibition. They may lose interest in socialization, self-care, and personal
responsibilities, or display socially inappropriate behaviors. Insight is usually impaired, and this
often delays medical consultation. The first referral is often to a psychiatrist. Individuals may
develop changes in social style, and in religious and political
beliefs, with repetitive movements, hoarding, changes in eating behavior, and hyperorality. In
later stages, loss of sphincter control may occur. Cognitive decline is less prominent, and formal
testing may show relatively few deficits in the early stages. Common neurocognitive symptoms
are lack of planning and organization, distractibility, and poor judgment. Deficits in executive
function, such as poor performance on tests of mental flexibility, abstract reasoning, and
response inhibition, are present, but learning and memory are relatively spared, and perceptualmotor abilities are almost always preserved in the early stages.
Individuals with language-variant major or mild frontotemporal NCD present with primary
progressive aphasia with gradual onset, with two subtypes commonly described: semantic variant
and agrammatic/nonfluent variant; each variant has distinctive features and corresponding
neuropathology. A third form of progressive language decline, called logopenic progressive
aphasia, is associated with left temporoparietal dysfunction and is often caused by Alzheimer’s
disease pathology.
“Probable” is distinguished from “possible” frontotemporal NCD by the presence of
causative genetic factors (e.g., mutations in the gene coding for microtubule-associated protein
tau) or by the presence of distinctive atrophy or reduced activity in frontotemporal regions on
structural or functional imaging.
Associated Features

Genetic and physiological.
Extrapyramidal features may be prominent in some cases, with an overlap with syndromes such
as progressive supranuclear palsy and corticobasal degeneration. Features of motor neuron
disease may be present in some cases (e.g., muscle atrophy, weakness). A subset of individuals
develop visual hallucinations.
Prevalence
Major or mild frontotemporal NCD is a common cause of early-onset NCD in individuals
younger than 65 years. In international studies, population prevalence estimates are in the range
of 2–31 per 100,000, with overall rates generally noted to be equal in men and women, although
variation exists among studies. Approximately 20%–25% of cases of frontotemporal NCD occur
in individuals older than 65 years. Frontotemporal NCD accounts for about 5% of all cases of
dementia in unselected autopsy series. The behavioral variant is the most common presentation
of NCD due to frontotemporal degeneration, occurring in approximately 60% of cases.
Development and Course
Individuals with major or mild frontotemporal NCD commonly present in their 50s, although the
age at onset varies from the 20s through the 80s. The disease is gradually progressive, with
median survival being 6–11 years after symptom onset and 3–4 years after diagnosis. Survival is
shorter and decline is faster in major or mild frontotemporal NCD than in typical Alzheimer’s
disease.
Risk and Prognostic Factors
Approximately 40% of individuals with major or mild frontotemporal
NCD have a family history of early-onset NCD, and approximately 10% show an autosomal
dominant inheritance pattern. A number of genetic factors have been identified, such as
mutations in the gene encoding the microtubule-associated protein tau (MAPT), the granulin
gene (GRN), and the C9ORF72 gene (C9orf72). A number of families with causative mutations
have been identified (see the section “Diagnostic Markers” for this disorder), but many
individuals with known familial transmission do not have a known mutation. The presence of
motor neuron disease is associated with a more rapid deterioration.
Diagnostic Markers
Computed tomography (CT) or structural magnetic resonance imaging (MRI) may show distinct
patterns of atrophy. In behavioral-variant major or mild frontotemporal NCD, both frontal lobes
(especially the medial frontal lobes) and the anterior temporal lobes are atrophic. In semantic
language–variant major or mild frontotemporal NCD, the middle, inferior, and anterior temporal
lobes are atrophic bilaterally but asymmetrically, with the left side usually being more affected.
Nonfluent language–variant major or mild frontotemporal NCD is associated with predominantly
left posterior frontal-insular atrophy. Functional imaging demonstrates hypoperfusion and/or
cortical hypometabolism in the corresponding brain regions, which may be present in the early
stages in the absence of structural abnormality. Emerging biomarkers for Alzheimer’s disease

Other neurocognitive disorders.
Other neurological conditions.
(e.g., cerebrospinal fluid amyloid-beta and tau levels, and amyloid imaging) may help in the
differential diagnosis, but the distinction from Alzheimer’s disease can remain difficult.
In familial cases of frontotemporal NCD, the identification of genetic mutations may help
confirm the diagnosis. Mutations associated with frontotemporal NCD include the genes
encoding microtubule-associated protein tau (MAPT) and granulin (GRN), C9ORF72,
transactive response DNA-binding protein of 43 kDa (TDP-43, or TARDBP), valosin-containing
protein (VCP), chromatin modifying protein 2B (CHMP2B), and fused in sarcoma protein
(FUS).
Functional Consequences of Major or Mild Frontotemporal
Neurocognitive Disorder
Because of the relative early age at onset of the disorder, the disorder often affects workplace and
family life. Because of the involvement of language and/or behavior, function is often more
severely impaired relatively early in the course. For individuals with the behavioral variant, prior
to diagnostic clarification there may be significant family disruption, legal involvement, and
problems in the workplace because of socially inappropriate behaviors. The functional
impairment attributable to behavioral change and language dysfunction, which can include
hyperorality, impulsive wandering, and other disinhibited behaviors, may far exceed that
attributable to the cognitive disturbance and may lead to nursing home placement or
institutionalization. These behaviors can be severely disruptive, even in structured care settings,
particularly when the individuals are otherwise healthy, nonfrail, and free of other medical
comorbidities.
Differential Diagnosis
Other neurodegenerative diseases may be distinguished from
major or mild frontotemporal NCD by their characteristic features. In major or mild NCD due to
Alzheimer’s disease, decline in learning and memory is an early feature. However, 10%–30% of
individuals presenting with a syndrome suggestive of major or mild frontotemporal NCD are
found at autopsy to have Alzheimer’s disease pathology. This occurs more frequently in
individuals who present with progressive dysexecutive syndromes in the absence of behavioral
changes or movement disorder or in those with the logopenic variant.
In major or mild NCD with Lewy bodies, core and suggestive features of Lewy bodies must
be present. In major or mild NCD due to Parkinson’s disease, spontaneous parkinsonism
emerges well before the cognitive decline. In major or mild vascular NCD, depending on
affected brain regions, there may also be loss of executive function and behavioral changes such
as apathy, and this disorder should be considered in the differential diagnosis. However, history
of a cerebrovascular event is temporally related to the onset of cognitive impairment in major or
mild vascular NCD, and neuroimaging reveals infarctions or white matter lesions sufficient to
account for the clinical picture.
Major or mild frontotemporal NCD overlaps with progressive
supranuclear palsy, corticobasal degeneration, and motor neuron disease clinically as well as

Other mental disorders and medical conditions.
pathologically. Progressive supranuclear palsy is characterized by supranuclear gaze palsies and
axial-predominant parkinsonism. Pseudobulbar signs may be present, and retropulsion (losing
balance in a backward direction) is often prominent. Neurocognitive assessment shows
psychomotor slowing, poor working memory, and executive dysfunction. Corticobasal
degeneration presents with asymmetric rigidity, limb apraxia, postural instability, myoclonus,
alien limb phenomenon, and cortical sensory loss. Many individuals with behavioral-variant
major or mild frontotemporal NCD show features of motor neuron disease, which tend to be
mixed upper and predominantly lower motor neuron disease.
Behavioral-variant major or mild frontotemporal
NCD may be mistaken for a primary mental disorder, such as major depression, bipolar
disorders, or schizophrenia, and individuals with this variant often present initially to psychiatry.
Over time, the development of progressive neurocognitive difficulties will help to make the
distinction. A careful medical evaluation will help to exclude treatable causes of NCDs, such as
metabolic disturbances, nutritional deficiencies, and infections. If the symptoms characteristic of
a primary mental disorder (e.g., delusions) are judged to be due to the physiological effects of
frontotemporal degeneration, a diagnosis of the appropriate mental disorder due to
frontotemporal degeneration should be given instead of the primary psychotic disorder (e.g.,
psychotic disorder due to frontotemporal degeneration, with delusions).
Major or Mild Neurocognitive Disorder With Lewy Bodies
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. The disorder has an insidious onset and gradual progression.
C. The disorder meets a combination of core diagnostic features and suggestive
diagnostic features for either probable or possible neurocognitive disorder with
Lewy bodies.
For probable major or mild neurocognitive disorder with Lewy bodies, the
individual has two core features, or one suggestive feature with one or more core
features. For possible major or mild neurocognitive disorder with Lewy
bodies, the individual has only one core feature, or one or more suggestive
features.
1. Core diagnostic features:
a. Fluctuating cognition with pronounced variations in attention and
alertness.
b. Recurrent visual hallucinations that are well formed and detailed.
c. Spontaneous features of parkinsonism, with onset subsequent to the
development of cognitive decline.
2. Suggestive diagnostic features:
a. Meets criteria for rapid eye movement sleep behavior disorder.

b. Severe neuroleptic sensitivity.
D. The disturbance is not better explained by cerebrovascular disease, another
neurodegenerative disease, the effects of a substance, or another mental,
neurological, or systemic disorder.
Coding note (see coding table on pp. 682–683):
For major neurocognitive disorder with probable or possible Lewy bodies, with
behavioral disturbance, code first G31.83 Lewy body disease, followed by F02.81.
For major neurocognitive disorder with probable or possible Lewy bodies, without
behavioral disturbance, code first G31.83 Lewy body disease, followed by F02.80.
Note: The severity specifiers “mild,” “moderate,” and “severe” cannot be coded for
major neurocognitive disorder but should still be recorded.
For mild neurocognitive disorder with Lewy bodies, code G31.84. (Note: Do not use
the additional code for Lewy body disease. “With behavioral disturbance” and
“without behavioral disturbance” cannot be coded but should still be recorded.)
For major or mild neurocognitive disorder with Lewy bodies: Use additional code(s)
to indicate clinically significant psychiatric symptoms due to Lewy body disease (e.g.,
F06.0 psychotic disorder due to Lewy body disease, with hallucinations; F06.31
depressive disorder due to Lewy body disease, with depressive features).
Diagnostic Features
Major neurocognitive disorder with Lewy bodies corresponds to the condition known as
dementia with Lewy bodies (DLB). The overall major or mild neurocognitive disorder with
Lewy bodies (NCDLB) category includes not only progressive cognitive impairment (with early
changes in attention, executive function, and visuoperceptual ability, rather than learning and
memory) but also recurrent, complex, visual hallucinations; and concurrent symptoms of rapid
eye movement (REM) sleep behavior disorder (which can be a very early manifestation); as well
as hallucinations in other sensory modalities, apathy, anxiety, depression, and delusions. The
cognitive symptoms may fluctuate in a pattern that can resemble a delirium, for which an
adequate precipitating factor may or may not be found. The variable presentation of NCDLB
symptoms reduces the likelihood of all symptoms being observed in a brief clinic visit and
necessitates a thorough assessment, including caregiver observations. The use of assessment
scales specifically designed to assess fluctuation may aid in diagnosis. Another core feature is
spontaneous parkinsonism; this can often be relatively mild, and the degree of response to
levodopa therapy is variable. Up to 25% of individuals with probable NCDLB may never
develop extrapyramidal signs, and they are not essential for diagnosis. The parkinsonism must be
distinguished from neuroleptic-induced extrapyramidal signs. Accurate diagnosis is essential to
safe treatment planning, as up to 50% of individuals with NCDLB have severe sensitivity to
neuroleptic drugs, and these medications should be used with extreme caution in individuals
suspected of having an NCDLB diagnosis.
The diagnosis of mild NCDLB is appropriate for individuals who present with the core

Genetic and physiological.
clinical features at a stage when cognitive or functional impairments are not of sufficient severity
to fulfill criteria for major NCD, particularly if nonamnestic cognitive deficits are prominent.
However, as for all mild NCDs, there will often be insufficient evidence to justify any single
etiology, and use of the unspecified diagnosis may be more appropriate.
Associated Features
Individuals with NCDLB frequently experience repeated falls, syncope, or other transient
episodes of unresponsiveness. Autonomic dysfunction may be observed, including orthostatic
hypotension, constipation, and urinary incontinence; hypersomnia and hyposmia may also be
observed.
Prevalence
Limited data from several high-income and low- and middle-income countries show that the
population-based prevalence estimates for NCDLB range from 0% to 1.2% of the general elderly
population, and from 0% to 9.7% of all dementia cases. The mean prevalence of major NCDLB
was 4.2% of all dementias in the community, and in clinic-based studies this increased to 7.5%
of all dementias. The clinical prevalence of major NCDLB among
individuals with dementia does not appear to be significantly affected by either age or sex. In
studies from the United States and United Kingdom, the pathological lesions known as Lewy
bodies are present in 20%–35% of cases of dementia. In a population-based study in Minnesota
that relied on medical records, the incidence of NCDLB was approximately three times higher in
men than in women age 65 or older.
Development and Course
NCDLB is a gradually progressive disorder with insidious onset. However, there is often a
prodromal history of confusional episodes (delirium) of acute onset, which may be precipitated
by illness or surgery. The distinction between NCDLB, in which Lewy bodies are primarily
limbic in location (with or without neocortical involvement), and major or mild NCD due to
Parkinson’s disease, which starts in the brain stem, is the order in which the cognitive and motor
symptoms emerge. In NCDLB, the cognitive decline is manifested early in the course of illness
(see the section “Differential Diagnosis” for this disorder).
Onset of symptoms is typically observed in individuals ages 50–89, with most cases having
onset in individuals in the mid-70s. Disease course may be characterized by occasional plateaus
but eventually progresses through severe dementia to death. Average duration of survival is 5.5–
7.7 years from the onset of cognitive decline.
Risk and Prognostic Factors
Familial aggregation may occur, and several risk genes have been
identified; but in most cases of NCDLB, there is no family history. The available studies suggest
that genetic risk factors are as important in NCDLB as in Alzheimer’s disease or Parkinson’s

Major or mild neurocognitive disorder due to Parkinson’s disease.
disease.
Diagnostic Markers
Biomarkers indicative of NCDLB may be considered to carry diagnostic weight equivalent to
core clinical features; these include low striatal dopamine transporter uptake on single photon
emission computed tomography (SPECT) or positron emission tomography (PET) scan,
abnormal (low uptake) (MIBG) myocardial scintigraphy suggesting cardiac sympathetic
denervation, and polysomnographic confirmation of REM sleep without atonia. The associated
condition REM sleep behavior disorder may be diagnosed through a formal sleep study or
identified by questioning the individual or informant about relevant symptoms. The underlying
neurodegenerative disease is primarily associated with misfolding and aggregation of αsynuclein, which may be confirmed via postmortem histopathological examination.
Neuropsychological testing beyond the use of a brief screening instrument may be necessary to
define cognitive deficits clearly. Assessment scales developed to measure fluctuation can be
useful.
Biomarkers supportive of NCDLB but with more limited evidence of diagnostic value
include the following: preservation of medial temporal volume relative to Alzheimer’s disease on
magnetic resonance imaging (MRI), generalized low uptake on SPECT/PET perfusion scan with
reduced occipital activity with or without the cingulate island sign (sparing of the posterior
cingulate cortex relative to the precuneus plus cuneus on fluorodeoxyglucose-PET imaging), and
prominent slow-wave activity on electroencephalogram with periodic fluctuations in the prealpha/theta range.
Functional Consequences of Major or Mild Neurocognitive Disorder
With Lewy Bodies
Individuals with NCDLB are more functionally impaired than would be expected for their
cognitive deficits when contrasted to individuals with other neurodegenerative diseases,
such as Alzheimer’s disease. This is largely a result of motor and autonomic impairments, which
cause problems with toileting, transferring, and eating. Sleep disorders and prominent psychiatric
symptoms may also add to functional difficulties. Consequently, the quality of life of individuals
with NCDLB is often significantly worse than that of individuals with Alzheimer’s disease.
Differential Diagnosis
The distinction between NCDLB
and NCD due to Parkinson’s disease is based on the timing and sequence of motor symptoms
and cognitive symptoms. Consensus criteria for DLB separate NCDLB from NCD due to
Parkinson’s disease by specifying that for dementia to be attributed to Parkinson’s disease, the
Parkinson’s disease diagnosis is present for at least 1 year before cognitive decline has reached
the level of major NCD, whereas for NCDLB, the cognitive symptoms may begin before, with,
or in the absence of parkinsonism. By contrast, expert consensus criteria for Parkinson’s disease
propose that if cognitive decline occurs prior to a motor diagnosis, the diagnosis of Parkinson’s

disease may still be made; therefore, a clinician may attribute the cognitive decline to the
Parkinson’s disease and diagnose NCD due to Parkinson’s disease. Consequently, the clinician
may choose to diagnose NCD due to Parkinson’s disease or NCDLB for individuals with major
NCD that starts either before or within 12 months of Parkinson’s disease. In such circumstances,
the clinician decides which diagnosis is more appropriate. If Parkinson’s disease has been
diagnosed for at least 1 year prior to the onset of cognitive symptoms, then both expert criteria
agree that NCD due to Parkinson’s disease would typically be the appropriate diagnosis. The
timing and sequence of parkinsonism and mild NCD may be particularly difficult to determine,
and unspecified NCD may need to be diagnosed until the order of clinical progression becomes
evident.
Comorbidity
Lewy body pathology frequently coexists with Alzheimer’s disease, transactive response DNA‐
binding protein 43 (TDP‐43)–related pathology, and cerebrovascular disease pathology,
particularly in the oldest age groups. TDP-43 is a protein that has been identified as a source of
the proteinopathies across a range of neurodegenerative disorders, including amyotrophic lateral
sclerosis and frontotemporal degeneration. The presence of multiple pathological lesions has
implications for disease prognosis and may be associated with a more rapid cognitive decline and
shorter survival time.
Major or Mild Vascular Neurocognitive Disorder
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. The clinical features are consistent with a vascular etiology, as suggested by
either of the following:
1. Onset of the cognitive deficits is temporally related to one or more
cerebrovascular events.
2. Evidence for decline is prominent in complex attention (including processing
speed) and frontal-executive function.
C. There is evidence of the presence of cerebrovascular disease from history,
physical examination, and/or neuroimaging considered sufficient to account for
the neurocognitive deficits.
D. The symptoms are not better explained by another brain disease or systemic
disorder.
Probable vascular neurocognitive disorder is diagnosed if one of the following is
present; otherwise possible vascular neurocognitive disorder should be
diagnosed:

1. Clinical criteria are supported by neuroimaging evidence of significant
parenchymal injury attributed to cerebrovascular disease (neuroimagingsupported).
2. The neurocognitive syndrome is temporally related to one or more documented
cerebrovascular events.
3. Both clinical and genetic (e.g., cerebral autosomal dominant arteriopathy with
subcortical infarcts and leukoencephalopathy) evidence of cerebrovascular
disease is present.
Possible vascular neurocognitive disorder is diagnosed if the clinical criteria are
met but neuroimaging is not available and the temporal relationship of the
neurocognitive syndrome with one or more cerebrovascular events is not
established.
Coding note (see coding table on pp. 682–683):
For major neurocognitive disorder probably or possibly due to vascular disease, with
behavioral disturbance, code F01.51.
For major neurocognitive disorder probably or possibly due to vascular disease,
without behavioral disturbance, code F01.50.
An additional medical code for the vascular disease is not used.
Note: The severity specifiers “mild,” “moderate,” and “severe” cannot be coded for
major neurocognitive disorder but should still be recorded.
For mild vascular neurocognitive disorder, code G31.84. (Note: Do not use an
additional code for the vascular disease. “With behavioral disturbance” and “without
behavioral disturbance” cannot be coded but should still be recorded.)
For major or mild vascular neurocognitive disorder: Use additional code(s) to
indicate clinically significant psychiatric symptoms due to the cerebrovascular
disease (e.g., F06.31 depressive disorder due to cerebrovascular disease, with
depressive features).
Diagnostic Features
The diagnosis of major or mild vascular neurocognitive disorder (NCD) requires the
establishment of an NCD (Criterion A) and the determination that cerebrovascular disease is the
dominant if not exclusive pathology that accounts for the cognitive deficits (Criteria B and C).
Vascular etiology may range from large vessel stroke to microvascular disease; the presentation
is therefore very heterogeneous, stemming from the types of vascular lesions and their extent and
location. The lesions may be focal, multifocal, or diffuse and occur in various combinations.
Pathogenic mechanisms responsible for brain parenchymal injury include hypoperfusion and
hypoxia, oxidative stress and inflammation leading to endothelial dysfunction, impairment of
autoregulation, and disruption of neurovascular coupling.
Many individuals with major or mild vascular NCD present with multiple infarctions, with an
acute stepwise or fluctuating decline in cognition, and intervening periods of stability and even
some improvement. Others may have gradual onset with slow progression, a rapid development
of deficits followed by relative stability, or another complex presentation. Major or mild vascular

NCD with a gradual onset and slow progression is generally attributable to small vessel disease
leading to lesions in the white matter, basal ganglia, or thalamus. The gradual progression in
these cases is often punctuated by acute
events that leave subtle neurological deficits. The cognitive deficits in these cases can be
attributed to disruption of cortical-subcortical circuits; complex attention, particularly speed of
information processing, and executive function are likely to be affected. Clinical subtypes of
vascular NCD have been described and include 1) poststroke NCD, manifesting immediately
after a stroke; 2) subcortical ischemic vascular NCD; 3) multi-infarct (cortical) NCD; and 4)
cortical-subcortical vascular NCD.
Assessing for the presence of sufficient cerebrovascular disease relies on history, physical
examination, and neuroimaging (Criterion C). Etiological certainty requires the demonstration of
abnormalities on neuroimaging. The lack of neuroimaging can result in significant diagnostic
inaccuracy by overlooking “silent” brain infarction and white matter lesions. However, if the
neurocognitive impairment is temporally associated with one or more well-documented strokes,
a probable diagnosis can be made in the absence of neuroimaging. Clinical evidence of
cerebrovascular disease includes documented history of stroke, with cognitive decline temporally
associated with the event, or physical signs consistent with stroke (e.g., hemiparesis;
pseudobulbar syndrome, visual field defect). Neuroimaging (magnetic resonance imaging [MRI]
or computed tomography [CT]) evidence of cerebrovascular disease comprises one or more of
the following: one or more large vessel infarcts or hemorrhages, a strategically placed single
infarct or hemorrhage (e.g., in angular gyrus, thalamus, basal forebrain), two or more lacunes
outside the brain stem, or extensive and confluent white matter lesions. The latter is often termed
small vessel disease or subcortical ischemic changes on clinical neuroimaging evaluations. MRI
is the preferred mode of neuroimaging, and there has been interest in using specialized MRI
techniques to detect cerebral microbleeds, cortical microinfarcts, dilated perivascular spaces, and
diffusion-based analyses of white matter tracts and network connectivity.
For mild vascular NCD, history of a single stroke or extensive white matter disease is
generally sufficient. For major vascular NCD, two or more strokes, a strategically placed stroke,
or a combination of white matter disease and one or more lacunes is generally necessary.
However, the relationship between identifiable vascular pathology in the brain on neuroimaging
and the cognitive symptoms is imperfect, and clinical judgment is generally needed to relate the
vascular lesions to the cognitive syndrome.
The neurocognitive symptoms must not be better explained by another medical condition or
mental disorder. For example, prominent memory deficit early in the course might suggest NCD
due to Alzheimer’s disease, early and prominent parkinsonian features would suggest NCD due
to Parkinson’s disease, and a close association between onset of cognitive and depressive
symptoms would suggest cognitive impairment as a result of depression.
A number of expert international groups have similarly defined and categorized the vascular
NCDs, with which DSM-5 criteria generally display good correspondence.
Associated Features

Environmental.
A neurological assessment often reveals history of stroke or transient ischemic episodes, and
signs indicative of brain infarctions. Also commonly associated are personality and mood
changes, abulia, depression, and emotional lability. The development of late-onset depressive
symptoms accompanied by psychomotor slowing and executive dysfunction is a common
presentation among older adults with progressive small vessel ischemic disease (so-called
vascular depression).
Prevalence
Vascular disease is the second most common cause of NCD after Alzheimer’s disease. In the
United States, population prevalence estimates for vascular dementia are 0.98% for individuals
ages 71–79 years, 4.09% for those ages 80–89 years, and 6.19% for those age 90 years or older.
Within 3 months following stroke, 20%–30% of individuals are diagnosed with
dementia. In a European autopsy series of decedents ages 60–103 years, the prevalence of pure
vascular dementia was 12.3%. Among those ages 60–69 years, the prevalence was higher
(15.0%) compared with those older than 90 years (8.7%). Mixed dementia (Alzheimer’s plus
vascular pathology) was present in 5.5% of the overall cohort, with a higher prevalence in those
older than 90 years (10.6%) compared with those ages 60–69 years (5.2%). Higher prevalence of
vascular dementia has been found among African Americans, Mexican Americans, and South
Asian Americans compared with non-Latinx Whites, possibly because of higher rates of risk
factors such as diabetes and cardiovascular disease. In Japan and several other Asian countries,
the prevalence of dementia due to Alzheimer’s disease has increased over time relative to
vascular dementia. Currently, the prevalence of dementia due to Alzheimer’s disease among
Japanese Americans is 2.6 times higher than that of vascular dementia.
Stroke is more common in men through age 65 years, but more common in women after age
65 years. Overall, the rate of vascular NCD was higher in men in some studies.
Development and Course
Major or mild vascular NCD can occur at any age, although the prevalence increases
exponentially after age 65 years. In older individuals, additional pathologies are almost always
present and partly account for the neurocognitive deficits. The course may vary from acute onset
with partial improvement to stepwise decline to progressive decline, with fluctuations and
plateaus of varying durations. Pure subcortical major or mild vascular NCD can have a slowly
progressive course that simulates major or mild NCD due to Alzheimer’s disease. The risk of an
ischemic stroke progressing to vascular NCD within 5 years was almost twice as high among
African Americans as among non-Latinx Whites in the United States and occurred at younger
ages. This is possibly a result of the impact of higher rates of hypertension, diabetes, and adverse
social determinants of mental health known to worsen dementia risk, such as limited formal
education and low socioeconomic status.
Risk and Prognostic Factors
The neurocognitive outcomes of vascular brain injury are influenced by

Genetic and physiological.
Other neurocognitive disorders.
Other medical conditions.
Other mental disorders.
neuroplasticity factors such as education, physical exercise, and mental activity.
The major risk factors for major or mild vascular NCD are the same as
those for cerebrovascular disease and stroke, including hypertension, diabetes, smoking, obesity,
high cholesterol levels, high homocysteine levels, other risk factors for atherosclerosis and
arteriolosclerosis, atrial fibrillation, and other conditions increasing the risk of cerebral emboli.
Cerebral amyloid angiopathy, leading to cerebral hemorrhage, is an important risk factor in
which amyloid deposits occur within arterial vessels. A genetic risk factor is the hereditary
condition 
cerebral 
autosomal 
dominant 
arteriopathy 
with 
subcortical 
infarcts 
and
leukoencephalopathy, or CADASIL. Other rarer forms of genetic disorders linked to vascular
NCD exist, but overall the contribution of genetics is small.
Diagnostic Markers
Structural neuroimaging, using MRI or CT, has an important role in the diagnostic process.
There are no other established biomarkers of major or mild vascular NCD.
Functional Consequences of Major or Mild Vascular Neurocognitive
Disorder
Major or mild vascular NCD is commonly associated with physical deficits that cause additional
disability.
Differential Diagnosis
Since incidental brain infarctions and white matter lesions are
common in older individuals, it is important to consider other possible etiologies when an NCD
is present in an individual with white matter lesions. A history of memory deficit early in the
course, and progressive worsening of memory, language, executive function, and perceptualmotor abilities in the absence of corresponding focal lesions on brain imaging, are suggestive of
Alzheimer’s disease as the primary diagnosis. Potential biomarkers currently being validated for
Alzheimer’s disease, such as cerebrospinal fluid levels of β-amyloid and phosphorylated tau, and
amyloid and tau imaging, may prove to be helpful in the differential diagnosis. NCD with Lewy
bodies is distinguished from major or mild vascular NCD by its core features of fluctuating
cognition, visual hallucinations, and spontaneous parkinsonism. While deficits in executive
function and language occur in major or mild vascular NCD, the insidious onset and gradual
progression of behavioral features or language impairment are characteristic of frontotemporal
NCD and are not typical of vascular etiology.
A diagnosis of major or mild vascular NCD is not made if other
diseases (e.g., brain tumor, multiple sclerosis, encephalitis, toxic or metabolic disorders) are
present and are of sufficient severity to account for the cognitive impairment.
A diagnosis of major or mild vascular NCD is inappropriate if the
symptoms can be entirely attributed to delirium, although delirium may sometimes be
superimposed on a preexisting major or mild vascular NCD, in which case both diagnoses can be
made. If the criteria for major depressive disorder are met and the cognitive impairment is

temporally related to the likely onset of the depression, major or mild vascular NCD should not
be diagnosed. However, if the NCD preceded the development of the depression, or the severity
of the cognitive impairment is out of proportion to the severity of the depression, depressive
disorder due to cerebrovascular disease should be diagnosed instead of major depressive
disorder.
Comorbidity
Major or mild NCD due to Alzheimer’s disease commonly co-occurs with major or mild
vascular NCD, in which case both diagnoses should be made. Major or mild vascular NCD and
depression frequently co-occur.
Major or Mild Neurocognitive Disorder Due to Traumatic
Brain Injury
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. There is evidence of a traumatic brain injury—that is, an impact to the head or
other mechanisms of rapid movement or displacement of the brain within the
skull, with one or more of the following:
1. Loss of consciousness.
2. Posttraumatic amnesia.
3. Disorientation and confusion.
4. Neurological signs (e.g., neuroimaging demonstrating injury; visual field cuts;
anosmia; hemiparesis; hemisensory loss; cortical blindness; aphasia; apraxia;
weakness;
loss of balance; other sensory loss that cannot be accounted for by peripheral
or other causes).
C. The neurocognitive disorder presents immediately after the occurrence of the
traumatic brain injury or immediately after recovery of consciousness and
persists past the acute post-injury period.
Coding note (see coding table on pp. 682–683):
For major neurocognitive disorder due to traumatic brain injury, with behavioral
disturbance: code first S06.2X9S diffuse traumatic brain injury with loss of
consciousness of unspecified duration, sequela; followed by F02.81 major
neurocognitive disorder due to traumatic brain injury, with behavioral disturbance.
For major neurocognitive disorder due to traumatic brain injury, without behavioral

disturbance: code first S06.2X9S diffuse traumatic brain injury with loss of
consciousness of unspecified duration, sequela; followed by F02.80 major
neurocognitive disorder due to traumatic brain injury, without behavioral disturbance.
Note: The severity specifiers “mild,” “moderate,” and “severe” cannot be coded for
major neurocognitive disorder but should still be recorded.
For mild neurocognitive disorder due to traumatic brain injury, code G31.84. (Note:
Do not use the additional code for traumatic brain injury. “With behavioral
disturbance” and “without behavioral disturbance” cannot be coded but should still
be recorded.)
For major or mild neurocognitive disorder due to traumatic brain injury: Use
additional code(s) to indicate clinically significant psychiatric symptoms due to the
traumatic brain injury (e.g., F06.34 bipolar and related disorder due to traumatic
brain injury, with mixed features; F07.0 personality change due to traumatic brain
injury, apathetic type).
Specifiers
Rate the severity of the neurocognitive disorder (NCD), not the underlying traumatic brain injury
(see the section “Development and Course” for this disorder).
Diagnostic Features
Major or mild NCD due to traumatic brain injury (TBI) denotes an acquired and persistent
disorder of cognition resulting from a traumatic brain injury. Traumatic brain injury is defined as
disruption of brain structure and/or function resulting from the application of biomechanical
forces (including acceleration/deceleration forces and blast-related forces), as manifested
immediately by one or more of the following clinical signs: loss of consciousness, loss of
memory for events immediately before or after the injury (posttraumatic amnesia), alteration in
mental state (e.g., confusion, disorientation, slowed thinking), or focal neurological signs (e.g.,
hemiparesis, hemisensory loss, cortical blindness, aphasia, apraxia, weakness, loss of balance,
other sensory loss that cannot be accounted for by peripheral or other causes) (Criterion B).
These manifestations of TBI must not be due to alcohol or other drugs or medications, other
injuries or treatment(s) for other injuries (e.g., facial injuries, intubation, or bodily/systemic
injuries), or psychological trauma, language barrier, or coexisting medical conditions.
The severity of a TBI is classified as mild, complicated mild, moderate, or severe according
to the thresholds in Table 2. An individual whose injury phenomenologically meets criteria for
mild TBI but whose computed tomographic or magnetic resonance imaging in the acute period
after TBI reveals traumatic intracranial abnormalities (i.e., traumatic epidural or subdural
hematoma, subarachnoid or intracerebral hemorrhage, cerebral contusions or laceration) is
classified as complicated mild TBI. Outcomes of individuals with complicated mild TBI are
more like those with moderate TBI than those with uncomplicated mild TBI.
TABLE 2 Classification of traumatic brain injury (TBI) severity

TBI severity
Mild TBI
Complicated
mild TBI
Moderate TBI
Severe TBI
Loss of consciousness duration
≤ 30 minutes
≤ 30 minutes
> 30 minutes to
< 24 hours
≥ 24 hours
Posttraumatic amnesia duration (densely
impaired new learning)
≤ 1 day
≤ 1 day
> 1 day to < 7
days
≥ 7 days
Alteration of consciousness duration (e.g.,
confusion, disorientation, slowed thinking)
≤ 1 day
≤ 1 day
> 1 day to < 7
days
≥ 7 days
Glasgow Coma Scale score (30 minutes after
the event)
13–15
13–15
9–12
3–8
Computed tomography or magnetic
resonance imaging of the brain
Normal
Abnormal
Normal or
abnormal
Normal or
abnormal
To be attributable to TBI, the NCD must manifest either immediately after the brain injury
occurs or immediately after the individual recovers consciousness after the injury, and persist
past the acute postinjury period (Criterion C).
While the specific cognitive impairments associated with major or mild NCD due to TBI are
variable, impairments in complex attention, processing speed, learning and memory, and
executive function are common, as are disturbances in social cognition. In more severe TBI in
which there is brain contusion, intracranial hemorrhage, or penetrating injury, there may be
additional neurocognitive impairments associated with the affected region of the brain and the
volume of brain tissue lost (e.g., aphasia, apraxia, disturbances in perceptual-motor function).
Associated Features
The diagnosis may also be supported by subtle neurological signs (e.g., multiple primitive
reflexes such as glabellar sign, snout response, palmomental reflex) or deficits in saccades and
smooth-pursuit eye movements co-occurring with frontally mediated cognitive impairments such
as complex attention problems, slow processing speed, impaired memory retrieval, or executive
dysfunction. Particularly in some cases of penetrating TBI, the diagnosis of NCD due to TBI
may be supported by posttraumatic epilepsy with focal onset in a location that corresponds to the
anatomy of a cognitive domain in which an individual demonstrates impairment (e.g., medial
temporal lobe–onset seizures and episodic memory impairment; frontal lobe seizures and
executive dysfunction or social cognitive impairment).
Prevalence
The prevalence of major and mild NCD due to TBI varies with injury severity and time since
injury, with the highest frequencies among individuals with more severe injury and during the
acute/subacute post-injury period. In the United States, more than 2.87 million TBIs occur
annually, including more than 837,000 TBIs in children. These TBIs account for 2.5 million
emergency department visits, 288,000 hospitalizations, and more than 56,000
deaths annually. Among individuals presenting to an emergency department with TBI, the rates
for men are 547.6 per 100,000 and for women are 385.9 per 100,000. The TBI rate is higher for
men than women in every age group up to age 75 years, after which the rates of TBI between

men and women approach parity. The leading causes of TBI in the United States are falls (178.4
per 100,000), collision with a moving or stationary object (termed “struck by/against” events)
(92.7 per 100,000), motor vehicle crashes (74.7 per 100,000), and assaults (50.6 per 100,000
persons). Concussion in sport is increasingly recognized as a cause of mild TBI.
Men are approximately 40% more likely to experience a TBI compared with women in the
young and adult populations; however, women may have higher risk of TBI after age 65 years. It
has been suggested that men with moderate or severe TBI may have a worse prognosis than
women with the same level of severity; however, the findings have been mixed. The cause of
TBI also differs by sex and gender. Men are more likely to experience injuries at work, in motor
vehicle accidents, and during military activities, whereas women are more likely to experience
injuries from assault and domestic violence.
Development and Course
The course of recovery from TBI is variable, depending not only on the specifics of the injury
but also on pre-injury and postinjury factors. These factors may favor or impede recovery and
include age; prior history of TBI; neurological, psychiatric, and substance use comorbidities and
complications; genetics; the timeliness and effectiveness of medical and rehabilitative
interventions; and psychosocial support, among others.
Neurocognitive impairments are most severe in the acute period following the TBI and may
be accompanied by disturbances of emotion and behavior. Across the spectrum of TBI severity,
substantial improvement in neurocognitive and associated psychiatric and neurological
symptoms and signs is expected. The extent of recovery and the variability in neurocognitive
outcomes tend to reflect the severity of TBI, with complete recovery being typical after mild TBI
and more variable, and often incomplete, recovery following more severe TBI.
Neurocognitive impairments associated with mild TBI typically resolve within days to weeks
after the injury, with complete resolution within 3–12 months post-injury. Other symptoms (e.g.,
depression, irritability, fatigue, headache, photosensitivity, sleep disturbance) that may
potentially co-occur with the neurocognitive symptoms also tend to resolve in the weeks
following mild TBI. Persistent symptoms after mild TBI or subsequent neurocognitive
deterioration should trigger consideration of other potential causes of neurocognitive symptoms
and functional limitations, including major depressive disorder, posttraumatic stress disorder
(PTSD), anxiety disorders, substance use disorders, sleep disturbances, negative injury
perceptions, and poor expectations for recovery. When neurocognitive symptoms and functional
limitations persist after mild TBI (including repetitive mild TBI) despite treatment of their other
potential causes, diagnosis of an NCD due to TBI may be appropriate.
Neurocognitive impairments and associated functional limitations produced by moderate and
severe TBI typically improve over weeks to months after the injury, although long-term
neurocognitive recovery is often incomplete among individuals with more severe injuries.
Nonetheless, neurocognitive and functional improvement may continue for years after moderate
or severe TBI, with more individuals cognitively improving than declining during the first 5
years postinjury. With moderate and severe TBI, in addition to persistence of neurocognitive
deficits, there may be associated neurological, medical, emotional, and behavioral complications.
These include seizures (particularly in the first year), photosensitivity, hyperacusis, irritability,
aggression, depression, sleep disturbance, fatigue, apathy, inability to resume occupational and

social functioning at preinjury level, and deterioration in interpersonal relationships. Moderate
and severe TBI have been
associated with increased risk of depression, aggression, and possibly neurodegenerative
diseases such as Alzheimer’s disease, Lewy body disease, and frontotemporal degeneration.
The features of persisting major or mild NCD due to TBI will vary by age, specifics of the
injury, and cofactors. Persisting TBI-related impairment in an infant or child may be reflected in
delays in reaching developmental milestones (e.g., language acquisition), worse academic
performance, and possibly impaired social development. Among older teenagers and adults,
persisting symptoms may include various neurocognitive deficits, irritability, hypersensitivity to
light and sound, easy fatigability, and mood changes, including depression, anxiety, hostility, or
apathy. In older individuals, mild TBI may produce neurocognitive outcomes like those
associated with moderate or severe TBI in younger adults.
Risk and Prognostic Factors
Risk factors for adverse cognitive outcomes after TBI include age older than 40 years, lower preinjury cognitive abilities (especially as indexed by education or academic competence), preinjury
depressive symptoms, possibly pre-injury unemployment, and injury severity. Other risk factors
for adverse cognitive outcomes include a longer duration of posttraumatic amnesia, evidence of
traumatic intracranial abnormalities on early computed tomography or magnetic resonance
imaging (MRI) studies (i.e., traumatic epidural or subdural hematoma, subarachnoid or
intracerebral hemorrhage, cerebral contusions or laceration, diffuse axonal injury) and
neurogenetic profile (e.g., APOE*E4 allele carrier status, catechol-O-methyltransferase
genotype, ANKK1 Taq1A allele status). Pre-injury alcohol or substance use disorders increase
the risk of sustaining a TBI as well as the risk of adverse cognitive outcomes, including memory
impairment and executive dysfunction.
Diagnostic Markers
The diagnosis of major or mild NCD due to TBI may be supported by contemporaneous
computed tomographic or MRI findings (e.g., focal atrophy, encephalomalacia, gliosis, white
matter abormalities) in brain areas or networks subserving specific cognitive domains in which
an individual demonstrates impairment. The diagnosis may also be supported by subtle
neurological signs (e.g., multiple primitive reflexes such as glabellar sign, snout response,
palmomental reflex) or deficits in saccades and smooth-pursuit eye movements co-occurring
with frontally mediated cognitive impairments such as complex attention problems, slow
processing speed, impaired memory retrieval, or executive dysfunction. Particularly in some
cases of penetrating TBI, the diagnosis of NCD due to TBI may be supported by posttraumatic
epilepsy with focal onset in a location that corresponds to the anatomy of a cognitive domain in
which an individual demonstrates impairment (e.g., medial temporal lobe–onset seizures and
episodic memory impairment; frontal lobe seizures and executive dysfunction or social cognitive
impairment).
Performance on commonly used general cognitive screening measures, particularly when

interpreted using large-scale, population-based normative data, may usefully identify individuals
in need of further neurodiagnostic assessment. However, the diagnosis of major or mild NCD
due to TBI rests on performance on domain-specific cognitive assessment interpreted in light of
the individual’s prior performance (e.g., neuropsychological estimates of pre-injury cognitive
ability or appropriate norms) and assessment of functional status.
While neuroimaging and other clinical assessments (e.g., subtle neurological signs) may
provide supportive information, they cannot independently diagnose NCD due to TBI. At
present, there are no other established biomarkers of major or mild NCD due to TBI.
Association With Suicidal Thoughts or Behavior
Individuals with TBI, including moderate or severe TBI, are at increased long-term risk for
suicide. While depression is a substantial contributor to this risk, it does not fully account for it.
Rates of suicidal ideation are as high as 10%, and rates of suicide attempt are 0.8%–1.7%
over the first 20 years after TBI. The development of depression and/or suicidal behavior at 1year post-injury is associated with consistently elevated rates of depression and suicidal behavior
5 years after TBI. While the relationship between cognitive impairments and suicide risk after
TBI is complex, assessing suicide risk is an important element in the evaluation of individuals
with major or mild NCD due to TBI.
Youth who have had concussions may be at higher risk for suicidal behavior. There is an
increased risk of suicide among both veteran and civilian cohorts with TBI, and individuals
seeking mental health care may have a history of TBI. Individuals seeking rehabilitative services
for TBI are also at heightened risk for suicidal thoughts and behavior.
Functional Consequences of Major or Mild Neurocognitive Disorder
Due to Traumatic Brain Injury
Approximately 3.17 million individuals in the United States (approximately 1.1% of the
population) live with a TBI-related disability, including neurocognitive impairments that
compromise the ability to work or perform daily activities and that are associated with the need
for ongoing medical care, rehabilitation, support, and services. Cognitive impairments interfere
with functional independence, productive employment, and community participation and may
reduce satisfaction with life. The influence of cognitive impairments on functional status varies
with the type and severity of those impairments; with the presence and severity of co-occurring
psychiatric, substance use, neurological, and medical conditions; and with family, other
psychosocial, and medical support.
With mild NCD due to TBI, individuals may report reduced cognitive efficiency, difficulty
concentrating, and lessened ability to perform usual activities. With major NCD due to TBI, an
individual may have difficulty in independent living and self-care. Prominent neuromotor
features, such as severe incoordination, ataxia, and motor slowing, may be present in major NCD
due to TBI and may add to functional difficulties.
Individuals with TBI histories report more depressive and anxious symptoms, and these can
amplify cognitive complaints and worsen functional outcome. Additionally, loss of emotional

Other mental disorders and medical conditions.
Factitious disorder and malingering.
control, including aggressive or inappropriate affect and apathy, may be present after more
severe TBI with greater neurocognitive impairment. These features may compound difficulties
with functional independence and self-care.
Differential Diagnosis
Mental disorders (e.g., major depressive disorder,
anxiety disorders, PTSD, alcohol and other substance use disorders, sleep disturbances),
prescribed medications (e.g., typical antipsychotics, benzodiazepines, drugs with anticholinergic
properties, antiepileptic drugs), and other medical conditions may contribute to or account for
cognitive impairments among individuals with TBI, and need to be considered in the differential
diagnosis of major or mild NCD due to TBI.
Alternative explanations for neurocognitive symptoms should
be considered when the severity of neurocognitive symptoms and functional limitations are
inconsistent with the cognitive outcomes expected after TBI—and particularly mild TBI—and
when neuropsychological assessment reveals poor effort or is otherwise not valid for
interpretation. In such circumstances, the possibility of factitious disorder or malingering
(especially in situations in which there might be external incentives such as obtaining financial
compensation) should be considered.
Comorbidity
Major or mild NCD due to TBI may be accompanied by other specified or unspecified
depressive or anxiety disorders characterized by disturbances in emotional function (e.g.,
irritability, easy frustration, tension and anxiety, affective lability). Other specified or
unspecified personality disorders may also occur as a result of symptoms such as disinhibition,
apathy, suspiciousness, or aggression. Medical comorbidities may occur with neurological and
physical disturbances characterized by headache, fatigue, sleep disorders, vertigo or dizziness,
tinnitus or hyperacusis, photosensitivity, anosmia, reduced tolerance to psychotropic
medications, and, particularly in more severe TBI, neurological symptoms and signs (e.g.,
seizures, hemiparesis, visual disturbances, cranial nerve deficits) and evidence of orthopedic
injuries. The most common medical and psychiatric comorbidities associated with moderate-tosevere TBI are (in order of frequency) back pain, depression, hypertension, anxiety, fractures,
high blood cholesterol, sleep disorders, panic attacks, osteoarthritis, and diabetes.
Among individuals with substance use disorders, the neurocognitive effects of the substance
contribute to or compound the TBI-associated cognitive disturbances, particularly among
individuals with two or more TBIs.
PTSD can co-occur with TBI in civilian, military, and veterans populations. TBI and PTSD
produce similar neurocognitive symptoms (e.g., disturbances of complex attention, processing
speed, learning and memory, and executive function), and either or both conditions, as well as
co-occurring depression and sleep disturbances, may explain neurocognitive symptoms in
individuals with such comorbidities.

Substance/Medication-Induced Major or Mild
Neurocognitive Disorder
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. The neurocognitive impairments do not occur exclusively during the course of a
delirium and persist beyond the usual duration of intoxication and acute
withdrawal.
C. The involved substance or medication and duration and extent of use are
capable of producing the neurocognitive impairment.
D. The temporal course of the neurocognitive deficits is consistent with the timing of
substance or medication use and abstinence (e.g., the deficits remain stable or
improve after a period of abstinence).
E. The neurocognitive disorder is not attributable to another medical condition or is
not better explained by another mental disorder.
Coding note (see also coding table on pp. 682–683): The ICD-10-CM codes for
the [specific substance/medication]-induced neurocognitive disorders are indicated
in the table below. Note that the ICD-10-CM code depends on whether or not there
is a comorbid substance use disorder present for the same class of substance. In
any case, an additional separate diagnosis of a substance use disorder is not given.
Substance-induced major neurocognitive disorder: If a mild substance use
disorder is comorbid with the substance-induced major neurocognitive disorder, the
4th position character is “1,” and the clinician should record “mild [substance] use
disorder” before the substance-induced major neurocognitive disorder (e.g., “mild
inhalant use disorder with inhalant-induced major neurocognitive disorder”). For
alcohol and sedative, hypnotic, or anxiolytic substances, a mild substance use
disorder is insufficient to cause a substance-induced major neurocognitive disorder;
thus, there are no available ICD-10-CM codes for this combination. If a moderate or
severe substance use disorder is comorbid with the substance-induced major
neurocognitive disorder, the 4th position character is “2,” and the clinician should
record “moderate [substance] use disorder” or “severe [substance] use disorder,”
depending on the severity of the comorbid substance use disorder. If there is no
comorbid substance use disorder, then the 4th position character is “9,” and the
clinician should record only the substance-induced major neurocognitive disorder.
Substance-induced mild neurocognitive disorder: If a mild substance use
disorder is comorbid with the substance-induced mild neurocognitive disorder, the
4th position character is “1,” and the clinician should record “mild [substance] use
disorder” before the substance-induced mild neurocognitive disorder (e.g., “mild

cocaine use disorder with cocaine-induced mild neurocognitive disorder”). If a
moderate or severe substance use disorder is comorbid with the substance-induced
mild neurocognitive disorder, the 4th position character is “2,” and the clinician
should record “moderate [substance] use disorder” or “severe [substance] use
disorder,” depending on the severity of the comorbid substance use disorder. If there
is no comorbid substance use disorder, then the 4th position character is “9,” and the
clinician should record only the substance-induced mild neurocognitive disorder.
The severity specifiers “mild,” “moderate,” and “severe” (for major neurocognitive
disorder) and the accompanying symptom specifiers “with behavioral disturbance”
and “without behavioral disturbance” (for major or mild neurocognitive disorder)
cannot be coded but should still be recorded.
ICD-10-CM
With mild use
disorder
With moderate or
severe use disorder
Without use
disorder
Substance-induced major neurocognitive disorder (NCD)
Alcohol (major NCD), nonamnesticconfabulatory type
NA
F10.27
F10.97
Alcohol (major NCD), amnesticconfabulatory type
NA
F10.26
F10.96
Inhalant (major NCD)
F18.17
F18.27
F18.97
Sedative, hypnotic, or anxiolytic (major
NCD)
NA
F13.27
F13.97
Other (or unknown) substance (major NCD)
F19.17
F19.27
F19.97
Substance-induced mild neurocognitive disorder (NCD)
Alcohol (mild NCD)
F10.188
F10.288
F10.988
Inhalant (mild NCD)
F18.188
F18.288
F18.988
Sedative, hypnotic, or anxiolytic (mild NCD)
F13.188
F13.288
F13.988
Amphetamine-type substance (or other
stimulant) (mild NCD)
F15.188
F15.288
F15.988
Cocaine (mild NCD)
F14.188
F14.288
F14.988
Other (or unknown) substance (mild NCD)
F19.188
F19.288
F19.988
Specify if:
Persistent: Neurocognitive impairment continues to be significant after an
extended period of abstinence.
Recording Procedures
The name of the substance/medication-induced neurocognitive disorder (NCD) begins with the
specific substance (e.g., alcohol) that is presumed to be causing the neurocognitive symptoms.
The ICD-10-CM code that corresponds to the applicable drug class is selected from the table
included in the criteria set. For substances that do not fit into any of the classes (e.g., intrathecal
methotrexate), the ICD-10-CM code for the other (or unknown) substance class should be used
and the name of the specific substance recorded (e.g., F19.988 intrathecal methotrexate-induced

mild neurocognitive disorder). In cases in which a substance is judged to be an etiological factor
but the specific substance is unknown, the ICD-10-CM code for the other (or unknown)
substance class is used, and the fact that the substance is unknown is recorded (e.g., F19.97
unknown substance-induced major neurocognitive disorder).
When recording the name of the disorder, the comorbid substance use disorder (if any) is
listed first, followed by the word “with,” followed by the name of the disorder (i.e., [specific
substance]–induced major neurocognitive disorder or [specific substance]–induced mild
neurocognitive disorder), followed by the type in the case of alcohol (i.e., nonamnesticconfabulatory type, amnestic-confabulatory type), followed by specification of duration (i.e.,
persistent). For example, in the case of persistent amnestic-confabulatory symptoms in a man
with a severe alcohol use disorder, the diagnosis is F10.26 severe alcohol use disorder with
alcohol-induced major neurocognitive disorder, amnestic-confabulatory type, persistent. A
separate diagnosis of the comorbid severe alcohol use disorder is not given. If the substanceinduced neurocognitive disorder occurs without a comorbid substance use disorder (e.g., after a
sporadic heavy use of inhalants), no accompanying substance use disorder is noted (e.g., F18.988
[specific inhalant]–induced mild neurocognitive disorder).
Diagnostic Features
Substance/medication-induced major or mild NCD is characterized by neurocognitive
impairments that persist beyond the usual duration of intoxication and acute withdrawal
(Criterion B). Initially, these manifestations can reflect slow recovery of brain functions from a
period of prolonged substance use, and improvements in neurocognitive as well as brain imaging
indicators may be seen over many months. If the disorder continues for an extended period,
persistent should be specified. The given substance and its use must be known to be capable of
causing the observed impairments (Criterion C). While nonspecific decrements in a range of
cognitive abilities can occur with nearly any substance of abuse and a variety of medications,
some patterns occur more frequently with selected drug classes. For example, NCD due to
sedative, hypnotic, or anxiolytic drugs (e.g., benzodiazepines, barbiturates) may show greater
disturbances in memory than in other cognitive functions. NCD induced by alcohol frequently
manifests with a combination of impairments in executive-function and memory and learning
domains. The temporal course of the substance-induced NCD must be consistent with that of use
of the given substance (Criterion D). Alcohol-induced, amnestic-confabulatory type
(Korsakoff’s) NCD is characterized by an impairment in recent memory that is out of proportion
to additional NCD symptoms. Features include prominent amnesia (severe difficulty learning
new information with rapid forgetting) and a tendency to confabulate, although confabulation
can be seen with any severe diminution of recent memory. These manifestations may co-occur
with signs of thiamine encephalopathy (Wernicke’s encephalopathy) with associated features
such as nystagmus and ataxia. Ophthalmoplegia of Wernicke’s encephalopathy is typically
characterized by a lateral gaze paralysis. The neurocognitive deficits associated with inhalant
misuse include diminished executive functioning, slower cognitive speed, and additional
impaired performance on aspects of the Wisconsin Card Sorting and the Stroop tests.
Neurocognitive symptoms associated with stimulant use include difficulties with learning and
memory and executive function. Methamphetamine use can also be associated with

715
evidence of vascular injury (e.g., focal weakness, unilateral incoordination, asymmetrical
reflexes). The most common neurocognitive profile approximates that seen in vascular NCD.
Substances that cause NCD included in the other (or unknown) substance category include
intrathecal methotrexate and organophosphate insecticides, as well as compounds that are
misused and known to induce adverse cognitive effects but are less well characterized (e.g.,
kratom/Mitragyna speciosa).
When one is determining the relationship between NCD conditions and any group of drugs, it
is important to consider whether the deficit was present before the use of the substance and
consequently would not be attributable to the substance—and may have even contributed to poor
judgment that resulted in the substance use. For example, evidence of decreased impulse control
and related impairment of executive functions have been reported as associated with the onset of
the use of stimulants and other drugs. In studies in which neurocognitive function is carefully
assessed prior to substance use, and then subjects are followed up over several months or more,
the ability of drugs other than alcohol, other depressants, and inhalants to cause clinically
significant persistent NCDs is not clear.
Associated Features
Inhalant-induced NCD conditions may be associated with the smell of the inhalant on an
individual’s breath or a rash around the individual’s nose or mouth from “huffing” the drug from
a container. These are most often seen in individuals with limited access to other drugs who have
histories of inhalant use as well as the early onset of use of multiple substances, especially if
their symptoms fulfill criteria for conduct or antisocial personality disorders. A high risk is also
seen in workers exposed to solvents in the workplace. Mild NCD induced by drugs with central
nervous system depressant effects may manifest with added symptoms of increased irritability,
anxiety, sleep disturbance, and dysphoria. NCD induced by stimulant drugs may manifest with
rebound depression, hypersomnia, and apathy. In severe forms of substance/medication-induced
major NCD (e.g., associated with long-term alcohol use), there may be prominent neuromotor
features, such as incoordination, ataxia related to cerebellar damage, and motor slowing, as well
as medical complications such as hypokalemia and cardiac arrhythmias. There may also be loss
of emotional control, including aggressive or inappropriate affect, or apathy.
Prevalence
The prevalence of these conditions is not well known. Prevalence figures are more available for
the use of these substances and for associated substance use disorders rather than for the
neurocognitive conditions. Substance/medication-induced major or mild NCDs are more likely
in those who are older, have longer duration of use, and have other risk factors such as
nutritional deficits.
For alcohol use disorder, the rate of mild NCD is approximately 30%–40% in the first 2
months of abstinence. Mild NCD may persist, particularly in those who do not achieve stable
abstinence until after age 50 years. Major NCD is rare and may result from concomitant
nutritional deficits, as in alcohol-induced amnestic-confabulatory NCD. Alcohol-induced major
NCD may be more common in men.

Few studies are available regarding the prevalence of NCD from other brain depressant drugs
(i.e., sedatives, hypnotics, or anxiolytics), likely reflecting the relative rarity of studies of
substance use disorders on these drugs and the relatively low level of heavy and persistent
“recreational” use of sedative, hypnotic, or anxiolytic drugs compared with alcohol, cannabis,
and many other drugs.
More data are available on the prevalence of inhalant use. Such exposure has been linked to
both major and mild NCD of varied duration in both higher- and lower-income populations.
However, persistent use to the point of developing an NCD is estimated to be less than 1% of the
U.S. population.
In the case of stimulants (methamphetamines and cocaine), cerebrovascular disease can also
occur, resulting in diffuse or focal brain injury that can be of mild or major neurocognitive
levels.
Development and Course
The onset of substance use disorders tends to occur during late adolescence and peak in the 20s
and 30s. Although longer history of severe substance use disorder is associated with greater
likelihood of NCD, the relationships are not straightforward, with substantial and even complete
recovery of neurocognitive functions being common among persons who achieve stable
abstinence prior to age 50 years. Substance/medication-induced major or mild NCD is most
likely to become persistent in individuals who continue to have substance use disorders past the
age of 50 years, presumably because of a combination of lessened neural plasticity and the onset
of other age-related brain changes.
NCD conditions may involve a fairly rapid onset of neurocognitive impairment in individuals
whose history includes the use of multiple types of drugs of abuse, especially with an early onset
of substance use. Earlier commencement of heavy use, particularly of alcohol, may lead to
defects in later neural development (e.g., later stages of maturation of frontal circuitries), which
may have effects on social cognition as well as other neurocognitive abilities. For alcoholinduced NCD, there may be an additive effect of aging and alcohol-induced brain injury.
Risk and Prognostic Factors
Risk factors for substance/medication-induced NCDs include older age, longer duration of use,
and persistent use past age 50 years.
For alcohol-induced NCD, long-term nutritional deficiencies, liver disease, vascular risk
factors, and cardiovascular and cerebrovascular disease may contribute to risk. An increased risk
for alcohol-induced, amnestic confabulatory–type NCD occurs in the context of a genetic
transketolase deficiency as well as in the context of poor nutrition.
Sedative-, hypnotic-, or anxiolytic-induced NCDs have not been well studied, but these
problems may be increased in individuals with long-term anxiety disorders or sleep impairment
who have been taking benzodiazepines or other hypnotic medications in increasing amounts for
months or years.

Diagnostic Markers
Magnetic resonance imaging (MRI) of individuals with chronic alcohol use disorder frequently
reveals cortical thinning, white matter loss, and enlargement of sulci and ventricles. While
neuroimaging abnormalities are more common in those with NCDs, it is possible to observe
NCDs without neuroimaging abnormalities, and vice versa. Specialized techniques (e.g.,
diffusion tensor imaging) may reveal damage to specific white matter tracts. Magnetic resonance
spectroscopy may reveal reduction in N-acetylaspartate, and increase in markers of inflammation
(e.g., myoinositol) or white matter injury (e.g., choline). Many of these brain imaging changes
and neurocognitive manifestations reverse following successful abstinence. In individuals with
methamphetamine use disorder, MRI may also reveal hyperintensities suggestive of
microhemorrhages or larger areas of infarction.
Functional Consequences of Substance/Medication-Induced Major or
Mild Neurocognitive Disorder
The functional consequences of substance/medication-induced mild NCD are sometimes
augmented by reduced cognitive efficiency and difficulty concentrating beyond that seen in
many other NCDs. In addition, at both major and mild levels, substance/medication-induced
NCDs may have associated motor syndromes that increase the level of functional impairment.
Differential Diagnosis
Individuals with substance use disorders, substance intoxication, and substance withdrawal are at
increased risk for other conditions that may independently, or through a compounding effect,
result in neurocognitive disturbance. These include history of traumatic brain injury and
infections that can accompany substance use disorder (e.g., HIV, hepatitis C virus, syphilis).
Therefore, presence of substance/medication-induced major or mild NCD should be
differentiated from NCDs arising outside the context of substance use, intoxication, and
withdrawal, including these accompanying conditions (e.g., traumatic brain injury).
Comorbidity
Substance use disorders, substance intoxication, and substance withdrawal are highly comorbid
with other mental disorders. In general, the higher the exposure to drugs of abuse, the greater the
risk for a substance- or medication-induced NCD. Comorbid posttraumatic stress disorder,
psychotic disorders, depressive and bipolar disorders, and neurodevelopmental disorders can
contribute to neurocognitive impairment in substance users. Traumatic brain injury occurs more
frequently with substance use, complicating efforts to determine the etiology of NCD in such
cases. Severe, long-term alcohol use disorder can be associated with major organ system disease,
including cerebrovascular disease and cirrhosis; inhalant use disorder is associated with higher
rates of kidney and liver damage; and amphetamine- and cocaine-induced NCD may be
accompanied by major or mild vascular NCD secondary to stimulant use.

Major or Mild Neurocognitive Disorder Due to HIV
Infection
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. There is documented infection with human immunodeficiency virus (HIV).
C. The neurocognitive disorder is not better explained by non-HIV conditions,
including 
secondary 
brain 
diseases 
such 
as 
progressive 
multifocal
leukoencephalopathy or cryptococcal meningitis.
D. The neurocognitive disorder is not attributable to another medical condition and
is not better explained by a mental disorder.
Coding note (see coding table on pp. 682–683):
For major neurocognitive disorder due to HIV infection, with behavioral disturbance,
code first B20 HIV infection, followed by F02.81 major neurocognitive disorder due
to HIV infection, with behavioral disturbance.
For major neurocognitive disorder due to HIV infection, without behavioral
disturbance, code first B20 HIV infection, followed by F02.80 major neurocognitive
disorder due to HIV infection, without behavioral disturbance.
Note: The severity specifiers “mild,” “moderate,” and “severe” cannot be coded for
major neurocognitive disorder but should still be recorded.
For mild neurocognitive disorder due to HIV infection, code G31.84. (Note: Do not
use the additional code for HIV infection. “With behavioral disturbance” and “without
behavioral disturbance” cannot be coded but should still be recorded.)
For major or mild neurocognitive disorder due to HIV infection: Use additional
code(s) to indicate clinically significant psychiatric symptoms due to HIV infection
(e.g., F06.34 bipolar and related disorder due to HIV infection, with mixed features;
F07.0 personality change due to traumatic brain injury, apathetic type).
Diagnostic Features
HIV disease is caused by infection with human immunodeficiency virus type-1 (HIV-1), which
is acquired through exposure to bodily fluids of an infected individual through injection
substance use, unprotected sexual contact, or accidental or iatrogenic exposure (e.g., needle
puncture injury to medical personnel). HIV infects several types of cells, most particularly “Thelper” (CD4) lymphocytes and monocytes. Over time, the infection can cause severe decreases
in the CD4 count, resulting in severe immunocompromise, often leading to opportunistic
infections and neoplasms. Infected monocytes can enter the central nervous system, leading to
infection of macrophages and microglia. A small percentage of astrocytes may harbor productive

HIV infection. The advanced form of HIV infection is termed acquired immune deficiency
syndrome (AIDS). Diagnosis of HIV is confirmed by established laboratory methods, such as the
reverse-transcription polymerase chain reaction (RT-PCR) assay for HIV RNA and the
antibody/antigen combination test. Of note, in-home self-testing for HIV is available.
Some individuals with HIV infection develop a neurocognitive disorder (NCD), which
generally shows a “subcortical pattern” with prominently impaired executive function, slowing
of processing speed, problems with more demanding attentional tasks, and difficulty in learning
new information, but fewer problems with recall of learned information. In major NCD, slowing
may be prominent. Language difficulties, such as aphasia, are uncommon, although reductions in
fluency may be observed. HIV pathogenic processes can affect any part of the brain; therefore,
other patterns are possible.
Associated Features
Major or mild NCD due to HIV infection is more prevalent in individuals of increasing age,
lower educational level, or female sex, and among those with major depressive disorder, alcohol
or other substance use disorders, and medical comorbidities (particularly diabetes and
hypertension). The NCD risk due to HIV infection is also increased with any of the following:
prior episodes of immunosuppression, high viral loads in the cerebrospinal fluid, and increased
levels of tumor necrosis factor–alpha (TNF-α), interleukin-6 (IL-6), C-reactive protein, D-dimer,
sCD14, sCD163, and neurofilament light chain in the peripheral blood or clinical laboratory
indicators of advanced HIV disease, such as a low CD4 cell nadir, anemia, and
hypoalbuminemia. Individuals with major NCD may show more prominent neuromotor features,
such as severe incoordination, ataxia, and motor slowing. These features may become more
prominent with NCD disease progression.
Prevalence
Depending on the clinical stage of HIV disease, approximately one-third to over one-half of
HIV-infected individuals have at least some evidence of a neurocognitive disturbance, but most
of these disturbances would not meet criteria for mild NCD and would instead represent
individuals with asymptomatic neurocognitive impairment (ANI), who may have substandard
performance on one or more tests of neurocognitive abilities but do not have any impairment in
functional status. Rates in North America and Western Europe have largely shown that ANI
accounts for the majority of neurocognitive disturbances, whereas mild NCD due to HIV
accounts for approximately one-quarter of individuals, and major NCD criteria are met for
typically less than 5% of individuals with HIV-related neurocognitive disturbances. In Germany,
the overall prevalence of HIV-associated NCDs among HIV
clinic participants was 43%, 90% of whom were in treatment: 20% had ANI, 17% had mild
NCD, and 6% had HIV-associated dementia. In low- and middle-income countries, prevalence of
HIV-associated NCDs is higher among untreated individuals with HIV. In other parts of the
world, and in cohorts composed mostly of individuals infected with HIV on effective
antiretroviral treatment tested with comprehensive cognitive test batteries, the overall rates of

cognitive impairment were found to be around 25%–35%.
In the United States, the incidence of HIV infection is higher in men than in women in every
ethnic group. However, evidence supports a sex difference in NCD due to HIV infection, with
more frequent neurocognitive impairment in women, including when sex is maintained as a risk
factor in a multivariate analysis. The higher rate of impairment in women may be associated with
differences in educational quality.
Development and Course
In the development and course of NCD due to HIV, individuals may have neurocognitive
impairment when the HIV infection is asymptomatic; the Centers for Disease Control and
Prevention classifies the underlying HIV infection in three stages: asymptomatic, early
symptomatic, and late symptomatic/AIDS. The course of NCD due to HIV infection can resolve,
improve, remain stable, slowly worsen, rapidly worsen, or have a fluctuating course. Rapid
progression of neurocognitive impairment is uncommon in the context of currently available
combination antiretroviral treatment, although it may still occur in the context of a subgroup
associated with older age, as well as in association with specific comorbidities promoting
cognitive impairment. Nevertheless, for the predominant proportion of individuals with HIV, an
abrupt change in mental status warrants an evaluation of other medical sources for the cognitive
change, including secondary infections. Because HIV infection preferentially affects subcortical
regions over the course of illness, including deep white matter, the progression of the disorder
follows a subcortical pattern. The subcortical pattern of cognitive impairment is characterized by
mental slowing associated with motor dysfunction, procedural learning deficits, and free recall
deficits, with relative sparing of recognition memory, verbal abstraction, and naming.
Because HIV infection can affect a variety of brain regions and the illness can take on many
different trajectories depending on associated comorbidities and the consequences of HIV
infection, the overall course of an NCD due to HIV infection has considerable heterogeneity. A
subcortical neurocognitive profile may interact with age over the life course, such that an
interaction occurs between age and clinical stage of HIV disease in the domains of episodic
memory and motor impairment (e.g., slowed gait). This interaction increases the overall
prevalence of neurocognitive impairment and the likelihood that it will be more pronounced in
later life.
Acquisition of HIV infection typically occurs in adults in high-income countries, via highrisk behaviors (e.g., unprotected sex; injection substance use) beginning in late adolescence and
peaking during young and middle adulthood, with a significant contribution persisting into older
age. In lower-income regions, where HIV testing and antiretroviral treatments for pregnant
women are not readily available, perinatal transmission is common. The NCD in such infants and
children may manifest primarily as neurodevelopmental delay. As individuals treated for HIV
survive into older age, additive and interactive neurocognitive effects of HIV and aging,
including other NCDs (e.g., due to Alzheimer’s disease, due to Parkinson’s disease), are
possible. More than 50% of individuals with HIV in the United States are older than 50 years.
Long-term antiretroviral therapy is indicated for the ongoing control of HIV infection. However,
some antiretroviral therapy may be associated with inflammation, neurotoxic effects, and
metabolic changes that can lead to vascular compromise and indirectly increase neurocognitive
impairment in conjunction with aging and medical comorbidities that may worsen cognition.

720
Risk and Prognostic Factors
Paradoxically, NCD due to HIV infection has not declined significantly with the advent of
effective antiretroviral therapy, although the most severe presentations (consistent with the
diagnosis of major NCD) have decreased sharply. Contributory factors may include inadequate
control of HIV in the central nervous system (CNS), the evolution of antiretroviral drug-resistant
viral strains, the effects of chronic long-term systemic and brain inflammation, and the effects of
comorbid factors such as aging, substance use disorder, hypertension, diabetes, past history of
CNS trauma, and co-infections, such as with the hepatitis C virus. Chronic exposure to
antiretroviral drugs has also been associated with neurotoxicity in its own right.
Diagnostic Markers
An HIV diagnosis may be made from a test conducted on the blood, oral fluids, or urine. In
addition, HIV characterization of the cerebrospinal fluid may be helpful if it reveals a
disproportionately high viral load in the cerebrospinal fluid versus in the plasma or if there are
indicators of a high level of neuroinflammation. Neuroimaging (e.g., magnetic resonance
imaging [MRI]) may reveal reduction in total brain volume, cortical thinning, reduction in white
matter volume, and patchy areas of abnormal white matter (hyperintensities). MRI of the brain or
lumbar puncture may be helpful to exclude a specific medical condition (e.g., cryptococcal
meningitis, meningoencephalitis, herpes simplex virus type 1 or type 2 encephalitis, progressive
multifocal leukoencephalopathy) that might contribute to CNS changes in the context of AIDS.
Specialized techniques such as diffusion tensor imaging may reveal damage to specific white
matter tracts. Arterial spin-labeling (ASL) developed as a new type of MRI (ASL-MRI) may
reveal regional changes in brain perfusion in 3–5 minutes without infusion of extrinsic tracers,
and translocator protein 18-kDa (TSPO) positron emission tomography scanning may reveal
neuroinflammation.
Functional Consequences of Major or Mild Neurocognitive Disorder
Due to HIV Infection
Functional consequences of major or mild NCD due to HIV infection are variable across
individuals. Thus, impaired executive functions and slowed information processing may
substantially interfere with adherence to the effective antiretroviral therapy regimens, although
these regimens have been greatly simplified since their inception. Thus, functional status must be
assessed and mapped directly to neurocognitive impairment in order to determine the severity of
the NCD. Functional status related to neurocognitive impairment due to HIV should be separated
from dysfunction attributable to other concomitant disorders that can affect neurocognitive
function.
Differential Diagnosis
In the presence of comorbidities, such as other infections (e.g., hepatitis C virus, syphilis),
substance use disorder (e.g., methamphetamine use disorder), prior traumatic brain injury, or
neurodevelopmental conditions, major or mild NCD due to HIV infection can be diagnosed

provided there is evidence that infection with HIV has worsened any NCDs because of such
preexisting or comorbid conditions. Among older adults, onset of neurocognitive decline related
to cerebrovascular disease or primary neurodegeneration (e.g., major or mild NCD due to
Alzheimer’s disease) may need to be differentiated; these conditions may be suggested by a
relatively more progressive course of decline than is seen in NCD due to HIV. HIV infection
itself has been shown to increase the risk of cerebrovascular disease. Because more severe
immunodeficiency can result in opportunistic infections of the brain (e.g., toxoplasmosis;
cryptococcosis) and neoplasia (e.g., CNS lymphoma), sudden
onset of an NCD or sudden worsening of an NCD demands active investigation of non-HIV
etiologies. Delirium is important to consider because it occurs frequently over the disease course
of individuals with HIV and may be due to multiple etiologies (including SARS-CoV-2 coinfection).
Comorbidity
HIV disease is accompanied by chronic systemic and CNS inflammation and diseases that can be
associated with an NCD. These complications can be part of the pathogenesis of major or mild
NCD as well as ANI due to HIV infection. HIV frequently co-occurs with conditions such as
substance use disorders and other sexually transmitted infections. Both medical and psychiatric
comorbidities have been identified that increase the likelihood of a diagnosis of NCD due to HIV
infection. Women and members of underserved ethnic and racialized groups may show variation
in the rates of the comorbidities associated with NCD due to HIV infection.
Major or Mild Neurocognitive Disorder Due to Prion
Disease
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. There is insidious onset, and rapid progression of impairment is common.
C. There are motor features of prion disease, such as myoclonus or ataxia, or
biomarker evidence.
D. The neurocognitive disorder is not attributable to another medical condition and
is not better explained by another mental disorder.
Coding note (see coding table on pp. 682–683):
For major neurocognitive disorder due to prion disease, with behavioral disturbance,
code first A81.9 prion disease, followed by F02.81 major neurocognitive disorder
due to prion disease, with behavioral disturbance.
For major neurocognitive disorder due to prion disease, without behavioral

disturbance, code first A81.9 prion disease, followed by F02.80 major neurocognitive
disorder due to prion disease, without behavioral disturbance.
Note: The severity specifiers “mild,” “moderate,” and “severe” cannot be coded for
major neurocognitive disorder but should still be recorded.
For mild neurocognitive disorder due to prion disease, code G31.84. (Note: Do not
use the additional code for prion disease. “With behavioral disturbance” and “without
behavioral disturbance” cannot be coded but should still be recorded.)
For major or mild neurocognitive disorder due to prion disease: Use additional
code(s) to indicate clinically significant psychiatric symptoms due to prion disease
(e.g., F06.2 psychotic disorder due to prion disease, with delusions; F06.32
depressive disorder due to prion disease with major depressive–like episode).
Diagnostic Features
The classification of major or mild neurocognitive disorder (NCD) due to prion disease includes
NCDs due to a group of subacute spongiform encephalopathies (including sporadic CreutzfeldtJakob disease, genetic Creutzfeldt-Jakob disease, iatrogenic Creutzfeldt-Jakob disease, variant
Creutzfeldt-Jakob disease, variably protease-sensitive prionopathy,
kuru [found among the Fore people in Papua New Guinea], Gerstmann-Sträussler-Scheinker
syndrome, and fatal insomnia) caused by transmissible agents known as prions. Given that the
most common type is sporadic Creutzfeldt-Jakob disease, it is typically referred to as simply
Creutzfeldt-Jakob disease (CJD). Variant CJD is much rarer and is associated with transmission
of bovine spongiform encephalopathy, also called “mad cow disease.” Typically, individuals
with CJD present with neurocognitive deficits, ataxia, and abnormal movements such as
myoclonus, chorea, or dystonia; a startle reflex is also common. The history often reveals rapid
progression to major NCD over as little as 6 months, and thus the disorder is typically seen only
at the major level. However, many individuals with the disorder may have atypical presentations,
and the disease can be confirmed only by biopsy or at autopsy. For example, individuals with
variant CJD may present with a greater preponderance of psychiatric symptoms than do
individuals with other types of prion disease, characterized by low mood, withdrawal, and
anxiety. Although biomarker evidence is not necessarily required for the diagnosis if the motor
features of prion disease (e.g., myoclonus, ataxia) are present, confidence that the NCD is due to
prion disease is greatly increased if characteristic biomarkers are present.
Prevalence
Prevalence is unknown but very low given the short survival. Based on data from nine highincome countries, the annual incidence of sporadic CJD is approximately one or two cases per
million people. Incidence varies by age and is highest in those age 65 years or older
(4.8/1,000,000 individuals) and is higher in Whites compared with Blacks. Incidence among
ethnic Chinese in Taiwan is lower than general population rates in the United States and other
reporting countries.

Environmental.
Genetic and physiological.
Development and Course
Prion disease may develop at any age in adults—the peak age for sporadic CJD is approximately
67 years—although it has been reported to occur in individuals spanning the teenage years to late
life. Non-Latinx Whites were found to have an older mean age at onset compared with other
ethnic and racialized populations in the United States. Prodromal symptoms of prion disease may
include fatigue, anxiety, problems with appetite or sleeping, or difficulties with concentration.
After several weeks, these symptoms may be followed by incoordination, altered vision, or
abnormal gait or other movements that may be myoclonic, choreoathetoid, or ballistic, along
with a rapidly progressive dementia. The disease typically progresses very rapidly to the major
level of impairment over several months. More rarely, it can progress over 2 years and appear
similar in its course to other NCDs.
Risk and Prognostic Factors
Cross-species transmission of prion infections, with agents that are closely related
to the human form, has been demonstrated (e.g., the outbreak of bovine spongiform
encephalopathy inducing variant CJD in the United Kingdom during the mid-1990s).
Transmission by corneal transplantation, cadaveric dura mater grafts, contaminated neurosurgical
instruments, cadaver-derived human growth hormone and pituitary gonadotropin injections, and
blood transfusion (only in the case of variant CJD) has been documented. Studies have not
demonstrated an increased risk of sporadic CJD in health care professionals.
In up to 15% of prion disease cases, there are autosomal dominant
genetic mutations in the prion protein gene (PRNP), which encodes for a normal neuronal
membrane–bound protein. The codon 129 polymorphism of PRNP mediates the risk
of sporadic and acquired prion diseases as well as modifies clinical manifestation, age at disease
onset, and disease duration.
Diagnostic Markers
Prion disease can be definitively confirmed only by brain biopsy or at autopsy. There are several
cerebrospinal fluid (CSF) proteins that are markers of neuronal injury and are frequently elevated
in prion disease; the ones most commonly used for diagnostic purposes are 14-3-3 and tau, which
have high sensitivity but variable specificity. Real-time quaking induced conversion (RT-QuIC)
is another CSF diagnostic test that is able to amplify minute amounts of disease-causing prion
proteins and has extremely high specificity. Magnetic resonance brain imaging is currently
considered the most sensitive diagnostic test when DWI (diffusion-weighted imaging) is
performed, with the most common finding being multifocal gray matter hyperintensities in
subcortical and/or cortical regions. In some individuals, the electroencephalogram reveals
periodic sharp, often triphasic and synchronous discharges at a rate of 0.5–2 Hz at some point
during the course of the disorder. It is important to note that the above diagnostic markers vary
across prion disease type (e.g., sporadic CJD, genetic CJD, variant CJD).

Other major neurocognitive disorders.
Differential Diagnosis
Major NCD due to prion disease may appear similar in its
course to other NCDs, but prion diseases are typically distinguished by their rapid progression
and prominent cerebellar and motor symptoms.
Major or Mild Neurocognitive Disorder Due to
Parkinson’s Disease
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. The disturbance occurs in the setting of established Parkinson’s disease.
C. There is insidious onset and gradual progression of impairment.
D. The neurocognitive disorder is not attributable to another medical condition and
is not better explained by another mental disorder.
Major or mild neurocognitive disorder probably due to Parkinson’s disease
should be diagnosed if 1 and 2 are both met. Major or mild neurocognitive
disorder possibly due to Parkinson’s disease should be diagnosed if 1 or 2 is
met:
1. There is no evidence of mixed etiology (i.e., absence of other neurodegenerative
or cerebrovascular disease or another neurological, mental, or systemic disease
or condition likely contributing to cognitive decline).
2. The Parkinson’s disease clearly precedes the onset of the neurocognitive
disorder.
Coding note (see coding table on pp. 682–683):
For major neurocognitive disorder probably or possibly due to Parkinson’s disease,
with behavioral disturbance, code first G20 Parkinson’s disease, followed by F02.81.
For major neurocognitive disorder probably or possibly due to Parkinson’s disease,
without behavioral disturbance, code first G20 Parkinson’s disease, followed by
F02.80.
Note: The severity specifiers “mild,” “moderate,” and “severe” cannot be coded for
major neurocognitive disorder but should still be recorded.
For mild neurocognitive disorder due to Parkinson’s disease, code G31.84. (Note:
Do not use the additional code for Parkinson’s disease. “With behavioral
disturbance” and “without behavioral disturbance” cannot be coded but should still
be recorded.)
For major or mild neurocognitive disorder due to Parkinson’s disease: Use additional
code(s) to indicate clinically significant psychiatric symptoms due to Parkinson’s

disease (e.g., F06.0 psychotic disorder due to Parkinson’s disease, with
hallucinations; F06.31 depressive disorder due to Parkinson’s disease, with
depressive features; F07.0 personality change due to traumatic brain injury,
apathetic type).
Diagnostic Features
The essential feature of major or mild neurocognitive disorder (NCD) due to Parkinson’s disease
is cognitive decline observed at the time of or following the onset of idiopathic Parkinson’s
disease. The disturbance must occur in the setting of established Parkinson’s disease (Criterion
B), and deficits must have developed gradually (Criterion C). The rate of progression of
cognitive deficits may vary; for some individuals with mild deficits there may be very minimal
change over time.
The NCD is viewed as probably due to Parkinson’s disease when there is no evidence of
another disorder that might be responsible for the cognitive decline and when the Parkinson’s
disease precedes onset of the NCD. The NCD is considered possibly due to Parkinson’s disease
when only one of these conditions is met but not both conditions. A diagnosis of Parkinson’s
disease prior to the onset of the cognitive change increases the diagnostic confidence that the
NCD is attributable to Parkinson’s disease, as denoted by the probable designation.
Associated Features
Frequently present features include apathy, depressed mood, anxious mood, hallucinations,
delusions, personality changes, rapid eye movement (REM) sleep behavior disorder, excessive
daytime sleepiness, freezing of gait, falls, bilateral involvement early in disease, postural
instability and gait disturbance (PIGD) subtype, and hyposmia. The combination of postural and
gait instability may occur early in the disease and may be described by the term PIGD subtype to
distinguish from tremor-predominant Parkinson’s disease.
Prevalence
The prevalence of Parkinson’s disease in the United States steadily increases with age from
approximately 0.4% between ages 60 and 69 years to 1.4% between ages 80 and 89 years.
Parkinson’s disease is more common in men than in women. Similarly, the prevalence of NCD
due to Parkinson’s disease is higher in men than in women. However, it is not clear if the
incidence of NCD due to Parkinson’s disease is higher in men than in women. Among
individuals with Parkinson’s disease, as many as 80% will eventually develop a major NCD.
Among those without a major NCD, the prevalence of mild NCD in Parkinson’s disease has been
estimated at 25%–27%. For individuals with incident-untreated Parkinson’s disease, a range of
9%–19% have mild NCD, whereas other studies have reported major NCD occurring in 24% of
newly diagnosed untreated Parkinson’s disease. Among African Americans, the risk of
Parkinson’s disease tends to be lower than among non-Latinx Whites, but the risk of dementia
among those with the disease tends to be higher.
Development and Course
Onset of Parkinson’s disease is typically between ages 50 and 89 years, with most expression in

Environmental.
Genetic and physiological.
Major or mild neurocognitive disorder with Lewy bodies (NCDLB).
the early 60s. Mild NCD often develops relatively early in the course of Parkinson’s disease,
whereas major impairment typically does not occur until individuals are older.
Risk and Prognostic Factors
Risk factors for Parkinson’s disease include exposure to pesticides, solvents, and
possibly traumatic brain injury.
Potential risk factors for NCD among individuals with Parkinson’s
disease include older age at disease onset, increasing severity of disease, prominent gait
symptoms, severe autonomic disturbance (particularly orthostatic hypotension), REM sleep
behavior disorder, and possibly being a man and having fewer years of formal education.
Individuals with Parkinson’s disease with glucocerebrosidase gene (GBA) mutations and
APOE*E4 genotype have been demonstrated to have worse cognition in cross-sectional and
longitudinal research.
Culture-Related Diagnostic Issues
Guam dementia is a late-onset NCD observed among 8.8% of Chamorros (the indigenous
population of Guam) age 65 years and older. Characterized by neurofibrillary tangles but without
the amyloid plaques found in Alzheimer’s disease, it is thought to be possibly related to a unique
parkinsonism-dementia complex and amyotrophic lateral sclerosis. An association has been
found with processing and eating fadang made with cycad seeds.
Diagnostic Markers
Neuropsychological testing, with a focus on tests that are not affected by motor slowing (i.e., not
timed or requiring use of hands), is critical in detecting the core cognitive deficits, particularly at
the mild NCD phase. Characteristic features observed in neuropsychological testing early in the
disorder may include reduced attention, executive dysfunction, slowed information processing,
and deficits in memory and visuospatial function, whereas many language skills may remain
intact.
Dopamine transporter scans, such as DaT scans, may differentiate Lewy body–related
dementias (i.e., NCD due to Parkinson’s disease, NCD with Lewy bodies) from non–Lewy
body–related dementias (e.g., NCD due to Alzheimer’s disease).
Differential Diagnosis
The distinction between NCDLB
and NCD due to Parkinson’s disease is based on the timing and sequence of motor symptoms
and cognitive symptoms. Consensus criteria for dementia with Lewy bodies separate NCDLB
from NCD due to Parkinson’s disease by specifying that for dementia to be attributed to
Parkinson’s disease, the Parkinson’s disease diagnosis must be present for at least 1 year before
cognitive decline has reached the level of major NCD, whereas for NCDLB, the cognitive

Major or mild neurocognitive disorder due to Alzheimer’s disease.
Major or mild vascular neurocognitive disorder.
Neurocognitive disorder due to another medical condition (e.g., neurodegenerative disorders).
Antipsychotic (or other dopamine receptor–blocking drug)–induced parkinsonism.
symptoms may begin before, with, or in the absence of parkinsonism. By contrast, expert
consensus criteria for Parkinson’s disease propose that if cognitive decline occurs prior to a
motor diagnosis, the diagnosis of Parkinson’s disease may still be made; therefore, a clinician
may attribute the cognitive decline to the Parkinson’s disease and diagnose NCD due to
Parkinson’s disease. Consequently, the clinician may choose to diagnose NCD due to
Parkinson’s disease or NCDLB for individuals with major NCD that starts either before or within
12 months of Parkinson’s disease. In such circumstances, the clinician decides which diagnosis
is more appropriate. If Parkinson’s disease has been diagnosed for at least 1 year prior to the
onset of cognitive symptoms, then both expert criteria agree that NCD due to Parkinson’s disease
would typically be the appropriate diagnosis. The timing and sequence of parkinsonism and mild
NCD may be particularly difficult to determine, and unspecified NCD may need to be diagnosed
until the order of clinical progression becomes evident.
The motor features are the key to
distinguishing major or mild NCD due to Parkinson’s disease from major or mild NCD due to
Alzheimer’s disease. However, the two disorders can co-occur, and individuals with wellestablished Alzheimer’s disease can develop mild parkinsonism.
Major or mild vascular NCD may manifest with
parkinsonian features that may occur as a consequence of diffuse cortical or subcortical small
vessel disease. However, the parkinsonian features typically are not sufficient for a diagnosis of
Parkinson’s disease, and the course of the NCD usually has a clear association with
cerebrovascular changes.
When 
a
diagnosis of major or mild NCD due to Parkinson’s disease is being considered, the distinction
must also be made from other brain disorders, such as progressive supranuclear palsy,
corticobasal degeneration, multiple system atrophy, tumors, and hydrocephalus.
Antipsychotic 
(or
other dopamine receptor–blocking drug)–induced parkinsonism can occur in individuals with
other NCDs, particularly when antipsychotic medications are prescribed for the behavioral
manifestations of such disorders.
Comorbidity
Parkinson’s disease may coexist with Alzheimer’s disease and cerebrovascular disease,
especially in older individuals. Individuals with NCD due to Parkinson’s disease may display
clinical or biomarker features that suggest the presence of both Parkinson’s disease and other
pathologies. Evidence for mixed etiology does not preclude the contribution of Parkinson’s
disease to an NCD. The compounding of multiple pathological features may diminish the
functional abilities of individuals with Parkinson’s disease. Motor symptoms and frequent cooccurrence of depression, psychosis, REM sleep behavior disorder, or apathy can make
functional impairment worse.
Major or Mild Neurocognitive Disorder Due to
Huntington’s Disease

Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. There is insidious onset and gradual progression.
C. There is clinically established Huntington’s disease, or risk for Huntington’s
disease based on family history or genetic testing.
D. The neurocognitive disorder is not attributable to another medical condition and
is not better explained by another mental disorder.
Coding note (see coding table on pp. 682–683):
For major neurocognitive disorder due to Huntington’s disease, with behavioral
disturbance, code first G10 Huntington’s disease, followed by F02.81 major
neurocognitive disorder due to Huntington’s disease, with behavioral disturbance.
For major neurocognitive disorder due to Huntington’s disease, without behavioral
disturbance, code first G10 Huntington’s disease, followed by F02.80 major
neurocognitive disorder due to Huntington’s disease, without behavioral disturbance.
Note: The severity specifiers “mild,” “moderate,” and “severe” cannot be coded for
major neurocognitive disorder but should still be recorded.
For mild neurocognitive disorder due to Huntington’s disease, code G31.84. (Note:
Do not use the additional code for Huntington’s disease. “With behavioral
disturbance” and “without behavioral disturbance” cannot be coded but should still
be recorded.)
For major or mild neurocognitive disorder due to Huntington’s disease: Use
additional code(s) to indicate clinically significant psychiatric symptoms due to
Huntington’s disease (e.g., F06.31 depressive disorder due to Huntington’s disease
with depressive features; F06.4 anxiety disorder due to Huntington’s disease).
Diagnostic Features
Progressive cognitive impairment is a core feature of Huntington’s disease, with early changes in
executive function (i.e., processing speed, organization, and planning) typically being more
prominent than decline in learning and memory. Cognitive and associated behavioral changes
often precede the emergence of the typical motor abnormalities of bradykinesia (i.e., slowing of
voluntary movement) and chorea (i.e., involuntary jerking movements). A diagnosis of definite
Huntington’s disease is given in the presence of unequivocal, extrapyramidal motor
abnormalities in an individual with either a family history of Huntington’s disease or genetic
testing showing a CAG trinucleotide repeat expansion in the HTT gene, located on chromosome
4.
Associated Features
Irritability, apathy, anxiety, obsessive-compulsive symptoms, depression, and, more rarely,

Genetic and physiological.
psychosis can all be associated with Huntington’s disease and often precede the onset of motor
symptoms.
Prevalence
Neurocognitive deficits are an eventual outcome of Huntington’s disease; the worldwide
prevalence is estimated to be 2.7 per 100,000. The prevalence of Huntington’s disease in North
America, Europe, and Australia is 5.7 per 100,000, with a much lower prevalence of 0.40 per
100,000 in Asia.
Development and Course
The age at diagnosis of Huntington’s disease varies widely, but symptoms are most often
observed between ages 35 and 45 years. Age at onset is inversely correlated with CAG
expansion length. Juvenile Huntington’s disease (onset before age 20) may present more
commonly with bradykinesia, dystonia, and rigidity than with the choreic movements
characteristic of the adult-onset disorder. The disease is gradually progressive, with the average
length of survival after clinical diagnosis estimated to be approximately 10–20 years, although
affected individuals may demonstrate significant variability in disease progression.
Phenotypic expression of Huntington’s disease varies by presence of motor, cognitive, and
psychiatric symptoms. Psychiatric and cognitive abnormalities can predate the motor
abnormality by a decade or more. Initial symptoms requiring care often include irritabity,
anxiety, or depressed mood. Other behavioral disturbances may include pronounced apathy,
disinhibition, impulsivity, and impaired insight, with apathy often becoming more progressive
over time. Early movement symptoms may involve the appearance of fidgetiness of the
extremities as well as mild apraxia (i.e., difficulty with purposeful movements), particularly with
fine motor tasks. As the disorder progresses, other motor problems include impaired gait (ataxia)
and postural instability. Motor impairment eventually affects speech production (dysarthria)
such that the speech becomes very difficult to understand, which may result in significant
distress resulting from the communication barrier in the context of comparatively intact
cognition. Advanced motor disease severely affects gait with
progressive ataxia. Eventually individuals become nonambulatory. End-stage motor disease
impairs motor control of eating and swallowing, typically a major contributor to the death of the
individual from aspiration pneumonia.
Risk and Prognostic Factors
The genetic basis of Huntington’s disease is a fully penetrant autosomal
dominant expansion of the CAG trinucleotide, often called a CAG repeat in the huntingtin gene.
A repeat length of 40 or more is invariably associated with Huntington’s disease, with longer
repeat lengths associated with early age at onset. A CAG repeat length in the 36–39 range is
considered to be partially penetrant, which means that this length could or could not lead to
Huntington’s disease. If Huntington’s disease does occur with repeat lengths in this range, it is
more often associated with onset late in life (diagnosis after age 70).

Diagnostic Markers
Genetic testing is the primary laboratory test for the determination of Huntington’s disease,
which is an autosomal dominant disorder with complete penetrance. The trinucleotide CAG is
observed to have a repeat expansion in the gene that encodes huntingtin protein on chromosome
4. A diagnosis of Huntington’s disease is not made in the presence of the gene expansion alone,
but the diagnosis is made only after motor symptoms become manifest. Some individuals with a
positive family history request genetic testing in a presymptomatic stage. Associated features
may also include neuroimaging changes; volume loss in the basal ganglia, particularly the
caudate nucleus and putamen, is well known to occur and progresses over the course of illness.
Other structural and functional changes have been observed in brain imaging but remain research
measures.
Association With Suicidal Thoughts or Behavior
In Huntington’s disease, an elevated suicide risk compared with the general population has been
well documented. A literature review and report of data from a large observational study found
that suicide is among the leading causes of death in Huntington’s disease. The elevated risk of
suicidal thoughts in Huntington’s disease has been shown in diagnosed individuals both prior to
and after manifesting the motor symptoms of Huntington’s disease. Risk factors for suicidal
thoughts include depressive symptoms, anxiety, irritability, psychosis, and apathy—emphasizing
the importance of treating depressive symptoms and assessing suicidal thoughts during clinical
monitoring. A large European cohort study of Huntington’s disease similarly found that the most
frequent causes of death were pneumonia (19.5%), other infections (6.9%), and suicide (6.6%).
Functional Consequences of Major or Mild Neurocognitive Disorder
Due to Huntington’s Disease
In the prodromal phase of illness and at early diagnosis, occupational decline is most common,
with most individuals reporting some loss of ability to engage in their typical work. The
emotional, behavioral, and cognitive aspects of Huntington’s disease, such as disinhibition and
personality changes, are highly associated with functional decline. Cognitive deficits that
contribute most to functional decline may include speed of processing, initiation, and attention
rather than memory impairment. Given that Huntington’s disease onset occurs in productive
years of life, it may have a very disruptive effect on performance in the work setting as well as
social life, family life, and important aspects of daily functioning such as driving. As the disease
progresses, disability from problems such as
impaired gait, dysarthria, and impulsive or irritable behaviors may substantially add to the level
of impairment and daily care needs, over and above the care needs attributable to cognitive
decline. Severe choreic movements may substantially interfere with provision of care such as
bathing, dressing, and toileting.
Differential Diagnosis

Other mental disorders.
Other neurocognitive disorders.
Other movement disorders.
Early symptoms of Huntington’s disease may include instability of mood,
irritability, or compulsive behaviors that may suggest another mental disorder. However, genetic
testing or the development of motor symptoms will distinguish the presence of Huntington’s
disease. In such cases, if the mood symptoms are a focus of clinical attention, they may be
indicated by an additional diagnosis of depressive disorder due to Huntington’s disease, with
depressive features.
The early symptoms of Huntington’s disease, particularly
symptoms of executive dysfunction and impaired psychomotor speed, may resemble other
neurocognitive disorders (NCDs), such as major or mild vascular NCD.
Huntington’s disease must also be differentiated from other disorders
or conditions associated with chorea, such as Wilson’s disease, drug-induced tardive dyskinesia,
Sydenham’s chorea, systemic lupus erythematosus, or senile chorea. Rarely, individuals may
present with a course similar to that of Huntington’s disease but without positive genetic testing;
this is considered to be a Huntington’s disease phenocopy that results from a variety of potential
genetic factors.
Major or Mild Neurocognitive Disorder Due to Another
Medical Condition
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. There is evidence from the history, physical examination, or laboratory findings
that the neurocognitive disorder is the pathophysiological consequence of
another medical condition (e.g., multiple sclerosis).
C. The cognitive deficits are not better explained by another mental disorder (e.g.,
major depressive disorder) or another specific neurocognitive disorder (e.g.,
major neurocognitive disorder due to Alzheimer’s disease).
Coding note (see coding table on pp. 682–683):
For major neurocognitive disorder due to another medical condition, with behavioral
disturbance, code first the other medical condition, followed by the major
neurocognitive disorder due to another medical condition, with behavioral
disturbance (e.g., G35 multiple sclerosis, F02.81 major neurocognitive disorder due
to multiple sclerosis, with behavioral disturbance).
For major neurocognitive disorder due to another medical condition, without
behavioral disturbance, code first the other medical condition, followed by the major
neurocognitive disorder due to another medical condition, without behavioral
disturbance (e.g., G35 multiple sclerosis, F02.80 major neurocognitive disorder due
to multiple sclerosis, without behavioral disturbance).
Note: The severity specifiers “mild,” “moderate,” and “severe” cannot be coded for
major neurocognitive disorder but should still be recorded.

Other major or mild neurocognitive disorder.
For mild neurocognitive disorder due to another medical condition, code G31.84.
(Note: Do not use the additional code for the other medical condition. “With
behavioral disturbance” and “without behavioral disturbance” cannot be coded but
should still be recorded.)
For major or mild neurocognitive disorder due to another medical condition: Use
additional code(s) to indicate clinically significant psychiatric symptoms due to
another medical condition (e.g., F06.32 depressive disorder due to multiple
sclerosis, with major depressive–like episode).
Diagnostic Features
A number of medical conditions can cause neurocognitive disorders (NCDs) other than those
specific etiologies (e.g., Alzheimer’s disease) already included in prior NCD criteria sets in this
chapter. These conditions include structural lesions (e.g., primary or secondary brain tumors,
subdural hematoma, slowly progressive or normal-pressure hydrocephalus), hypoxia related to
hypoperfusion from heart failure, endocrine conditions (e.g., hypothyroidism, hypercalcemia,
hypoglycemia), nutritional conditions (e.g., deficiencies of thiamine or niacin), other infectious
conditions (e.g., neurosyphilis, cryptococcosis), immune disorders (e.g., temporal arteritis,
systemic lupus erythematosus), hepatic or renal failure, metabolic conditions (e.g., Kufs’ disease,
adrenoleukodystrophy, metachromatic leukodystrophy, other storage diseases of adulthood and
childhood), and other neurological conditions (e.g., epilepsy, multiple sclerosis). Unusual causes
of central nervous system injury, such as electrical shock or intracranial radiation, are generally
evident from the history. The temporal association between the onset or exacerbation of the
medical condition and the development of the cognitive deficit offers the greatest support that the
NCD is a pathophysiological consequence of the medical condition. Diagnostic certainty
regarding this relationship may be increased if the neurocognitive deficits ameliorate partially or
stabilize in the context of treatment of the medical condition.
Development and Course
Typically the course of the NCD progresses in a manner that is commensurate with progression
of the underlying medical condition. In circumstances where the medical condition is treatable
(e.g., hypothyroidism), the neurocognitive deficit may improve or at least not progress. When the
medical condition has a deteriorative course (e.g., secondary progressive multiple sclerosis), the
neurocognitive deficits will progress along with the temporal course of illness.
Diagnostic Markers
Associated physical examination and laboratory findings and other clinical features depend on
the nature and severity of the medical condition.
Differential Diagnosis
The presence of an attributable medical condition does
not entirely exclude the possibility of another etiological type of major or mild NCD. If cognitive

deficits persist following successful treatment of an associated medical condition, then another
etiology may be responsible for the cognitive decline.
Major or Mild Neurocognitive Disorder Due to Multiple
Etiologies
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. There is evidence from the history, physical examination, or laboratory findings
that the neurocognitive disorder is the pathophysiological consequence of more
than one etiological process, excluding substances (e.g., neurocognitive disorder
due to Alzheimer’s disease with subsequent development of vascular
neurocognitive disorder).
Note: Refer to the diagnostic criteria for the various neurocognitive disorders
due to specific medical conditions for guidance on establishing the particular
etiologies.
C. The cognitive deficits are not better explained by another mental disorder and do
not occur exclusively during the course of a delirium.
Coding note (see coding table on pp. 682–683):
For major neurocognitive disorder due to multiple etiologies, code first all of the
etiological medical conditions (with the exception of vascular disease, which is not
coded), followed by either F02.81 for major neurocognitive disorder due to multiple
etiologies, with behavioral disturbance; or F02.80 for major neurocognitive disorder
due to multiple etiologies, without behavioral disturbance.
If vascular disease is among the multiple etiological medical conditions, code next
either F01.51 for major vascular neurocognitive disorder, with behavioral
disturbance; or F01.50 for major vascular neurocognitive disorder, without behavioral
disturbance. Note: The severity specifiers “mild,” “moderate,” and “severe” cannot be
coded for major neurocognitive disorder but should still be recorded.
For example, for a presentation of major neurocognitive disorder, moderate, with a
behavioral disturbance, that is judged to be due to Alzheimer’s disease, vascular
disease, and HIV infection, and in which heavy chronic alcohol use is judged to be a
contributing factor, code the following: G30.9 Alzheimer’s disease, B20 HIV
infection; F02.81 major neurocognitive disorder due to Alzheimer’s disease and HIV
infection, 
moderate, 
with 
behavioral 
disturbance; 
F01.51 
major 
vascular
neurocognitive disorder, moderate, with behavioral disturbance; and F10.27 severe
alcohol use disorder with alcohol-induced major neurocognitive disorder, moderate,
nonamnestic-confabulatory type.

For mild neurocognitive disorder due to multiple etiologies, code G31.84. (Note: Do
not use the additional codes for the etiologies. “With behavioral disturbance” and
“without behavioral disturbance” cannot be coded but should still be recorded.)
For major or mild neurocognitive disorder due to multiple etiologies: Use additional
code(s) to indicate clinically significant psychiatric symptoms due to the various
etiologies (e.g., F06.2 psychotic disorder due to Alzheimer’s disease, with delusions;
F06.31 depressive disorder due to cerebrovascular disease, with depressive
features).
This category is included to cover the clinical presentation of a neurocognitive disorder (NCD)
for which there is evidence that multiple medical conditions have played a probable role in the
development of the NCD. In addition to evidence indicative of the presence of multiple medical
conditions that are known to cause NCD (i.e., findings from the history and physical
examination, and laboratory findings), it may be helpful to refer to the diagnostic criteria and text
for the various medical etiologies (e.g., NCD due to Parkinson’s disease) for more information
on establishing the etiological connection for that particular medical condition.
Unspecified Neurocognitive Disorder
R41.9
This category applies to presentations in which symptoms characteristic of a
neurocognitive disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for any of the disorders in the neurocognitive disorders
diagnostic class. The unspecified neurocognitive disorder category is used in
situations in which the precise etiology cannot be determined with sufficient certainty
to make an etiological attribution.
Coding note: For unspecified major or mild neurocognitive disorder, code R41.9.
(Note: Do not use additional codes for any presumed etiological medical conditions.
“With behavioral disturbance” and “without behavioral disturbance” cannot be coded
but should still be recorded.)

# 18 - Personality Disorders

# Personality Disorders

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Personality Disorders
This chapter begins with a general definition of personality disorder that applies to each of
the 10 specific personality disorders. A personality disorder is an enduring pattern of inner
experience and behavior that deviates markedly from the norms and expectations of the
individual’s culture, is pervasive and inflexible, has an onset in adolescence or early adulthood,
is stable over time, and leads to distress or impairment.
With any ongoing review process, especially one of this complexity, different viewpoints
emerge, and an effort was made to accommodate them. Thus, personality disorders are included
in both Sections II and III. The material in Section II represents an update of text associated with
the same criteria found in DSM-5 (which were carried over from DSM-IV-TR), whereas Section
III includes the proposed model for personality disorder diagnosis and conceptualization
developed by the DSM-5 Personality and Personality Disorders Work Group. As this field
evolves, it is hoped that both versions will serve clinical practice and research initiatives,
respectively.
The following personality disorders are included in this chapter.
Paranoid personality disorder is a pattern of distrust and suspiciousness such that others’ motives are interpreted as
malevolent.
Schizoid personality disorder is a pattern of detachment from social relationships and a restricted range of emotional
expression.
Schizotypal personality disorder is a pattern of acute discomfort in close relationships, cognitive or perceptual distortions,
and eccentricities of behavior.
Antisocial personality disorder is a pattern of disregard for, and violation of, the rights of others, criminality, impulsivity,
and a failure to learn from experience.
Borderline personality disorder is a pattern of instability in interpersonal relationships, self-image, and affects, and
marked impulsivity.
Histrionic personality disorder is a pattern of excessive emotionality and attention seeking.
Narcissistic personality disorder is a pattern of grandiosity, need for admiration, and lack of empathy.
Avoidant personality disorder is a pattern of social inhibition, feelings of inadequacy, and hypersensitivity to negative
evaluation.
Dependent personality disorder is a pattern of submissive and clinging behavior related to an excessive need to be taken
care of.
Obsessive-compulsive personality disorder is a pattern of preoccupation with orderliness, perfectionism, and control.
Personality change due to another medical condition is a persistent personality disturbance that is judged to be the direct
pathophysiological consequence of another medical condition (e.g., frontal lobe lesion).
Other specified personality disorder is a category provided for two situations: 1) the individual’s personality pattern meets

734
the general criteria for a personality disorder, and traits of several different personality disorders are present, but the criteria
for any specific personality disorder are not met; or 2) the individual’s personality pattern meets the general criteria for a
personality disorder, but the individual is considered to have a personality disorder that is not included in the DSM-5
classification (e.g., passive-aggressive personality disorder). Unspecified personality disorder is for presentations in which
symptoms characteristic of a personality disorder are present but there is insufficient information to make a more specific
diagnosis.
The personality disorders are grouped into three clusters based on descriptive similarities.
Cluster A includes paranoid, schizoid, and schizotypal personality disorders. Individuals with
these disorders often appear odd or eccentric. Cluster B includes antisocial, borderline, histrionic,
and narcissistic personality disorders. Individuals with these disorders often appear dramatic,
emotional, or erratic. Cluster C includes avoidant, dependent, and obsessive-compulsive
personality disorders. Individuals with these disorders often appear anxious or fearful. It should
be noted that this clustering system, although useful in some research and educational situations,
has serious limitations and has not been consistently validated. For instance, two or more
disorders from different clusters, or traits from several of them, can often co-occur and vary in
intensity and pervasiveness.
A review of epidemiological studies from several countries found a median prevalence of
3.6% for disorders in Cluster A, 4.5% for Cluster B, 2.8% for Cluster C, and 10.5% for any
personality disorder. Prevalence appears to vary across countries and by ethnicity, raising
questions about true cross-cultural variation and about the impact of diverse definitions and
diagnostic instruments on prevalence assessments.
Dimensional Models for Personality Disorders
The diagnostic approach used in this manual represents the categorical perspective that
personality disorders are qualitatively distinct clinical syndromes. An alternative to the
categorical approach is the dimensional perspective that personality disorders represent
maladaptive variants of personality traits that merge imperceptibly into normality and into one
another. See Section III for a full description of a dimensional model for personality disorders.
The DSM-5 personality disorder clusters (i.e., odd-eccentric, dramatic-emotional, and anxiousfearful) may also be viewed as dimensions representing spectra of personality dysfunction on a
continuum with other mental disorders. The alternative dimensional models have much in
common and together appear to cover the important areas of personality dysfunction. Their
integration, clinical utility, and relationship with the personality disorder diagnostic categories
and various aspects of personality dysfunction continue to be under active investigation. This
includes research on whether the dimensional model can clarify the cross-cultural prevalence
variations seen with the categorical model.
General Personality Disorder

Criteria
A. An enduring pattern of inner experience and behavior that deviates markedly
from the expectations of the individual’s culture. This pattern is manifested in two
(or more) of the following areas:
1. Cognition (i.e., ways of perceiving and interpreting self, other people, and
events).
2. Affectivity (i.e., the range, intensity, lability, and appropriateness of emotional
response).
3. Interpersonal functioning.
4. Impulse control.
B. The enduring pattern is inflexible and pervasive across a broad range of
personal and social situations.
C. The enduring pattern leads to clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
D. The pattern is stable and of long duration, and its onset can be traced back at
least to adolescence or early adulthood.
E. The enduring pattern is not better explained as a manifestation or consequence
of another mental disorder.
F. The enduring pattern is not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication) or another medical condition
(e.g., head trauma).
Diagnostic Features
Personality traits are enduring patterns of perceiving, relating to, and thinking about the
environment and oneself that are exhibited in a wide range of social and personal contexts. Only
when personality traits are inflexible and maladaptive and cause significant functional
impairment or subjective distress do they constitute personality disorders. The essential feature
of a personality disorder is an enduring pattern of inner experience and behavior that deviates
markedly from the norms and expectations of the individual’s culture and is manifested in at
least two of the following areas: cognition, affectivity, interpersonal functioning, or impulse
control (Criterion A). This enduring pattern is inflexible and pervasive across a broad range of
personal and social situations (Criterion B) and leads to clinically significant distress or
impairment in social, occupational, or other important areas of functioning (Criterion C). The
pattern is stable and of long duration, and its onset can be traced back at least to adolescence or
early adulthood (Criterion D). The pattern is not better explained as a manifestation or
consequence of another mental disorder (Criterion E) and is not attributable to the physiological
effects of a substance (e.g., a drug of abuse, a medication, exposure to a toxin) or another

medical condition (e.g., head trauma) (Criterion F). Specific diagnostic criteria are also provided
for each of the personality disorders included in this chapter.
The diagnosis of personality disorders requires an evaluation of the individual’s long-term
patterns of functioning, and the particular personality features must be evident by early
adulthood. The personality traits that define these disorders must also be distinguished from
characteristics that emerge in response to specific situational stressors or more transient mental
states (e.g., bipolar, depressive, or anxiety disorders; substance intoxication). The clinician
should assess the stability of personality traits over time and across different situations. Although
a single interview with the individual is sometimes sufficient for making the diagnosis, it is often
necessary to conduct more than one interview and to space these over time. Assessment can also
be complicated by the fact that the characteristics that define a personality disorder may not be
considered problematic by the individual (i.e., the traits are often ego-syntonic). To help
overcome this difficulty, supplementary information from other informants may be helpful.
Development and Course
The features of a personality disorder usually become recognizable during adolescence or early
adult life. By definition, a personality disorder is an enduring pattern of thinking, feeling, and
behaving that is relatively stable over time. Some types of personality disorder (notably,
antisocial and borderline personality disorders) tend to become less evident or to remit with age,
whereas this appears to be less true for some other types (e.g., obsessive-compulsive and
schizotypal personality disorders).
Personality disorder categories may be applied with children or adolescents in those
relatively unusual instances in which the individual’s particular maladaptive personality traits
appear to be pervasive, persistent, and unlikely to be limited to a particular
developmental stage or attributable to another mental disorder. It should be recognized that
the traits of a personality disorder that appear in childhood will often not persist unchanged into
adult life. For a personality disorder to be diagnosed in an individual younger than 18 years, the
features must have been present for at least 1 year. The one exception to this is antisocial
personality disorder, which cannot be diagnosed in individuals younger than 18 years. Although,
by definition, a personality disorder requires an onset no later than early adulthood, individuals
may not come to clinical attention until relatively late in life. A personality disorder may be
exacerbated following the loss of significant supporting persons (e.g., a spouse) or previously
stabilizing social situations (e.g., a job). However, the development of a change in personality in
middle adulthood or later life warrants a thorough evaluation to determine the possible presence
of a personality change due to another medical condition or an unrecognized substance use
disorder.
Culture-Related Diagnostic Issues
Core aspects of personality like emotion regulation and interpersonal functioning are influenced
by culture, which also provides means of protection and assimilation and norms for acceptance
and denunciation of specific behaviors and personality traits. Judgments about personality

Other mental disorders and personality traits.
functioning must take into account the individual’s ethnic, cultural, and social background.
Personality disorders should not be confused with problems associated with acculturation
following migration or with the expression of habits, customs, or religious and political values
based on the individual’s cultural background or context. Behavioral patterns that appear to be
rigid and dysfunctional aspects of personality disorder may reflect instead adaptive responses to
cultural constraints. For example, reliance on an abusive relationship in a small community
where divorce is proscribed may not reflect pathological dependence; conscientious political
protest that puts friends and family members at risk with authorities or in conflict with legal
norms does not necessarily reflect pathological callousness. There are marked variations in the
recognition and diagnosis of personality disorders across cultural, ethnic, and racialized groups.
Accuracy of diagnosis can be enhanced by attention to culturally patterned conceptions of self
and attachment, assessment biases resulting from clinicians’ own cultural backgrounds or use of
diagnostic instruments that are not normed to the population being assessed, and the impact of
social determinants such as poverty, acculturative stress, racism, and discrimination on feelings,
cognitions, and behaviors. It is useful for the clinician, especially when evaluating someone from
a different background, to obtain additional information from informants who are familiar with
the person’s cultural background.
Sex- and Gender-Related Diagnostic Issues
Certain personality disorders (e.g., antisocial personality disorder) are diagnosed more frequently
in men. Others (e.g., borderline, histrionic, and dependent personality disorders) are diagnosed
more frequently in women; however, in the case of borderline personality disorder, this may be
due to higher help-seeking among women. Nonetheless, clinicians must be cautious not to
overdiagnose or underdiagnose certain personality disorders in women or in men because of
social stereotypes about typical gender roles and behaviors. There is currently insufficient
evidence on differences between cis- and transgender individuals with respect to the
epidemiology or clinical presentations of personality disorders to draw meaningful conclusions.
Differential Diagnosis
Many of the specific criteria for the personality
disorders describe features (e.g., suspiciousness, dependency, insensitivity) that are also
characteristic of episodes of other mental disorders. A personality disorder should
be diagnosed only when the defining characteristics appeared before early adulthood, are typical
of the individual’s long-term functioning, and do not occur exclusively during an episode of
another mental disorder. It may be particularly difficult (and not particularly useful) to
distinguish personality disorders from persistent mental disorders such as persistent depressive
disorder that have an early onset and an enduring, relatively stable course. Some personality
disorders may have a “spectrum” relationship to other mental disorders (e.g., schizotypal
personality disorder with schizophrenia; avoidant personality disorder with social anxiety
disorder) based on phenomenological or biological similarities or familial aggregation.
Personality disorders must be distinguished from personality traits that do not reach the

Psychotic disorders.
Anxiety and depressive disorders.
Posttraumatic stress disorder.
Substance use disorders.
Personality change due to another medical condition.
F60.0
threshold for a personality disorder. Personality traits are diagnosed as a personality disorder
only when they are inflexible, maladaptive, and persisting and cause significant functional
impairment or subjective distress.
For the three personality disorders that may be related to the psychotic
disorders (i.e., paranoid, schizoid, and schizotypal), there is an exclusion criterion stating that the
pattern of behavior must not have occurred exclusively during the course of schizophrenia, a
bipolar or depressive disorder with psychotic features, or another psychotic disorder. When an
individual has a persistent mental disorder (e.g., schizophrenia) that was preceded by a
preexisting personality disorder, the personality disorder should also be recorded, followed by
“premorbid” in parentheses.
The clinician must be cautious in diagnosing personality
disorders during an episode of a depressive disorder or an anxiety disorder, because these
conditions may have cross-sectional symptom features that mimic personality traits and may
make it more difficult to evaluate retrospectively the individual’s long-term patterns of
functioning.
When personality changes emerge and persist after an individual
has been exposed to extreme stress, a diagnosis of posttraumatic stress disorder should be
considered.
When an individual has a substance use disorder, it is important not to
make a personality disorder diagnosis based solely on behaviors that are consequences of
substance intoxication or withdrawal or that are associated with activities in the service of
sustaining substance use (e.g., antisocial behavior).
When enduring changes in personality arise as
a result of the physiological effects of another medical condition (e.g., brain tumor), a diagnosis
of personality change due to another medical condition should be considered.
Cluster A Personality Disorders
Paranoid Personality Disorder
Diagnostic Criteria
A. A pervasive distrust and suspiciousness of others such that their motives are
interpreted as malevolent, beginning by early adulthood and present in a variety
of contexts, as indicated by four (or more) of the following:
1. Suspects, without sufficient basis, that others are exploiting, harming, or
deceiving him or her.

2. Is preoccupied with unjustified doubts about the loyalty or trustworthiness of
friends or associates.
3. Is reluctant to confide in others because of unwarranted fear that the
information will be used maliciously against him or her.
4. Reads hidden demeaning or threatening meanings into benign remarks or
events.
5. Persistently bears grudges (i.e., is unforgiving of insults, injuries, or slights).
6. Perceives attacks on his or her character or reputation that are not apparent
to others and is quick to react angrily or to counterattack.
7. Has recurrent suspicions, without justification, regarding fidelity of spouse or
sexual partner.
B. Does not occur exclusively during the course of schizophrenia, a bipolar disorder
or depressive disorder with psychotic features, or another psychotic disorder and
is not attributable to the physiological effects of another medical condition.
Note: If criteria are met prior to the onset of schizophrenia, add “premorbid,” i.e.,
“paranoid personality disorder (premorbid).”
Diagnostic Features
The essential feature of paranoid personality disorder is a pattern of pervasive distrust and
suspiciousness of others such that their motives are interpreted as malevolent. This pattern begins
by early adulthood and is present in a variety of contexts.
Individuals with this disorder assume that other people will exploit, harm, or deceive them,
even if no evidence exists to support this expectation (Criterion A1). They suspect on the basis of
little or no evidence that others are plotting against them and may attack them suddenly, at any
time and without reason. They often feel that they have been deeply and irreversibly injured by
another person or persons even when there is no objective evidence for this. They are
preoccupied with unjustified doubts about the loyalty or trustworthiness of their friends and
associates, whose actions are minutely scrutinized for evidence of hostile intentions (Criterion
A2). Any perceived deviation from trustworthiness or loyalty serves to support their underlying
assumptions. They are so amazed when a friend or associate shows loyalty that they cannot trust
or believe it. If they get into trouble, they expect that friends and associates will either attack or
ignore them.
Individuals with paranoid personality disorder are reluctant to confide in or become close to
others because they fear that the information they share will be used against them (Criterion A3).
They may refuse to answer personal questions, saying that the information is “nobody’s
business.” They read hidden meanings that are demeaning and threatening into benign remarks
or events (Criterion A4). For example, an individual with this disorder may misinterpret an
honest mistake by a store clerk as a deliberate attempt to shortchange, or view a casual humorous
remark by a coworker as a serious character attack. Compliments are often misinterpreted (e.g., a
compliment on a new acquisition is misinterpreted as a criticism for selfishness; a compliment on
an accomplishment is misinterpreted as an attempt to coerce more and better performance). They
may view an offer of help as a criticism that they are not doing well enough on their own.

Individuals with this disorder persistently bear grudges and are unwilling to forgive the
insults, injuries, or slights that they think they have received (Criterion A5). Minor slights arouse
major hostility, and the hostile feelings persist for a long time. Because they are constantly
vigilant to the harmful intentions of others, they very often feel that their character or reputation
has been attacked or that they have been slighted in some other way. They are quick to
counterattack and react with anger to perceived insults (Criterion A6). Individuals with this
disorder may be pathologically jealous, often suspecting that their spouse
or sexual partner is unfaithful without any adequate justification (Criterion A7). They may
gather trivial and circumstantial “evidence” to support their jealous beliefs. They want to
maintain complete control of intimate relationships to avoid being betrayed and may constantly
question and challenge the whereabouts, actions, intentions, and fidelity of their spouse or
partner.
Paranoid personality disorder should not be diagnosed if the pattern of behavior occurs
exclusively during the course of schizophrenia, a bipolar disorder or depressive disorder with
psychotic features, or another psychotic disorder, or if it is attributable to the physiological
effects of a neurological (e.g., temporal lobe epilepsy) or another medical condition (Criterion
B).
Associated Features
Individuals with paranoid personality disorder are generally difficult to get along with and often
have problems with close relationships. Their excessive suspiciousness and hostility may be
expressed in overt argumentativeness, in recurrent complaining, or by hostile aloofness. They
display a labile range of affect, with hostile, stubborn, and sarcastic expressions predominating.
Their combative and suspicious nature may elicit a hostile response in others, which then serves
to confirm their original expectations.
Because individuals with paranoid personality disorder lack trust in others, they need to have
a high degree of control over those around them. They are often rigid, critical of others, and
unable to collaborate, although they have great difficulty accepting criticism themselves. They
may blame others for their own shortcomings. Because of their quickness to counterattack in
response to the threats they perceive around them, they may be litigious and frequently become
involved in legal disputes. Individuals with this disorder seek to confirm their preconceived
negative notions regarding people or situations they encounter, attributing malevolent
motivations to others that are projections of their own fears. They may exhibit thinly hidden,
unrealistic grandiose fantasies, are often attuned to issues of power and rank, and tend to develop
negative stereotypes of others, particularly those from population groups distinct from their own.
Attracted by simplistic formulations of the world, they are often wary of ambiguous situations.
They may be perceived as “fanatics” and form tightly knit “cults” or groups with others who
share their paranoid belief systems.
Prevalence
The estimated prevalence of paranoid personality based on a probability subsample from Part II

Environmental.
Genetic and physiological.
of the National Comorbidity Survey Replication was 2.3%. The prevalence of paranoid
personality disorder in the National Epidemiologic Survey on Alcohol and Related Conditions
was 4.4%. A review of six epidemiological studies (four in the United States) found a median
prevalence of 3.2%. In forensic settings, the estimated prevalence may be as high as 23%.
Development and Course
Paranoid personality disorder may be first apparent in childhood and adolescence with
solitariness, poor peer relationships, social anxiety, underachievement in school, and
interpersonal hypersensitivity. Adolescent onset of paranoid personality disorder is associated
with a prior history of childhood maltreatment, externalizing symptoms, bullying of peers, and
adult appearance of interpersonal aggression.
Risk and Prognostic Factors
Exposure to social stressors such as socioeconomic inequality, marginalization,
and racism is associated with decreased trust, which in some cases is adaptive.
The combination of social stress and childhood maltreatment accounts for the increased
prevalence of paranoid symptoms in social groups facing racial discrimination. Both longitudinal
and cross-sectional studies confirm that childhood trauma is a risk factor for paranoid personality
disorder.
There is some evidence for an increased prevalence of paranoid
personality disorder in relatives of probands with schizophrenia and for a more specific familial
relationship with delusional disorder, persecutory type.
Culture-Related Diagnostic Issues
Some behaviors that are influenced by sociocultural contexts or specific life circumstances may
be erroneously labeled paranoid and may even be reinforced by the process of clinical
evaluation. Migrants, members of socially oppressed ethnic and racialized populations, and other
groups facing social adversity, racism, and discrimination may display guarded or defensive
behaviors because of unfamiliarity (e.g., language barriers or lack of knowledge of rules and
regulations) or in response to the neglect, hostility, or indifference of the majority society. Some
cultural groups develop low generalized trust, especially of outgroup members, which may lead
to behaviors that can be misjudged as paranoid. These include guardedness, limited outward
emotionality, cognitive rigidity, social distance, and hostility or defensiveness in situations
experienced as unfair or discriminatory. These behaviors can, in turn, generate anger and
frustration in others, including clinicians, thus setting up a vicious cycle of mutual mistrust,
which should not be confused with paranoid traits or paranoid personality disorder.
Sex- and Gender-Related Diagnostic Issues
While paranoid personality disorder was found to be more common in men than in women in a
meta-analysis relying on clinical and community samples, the National Epidemiologic Survey on

Other mental disorders with psychotic symptoms.
Personality change due to another medical condition.
Substance use disorders.
Paranoid traits associated with physical handicaps.
Other personality disorders and personality traits.
Alcohol and Related Conditions found it to be more common in women.
Differential Diagnosis
Paranoid personality disorder can be distinguished
from delusional disorder, persecutory type; schizophrenia; and a bipolar or depressive disorder
with psychotic features because these disorders are all characterized by a period of persistent
psychotic symptoms (e.g., delusions and hallucinations). For an additional diagnosis of paranoid
personality disorder to be given, the personality disorder must have been present before the onset
of psychotic symptoms and must persist when the psychotic symptoms are in remission. When
an individual has another persistent mental disorder (e.g., schizophrenia) that was preceded by
paranoid personality disorder, paranoid personality disorder should also be recorded, followed by
“premorbid” in parentheses.
Paranoid 
personality 
disorder 
must 
be
distinguished from personality change due to another medical condition, in which the traits that
emerge are a direct physiological consequence of another medical condition.
Paranoid personality disorder must be distinguished from symptoms that
may develop in association with persistent substance use.
The disorder must also be distinguished from
paranoid traits associated with the development of physical handicaps (e.g., a hearing
impairment).
Other personality disorders may be confused with
paranoid personality disorder because they have certain features in common. It is therefore
important to distinguish among these disorders based on differences in their characteristic
features. However, if an individual has personality features that meet criteria for one or more
personality disorders in addition to paranoid personality disorder, all can be diagnosed. Paranoid
personality disorder and schizotypal personality disorder share the traits of suspiciousness,
interpersonal aloofness, and paranoid ideation, but schizotypal personality disorder also includes
symptoms such as magical thinking, unusual perceptual experiences, and odd thinking and
speech. Individuals with behaviors that meet criteria for schizoid personality disorder are often
perceived as strange, eccentric, cold, and aloof, but they do not usually have prominent paranoid
ideation. The tendency of individuals with paranoid personality disorder to react to minor stimuli
with anger is also seen in borderline and histrionic personality disorders. However, these
disorders are not necessarily associated with pervasive suspiciousness, and borderline personality
disorder exhibits higher levels of impulsivity and self-destructive behavior. People with avoidant
personality disorder may also be reluctant to confide in others, but more from fear of being
embarrassed or found inadequate than from fear of others’ malicious intent. Although antisocial
behavior may be present in some individuals with paranoid personality disorder, it is not usually
motivated by a desire for personal gain or to exploit others as in antisocial personality disorder,
but rather is more often attributable to a desire for revenge. Individuals with narcissistic
personality disorder may occasionally display suspiciousness, social withdrawal, or alienation,
but this derives primarily from fears of having their imperfections or flaws revealed.

F60.1
Paranoid traits may be adaptive, particularly in threatening environments. Paranoid
personality disorder should be diagnosed only when these traits are inflexible, maladaptive, and
persisting and cause significant functional impairment or subjective distress.
Comorbidity
Particularly in response to stress, individuals with this disorder may experience very brief
psychotic episodes (lasting minutes to hours). In some instances, paranoid personality disorder
may appear as the premorbid antecedent of delusional disorder or schizophrenia. Individuals
with paranoid personality disorder may develop major depressive disorder and may be at
increased risk for agoraphobia and obsessive-compulsive disorder. Alcohol and other substance
use disorders frequently occur. The most common co-occurring personality disorders appear to
be schizotypal, schizoid, narcissistic, avoidant, and borderline.
Schizoid Personality Disorder
Diagnostic Criteria
A. A pervasive pattern of detachment from social relationships and a restricted
range of expression of emotions in interpersonal settings, beginning by early
adulthood and present in a variety of contexts, as indicated by four (or more) of
the following:
1. Neither desires nor enjoys close relationships, including being part of a
family.
2. Almost always chooses solitary activities.
3. Has little, if any, interest in having sexual experiences with another person.
4. Takes pleasure in few, if any, activities.
5. Lacks close friends or confidants other than first-degree relatives.
6. Appears indifferent to the praise or criticism of others.
7. Shows emotional coldness, detachment, or flattened affectivity.
B. Does not occur exclusively during the course of schizophrenia, a bipolar disorder
or depressive disorder with psychotic features, another psychotic disorder, or
autism spectrum disorder and is not attributable to the physiological effects of
another medical condition.
Note: If criteria are met prior to the onset of schizophrenia, add “premorbid,” i.e.,
“schizoid personality disorder (premorbid).”
Diagnostic Features

The essential feature of schizoid personality disorder is a pervasive pattern of detachment from
social relationships and a restricted range of expression of emotions in interpersonal settings.
This pattern begins by early adulthood and is present in a variety of contexts.
Individuals with schizoid personality disorder appear to lack a desire for intimacy, seem
indifferent to opportunities to develop close relationships, and do not seem to derive much
satisfaction from being part of a family or other social group (Criterion A1). They prefer
spending time by themselves, rather than being with other people. They often appear to be
socially isolated or “loners” and almost always choose solitary activities or hobbies that do not
include interaction with others (Criterion A2). They prefer mechanical or abstract tasks, such as
computer or mathematical games. They may have very little interest in having sexual
experiences with another person (Criterion A3) and take pleasure in few, if any, activities
(Criterion A4). There is usually a reduced experience of pleasure from sensory, bodily, or
interpersonal experiences, such as walking on a beach at sunset or having sex. These individuals
have no close friends or confidants, except possibly a first-degree relative (Criterion A5).
Individuals with schizoid personality disorder often seem indifferent to the approval or
criticism of others and do not appear to be bothered by what others may think of them (Criterion
A6). They may be oblivious to the normal subtleties of social interaction and often do not
respond appropriately to social cues so that they seem socially inept or superficial and selfabsorbed. They usually display a “bland” exterior without visible emotional reactivity and rarely
reciprocate gestures or facial expressions, such as smiles or nods (Criterion A7). They claim that
they rarely experience strong emotions such as anger and joy. They often display a constricted
affect and appear cold and aloof. However, in those very unusual circumstances in which these
individuals become at least temporarily comfortable in revealing themselves, they may
acknowledge having painful feelings, particularly related to social interactions.
Schizoid personality disorder should not be diagnosed if the pattern of behavior occurs
exclusively during the course of schizophrenia, a bipolar or depressive disorder with psychotic
features, another psychotic disorder, or autism spectrum disorder, or if it is attributable to the
physiological effects of a neurological (e.g., temporal lobe epilepsy) or another medical
condition (Criterion B).
Associated Features
Individuals with schizoid personality disorder may have particular difficulty expressing anger,
even in response to direct provocation, which contributes to the impression that they lack
emotion. Their lives sometimes seem directionless, and they may appear to “drift” in their goals.
Such individuals often react passively to adverse circumstances and have difficulty responding
appropriately to important life events. Because of their lack of social skills and lack of desire for
sexual experiences, individuals with this disorder have few friendships, date infrequently, and
often do not marry. Occupational functioning may be impaired, particularly if interpersonal
involvement is required, but individuals with this disorder may do well when they work under
conditions of social isolation.
Prevalence

Genetic and physiological.
Other mental disorders with psychotic symptoms.
Autism spectrum disorder.
Personality change due to another medical condition.
Schizoid personality disorder is uncommon in clinical settings. The estimated prevalence of
schizoid personality disorder based on a probability subsample from Part II of the National
Comorbidity Survey Replication was 4.9%. The prevalence of schizoid personality disorder in
the National Epidemiologic Survey on Alcohol and Related Conditions was 3.1%. A review of
six epidemiological studies (four in the United States) found a median prevalence of 1.3%.
Development and Course
Schizoid personality disorder may be first apparent in childhood and adolescence with
solitariness, poor peer relationships, and underachievement in school, which mark these children
or adolescents as different and make them subject to teasing.
Risk and Prognostic Factors
Schizoid personality disorder may have increased prevalence in the
relatives of individuals with schizophrenia or schizotypal personality disorder.
Culture-Related Diagnostic Issues
Individuals from a variety of cultural backgrounds sometimes exhibit defensive behaviors and
interpersonal styles that may be erroneously labeled as “schizoid.” For example, those who have
moved from rural to metropolitan environments may react with “emotional freezing” that may
last for several months and manifest as solitary activities, constricted affect, and other deficits in
communication. Immigrants from other countries are sometimes mistakenly perceived as cold,
hostile, or indifferent, which may be a response to social ostracism from the host society.
Sex- and Gender-Related Diagnostic Issues
While some research suggests that schizoid personality disorder may be more common in men,
other research suggests that there is no gender difference in prevalence.
Differential Diagnosis
Schizoid personality disorder can be distinguished
from delusional disorder, schizophrenia, and a bipolar or depressive disorder with psychotic
features because these disorders are all characterized by a period of persistent psychotic
symptoms (e.g., delusions and hallucinations). To give an additional diagnosis of schizoid
personality disorder, the personality disorder must have been present before the onset of
psychotic symptoms and must persist when the psychotic symptoms are in remission. When an
individual has a persistent psychotic disorder (e.g., schizophrenia) that was preceded by schizoid
personality disorder, schizoid personality disorder should also be recorded, followed by
“premorbid” in parentheses.
There may be great difficulty differentiating individuals with schizoid
personality disorder from individuals with autism spectrum disorder, particularly with milder
forms of either disorder, as both include a seeming indifference to companionship with others.
However, autism spectrum disorder may be differentiated by stereotyped behaviors and interests.
Schizoid 
personality 
disorder 
must 
be

Substance use disorders.
Other personality disorders and personality traits.
F21
distinguished from personality change due to another medical condition, in which the traits that
emerge are a direct physiological consequence of another medical condition.
Schizoid personality disorder must also be distinguished from symptoms
that may develop in association with persistent substance use.
Other personality disorders may be confused with
schizoid personality disorder because they have certain features in common. It is, therefore,
important to distinguish among these disorders based on differences in their characteristic
features. However, if an individual has personality features that meet criteria for one or more
personality disorders in addition to schizoid personality disorder, all can be diagnosed. Although
characteristics of social isolation and restricted affectivity are common to schizoid, schizotypal,
and paranoid personality disorders, schizoid personality disorder can be distinguished from
schizotypal personality disorder by the lack of cognitive and perceptual distortions and from
paranoid personality disorder by the lack of suspiciousness and paranoid ideation. The social
isolation of schizoid personality disorder can be distinguished from that of avoidant personality
disorder, which is attributable to fear of being embarrassed or found inadequate and excessive
anticipation of rejection. In contrast, people with schizoid personality disorder have a more
pervasive detachment and limited desire for social intimacy. Individuals with obsessivecompulsive personality disorder may also show an apparent social detachment stemming from
devotion to work and discomfort with emotions, but they do have an underlying capacity for
intimacy.
Individuals who are “loners” or quite introverted may display personality traits that might be
considered schizoid, consistent with the broader conceptualization of schizoid personality
disorder as a disorder defined by pathological introversion/detachment. Only when these traits
are inflexible and maladaptive and cause significant functional impairment or subjective distress
do they constitute schizoid personality disorder.
Comorbidity
Particularly in response to stress, individuals with this disorder may experience very brief
psychotic episodes (lasting minutes to hours). In some instances, schizoid personality disorder
may appear as the premorbid antecedent of delusional disorder or schizophrenia. Individuals
with this disorder may sometimes develop major depressive disorder. Schizoid personality
disorder most often co-occurs with schizotypal, paranoid, and avoidant personality disorders.
Schizotypal Personality Disorder
Diagnostic Criteria
A. A pervasive pattern of social and interpersonal deficits marked by acute
discomfort with, and reduced capacity for, close relationships as well as by

cognitive or perceptual distortions and eccentricities of behavior, beginning by
early adulthood and present in a variety of contexts, as indicated by five (or
more) of the following:
1. Ideas of reference (excluding delusions of reference).
2. Odd beliefs or magical thinking that influences behavior and is inconsistent
with subcultural norms (e.g., superstitiousness, belief in clairvoyance,
telepathy, or “sixth sense”; in children and adolescents, bizarre fantasies or
preoccupations).
3. Unusual perceptual experiences, including bodily illusions.
4. Odd thinking and speech (e.g., vague, circumstantial, metaphorical,
overelaborate, or stereotyped).
5. Suspiciousness or paranoid ideation.
6. Inappropriate or constricted affect.
7. Behavior or appearance that is odd, eccentric, or peculiar.
8. Lack of close friends or confidants other than first-degree relatives.
9. Excessive social anxiety that does not diminish with familiarity and tends to
be associated with paranoid fears rather than negative judgments about self.
B. Does not occur exclusively during the course of schizophrenia, a bipolar disorder
or depressive disorder with psychotic features, another psychotic disorder, or
autism spectrum disorder.
Note: If criteria are met prior to the onset of schizophrenia, add “premorbid,” e.g.,
“schizotypal personality disorder (premorbid).”
Diagnostic Features
The essential feature of schizotypal personality disorder is a pervasive pattern of social and
interpersonal deficits marked by acute discomfort with, and reduced capacity for, close
relationships as well as by cognitive or perceptual distortions and eccentricities of behavior. This
pattern begins by early adulthood and is present in a variety of contexts.
Individuals with schizotypal personality disorder often have ideas of reference (i.e., incorrect
interpretations of casual incidents and external events as having a particular and unusual
meaning specifically for the person) (Criterion A1). These should be distinguished from
delusions of reference, in which the beliefs are held with delusional conviction. These
individuals may be superstitious or preoccupied with paranormal phenomena that are outside the
norms of their subculture (Criterion A2). They may feel that they have special powers to sense
events before they happen or to read others’ thoughts. They may believe that they have magical
control over others, which can be implemented directly (e.g., believing that their spouse’s taking
the dog out for a walk is the direct result of thinking an hour earlier it should be done) or
indirectly through compliance with magical rituals (e.g., walking past a specific object three
times to avoid a certain harmful outcome). Perceptual alterations may be present (e.g., sensing

that another person is present or hearing a voice murmuring their name) (Criterion A3). Their
speech may include unusual or idiosyncratic phrasing and construction. It is often loose,
digressive, or vague, but without actual derailment or incoherence (Criterion A4). Responses can
be either overly concrete or overly abstract, and words or concepts are sometimes applied in
unusual ways (e.g., the individual may state that he or she was not “talkable” at work).
Individuals with this disorder are often suspicious and may have paranoid ideation (e.g.,
believing their colleagues at work are intent on undermining their reputation with the boss)
(Criterion A5). They are usually not able to negotiate the full range of affects and interpersonal
cuing required for successful relationships and thus often appear to interact with others in an
inappropriate, stiff, or constricted fashion (Criterion A6). These individuals are often considered
to be odd or eccentric because of unusual mannerisms, an often unkempt manner of dress that
does not quite “fit together,” and inattention to the usual social conventions (e.g., the individual
may avoid eye contact, wear clothes that are ink stained and ill-fitting, and be unable to join in
the give-and-take banter of co-workers) (Criterion A7).
Individuals with schizotypal personality disorder experience interpersonal relatedness as
problematic and are uncomfortable relating to other people. Although they may express
unhappiness about their lack of relationships, their behavior suggests a decreased desire for
intimate contacts. As a result, they usually have no or few close friends or confidants other than a
first-degree relative (Criterion A8). They are anxious in social situations, particularly those
involving unfamiliar people (Criterion A9). They will interact with other individuals when they
have to but prefer to keep to themselves because they feel that they are different and just do not
“fit in.” Their social anxiety does not easily abate, even when they spend more time in the setting
or become more familiar with the other people, because their anxiety tends to be associated with
suspiciousness regarding others’ motivations. For example, when attending a dinner party, the
individual with schizotypal
personality disorder will not become more relaxed as time goes on, but rather may become
increasingly tense and suspicious.
Schizotypal personality disorder should not be diagnosed if the pattern of behavior occurs
exclusively during the course of schizophrenia, a bipolar or depressive disorder with psychotic
features, another psychotic disorder, or autism spectrum disorder (Criterion B).
Associated Features
Individuals with schizotypal personality disorder often seek treatment for the associated
symptoms of anxiety or depression rather than for the personality disorder features per se.
Prevalence
The estimated prevalence of schizotypal personality disorder based on a probability subsample
from Part II of the National Comorbidity Survey Replication was 3.3%.The prevalence of
schizotypal personality disorder in the National Epidemiologic Survey on Alcohol and Related
Conditions data was 3.9%. A review of five epidemiological studies (three in the United States)
found a median prevalence of 0.6%.

Genetic and physiological.
Other mental disorders with psychotic symptoms.
Development and Course
Schizotypal personality disorder has a relatively stable course, with only a small proportion of
individuals going on to develop schizophrenia or another psychotic disorder. Schizotypal
personality disorder may be first apparent in childhood and adolescence with solitariness, poor
peer relationships, social anxiety, underachievement in school, hypersensitivity, peculiar
thoughts and language, and bizarre fantasies. These children may appear “odd” or “eccentric”
and attract teasing.
Risk and Prognostic Factors
Schizotypal personality disorder appears to aggregate familially and is
more prevalent among the first-degree biological relatives of individuals with schizophrenia than
among the general population. There may also be a modest increase in schizophrenia and other
psychotic disorders in the relatives of probands with schizotypal personality disorder. Twin
studies indicate highly stable genetic factors and rather transient environmental factors for an
increased risk for the schizotypal syndrome, and genetic risk variants for schizophrenia may be
linked to schizotypal personality disorder. Neuroimaging studies detect group-level differences
in the size and function of specific brain regions in individuals with schizotypal personality
disorder in comparison with healthy persons, individuals with schizophrenia, and individuals
with other personality disorders.
Culture-Related Diagnostic Issues
Cognitive and perceptual distortions must be evaluated in the context of the individual’s cultural
milieu. Pervasive culturally determined characteristics, particularly those regarding supernatural
and religious beliefs and practices (life beyond death, speaking in tongues, voodoo, shamanism,
mind reading, sixth sense, evil eye, magical beliefs related to health and illness), can appear to be
schizotypal to the uninformed clinician. Thus, observed cross-national and cross-ethnic
variations in the prevalence and expression of schizotypal traits may be a true epidemiological
finding or one due to differences in the cultural acceptance of these experiences.
Sex- and Gender-Related Diagnostic Issues
Schizotypal personality disorder appears to be slightly more common in men than in women.
Differential Diagnosis
Schizotypal 
personality 
disorder 
can 
be
distinguished from delusional disorder, schizophrenia, and a bipolar or depressive disorder with
psychotic features because these disorders are all characterized by a period of persistent
psychotic symptoms (e.g., delusions and hallucinations). To give an additional diagnosis of
schizotypal personality disorder, the personality disorder must have been present before the onset
of psychotic symptoms and persist when the psychotic symptoms are in remission. When an
individual has a persistent psychotic disorder (e.g., schizophrenia) that was preceded by
schizotypal personality disorder, schizotypal personality disorder should also be recorded,

Neurodevelopmental disorders.
Personality change due to another medical condition.
Substance use disorders.
Other personality disorders and personality traits.
followed by “premorbid” in parentheses.
There may be great difficulty differentiating children with
schizotypal personality disorder from the heterogeneous group of solitary, odd children whose
behavior is characterized by marked social isolation, eccentricity, or peculiarities of language
and whose diagnoses would probably include milder forms of autism spectrum disorder or
language communication disorders. Communication disorders may be differentiated by the
primacy and severity of the disorder in language and by the characteristic features of impaired
language found in a specialized language assessment. Milder forms of autism spectrum disorder
are differentiated by the even greater lack of social awareness and emotional reciprocity and
stereotyped behaviors and interests.
Schizotypal personality disorder must be
distinguished from personality change due to another medical condition, in which the traits that
emerge are a direct physiological consequence of another medical condition.
Schizotypal personality disorder must also be distinguished from
symptoms that may develop in association with persistent substance use.
Other personality disorders may be confused with
schizotypal personality disorder because they have certain features in common. It is, therefore,
important to distinguish among these disorders based on differences in their characteristic
features. However, if an individual has personality features that meet criteria for one or more
personality disorders in addition to schizotypal personality disorder, all can be diagnosed.
Although paranoid and schizoid personality disorders may also be characterized by social
detachment and restricted affect, schizotypal personality disorder can be distinguished from these
two diagnoses by the presence of cognitive or perceptual distortions and marked eccentricity or
oddness. Close relationships are limited in both schizotypal personality disorder and avoidant
personality disorder; however, in avoidant personality disorder an active desire for relationships
is constrained by a fear of rejection, whereas in schizotypal personality disorder there is a lack of
desire for relationships and persistent detachment. Individuals with narcissistic personality
disorder may also display suspiciousness, social withdrawal, or alienation, but in narcissistic
personality disorder these qualities derive primarily from fears of having imperfections or flaws
revealed. Individuals with borderline personality disorder may also have transient, psychotic-like
symptoms, but these are usually more closely related to affective shifts in response to stress (e.g.,
intense anger, anxiety, disappointment) and are usually more dissociative (e.g., derealization,
depersonalization). In contrast, individuals with schizotypal personality disorder are more likely
to have enduring psychotic-like symptoms that may worsen under stress but are less likely to be
invariably associated with pronounced affective symptoms. Although social isolation may occur
in borderline personality disorder, it is usually secondary to repeated interpersonal failures due to
angry outbursts and frequent mood shifts, rather than a result of a persistent lack of social
contacts and desire for intimacy. Furthermore, individuals with schizotypal personality disorder
do not usually demonstrate the impulsive or manipulative behaviors of the individual with
borderline personality disorder. However, there is a high rate of co-occurrence between the two
disorders, so that making such distinctions is not always feasible. Schizotypal features during

F60.2
adolescence may be reflective of transient emotional turmoil rather than an enduring personality
disorder.
Comorbidity
Particularly in response to stress, individuals with this disorder may experience transient
psychotic episodes (lasting minutes to hours), although they usually are insufficient in duration
to warrant an additional diagnosis such as brief psychotic disorder or schizophreniform disorder.
In some cases, clinically significant psychotic symptoms may develop that meet criteria for brief
psychotic disorder, schizophreniform disorder, delusional disorder, or schizophrenia. There is
considerable co-occurrence with schizoid, paranoid, avoidant, and borderline personality
disorders.
Cluster B Personality Disorders
Antisocial Personality Disorder
Diagnostic Criteria
A. A pervasive pattern of disregard for and violation of the rights of others,
occurring since age 15 years, as indicated by three (or more) of the following:
1. Failure to conform to social norms with respect to lawful behaviors, as
indicated by repeatedly performing acts that are grounds for arrest.
2. Deceitfulness, as indicated by repeated lying, use of aliases, or conning
others for personal profit or pleasure.
3. Impulsivity or failure to plan ahead.
4. Irritability and aggressiveness, as indicated by repeated physical fights or
assaults.
5. Reckless disregard for safety of self or others.
6. Consistent irresponsibility, as indicated by repeated failure to sustain
consistent work behavior or honor financial obligations.
7. Lack of remorse, as indicated by being indifferent to or rationalizing having
hurt, mistreated, or stolen from another.
B. The individual is at least age 18 years.
C. There is evidence of conduct disorder with onset before age 15 years.
D. The occurrence of antisocial behavior is not exclusively during the course of
schizophrenia or bipolar disorder.
Diagnostic Features

The essential feature of antisocial personality disorder is a pervasive pattern of disregard for, and
violation of, the rights of others that begins in childhood or early adolescence and continues into
adulthood. This pattern has also been referred to as psychopathy, sociopathy, or dyssocial
personality disorder. Because deceit and manipulation are central features of antisocial
personality disorder, it may be especially helpful to integrate information acquired from
systematic clinical assessment with information collected from collateral sources.
For this diagnosis to be given, the individual must be at least age 18 years (Criterion B) and
must have had evidence of conduct disorder with onset before age 15 years (Criterion C).
Conduct disorder involves a repetitive and persistent pattern of behavior in which the basic rights
of others or major age-appropriate societal norms or rules are violated. The specific behaviors
characteristic of conduct disorder fall into one of four categories: aggression to people and
animals, destruction of property, deceitfulness or theft, or serious violation of rules.
The pattern of antisocial behavior continues into adulthood. Individuals with antisocial
personality disorder fail to conform to social norms with respect to lawful behavior (Criterion
A1). They may repeatedly perform acts that are grounds for arrest (whether they are arrested or
not), such as destroying property, harassing others, stealing, or pursuing illegal occupations.
Persons with this disorder disregard the wishes, rights, or feelings of others. They are frequently
deceitful and manipulative in order to gain personal profit or pleasure (e.g., to obtain money, sex,
or power) (Criterion A2). They may repeatedly lie, use an alias, con others, or malinger. A
pattern of impulsivity may be manifested by a failure to plan ahead (Criterion A3). Decisions are
made on the spur of the moment, without forethought and without consideration for the
consequences to self or others; this may lead to sudden changes of jobs, residences, or
relationships. Individuals with antisocial personality disorder tend to be irritable and aggressive
and may repeatedly get into physical fights or commit acts of physical assault (including spouse
beating or child beating) (Criterion A4). (Aggressive acts that are required to defend oneself or
someone else are not considered to be evidence for this item.) These individuals also display a
reckless disregard for the safety of themselves or others (Criterion A5). This may be evidenced
in their driving behavior (i.e., recurrent speeding, driving while intoxicated, multiple accidents).
They may engage in sexual behavior or substance use that has a high risk for harmful
consequences. They may neglect or fail to care for a child in a way that puts the child in danger.
Individuals with antisocial personality disorder also tend to be consistently and extremely
irresponsible (Criterion A6). Irresponsible work behavior may be indicated by significant periods
of unemployment despite available job opportunities, or by abandonment of several jobs without
a realistic plan for getting another job. There may also be a pattern of repeated absences from
work that are not explained by illness either in themselves or in their family. Financial
irresponsibility is indicated by acts such as defaulting on debts, failing to provide child support,
or failing to support other dependents on a regular basis. Individuals with antisocial personality
disorder show little remorse for the consequences of their acts (Criterion A7). They may be
indifferent to, or provide a superficial rationalization for, having hurt, mistreated, or stolen from
someone (e.g., “life’s unfair,” “losers deserve to lose”). These individuals may blame the victims
for being foolish, helpless, or deserving their fate (e.g., “he had it coming anyway”); they may
minimize the harmful consequences of their actions; or they may simply indicate complete

indifference. They generally fail to compensate or make amends for their behavior. They may
believe that everyone is out to “help number one” and that one should stop at nothing to avoid
being pushed around.
The antisocial behavior must not occur exclusively during the course of schizophrenia or
bipolar disorder (Criterion D).
Associated Features
Individuals with antisocial personality disorder frequently lack empathy and tend to be callous,
cynical, and contemptuous of the feelings, rights, and sufferings of others. They may have an
inflated and arrogant self-appraisal (e.g., feel that ordinary work is beneath them or lack a
realistic concern about their current problems or their future) and may be excessively
opinionated, self-assured, or cocky. Some antisocial individuals may display a glib, superficial
charm and can be quite voluble and verbally facile (e.g., using technical terms or jargon that
might impress someone who is unfamiliar with the topic). Lack of
empathy, inflated self-appraisal, and superficial charm are features that have been commonly
included in traditional conceptions of psychopathy that may be particularly distinguishing of the
disorder and more predictive of recidivism in prison or forensic settings, where criminal,
delinquent, or aggressive acts are likely to be nonspecific. These individuals may also be
irresponsible and exploitative in their sexual relationships. They may have a history of many
sexual partners and may never have sustained a monogamous relationship. They may be
irresponsible as parents, as evidenced by malnutrition of a child, an illness in the child resulting
from a lack of minimal hygiene, a child’s dependence on neighbors or nonresident relatives for
food or shelter, a failure to arrange for a caretaker for a young child when the individual is away
from home, or repeated squandering of money required for household necessities. These
individuals may receive dishonorable discharges from the armed services, may fail to be selfsupporting, may become impoverished or even homeless, or may spend many years in penal
institutions. Individuals with antisocial personality disorder are more likely than individuals in
the general population to die prematurely from natural causes and suicide.
Prevalence
The estimated prevalence of antisocial personality disorder based on a probability subsample
from Part II of the National Comorbidity Survey Replication was 0.6%.The prevalence of
antisocial personality disorder in the National Epidemiologic Survey on Alcohol and Related
Conditions data was 3.6%. A review of seven epidemiological studies (six in the United States)
found a median prevalence of 3.6%. The highest prevalence of antisocial personality disorder
(greater than 70%) is among samples of men with the most severe alcohol use disorders and from
substance abuse clinics, prisons, or other forensic settings. Lifetime prevalence appears to be
similar across non-Latinx White and Black individuals and lower in Latinx and Asian
Americans. Prevalence may be higher in samples affected by adverse socioeconomic (i.e.,
poverty) or sociocultural (i.e., migration) factors.

Environmental.
Genetic and physiological.
Development and Course
Antisocial personality disorder has a chronic course but may become less evident or remit as the
individual grows older, often by age 40. Although this remission tends to be particularly evident
with respect to engaging in criminal behavior, there is likely to be a decrease in the full spectrum
of antisocial behaviors and substance use. By definition, antisocial personality cannot be
diagnosed before age 18 years.
Risk and Prognostic Factors
Child abuse or neglect, unstable or erratic parenting, or inconsistent parental
discipline may increase the likelihood that conduct disorder will evolve into antisocial
personality disorder.
Antisocial personality disorder is more common among the first-degree
biological relatives of those with the disorder than in the general population. Biological relatives
of individuals with this disorder are also at increased risk for somatization disorder (a diagnosis
that was replaced in DSM-5 with somatic symptom disorder) and substance use disorders.
Within a family that has a member with antisocial personality disorder, males more often have
antisocial personality disorder and substance use disorders, whereas females more often have
somatization disorder.
Culture-Related Diagnostic Issues
Antisocial personality disorder has been associated with low socioeconomic status and urban
settings. The diagnosis may at times be misapplied to individuals in settings in which
seemingly antisocial behavior may be part of a protective survival strategy (e.g., formation of
youth gangs in urban areas with high rates of violence and discrimination). Sociocultural
contexts with high rates of child maltreatment or exposure to violence also tend to have elevated
prevalence of antisocial behaviors, suggesting either a potential risk factor for the development
of antisocial personality disorder or an adverse environment that evokes reactive and contextual
antisocial behaviors that do not represent pervasive and enduring traits consistent with a
personality disorder. In assessing antisocial traits, it is helpful for the clinician to consider the
social and economic context in which the behaviors occur. In the National Epidemiologic Survey
on Alcohol and Related Conditions, prevalence appears to vary across U.S. ethnic and racialized
groups, possibly because of a combination of true prevalence differences, measurement artifacts,
and the impact of adverse environments that generate behaviors that resemble those of antisocial
personality disorder but are instead reactive and contextual. Individuals from some socially
oppressed groups may be at higher risk for misdiagnosis or overdiagnosis of antisocial
personality disorder because they are more likely to be misdiagnosed with conduct disorder in
adolescence, which is a requirement for a diagnosis of antisocial personality disorder.
Sex- and Gender-Related Diagnostic Issues
Antisocial personality disorder is three times as common in men than in women. Women with

Substance use disorders.
Schizophrenia and bipolar disorders.
Other personality disorders.
antisocial personality disorder are more likely to have experienced childhood and adult adverse
experiences such as sexual abuse compared with men. Clinical presentation may vary, with men
more often presenting with irritability/aggression and reckless disregard for the safety of others
compared with women. Comorbid substance use disorders are more common in men, while
comorbid mood and anxiety disorders are more common in women. There has been some
concern that antisocial personality disorder may be underdiagnosed in females, particularly
because of the emphasis on aggressive items in the definition of conduct disorder.
Differential Diagnosis
The diagnosis of antisocial personality disorder is not given to individuals younger than 18 years
and is given only if there is evidence of conduct disorder before age 15 years. For individuals
older than 18 years, a diagnosis of conduct disorder is given only if the criteria for antisocial
personality disorder are not met.
When antisocial behavior in an adult is associated with a substance use
disorder, the diagnosis of antisocial personality disorder is not made unless the signs of antisocial
personality disorder were also present in childhood and have continued into adulthood. When
substance use and antisocial behavior both began in childhood and continued into adulthood,
both a substance use disorder and antisocial personality disorder should be diagnosed if the
criteria for both are met, even though some antisocial acts may be a consequence of the
substance use disorder (e.g., illegal selling of drugs, thefts to obtain money for drugs).
Antisocial behavior that occurs exclusively during the course
of schizophrenia or a bipolar disorder should not be diagnosed as antisocial personality disorder.
Other personality disorders may be confused with antisocial
personality disorder because they have certain features in common. It is therefore important to
distinguish among these disorders based on differences in their characteristic features. However,
if an individual has personality features that meet criteria for one or more personality disorders in
addition to antisocial personality disorder, all can be diagnosed. Individuals with antisocial
personality disorder and narcissistic personality disorder share a tendency to be tough-minded,
glib, superficial, exploitative, and lack empathy. However,
narcissistic personality disorder does not include characteristics of impulsivity, aggression, and
deceit. In addition, individuals with antisocial personality disorder may not be as needy of the
admiration and envy of others, and persons with narcissistic personality disorder usually lack the
history of conduct disorder in childhood or criminal behavior in adulthood. Individuals with
antisocial personality disorder and histrionic personality disorder share a tendency to be
impulsive, superficial, excitement seeking, reckless, seductive, and manipulative, but persons
with histrionic personality disorder tend to be more exaggerated in their emotions and do not
characteristically engage in antisocial behaviors. Individuals with histrionic and borderline
personality disorders are manipulative to gain nurturance, whereas those with antisocial
personality disorder are manipulative to gain profit, power, or some other material gratification.
Individuals with antisocial personality disorder tend to be less emotionally unstable and more
aggressive than those with borderline personality disorder. Although antisocial behavior may be

Criminal behavior not associated with a mental disorder.
F60.3
present in some individuals with paranoid personality disorder, it is not usually motivated by a
desire for personal gain or to exploit others as in antisocial personality disorder, but rather is
more often attributable to a desire for revenge.
Antisocial personality disorder must be
distinguished from antisocial behavior not due to a mental disorder, for example, criminal
behavior undertaken for gain that is not accompanied by the personality features characteristic of
this disorder. In these cases, the condition adult antisocial behavior may be coded (see “Other
Conditions That May Be a Focus of Clinical Attention”).
Comorbidity
Individuals with antisocial personality disorder may also experience dysphoria, including
complaints of tension, inability to tolerate boredom, and depressed mood. They may have
associated anxiety disorders, mood disorders, substance use disorders, somatic symptom
disorder, and gambling disorder. Individuals with antisocial personality disorder also often have
personality features that meet criteria for other personality disorders, particularly borderline,
histrionic, and narcissistic personality disorders. The likelihood of developing antisocial
personality disorder in adult life is increased if the individual experienced childhood onset of
conduct disorder (before age 10 years) and accompanying attention-deficit/hyperactivity
disorder.
Borderline Personality Disorder
Diagnostic Criteria
A pervasive pattern of instability of interpersonal relationships, self-image, and
affects, and marked impulsivity, beginning by early adulthood and present in a
variety of contexts, as indicated by five (or more) of the following:
1. Frantic efforts to avoid real or imagined abandonment. (Note: Do not include
suicidal or self-mutilating behavior covered in Criterion 5.)
2. A pattern of unstable and intense interpersonal relationships characterized by
alternating between extremes of idealization and devaluation.
3. Identity disturbance: markedly and persistently unstable self-image or sense of
self.
4. Impulsivity in at least two areas that are potentially self-damaging (e.g.,
spending, sex, substance abuse, reckless driving, binge eating). (Note: Do not
include suicidal or self-mutilating behavior covered in Criterion 5.)
5. Recurrent suicidal behavior, gestures, or threats, or self-mutilating behavior.
6. Affective instability due to a marked reactivity of mood (e.g., intense episodic
dysphoria, irritability, or anxiety usually lasting a few hours and only rarely more

than a few days).
7. Chronic feelings of emptiness.
8. Inappropriate, intense anger or difficulty controlling anger (e.g., frequent displays
of temper, constant anger, recurrent physical fights).
9. Transient, stress-related paranoid ideation or severe dissociative symptoms.
Diagnostic Features
The essential feature of borderline personality disorder is a pervasive pattern of instability of
interpersonal relationships, self-image, and affects, and marked impulsivity that begins by early
adulthood and is present in a variety of contexts.
Individuals with borderline personality disorder make frantic efforts to avoid real or
imagined abandonment (Criterion 1). The perception of impending separation or rejection, or the
loss of external structure, can lead to profound changes in self-image, affect, cognition, and
behavior. These individuals are very sensitive to environmental circumstances. They experience
intense abandonment fears and inappropriate anger even when faced with a realistic time-limited
separation or when there are unavoidable changes in plans (e.g., sudden despair in reaction to a
clinician’s announcing the end of the hour; panic or fury when someone important to them is just
a few minutes late or must cancel an appointment). They may believe that this “abandonment”
implies they are “bad.” These abandonment fears are related to an intolerance of being alone and
a need to have other people with them. Their frantic efforts to avoid abandonment may include
impulsive actions such as self-mutilating or suicidal behaviors, which are described separately in
Criterion 5 (see also “Association With Suicidal Thoughts or Behavior”).
Individuals with borderline personality disorder have a pattern of unstable and intense
relationships (Criterion 2). They may idealize potential caregivers or lovers at the first or second
meeting, demand to spend a lot of time together, and share the most intimate details early in a
relationship. However, they may switch quickly from idealizing other people to devaluing them,
feeling that the other person does not care enough, does not give enough, or is not “there”
enough. These individuals can empathize with and nurture other people, but only with the
expectation that the other person will “be there” in return to meet their own needs on demand.
These individuals are prone to sudden and dramatic shifts in their view of others, who may
alternatively be seen as beneficent supports or as cruelly punitive. Such shifts often reflect
disillusionment with a caregiver whose nurturing qualities had been idealized or whose rejection
or abandonment is expected.
There may be an identity disturbance characterized by markedly and persistently unstable
self-image or sense of self (Criterion 3). There are sudden and dramatic shifts in self-image (e.g.,
suddenly changing from the role of a needy supplicant for help to that of a righteous avenger of
past mistreatment). Although they usually have a self-image that is based on the feeling of being
bad or evil, individuals with this disorder may at times have feelings that they do not exist at all.
This can be both painful and frightening to those with this disorder. Such experiences usually
occur in situations in which the individual feels a lack of a meaningful relationship, nurturing,
and support. These individuals may show worse performance in unstructured work or school
situations. This lack of a full and enduring identity makes it difficult for the individual with
borderline personality disorder to identify maladaptive patterns of behavior and can lead to
repetitive patterns of troubled relationships.

Individuals with borderline personality disorder display impulsivity in at least two areas that
are potentially self-damaging (Criterion 4). They may gamble, spend money irresponsibly, binge
eat, abuse substances, engage in unsafe sex, or drive recklessly.
Individuals with this disorder display recurrent suicidal behavior, gestures, or threats, or selfmutilating behavior (Criterion 5). Recurrent suicidal thoughts or behavior are often the reason
that these individuals present for help. These self-destructive acts are usually precipitated by
threats of separation or rejection or by expectations that the individual assume increased
responsibility. Self-mutilative acts (e.g., cutting or burning) are very common and may occur
during periods in which the individual is experiencing dissociative symptoms. These acts often
bring relief by reaffirming the individual’s ability to feel or by expiating the individual’s sense of
being evil.
Individuals with borderline personality disorder may display affective instability that is due
to a marked reactivity of mood (e.g., intense episodic dysphoria, irritability, or anxiety usually
lasting a few hours and only rarely more than a few days) (Criterion 6). The basic dysphoric
mood of those with borderline personality disorder is often disrupted by periods of anger, panic,
or despair and is rarely relieved by periods of well-being or satisfaction. These episodes may
reflect the individual’s extreme reactivity to interpersonal stresses.
Individuals with borderline personality disorder may be troubled by chronic feelings of
emptiness, which can co-occur with painful feelings of aloneness (Criterion 7). Easily bored,
they may frequently seek excitement to avoid their feelings of emptiness.
Individuals with this disorder frequently express inappropriate, intense anger or have
difficulty controlling their anger (Criterion 8). They may display extreme sarcasm, enduring
bitterness, or verbal outbursts. The anger is often elicited when a caregiver or lover is seen as
neglectful, withholding, uncaring, or abandoning. Such expressions of anger are often followed
by shame and guilt and contribute to the feeling they have of being evil.
During periods of extreme stress, transient paranoid ideation or dissociative symptoms (e.g.,
depersonalization) may occur (Criterion 9), but these are generally of insufficient severity or
duration to warrant an additional diagnosis. These episodes occur most frequently in response to
a real or imagined abandonment. Symptoms tend to be transient, lasting minutes or hours. The
real or perceived return of the caregiver’s nurturance may result in a remission of symptoms.
Associated Features
Individuals with borderline personality disorder may have a pattern of undermining themselves
at the moment a goal is about to be realized (e.g., dropping out of school just before graduation;
regressing severely after a discussion of how well therapy is going; destroying a good
relationship just when it is clear that the relationship could last). Some individuals develop
psychotic-like symptoms (e.g., hallucinations, body-image distortions, ideas of reference,
hypnagogic phenomena) during times of stress. Individuals with this disorder may feel more
secure with transitional objects (i.e., a pet or inanimate possession) than in interpersonal
relationships. Premature death from suicide may occur in individuals with borderline personality
disorder, especially in those with co-occurring depressive disorders or substance use disorders.

Environmental.
Genetic and physiological.
However, deaths from other causes. such as accidents or illness, are more than twice as common
as deaths by suicide in individuals with borderline personality disorder. Physical handicaps may
result from self-inflicted abuse behaviors or failed suicide attempts. Recurrent job losses,
interrupted education, and separation or divorce are common. Physical and sexual abuse, neglect,
hostile conflict, and early parental loss are more common in the childhood histories of those with
borderline personality disorder.
Prevalence
The estimated prevalence of borderline personality disorder based on a probability subsample
from Part II of the National Comorbidity Survey Replication was 1.4%. The prevalence of
borderline personality disorder in the National Epidemiologic Survey on Alcohol and Related
Conditions data was 5.9%. A review of seven epidemiological studies (six in
the United States) found a median prevalence of 2.7%. The prevalence of borderline personality
disorder is about 6% in primary care settings, about 10% among individuals seen in outpatient
mental health clinics, and about 20% among psychiatric inpatients.
Development and Course
Borderline personality disorder has typically been thought of as an adult-onset disorder.
However, it has been found in treatment settings that symptoms in adolescents as young as age
12 or 13 years can meet full criteria for the disorder. It is not yet known what percentage of
adults first entering treatment actually have such an early onset of borderline personality
disorder.
Borderline personality disorder has long been thought of as a disorder with a poor
symptomatic course, which tended to lessen in severity as those with borderline personality
disorder entered their 30s and 40s. However, prospective follow-up studies have found that
stable remissions of 1–8 years are very common. Impulsive symptoms of borderline personality
disorder remit the most rapidly, while affective symptoms remit at a substantially slower rate. In
contrast, recovery from borderline personality disorder (i.e., concurrent symptomatic remission
and good psychosocial functioning) is more difficult to achieve and less stable over time. Lack of
recovery is associated with supporting oneself on disability benefits and suffering from poor
physical health.
Risk and Prognostic Factors
Borderline personality disorder has also been found to be associated with high
rates of various forms of reported childhood abuse and emotional neglect. However, reported
rates of sexual abuse are higher in inpatients than in outpatients with this disorder, suggesting
that a history of sexual abuse is as much a risk factor for severity of borderline psychopathology
as it is for the disorder itself. In addition, an empirically based consensus has arisen that suggests
that a childhood history of reported sexual abuse is neither necessary nor sufficient for the
development of borderline personality disorder.
Borderline personality disorder is about five times more common

Depressive and bipolar disorders.
among first-degree biological relatives of those with the disorder than in the general population.
There is also an increased familial risk for substance use disorders, anxiety disorders, antisocial
personality disorder, and depressive or bipolar disorders.
Culture-Related Diagnostic Issues
The pattern of behavior seen in borderline personality disorder has been identified in many
settings around the world. Sociocultural contexts characterized by social demands that evoke
attempts at self-affirmation and acceptance by others, ambiguous or conflictual relationships
with authority figures, or marked uncertainties in adaptation can foster impulsivity, emotional
instability, explosive or aggressive behaviors, and dissociative experiences that are associated
with borderline personality disorder or with transient and contextual reactions to those
environments that can be confused with borderline personality disorder. Given that
psychodynamic, cognitive, behavioral, and mindfulness aspects of models of mind and self vary
cross-culturally, symptoms or traits that suggest the presence of borderline personality disorder
(e.g., number of sexual partners, shifting between relationships, substance use) must be evaluated
in light of cultural norms to make a valid diagnosis.
Sex- and Gender-Related Diagnostic Issues
While borderline personality disorder is more common among women than men in clinical
samples, community samples demonstrate no difference in prevalence between men and women.
This discrepancy may reflect a higher degree of help-seeking among women,
leading them to clinical settings. Clinical characteristics of men and women with borderline
personality disorder appear to be similar, with potentially a higher degree of externalizing
behaviors in boys and men and internalizing behaviors in girls and women.
Association With Suicidal Thoughts or Behavior
ln a longitudinal study, impulsive and antisocial behaviors of individuals with borderline
personality disorder were associated with increased suicide risk. In a sample of hospitalized
patients with borderline personality disorder followed prospectively for 24 years, around 6%
died by suicide, compared with 1.4% in a comparison sample of individuals with personality
disorders other than borderline personality disorder. A study of individuals with borderline
personality disorder followed for 10 years found that recurrent suicidal behavior was a defining
characteristic of borderline personality disorder, associated with declining rates of suicide
attempts from 79% to 13% over time.
Differential Diagnosis
Borderline personality disorder often co-occurs with depressive
or bipolar disorders, and when criteria for both are met, both should be diagnosed. Because the
cross-sectional presentation of borderline personality disorder can be mimicked by an episode of
depressive or bipolar disorder, the clinician should avoid giving an additional diagnosis of

Separation anxiety disorder in adults.
Other personality disorders.
Personality change due to another medical condition.
Substance use disorders.
Identity problems.
borderline personality disorder based only on cross-sectional presentation without having
documented that the pattern of behavior had an early onset and a long-standing course.
Separation anxiety disorder and borderline personality
disorder are characterized by fear of abandonment by loved ones, but problems in identity, selfdirection, interpersonal functioning, and impulsivity are additionally central to borderline
personality disorder.
Other personality disorders may be confused with borderline
personality disorder because they have certain features in common. It is therefore important to
distinguish among these disorders based on differences in their characteristic features. However,
if an individual has personality features that meet criteria for one or more personality disorders in
addition to borderline personality disorder, all can be diagnosed. Although histrionic personality
disorder can also be characterized by attention seeking, manipulative behavior, and rapidly
shifting emotions, borderline personality disorder is distinguished by self-destructiveness, angry
disruptions in close relationships, and chronic feelings of deep emptiness and loneliness.
Paranoid ideas or illusions may be present in both borderline personality disorder and
schizotypal personality disorder, but these symptoms are more transient, interpersonally reactive,
and responsive to external structuring in borderline personality disorder. Although paranoid
personality disorder and narcissistic personality disorder may also be characterized by an angry
reaction to minor stimuli, the relative stability of self-image, as well as the relative lack of
physical self-destructiveness, repetitive impulsivity, and profound abandonment concerns,
distinguishes these disorders from borderline personality disorder. Although antisocial
personality disorder and borderline personality disorder are both characterized by manipulative
behavior, individuals with antisocial personality disorder are manipulative to gain profit, power,
or some other material gratification, whereas the goal in borderline personality disorder is
directed more toward gaining the concern of caretakers. Both dependent personality disorder and
borderline personality disorder are characterized by fear of abandonment; however, the
individual with borderline personality disorder reacts to abandonment with feelings of emotional
emptiness, rage, and demands, whereas the individual with dependent personality disorder reacts
with increasing appeasement and submissiveness and urgently seeks a replacement relationship
to provide caregiving and support. Borderline personality disorder can
further be distinguished from dependent personality disorder by the typical pattern of unstable
and intense relationships.
Borderline 
personality 
disorder 
must 
be
distinguished from personality change due to another medical condition, in which the traits that
emerge are a direct physiological consequence of another medical condition.
Borderline personality disorder must also be distinguished from
symptoms that may develop in association with persistent substance use.
Borderline personality disorder should be distinguished from an identity
problem, which is reserved for identity concerns related to a developmental phase (e.g.,
adolescence) and does not qualify as a mental disorder. Adolescents and young adults with
identity problems (especially when accompanied by substance use) may transiently display

F60.4
behaviors that misleadingly give the impression of borderline personality disorder. Such
situations are characterized by emotional instability, existential dilemmas, uncertainty, anxietyprovoking choices, conflicts about sexual orientation, and competing social pressures to decide
on careers.
Comorbidity
Common co-occurring disorders include depressive and bipolar disorders, substance use
disorders, anxiety disorders (particularly panic disorder and social anxiety disorder), eating
disorders (notably bulimia nervosa and binge-eating disorder), posttraumatic stress disorder, and
attention-deficit/hyperactivity disorder. Borderline personality disorder also frequently co-occurs
with the other personality disorders.
Histrionic Personality Disorder
Diagnostic Criteria
A pervasive pattern of excessive emotionality and attention seeking, beginning by
early adulthood and present in a variety of contexts, as indicated by five (or more) of
the following:
1. Is uncomfortable in situations in which he or she is not the center of attention.
2. Interaction with others is often characterized by inappropriate sexually seductive
or provocative behavior.
3. Displays rapidly shifting and shallow expression of emotions.
4. Consistently uses physical appearance to draw attention to self.
5. Has a style of speech that is excessively impressionistic and lacking in detail.
6. Shows self-dramatization, theatricality, and exaggerated expression of emotion.
7. Is suggestible (i.e., easily influenced by others or circumstances).
8. Considers relationships to be more intimate than they actually are.
Diagnostic Features
The essential feature of histrionic personality disorder is pervasive and excessive emotionality
and attention-seeking behavior. This pattern begins by early adulthood and is present in a variety
of contexts.
Individuals with histrionic personality disorder are uncomfortable or feel unappreciated when
they are not the center of attention (Criterion 1). Often lively and dramatic, they tend to draw
attention to themselves and may initially charm new acquaintances by their enthusiasm, apparent
openness, or flirtatiousness. These qualities wear thin, however, as these individuals continually
demand to be the center of attention. They commandeer the
role of “the life of the party.” If they are not the center of attention, they may do something

dramatic (e.g., make up stories, create a scene) to draw the focus of attention to themselves. This
need is often apparent in their behavior with a clinician (e.g., being flattering, bringing gifts,
providing dramatic descriptions of physical and psychological symptoms that are replaced by
new symptoms each visit).
The appearance and behavior of individuals with this disorder are often inappropriately
sexually provocative or seductive (Criterion 2). This behavior not only is directed toward persons
in whom the individual has a sexual or romantic interest but also occurs in a wide variety of
social, occupational, and professional relationships beyond what is appropriate for the social
context. Emotional expression may be shallow and rapidly shifting (Criterion 3). Individuals
with this disorder consistently use physical appearance to draw attention to themselves (Criterion
4). They are overly concerned with impressing others by their appearance and expend an
excessive amount of time, energy, and money on clothes and grooming. They may “fish for
compliments” regarding appearance and may be easily and excessively upset by a critical
comment about how they look or by a photograph that they regard as unflattering.
These individuals have a style of speech that is excessively impressionistic and lacking in
detail (Criterion 5). Strong opinions are expressed with dramatic flair, but underlying rationales
are usually vague and diffuse, without supporting facts and details. For example, an individual
with histrionic personality disorder may comment that a certain individual is a wonderful human
being, yet be unable to provide any specific examples of good qualities to support this opinion.
Individuals with this disorder are characterized by self-dramatization, theatricality, and an
exaggerated expression of emotion (Criterion 6). They may embarrass friends and acquaintances
by an excessive public display of emotions (e.g., embracing casual acquaintances with excessive
ardor, sobbing uncontrollably on minor sentimental occasions, having temper tantrums).
However, their emotions often seem to be turned on and off too quickly to be deeply felt, which
may lead others to accuse the individual of faking these feelings.
Individuals with histrionic personality disorder have a high degree of suggestibility (Criterion
7). Their opinions and feelings are easily influenced by others and by current fads. They may be
overly trusting, especially of strong authority figures whom they see as magically solving their
problems. They have a tendency to play hunches and to adopt convictions quickly. Individuals
with this disorder often consider relationships more intimate than they actually are, describing
almost every acquaintance as “my dear, dear friend” or referring to physicians met only once or
twice under professional circumstances by their first names (Criterion 8).
Associated Features
Impairment in general tends to be lower in histrionic personality disorder than in many other
personality disorders. However, the impairment most associated with histrionic personality
disorder appears to be interpersonal in nature. Individuals with histrionic personality disorder
have an interpersonal style characterized by social dominance, which can span a spectrum of
behaviors that include a “warmer dominance” that can be intrusive in nature (e.g., need to be
center of attention; exhibitionistic) to a “colder dominance” that can include arrogant,
controlling, and aggressive behaviors. Romantic relationships appear to be particularly impaired,
with evidence suggesting that individuals with histrionic personality disorder symptoms are more
likely to get divorced or never get married. Individuals with histrionic personality disorder may
have difficulty achieving emotional intimacy in romantic or sexual relationships. Individuals

with this disorder often have impaired relationships with same-sex friends because their sexually
provocative interpersonal style may seem a threat to their friends’ relationships. These
individuals may also alienate friends with demands for constant attention. They often become
depressed and
upset when they are not the center of attention. They may crave novelty, stimulation, and
excitement and have a tendency to become bored with their usual routine. These individuals are
often intolerant of, or frustrated by, situations that involve delayed gratification, and their actions
are often directed at obtaining immediate satisfaction. Although they often initiate a job or
project with great enthusiasm, their interest may lag quickly. Longer-term relationships may be
neglected to make way for the excitement of new relationships.
Prevalence
The estimated prevalence of histrionic personality disorder based on a probability subsample
from Part II of the National Comorbidity Survey Replication was 0.0%.The prevalence of
histrionic personality disorder in the National Epidemiologic Survey on Alcohol and Related
Conditions data was 1.8%. A review of five epidemiological studies (four in the United States)
found a median prevalence of 0.9%.
Culture-Related Diagnostic Issues
Norms for interpersonal behavior, personal appearance, and emotional expressiveness vary
widely across cultures, genders, and age groups. Before considering the various traits (e.g.,
emotionality, seductiveness, dramatic interpersonal style, novelty seeking, sociability, charm,
impressionability, a tendency to somatization) to be evidence of histrionic personality disorder, it
is important to evaluate whether they cause clinically significant impairment or distress. The
presence of histrionic personality disorder should be distinguished from reactive and contextual
expression of these traits, arising in response to socialization pressures in competitive peer
groups, including the “need to be liked,” that do not represent pervasive and enduring traits
consistent with a personality disorder.
Sex- and Gender-Related Diagnostic Issues
In clinical settings, this disorder has been diagnosed more frequently in females; however, the
gender ratio is not significantly different from the gender ratio of females within the respective
clinical setting. In contrast, some studies using structured assessments report similar prevalence
rates among males and females.
Association With Suicidal Thoughts or Behavior
The actual risk of suicide is not known, but clinical experience suggests that individuals with this
disorder may be at increased risk for suicidal gestures and threats.
Differential Diagnosis

Other personality disorders and personality traits.
Personality change due to another medical condition.
Substance use disorders.
Other personality disorders may be confused with
histrionic personality disorder because they have certain features in common. It is therefore
important to distinguish among these disorders based on differences in their characteristic
features. However, if an individual has personality features that meet criteria for one or more
personality disorders in addition to histrionic personality disorder, all can be diagnosed.
Although borderline personality disorder can also be characterized by attention seeking,
manipulative behavior, and rapidly shifting emotions, it is distinguished by self-destructiveness,
angry disruptions in close relationships, and chronic feelings of deep emptiness and identity
disturbance. Individuals with antisocial personality disorder and histrionic personality disorder
share a tendency to be impulsive, superficial, excitement seeking, reckless, seductive, and
manipulative, but persons with histrionic personality disorder tend to be more exaggerated in
their emotions and do not characteristically engage in antisocial behaviors. Individuals with
histrionic personality disorder are manipulative to gain nurturance, whereas those with antisocial
personality disorder are manipu
lative to gain profit, power, or some other material gratification. Although individuals with
narcissistic personality disorder also crave attention from others, they usually want praise for
their “superiority,” whereas individuals with histrionic personality disorder are willing to be
viewed as fragile or dependent if this is instrumental in getting attention. Individuals with
narcissistic personality disorder may exaggerate the intimacy of their relationships with other
people, but they are more apt to emphasize the “VIP” status or wealth of their friends. In
dependent personality disorder, the individual is excessively dependent on others for praise and
guidance, but is without the flamboyant, exaggerated, emotional features of individuals with
histrionic personality disorder.
Many individuals may display histrionic personality traits. Only when these traits are
inflexible, maladaptive, and persisting and cause significant functional impairment or subjective
distress do they constitute histrionic personality disorder.
Histrionic 
personality 
disorder 
must 
be
distinguished from personality change due to another medical condition, in which the traits that
emerge are a direct physiological consequence of another medical condition.
The disorder must also be distinguished from symptoms that may
develop in association with persistent substance use.
Comorbidity
Histrionic personality disorder has been associated with higher rates of borderline, narcissistic,
paranoid, dependent, and antisocial personality disorders; alcohol and other substance use and
misuse; as well as aggression and violence. Histrionic personality disorder is also thought to be
related to somatic symptom disorder, functional neurological symptom disorder (conversion
disorder), and major depressive disorder.
Narcissistic Personality Disorder

F60.81
Diagnostic Criteria
A pervasive pattern of grandiosity (in fantasy or behavior), need for admiration, and
lack of empathy, beginning by early adulthood and present in a variety of contexts,
as indicated by five (or more) of the following:
1. Has a grandiose sense of self-importance (e.g., exaggerates achievements and
talents, expects to be recognized as superior without commensurate
achievements).
2. Is preoccupied with fantasies of unlimited success, power, brilliance, beauty, or
ideal love.
3. Believes that he or she is “special” and unique and can only be understood by, or
should associate with, other special or high-status people (or institutions).
4. Requires excessive admiration.
5. Has a sense of entitlement (i.e., unreasonable expectations of especially
favorable treatment or automatic compliance with his or her expectations).
6. Is interpersonally exploitative (i.e., takes advantage of others to achieve his or
her own ends).
7. Lacks empathy: is unwilling to recognize or identify with the feelings and needs
of others.
8. Is often envious of others or believes that others are envious of him or her.
9. Shows arrogant, haughty behaviors or attitudes.
Diagnostic Features
The essential feature of narcissistic personality disorder is a pervasive pattern of grandiosity,
need for admiration, and lack of empathy that begins by early adulthood and is present in a
variety of contexts.
Individuals with this disorder have a grandiose sense of self-importance, which may be
manifest as an exaggerated or unrealistic sense of superiority, value, or capability (Criterion 1).
They tend to overestimate their abilities and amplify their accomplishments, often appearing
boastful and pretentious. They may blithely assume that others attribute the same value to their
efforts and may be surprised when the praise they expect and feel they deserve is not
forthcoming. Often implicit in the inflated judgments of their own accomplishments is an
underestimation or devaluation of the contributions of others. Individuals with narcissistic
personality disorder are often preoccupied with fantasies of unlimited success, power, brilliance,
beauty, or ideal love (Criterion 2). They may ruminate about “long overdue” admiration and
privilege and compare themselves favorably with famous or privileged people.
Individuals with narcissistic personality disorder believe that they are special or unique and
expect others to recognize them as such (Criterion 3). They can be surprised or even devastated
when the recognition of acclaim they expect and feel they deserve from others is not
forthcoming. They may feel that they can only be understood by, and should only associate with,
people of high status and may attribute “unique,” “perfect,” or “gifted” qualities to those with

whom they associate. Individuals with this disorder believe that their needs are special and
beyond the ken of ordinary people. Their own self-esteem is enhanced (i.e., “mirrored”) by the
idealized value that they assign to those with whom they associate. They are likely to insist on
having only the “top” person (doctor, lawyer, hairdresser, instructor) or being affiliated with the
“best” institutions but may devalue the credentials of those who disappoint them.
Individuals with this disorder generally require excessive admiration (Criterion 4). Their selfesteem is almost invariably very fragile, and their struggle with severe internal self-doubt, selfcriticism, and emptiness results in their need to actively seek others’ admiration. They may be
preoccupied with how well they are doing and how favorably they are regarded by others. They
may expect their arrival to be greeted with great fanfare and are astonished if others do not covet
their possessions. They may constantly fish for compliments, often with great charm.
A sense of entitlement, which is rooted in their distorted sense of self-worth, is evident in
these individuals’ unreasonable expectation of especially favorable treatment (Criterion 5). They
expect to be catered to and are puzzled or furious when this does not happen. For example, they
may assume that they do not have to wait in line and that their priorities are so important that
others should defer to them, and then get irritated when others fail to assist “in their very
important work.” They expect to be given whatever they want or feel they need, no matter what
it might mean to others. For example, these individuals may expect great dedication from others
and may overwork them without regard for the impact on their lives. This sense of entitlement,
combined with a lack of understanding and sensitivity to the wants and needs of others, may
result in the conscious or unwitting exploitation of others (Criterion 6). They tend to form
friendships or romantic relationships only if the other person seems likely to advance their
purposes or otherwise enhance their self-esteem. They often usurp special privileges and extra
resources that they believe they deserve. Some individuals with narcissistic personality disorder
intentionally and purposefully take advantage of others emotionally, socially, intellectually, or
financially for their own purposes and gains.
Individuals with narcissistic personality disorder generally have a lack of empathy and are
unwilling to recognize or identify with the desires, subjective experiences, and feelings of others
(Criterion 7). They tend to have some degree of cognitive empathy
(understanding another person’s perspective on an intellectual level) but lack emotional
empathy (directly feeling the emotions that another person is feeling). These individuals may be
oblivious to the hurt their remarks may inflict (e.g., exuberantly telling a former lover that “I am
now in the relationship of a lifetime!”; boasting of health in front of someone who is sick). When
recognized, the needs, desires, or feelings of others are likely to be viewed disparagingly as signs
of weakness or vulnerability. Those who relate to individuals with narcissistic personality
disorder typically find an emotional coldness and lack of reciprocal interest.
These individuals are often envious of others or believe that others are envious of them
(Criterion 8). They may begrudge others their successes or possessions, feeling that they better
deserve those achievements, admiration, or privileges. They may harshly devalue the
contributions of others, particularly when those individuals have received acknowledgment or
praise for their accomplishments. Arrogant, haughty behaviors characterize these individuals;
they often display snobbish, disdainful, or patronizing attitudes (Criterion 9).

Associated Features
Vulnerability in self-esteem makes individuals with narcissistic personality disorder very
sensitive to criticism or defeat. Although they may not show it outwardly, such experiences may
leave them feeling ashamed, humiliated, degraded, hollow, and empty. They may react with
disdain, rage, or defiant counterattack. However, such experiences can also lead to social
withdrawal or an appearance of humility that may mask and protect the grandiosity.
Interpersonal relations are typically impaired because of problems related to self-preoccupation,
entitlement, need for admiration, and relative disregard for the sensitivities of others.
Individuals with narcissistic personality disorder can be competent and high functioning with
professional and social success, while others can have various levels of functional impairment.
Professional capability combined with self-control, stoicism, and interpersonal distancing with
minimal self-disclosure can support sustained life engagement and even enable marriage and
social affiliations. Sometimes ambition and temporary confidence lead to high achievements, but
performance can be disrupted because of fluctuating self-confidence and intolerance of criticism
or defeat. Some individuals with narcissistic personality disorder have very low vocational
functioning, reflecting an unwillingness to take a risk in competitive or other situations in which
failure or defeat can be possible.
Low self-esteem with inferiority, vulnerability, and sustained feelings of shame, envy, and
humiliation accompanied by self-criticism and insecurity can make individuals with narcissistic
personality disorder susceptible to social withdrawal, emptiness, and depressed mood. High
perfectionist standards are often associated with significant fear of exposure to imperfection,
failure, and overwhelming emotions.
Prevalence
The estimated prevalence of narcissistic personality disorder based on a probability subsample
from Part II of the National Comorbidity Survey Replication was 0.0%.The prevalence of
narcissistic personality disorder in the National Epidemiologic Survey on Alcohol and Related
Conditions data was 6.2%. A review of five epidemiological studies (four in the United States)
found a median prevalence of 1.6%.
Development and Course
Narcissistic traits may be particularly common in adolescents but do not necessarily indicate that
the individual will develop narcissistic personality disorder in adulthood. Predominant
narcissistic traits or manifestations of the full disorder may first come to clinical attention or be
exacerbated in the context of unexpected or extremely challenging life
experiences or crises, such as bankruptcies, demotions or loss of work, or divorces. In addition,
individuals with narcissistic personality disorder may have specific difficulties adjusting to the
onset of physical and occupational limitations that are inherent in the aging process. However,
life experiences, such as new durable relationships, real successful achievements, and tolerable
disappointments and setbacks, can all be corrective and contribute to changes and improvements
in individuals with this disorder.

Other personality disorders and personality traits.
Culture-Related Diagnostic Issues
Narcissistic traits may be elevated in sociocultural contexts that emphasize individualism and
personal autonomy over collectivistic goals. Compared with collectivistic contexts, in
individualistic contexts, narcissistic traits may warrant less clinical attention or less frequently
lead to social impairment.
Sex- and Gender-Related Diagnostic Issues
Among adults age 18 and older diagnosed with narcissistic personality disorder, 50%–75% are
men. Gender differences in adults with this disorder include stronger reactivity in response to
stress and compromised empathic processing in men as opposed to self-focus and withdrawal in
women. Culturally based gender patterns and expectations may also contribute to gender
differences in narcissistic personality disorder traits and patterns.
Association With Suicidal Thoughts or Behavior
In the context of severe stress, and given the perfectionism often associated with narcissistic
personality disorder, exposure to imperfection, failure, and overwhelming emotions can evoke
suicidal ideation. Suicide attempts in individuals with narcissistic personality disorder tend to be
less impulsive and are characterized by higher lethality compared with suicide attempts by
individuals with other personality disorders.
Differential Diagnosis
Other personality disorders may be confused with
narcissistic personality disorder because they have certain features in common. It is, therefore,
important to distinguish among these disorders based on differences in their characteristic
features. However, if an individual has personality features that meet criteria for one or more
personality disorders in addition to narcissistic personality disorder, all can be diagnosed. The
most useful feature in discriminating narcissistic personality disorder from histrionic, antisocial,
and borderline personality disorders, in which the interactive styles are coquettish, callous, and
needy, respectively, is the grandiosity characteristic of narcissistic personality disorder. The
relative stability of self-image and self-control as well as the relative lack of self-destructiveness,
impulsivity, separation insecurity, and emotional hyperreactivity also help distinguish
narcissistic personality disorder from borderline personality disorder.
Excessive pride in achievements, a relative lack of emotional display, and ignorance of or
disdain for others’ sensitivities help distinguish narcissistic personality disorder from histrionic
personality disorder. Although individuals with borderline, histrionic, and narcissistic personality
disorders may require much attention, those with narcissistic personality disorder specifically
need that attention to be admiring. Individuals with antisocial and narcissistic personality
disorders share a tendency to be tough-minded, glib, superficial, exploitative, and unempathic.
However, narcissistic personality disorder does not necessarily include characteristics of
impulsive aggressivity and deceitfulness. In addition, individuals with antisocial personality
disorder may be more indifferent and less sensitive to others’ reactions or criticism, and
individuals with narcissistic personality disorder usually lack the history of conduct disorder in
childhood or criminal behavior in adulthood.

Mania or hypomania.
Substance use disorders.
Persistent depressive disorder.
F60.6
In both narcissistic personality disorder and obsessive-compulsive personality disorder, the
individual may profess a commitment to perfectionism and believe that others cannot do things
as well. However, while those with obsessive-compulsive personality disorder tend to be more
immersed in perfectionism related to order and rigidity, individuals with narcissistic personality
disorder tend to set high perfectionistic standards, especially for appearance and performance,
and to be critically concerned if they are not measuring up.
Suspiciousness and social withdrawal usually distinguish those with schizotypal, avoidant, or
paranoid personality disorder from those with narcissistic personality disorder. When these
qualities are present in individuals with narcissistic personality disorder, they derive primarily
from shame and fear of failure, or fear of having imperfections or flaws revealed.
Many highly successful individuals display personality traits that might be considered
narcissistic. Only when these traits are inflexible, maladaptive, and persisting and cause
significant functional impairment or subjective distress do they constitute narcissistic personality
disorder.
Grandiosity may emerge as part of manic or hypomanic episodes, but the
association with mood change or functional impairments helps distinguish these episodes from
narcissistic personality disorder.
Narcissistic personality disorder must also be distinguished from
symptoms that may develop in association with persistent substance use.
Experiences that threaten self-esteem can evoke a deep sense of
inferiority and sustained feelings of shame, envy, self-criticism, and insecurity in individuals
with narcissistic personality disorder that can result in persistent negative feelings resembling
those seen in persistent depressive disorder. If criteria are also met for persistent depressive
disorder, both conditions can be diagnosed.
Comorbidity
Narcissistic personality disorder is associated with depressive disorders (persistent depressive
disorder and major depressive disorder), anorexia nervosa, and substance use disorders
(especially related to cocaine). Histrionic, borderline, antisocial, and paranoid personality
disorders may also be associated with narcissistic personality disorder.
Cluster C Personality Disorders
Avoidant Personality Disorder
Diagnostic Criteria
A pervasive pattern of social inhibition, feelings of inadequacy, and hypersensitivity

to negative evaluation, beginning by early adulthood and present in a variety of
contexts, as indicated by four (or more) of the following:
1. Avoids occupational activities that involve significant interpersonal contact
because of fears of criticism, disapproval, or rejection.
2. Is unwilling to get involved with people unless certain of being liked.
3. Shows restraint within intimate relationships because of the fear of being shamed
or ridiculed.
4. Is preoccupied with being criticized or rejected in social situations.
5. Is inhibited in new interpersonal situations because of feelings of inadequacy.
6. Views self as socially inept, personally unappealing, or inferior to others.
7. Is unusually reluctant to take personal risks or to engage in any new activities
because they may prove embarrassing.
Diagnostic Features
The essential feature of avoidant personality disorder is a pervasive pattern of social inhibition,
feelings of inadequacy, and hypersensitivity to negative evaluation that begins by early
adulthood and is present in a variety of contexts.
Individuals with avoidant personality disorder avoid work activities that involve significant
interpersonal contact because of fears of criticism, disapproval, or rejection (Criterion 1). Offers
of job promotions may be declined because failure to manage the new responsibilities might
result in criticism from coworkers. These individuals avoid making new friends unless they are
certain they will be liked and accepted without criticism (Criterion 2). Until they pass stringent
tests proving the contrary, other people are assumed to be critical and disapproving. Individuals
with this disorder are highly avoidant of group activities. Interpersonal intimacy is often difficult
for these individuals, although they are able to establish intimate relationships when there is
assurance of uncritical acceptance. They may act with restraint, be reluctant to talk about
themselves, and withhold intimate feelings for fear of being exposed, ridiculed, or shamed
(Criterion 3).
Because individuals with this disorder are preoccupied with being criticized or rejected in
social situations, they may have a markedly low threshold for detecting such reactions (Criterion
4). If someone is even slightly disapproving or critical, they may feel extremely hurt. They tend
to be shy, quiet, inhibited, and “invisible” because of the fear that any attention would be critical
or rejecting. They expect that no matter what they say, others will see it as “wrong,” and so they
may say nothing at all. They react strongly to subtle cues that are suggestive of mockery or
derision, and may misinterpret a neutral gesture or statement as critical or rejecting. Despite their
longing to be active participants in social life, they fear placing their psychological welfare in the
hands of others. Individuals with avoidant personality disorder are inhibited in new interpersonal
situations because they feel inadequate and have low self-esteem (Criterion 5). These individuals
believe themselves to be socially inept, personally unappealing, or inferior to others (Criterion
6). Doubts concerning social competence and personal appeal may be most intense for some
individuals in settings involving interactions with strangers. But many others report more

difficulties with repeated interaction, when sharing of personal information would normally
occur, thus, in the individual’s perception, increasing the chances that their inferiority would be
revealed and that they would be rejected. When commencing a new ongoing social or
occupational commitment requiring repeated interpersonal interaction, individuals may over
weeks or months develop a growing conviction that others or colleagues view them as inferior or
lacking worth, resulting in intolerable distress or anxiety that prompts resignation. Thus, a
history of repeated job changes may be present. Individuals with this disorder are unusually
reluctant to take personal risks or to engage in any new activities because these may prove
embarrassing (Criterion 7). They are prone to exaggerate the potential dangers of ordinary
situations, and a restricted lifestyle may result from their need for certainty and security.
Associated Features
Individuals with avoidant personality disorder often vigilantly appraise the movements and
expressions of those with whom they come into contact. They are likely to
misinterpret social responses as critical, which in turn confirms their self-doubts. They are
described by others as being “shy,” “timid,” “lonely,” and “isolated.” The major problems
associated with this disorder occur in social and occupational functioning. The low self-esteem
and hypersensitivity to rejection are associated with restricted interpersonal contacts. These
individuals may become relatively isolated and usually do not have a large social support
network that can help them weather crises. They desire affection and acceptance and may
fantasize about idealized relationships with others. Avoidant behaviors can also adversely affect
occupational functioning because these individuals try to avoid the types of social situations that
may be important for meeting the basic demands of the job or for advancement.
Individuals with avoidant personality disorder have been reported as having insecure
attachment styles characterized by a desire for emotional attachment (which may include a
preoccupation with previous and current relationships), but their fears that others may not value
them or may hurt them may lead them to respond with passivity, anger, or fear. These attachment
patterns have been referred to variously as “preoccupied” or “fearful” depending on the model
employed by researchers.
Prevalence
The estimated prevalence of avoidant personality disorder based on a probability subsample from
Part II of the National Comorbidity Survey Replication was 5.2%. The prevalence of avoidant
personality disorder in the National Epidemiologic Survey on Alcohol and Related Conditions
was 2.4%. A review of six epidemiological studies (four in the United States) found a median
prevalence of 2.1%.
Development and Course
The avoidant behavior often starts in infancy or childhood with shyness, isolation, and fear of
strangers and new situations. Although shyness in childhood is a common precursor of avoidant
personality disorder, in most individuals it tends to gradually dissipate as they get older. In

Social anxiety disorder.
Agoraphobia.
Other personality disorders and personality traits.
contrast, individuals who go on to develop avoidant personality disorder may become
increasingly shy and avoidant during adolescence and early adulthood, when social relationships
with new people become especially important. There is some evidence that in adults, avoidant
personality disorder tends to become less evident or to remit with age; the prevalence in adults
older than 65 years has been estimated at 0.8%. This diagnosis should be used with great caution
in children and adolescents, for whom shy and avoidant behavior may be developmentally
appropriate.
Culture-Related Diagnostic Issues
There may be variation in the degree to which different cultural and ethnic groups regard
diffidence and avoidance as appropriate. Moreover, avoidant behavior may be the result of
problems in acculturation following migration. In some sociocultural contexts, marked avoidance
might occur following social embarrassment (“loss of face”) or failure to meet major life goals
rather than temperamental shyness. In these settings, the goal of avoidance includes deliberate
minimization of social interactions in order to preserve social harmony or prevent public offense.
Sex- and Gender-Related Diagnostic Issues
Avoidant personality disorder appears to be more common in women than in men in community
surveys. This gender difference in prevalence is small but consistently found in large populationbased samples.
Differential Diagnosis
There appears to be a great deal of overlap between avoidant personality
disorder and social anxiety disorder. It has been suggested that they may represent different
manifestations of similar underlying problems, or avoidant personality disorder may be a more
severe form of social anxiety disorder. However, differences have also been described, especially
in relation to self-concept (such as self-esteem and the sense of inferiority in avoidant personality
disorder); the latter is indirect evidence as it shows that negative self-concept in social anxiety
disorder may be unstable and thus less pervasive and entrenched than in avoidant personality
disorder. Additionally, studies have shown that avoidant personality disorder frequently occurs
in the absence of social anxiety disorder, and some separate risk factors have been identified,
providing support for retaining two separate diagnostic categories.
Avoidance characterizes both avoidant personality disorder and agoraphobia, and
they often co-occur. They can be distinguished by the motivation for the avoidance (e.g., fear of
panic or physical harm in agoraphobia).
Other personality disorders may be confused with
avoidant personality disorder because they have certain features in common. It is, therefore,
important to distinguish among these disorders based on differences in their characteristic
features. However, if an individual has personality features that meet criteria for one or more
personality disorders in addition to avoidant personality disorder, all can be diagnosed. Both
avoidant personality disorder and dependent personality disorder are characterized by feelings of

Personality change due to another medical condition.
Substance use disorders.
F60.7
inadequacy, hypersensitivity to criticism, and a need for reassurance. Similar behaviors (e.g.,
unassertiveness) and attributes (e.g., low self-esteem and low self-confidence) may be observed
in both dependent personality disorder and avoidant personality disorder, although other
behaviors are notably divergent, such as avoidance of social proximity in avoidant personality
disorder but proximity-seeking in dependent personality disorder. The motivations behind
similar behaviors may be quite different. For example, the unassertiveness in avoidant
personality disorder is described as more closely related to fears of being rejected or humiliated,
whereas in dependent personality disorder it is motivated by the desire to avoid being left to fend
for oneself. However, avoidant personality disorder and dependent personality disorder may be
particularly likely to co-occur. Like avoidant personality disorder, schizoid personality disorder
and schizotypal personality disorder are characterized by social isolation. However, individuals
with avoidant personality disorder want to have relationships with others and feel their loneliness
deeply, whereas those with schizoid or schizotypal personality disorder may be content with and
even prefer their social isolation. Paranoid personality disorder and avoidant personality disorder
are both characterized by a reluctance to confide in others. However, in avoidant personality
disorder, this reluctance is attributable more to a fear of humiliation or being found inadequate
than to a fear of others’ malicious intent.
Many individuals display avoidant personality traits. Only when these traits are inflexible,
maladaptive, and persisting and cause significant functional impairment or subjective distress do
they constitute avoidant personality disorder.
Avoidant 
personality 
disorder 
must 
be
distinguished from personality change due to another medical condition, in which the traits that
emerge are a direct physiological consequence of another medical condition.
Avoidant personality disorder must also be distinguished from
symptoms that may develop in association with persistent substance use.
Comorbidity
Other disorders that are commonly diagnosed with avoidant personality disorder include
depressive disorders and anxiety disorders, especially social anxiety disorder. Avoidant
personality disorder also tends to be diagnosed with schizoid personality disorder. Avoidant
personality disorder is associated with increased rates of substance use disorders at a similar rate
to the generalized form of social anxiety disorder.
Dependent Personality Disorder
Diagnostic Criteria
A pervasive and excessive need to be taken care of that leads to submissive and
clinging behavior and fears of separation, beginning by early adulthood and present
in a variety of contexts, as indicated by five (or more) of the following:

1. Has difficulty making everyday decisions without an excessive amount of advice
and reassurance from others.
2. Needs others to assume responsibility for most major areas of his or her life.
3. Has difficulty expressing disagreement with others because of fear of loss of
support or approval. (Note: Do not include realistic fears of retribution.)
4. Has difficulty initiating projects or doing things on his or her own (because of a
lack of self-confidence in judgment or abilities rather than a lack of motivation or
energy).
5. Goes to excessive lengths to obtain nurturance and support from others, to the
point of volunteering to do things that are unpleasant.
6. Feels uncomfortable or helpless when alone because of exaggerated fears of
being unable to care for himself or herself.
7. Urgently seeks another relationship as a source of care and support when a
close relationship ends.
8. Is unrealistically preoccupied with fears of being left to take care of himself or
herself.
Diagnostic Features
The essential feature of dependent personality disorder is a pervasive and excessive need to be
taken care of that leads to submissive and clinging behavior and fears of separation. This pattern
begins by early adulthood and is present in a variety of contexts. The dependent and submissive
behaviors are designed to elicit caregiving and arise from a self-perception of being unable to
function adequately without the help of others.
Individuals with dependent personality disorder have great difficulty making everyday
decisions (e.g., what color shirt to wear to work or whether to carry an umbrella) without an
excessive amount of advice and reassurance from others (Criterion 1). These individuals tend to
be passive and to allow other people (often a single other person) to take the initiative and
assume responsibility for most major areas of their lives (Criterion 2). Adults with this disorder
typically depend on a parent or spouse to decide where they should live, what kind of job they
should have, and which neighbors to befriend. Adolescents with this disorder may allow their
parent(s) to decide what they should wear, with whom they should associate, how they should
spend their free time, and what school or college they should attend. This need for others to
assume responsibility goes beyond age-appropriate and situation-appropriate requests for
assistance from others (e.g., the specific needs of children, elderly persons, and handicapped
persons). Dependent personality disorder may occur in an individual who has a serious medical
condition or disability, but in such cases the difficulty in taking responsibility must go beyond
what would normally be associated with that condition or disability.
Because they fear losing support or approval, individuals with dependent personality disorder
often have difficulty expressing disagreement with other individuals, especially those on whom
they are dependent (Criterion 3). These individuals feel so unable to function alone that they will
agree with things that they feel are wrong rather than risk losing the help of those to whom they

look for guidance. They do not express anger toward others whose support and nurturance they
need for fear of alienating them. If the individual’s concerns regarding the consequences of
expressing disagreement are realistic (e.g., realistic fears of retribution from an abusive spouse),
the behavior should not be considered to be evidence of dependent personality disorder.
Individuals with this disorder have difficulty initiating projects or doing things independently
(Criterion 4). They lack self-confidence and believe that they need help to begin and carry
through tasks. They will wait for others to start things because they believe that as a rule others
can do them better. These individuals are convinced that they are incapable of functioning
independently and present themselves as inept and requiring constant assistance. They are,
however, likely to function adequately if given the assurance that someone else is supervising
and approving. There may be a fear of becoming or appearing to be more competent, because
they may believe that this will lead to loss of support. Because they rely on others to handle their
problems, they often do not learn the skills of independent living, thus perpetuating dependency.
Individuals with dependent personality disorder may go to excessive lengths to obtain
nurturance and support from others, even to the point of volunteering for unpleasant tasks if such
behavior will bring the care they need (Criterion 5). They are willing to submit to what others
want, even if the demands are unreasonable. Their need to maintain an important bond will often
result in imbalanced or distorted relationships. They may make extraordinary self-sacrifices or
tolerate verbal, physical, or sexual abuse. (It should be noted that this behavior should be
considered evidence of dependent personality disorder only when it can clearly be established
that other options are available to the individual.) Individuals with this disorder feel
uncomfortable or helpless when alone because of their exaggerated fears of being unable to care
for themselves (Criterion 6).
When a close relationship ends (e.g., a breakup with a lover; the death of a caregiver),
individuals with dependent personality disorder may urgently seek another relationship to
provide the care and support they need (Criterion 7). Their belief that they are unable to function
in the absence of a close relationship motivates these individuals to become quickly and
indiscriminately attached to another individual. Individuals with this disorder are often
preoccupied with fears of being left to care for themselves (Criterion 8). They see themselves as
so totally dependent on the advice and help of an important other person that they worry about
losing the support of that person when there are no grounds to justify such fears. To be
considered as evidence of this criterion, the fears must be excessive and unrealistic. For example,
an elderly man with cancer who moves into his son’s household for care is exhibiting dependent
behavior that is appropriate given this person’s life circumstances.
Associated Features
Individuals with dependent personality disorder are often characterized by pessimism and selfdoubt and tend to belittle their abilities and assets. They take criticism and disapproval as proof
of their worthlessness and lose faith in themselves. They may seek overprotection and
dominance from others. Occupational functioning may be impaired if independent initiative is
required. They may avoid positions of responsibility and become anxious when faced with
decisions.
Prevalence

Separation anxiety disorder in adults.
Other mental disorders and medical conditions.
Other personality disorders and personality traits.
The estimated prevalence of dependent personality disorder based on a probability subsample
from Part II of the National Comorbidity Survey Replication was 0.6%. The
prevalence of dependent personality disorder in the National Epidemiologic Survey on Alcohol
and Related Conditions was 0.5%. A review of six epidemiological studies (four in the United
States) found a median prevalence of 0.4%.
Development and Course
This diagnosis should be used with great caution, if at all, in children and adolescents, for whom
dependent behavior may be developmentally appropriate.
Culture-Related Diagnostic Issues
The degree to which dependent behaviors are considered to be appropriate varies substantially
across different age and sociocultural groups. Age and cultural factors need to be considered in
evaluating the diagnostic threshold of each criterion. Dependent behavior should be considered
characteristic of the disorder only when it is clearly in excess of the individual’s cultural norms
or reflects unrealistic concerns. An emphasis on passivity, politeness, and deferential treatment is
characteristic of some societies and may be misinterpreted as traits of dependent personality
disorder. Similarly, societies may differentially foster and discourage dependent behavior in
males and females. Individuals with dependent personality disorder exhibit a pervasive inability
to make decisions, continuous feelings of subjugation, lack of initiative, silence, and social
distancing that are far in excess of usual cultural norms of politeness and purposeful passivity.
Sex- and Gender-Related Diagnostic Issues
In clinical and community settings, dependent personality disorder has been diagnosed more
frequently in women compared with men.
Differential Diagnosis
Adults with separation anxiety disorder are typically
overconcerned about their offspring, spouses, parents, and pets, and experience marked
discomfort when separated from them. In contrast, individuals with dependent personality
disorder feel uncomfortable or helpless when alone because of exaggerated fears of being unable
to take care of themselves.
Dependent 
personality 
disorder 
must 
be
distinguished from dependency arising as a consequence of other mental disorders (e.g.,
depressive disorders, panic disorder, agoraphobia) and as a result of other medical conditions.
Other personality disorders may be confused with
dependent personality disorder because they have certain features in common. It is therefore
important to distinguish among these disorders based on differences in their characteristic
features. However, if an individual has personality features that meet criteria for one or more
personality disorders in addition to dependent personality disorder, all can be diagnosed.

Personality change due to another medical condition.
Substance use disorders.
Although many personality disorders are characterized by dependent features, dependent
personality disorder can be distinguished by its predominantly submissive and clinging behavior
and by the person’s self-perception of not being able to function adequately without the help and
support of others. Both dependent personality disorder and borderline personality disorder are
characterized by fear of abandonment; however, the individual with borderline personality
disorder reacts to abandonment with feelings of emotional emptiness, rage, and demands,
whereas the individual with dependent personality disorder reacts with increasing appeasement
and submissiveness and urgently seeks a replacement relationship to provide caregiving and
support. Borderline personality disorder can further be distinguished from dependent
personality disorder by a typical pattern of unstable and intense relationships. Individuals with
histrionic personality disorder, like those with dependent personality disorder, have a strong need
for reassurance and approval and may appear childlike and clinging. However, unlike dependent
personality disorder, which is characterized by self-effacing and docile behavior, histrionic
personality disorder is characterized by gregarious flamboyance with active demands for
attention. Moreover, individuals with histrionic personality disorder typically have less insight
regarding their underlying dependency needs than do people with dependent personality
disorder. Both dependent personality disorder and avoidant personality disorder are characterized
by feelings of inadequacy, hypersensitivity to criticism, and a need for reassurance; however,
individuals with avoidant personality disorder have such a strong fear of humiliation and
rejection that they withdraw until they are certain they will be accepted. In contrast, individuals
with dependent personality disorder have a pattern of seeking and maintaining connections to
important others, rather than avoiding and withdrawing from relationships.
Many individuals display dependent personality traits. Only when these traits are inflexible,
maladaptive, and persisting and cause significant functional impairment or subjective distress do
they constitute dependent personality disorder.
Dependent 
personality 
disorder 
must 
be
distinguished from personality change due to another medical condition, in which the traits that
emerge are a direct physiological consequence of another medical condition.
Dependent personality disorder must also be distinguished from
symptoms that may develop in association with persistent substance use.
Comorbidity
There may be an increased risk of depressive disorders, anxiety disorders, and adjustment
disorders. Dependent personality disorder often co-occurs with other personality disorders,
especially borderline, avoidant, and histrionic personality disorders. Chronic physical illness or
persistent separation anxiety disorder in childhood or adolescence may predispose the individual
to the development of this disorder.
Obsessive-Compulsive Personality Disorder

F60.5
Diagnostic Criteria
A pervasive pattern of preoccupation with orderliness, perfectionism, and mental and
interpersonal control, at the expense of flexibility, openness, and efficiency,
beginning by early adulthood and present in a variety of contexts, as indicated by
four (or more) of the following:
1. Is preoccupied with details, rules, lists, order, organization, or schedules to the
extent that the major point of the activity is lost.
2. Shows perfectionism that interferes with task completion (e.g., is unable to
complete a project because his or her own overly strict standards are not met).
3. Is excessively devoted to work and productivity to the exclusion of leisure
activities and friendships (not accounted for by obvious economic necessity).
4. Is overconscientious, scrupulous, and inflexible about matters of morality, ethics,
or values (not accounted for by cultural or religious identification).
5. Is unable to discard worn-out or worthless objects even when they have no
sentimental value.
6. Is reluctant to delegate tasks or to work with others unless they submit to exactly
his or her way of doing things.
7. Adopts a miserly spending style toward both self and others; money is viewed as
something to be hoarded for future catastrophes.
8. Shows rigidity and stubbornness.
Diagnostic Features
The essential feature of obsessive-compulsive personality disorder is a preoccupation with
orderliness, perfectionism, and mental and interpersonal control, at the expense of flexibility,
openness, and efficiency. This pattern begins by early adulthood and is present in a variety of
contexts.
Individuals with obsessive-compulsive personality disorder attempt to maintain a sense of
control through painstaking attention to rules, trivial details, procedures, lists, schedules, or form
to the extent that the major point of the activity is lost (Criterion 1). They are excessively careful
and prone to repetition, paying extraordinary attention to detail and repeatedly checking for
possible mistakes, losing track of time in the process. For example, when such individuals
misplace a list of things to be done, they will spend an inordinate amount of time looking for the
list rather than spending a few moments trying their best to recreate it from memory and
proceeding to accomplish the tasks. They dismiss the fact that other people tend to become very
annoyed at the delays and inconveniences that result from this behavior because they
preferentially respond to either their anxiety about making a mistake or their insistence on how
things should be done. Time is poorly allocated, and the most important tasks are left to the last
moment. The perfectionism and self-imposed high standards of performance cause significant
dysfunction and distress in these individuals. They may become so involved in making every

detail of a project absolutely perfect that the project is never finished (Criterion 2). For example,
the completion of a written report is delayed by numerous time-consuming rewrites that all come
up short of “perfection.” Deadlines are routinely missed or the individual has a pattern of
exerting extraordinary effort (e.g., working through the night, skipping meals) in order to make
the deadline at the last moment, and aspects of the individual’s life that are not the current focus
of activity may fall into disarray.
Individuals with obsessive-compulsive personality disorder display excessive devotion to
work and productivity to the exclusion or devaluing of leisure activities and friendships
(Criterion 3). This behavior is not accounted for by economic necessity. They often feel that they
do not have time to take an evening or a weekend day off to go on an outing or to just relax.
They may keep postponing a pleasurable activity, such as a vacation, so that it may never occur.
When they reluctantly take time for leisure activities or vacations, they are very uncomfortable
unless they have taken along something to work on so they do not “waste time.” There may be a
great concentration on household chores (e.g., repeated excessive cleaning so that “one could eat
off the floor”). If they spend time with friends, it is likely to be in some kind of formally
organized activity (e.g., sports). Hobbies or recreational activities are approached as serious tasks
or with methodical intensity, requiring careful organization and hard work to master. The
emphasis is on perfect performance. These individuals turn play into a structured work-like task
(e.g., correcting an infant for not putting rings on the post in the right order; telling a toddler to
ride their tricycle in a straight line; turning a baseball game into a harsh “lesson”).
Individuals 
with 
obsessive-compulsive 
personality 
disorder 
may 
be 
excessively
conscientious, scrupulous, and inflexible about matters of morality, ethics, or values (Criterion
4). They may force themselves and others to follow rigid moral principles and very strict
standards of performance. They may also be mercilessly self-critical about their own
mistakes or harshly judgmental of others’ moral or ethical missteps. Individuals with this
disorder are rigidly deferential to authority and rules and insist on quite literal compliance, with
no rule bending for extenuating circumstances. For example, the individual will not lend a dollar
to a friend who is short of the fare needed to get on a bus because “neither a borrower nor a
lender be” or because it would be “bad” for the friend’s character. These qualities should not be
accounted for by the individual’s cultural or religious identification.
Individuals with this disorder may be unable to discard worn-out or worthless objects, even
when they have no sentimental value (Criterion 5). Often these individuals will admit to being
“pack rats.” They regard discarding objects as wasteful because “you never know when you
might need something.” The clutter may also result from an accumulation of partially read
learning material or unfinished projects that the individual intends to get to someday but that
have been sidelined because of procrastination and/or a meticulous yet slow work style. These
individuals will become upset if someone tries to get rid of the things they have saved. Their
spouses or roommates may complain about the amount of space taken up by old parts, piles of
reading material, broken appliances, and so on.
Individuals with obsessive-compulsive personality disorder are reluctant to delegate tasks or
to work with others (Criterion 6). They stubbornly and unreasonably insist that everything be
done their way and that people conform to their way of doing things. They often give very

detailed instructions about how things should be done (e.g., there is one and only one way to
mow the lawn, wash the dishes, load the dishwasher, build a doghouse), even to the point of
micromanaging others, and are surprised and irritated if others suggest creative alternatives. At
other times they may reject offers of help even when behind schedule because they believe no
one else can do it right.
Individuals with this disorder may be miserly and stingy (having difficulty spending money
on both themselves and others) and maintain a standard of living far below what they can afford,
believing that spending must be tightly controlled to provide for future catastrophes (Criterion 7).
Obsessive-compulsive personality disorder is characterized by rigidity and stubbornness
(Criterion 8). Individuals with this disorder are so concerned about having things done the one
“correct” way that they have trouble going along with anyone else’s ideas. These individuals
plan ahead in meticulous detail and are unwilling to consider changes to these plans or their
usual routines. Totally wrapped up in their own perspective, they have difficulty acknowledging
the viewpoints of others. Friends and colleagues may become frustrated by this constant rigidity.
Even when individuals with obsessive-compulsive personality disorder recognize that it may be
in their interest to compromise, they may stubbornly refuse to do so, arguing that it is “the
principle of the thing.”
Associated Features
When rules and established procedures do not dictate the correct answer, decision-making may
become a time-consuming, often painful process (e.g., exhaustively researching options before
making a purchase). Individuals with obsessive-compulsive personality disorder may have such
difficulty deciding which tasks take priority or what is the best way of doing some particular task
that they may never get started on anything. They are prone to become upset or angry in
situations in which they are not able to maintain control of their physical or interpersonal
environment, although the anger is typically not expressed directly. For example, an individual
may be angry when service in a restaurant is poor, but instead of complaining to the
management, the individual ruminates about how much to leave as a tip. On other occasions,
anger may be expressed with righteous indignation over a seemingly minor matter. Individuals
with this disorder may be especially attentive to their relative status in dominance-submission
relationships and may display excessive deference to an authority they respect and excessive
resistance to authority they do not respect.
Individuals with this disorder have difficulty relating to and sharing emotions. For example,
they may express affection in a highly controlled or stilted fashion and may be very
uncomfortable in the presence of others who are emotionally expressive. Their everyday
relationships have a formal and serious quality, and they may be stiff in situations in which
others would smile and be happy (e.g., greeting a lover at the airport). They carefully hold
themselves back until they are sure that whatever they say will be perfect. They may be
preoccupied with logic and intellect and intolerant of displays of emotion in others. They often
have difficulty expressing tender feelings, rarely paying compliments. Individuals with this
disorder may experience occupational difficulties and distress, particularly when confronted with

Obsessive-compulsive disorder (OCD).
Hoarding disorder.
Other personality disorders and personality traits.
new situations that demand flexibility and compromise.
Prevalence
The estimated prevalence of obsessive-compulsive personality disorder based on a probability
subsample from Part II of the National Comorbidity Survey Replication was 2.4%. The
prevalence of obsessive-compulsive personality disorder in the National Epidemiologic Survey
on Alcohol and Related Conditions was 7.9%. A review of five epidemiological studies (three in
the United States) found a median prevalence of 4.7%.
Culture-Related Diagnostic Issues
In assessing an individual for obsessive-compulsive personality disorder, the clinician should not
include those behaviors that reflect habits, customs, or interpersonal styles that are culturally
sanctioned by the individual’s reference group. Certain cultural communities place substantial
emphasis on work and productivity, and some members of sociocultural groups (e.g., certain
religious groups, professions, migrants) may at times rigidly embrace codes of conduct; work
demands; restrictive social environments; rules of behavior; or standards that emphasize
overconscientiousness, moral scrupulosity, and striving for perfectionism that may be reinforced
by norms of the cultural group. Such behaviors should not on their own be considered indications
of obsessive-compulsive personality disorder.
Sex- and Gender-Related Diagnostic Issues
In large population-based studies, obsessive-compulsive personality disorder appears to be
equally prevalent in men and women.
Differential Diagnosis
Despite the similarity in names, OCD is usually easily
distinguished from obsessive-compulsive personality disorder by the presence of true obsessions
and compulsions in OCD. When criteria for both obsessive-compulsive personality disorder and
OCD are met, both diagnoses should be recorded.
A diagnosis of hoarding disorder should be considered especially when
hoarding is extreme (e.g., accumulated stacks of worthless objects present a fire hazard and make
it difficult for others to walk through the house). When criteria for both obsessive-compulsive
personality disorder and hoarding disorder are met, both diagnoses should be recorded.
Other personality disorders may be confused with
obsessive-compulsive personality disorder because they have certain features in common. It is,
therefore, important to distinguish among these disorders based on differences in their
characteristic features. However, if an individual has personality
features that meet criteria for one or more personality disorders in addition to obsessivecompulsive personality disorder, all can be diagnosed. Individuals with narcissistic personality
disorder may also profess a commitment to perfectionism and believe that others cannot do

Personality change due to another medical condition.
Substance use disorders.
F07.0
things as well, but these individuals are more likely to believe that they have achieved perfection,
whereas those with obsessive-compulsive personality disorder are usually self-critical.
Individuals with narcissistic or antisocial personality disorder lack generosity but will indulge
themselves, whereas those with obsessive-compulsive personality disorder adopt a miserly
spending style toward both self and others. Both schizoid personality disorder and obsessivecompulsive personality disorder may be characterized by an apparent formality and social
detachment. In obsessive-compulsive personality disorder, this stems from discomfort with
emotions and excessive devotion to work, whereas in schizoid personality disorder there is a
fundamental lack of capacity for intimacy.
Obsessive-compulsive personality traits in moderation may be especially adaptive,
particularly in situations that reward high performance. Only when these traits are inflexible,
maladaptive, and persisting and cause significant functional impairment or subjective distress do
they constitute obsessive-compulsive personality disorder.
Obsessive-compulsive 
personality 
disorder
must be distinguished from personality change due to another medical condition, in which the
traits are a direct physiological consequence of another medical condition.
Obsessive-compulsive personality disorder must also be distinguished
from symptoms that may develop in association with persistent substance use.
Comorbidity
Individuals with anxiety disorders (e.g., generalized anxiety disorder, separation anxiety
disorder, social anxiety disorder, specific phobias) and OCD have an increased likelihood of
having a personality disturbance that meets criteria for obsessive-compulsive personality
disorder. Even so, it appears that the majority of individuals with OCD do not have a pattern of
behavior that meets criteria for this personality disorder. Many of the features of obsessivecompulsive personality disorder overlap with “type A” personality characteristics (e.g.,
preoccupation with work, competitiveness, time urgency), and these features may be present in
individuals at risk for myocardial infarction. There may be an association between obsessivecompulsive personality disorder and depressive and bipolar disorders and eating disorders.
Other Personality Disorders
Personality Change Due to Another Medical Condition
Diagnostic Criteria
A. A persistent personality disturbance that represents a change from the
individual’s previous characteristic personality pattern.
Note: In children, the disturbance involves a marked deviation from normal
development or a significant change in the child’s usual behavior patterns, lasting

at least 1 year.
B. There is evidence from the history, physical examination, or laboratory findings
that the disturbance is the direct pathophysiological consequence of another
medical condition.
C. The disturbance is not better explained by another mental disorder (including
another mental disorder due to another medical condition).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Specify whether:
Labile type: If the predominant feature is affective lability.
Disinhibited type: If the predominant feature is poor impulse control as
evidenced by sexual indiscretions, etc.
Aggressive type: If the predominant feature is aggressive behavior.
Apathetic type: If the predominant feature is marked apathy and indifference.
Paranoid type: If the predominant feature is suspiciousness or paranoid
ideation.
Other type: If the presentation is not characterized by any of the above
subtypes.
Combined type: If more than one feature predominates in the clinical picture.
Unspecified type
Coding note: Include the name of the other medical condition (e.g., F07.0
personality change due to temporal lobe epilepsy). The other medical condition
should be coded and listed separately immediately before the personality change
due to another medical condition (e.g., G40.209 temporal lobe epilepsy; F07.0
personality change due to temporal lobe epilepsy).
Subtypes
The particular personality change can be specified by indicating the symptom presentation that
predominates in the clinical presentation.
Diagnostic Features
The essential feature of a personality change due to another medical condition is a persistent
personality disturbance that is judged to be a physiological consequence of another medical
condition. The personality disturbance represents a change from the individual’s previous
characteristic personality pattern. In children, this condition may be manifested as a marked
deviation from normal development rather than as a change in a stable personality pattern
(Criterion A). There must be evidence from the history, physical examination, or laboratory

Chronic medical conditions associated with pain and disability.
Delirium or major neurocognitive disorder.
findings that the personality change is the direct physiological consequence of another medical
condition (Criterion B). The diagnosis is not given if the disturbance is better explained by
another mental disorder (Criterion C). The diagnosis is not given if the disturbance occurs
exclusively during the course of a delirium (Criterion D). The disturbance must also cause
clinically significant distress or impairment in social, occupational, or other important areas of
functioning (Criterion E).
Common manifestations of the personality change include affective instability, poor impulse
control, outbursts of aggression or rage grossly out of proportion to any precipitating
psychosocial stressor, marked apathy, suspiciousness, or paranoid ideation. The phenomenology
of the change is indicated using the subtypes listed in the criteria set. An individual with the
disorder is often characterized by others as “not himself [or herself].” Although it shares the term
“personality” with the other personality disorders, this diagnosis is distinct by virtue of its
specific etiology, different phenomenology, and more variable onset and course.
The clinical presentation in a given individual may depend on the nature and localization of
the pathological process. For example, injury to the frontal lobes may yield
symptoms such as lack of judgment or foresight, facetiousness, disinhibition, and euphoria.
In this example, the diagnosis of personality change due to frontal lobe injury would be made if a
persistent personality disturbance is a deviation from the individual’s previous characteristic
personality pattern prior to the injury (Criterion A). Right hemisphere strokes have often been
shown to evoke personality changes in association with unilateral spatial neglect, anosognosia
(i.e., inability of the individual to recognize a bodily or functional deficit, such as the existence
of hemiparesis), motor impersistence, and other neurological deficits.
Associated Features
A variety of neurological and other medical conditions may cause personality changes, including
central nervous system neoplasms, head trauma, cerebrovascular disease, Huntington’s disease,
epilepsy, infectious conditions with central nervous system involvement (e.g., HIV), endocrine
conditions (e.g., hypothyroidism, hypo- and hyperadrenocorticism), and autoimmune conditions
with central nervous system involvement (e.g., systemic lupus erythematosus). The associated
physical examination findings, laboratory findings, and patterns of prevalence and onset reflect
those of the neurological or other medical condition involved.
Differential Diagnosis
Chronic medical conditions associated
with pain and disability can also be associated with changes in personality. The diagnosis of
personality change due to another medical condition is given only if a direct pathophysiological
mechanism can be established. This diagnosis is not given if the change is due to a behavioral or
psychological adjustment or response to another medical condition (e.g., dependent behaviors
that result from a need for the assistance of others following a severe head trauma,
cardiovascular disease, or dementia).
Personality change is a frequently associated feature of a

Another mental disorder due to another medical condition.
Substance use disorders.
Other mental disorders.
Other personality disorders.
delirium or major neurocognitive disorder. A separate diagnosis of personality change due to
another medical condition is not given if the change occurs exclusively during the course of a
delirium. However, the diagnosis of personality change due to another medical condition may be
given in addition to the diagnosis of major neurocognitive disorder if the personality change is
judged to be a physiological consequence of the pathological process causing the neurocognitive
disorder and if the personality change is a prominent part of the clinical presentation.
The diagnosis of personality change due to
another medical condition is not given if the disturbance is better explained by another mental
disorder due to another medical condition (e.g., depressive disorder due to brain tumor).
Personality changes may also occur in the context of substance use
disorders, especially if the disorder is long-standing. The clinician should inquire carefully about
the nature and extent of substance use. If the clinician wishes to indicate an etiological
relationship between the personality change and substance use, the other specified category for
the specific substance can be used (e.g., other specified stimulant-related disorder with
personality change).
Marked personality changes may also be an associated feature of other
mental disorders (e.g., schizophrenia; delusional disorder; depressive and bipolar disorders; other
specified and unspecified disruptive behavior, impulse-control, and conduct disorders; panic
disorder). However, in these disorders, no specific physiological factor is judged to be
etiologically related to the personality change.
Personality change due to another medical condition can be
distinguished from a personality disorder by the requirement for a clinically significant change
from baseline personality functioning and the presence of a specific etiological medical
condition.
Other Specified Personality Disorder
F60.89
This category applies to presentations in which symptoms characteristic of a
personality disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the personality disorders diagnostic class.
The other specified personality disorder category is used in situations in which the
clinician chooses to communicate the specific reason that the presentation does not
meet the criteria for any specific personality disorder. This is done by recording
“other specified personality disorder” followed by the specific reason (e.g., “mixed
personality features”).

Unspecified Personality Disorder
F60.9
This category applies to presentations in which symptoms characteristic of a
personality disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the personality disorders diagnostic class.
The unspecified personality disorder category is used in situations in which the
clinician chooses not to specify the reason that the criteria are not met for a specific
personality disorder and includes presentations in which there is insufficient
information to make a more specific diagnosis.

# 19 - Paraphilic Disorders

# Paraphilic Disorders

779

Paraphilic Disorders
Paraphilic disorders included in this manual are voyeuristic disorder (spying on others
in private activities), exhibitionistic disorder (exposing the genitals), frotteuristic disorder
(touching or rubbing against a nonconsenting person), sexual masochism disorder (undergoing
humiliation, bondage, or suffering), sexual sadism disorder (inflicting humiliation, bondage, or
suffering), pedophilic disorder (sexual focus on children), fetishistic disorder (using nonliving
objects or having a highly specific focus on nongenital body parts), and transvestic disorder
(engaging in sexually arousing cross-dressing). These disorders have traditionally been selected
for specific listing and assignment of explicit diagnostic criteria in DSM for two main reasons:
they are relatively common, in relation to other paraphilic disorders, and some of them entail
actions for their satisfaction that, because of their noxiousness or potential harm to others, are
classed as criminal offenses. The eight listed disorders do not exhaust the list of possible
paraphilic disorders. Many dozens of distinct paraphilias have been identified and named, and
almost any of them could, by virtue of its negative consequences for the individual or for others,
rise to the level of a paraphilic disorder.
In this chapter, the order of presentation of the listed paraphilic disorders generally
corresponds to common classification schemes for these conditions. The first group of disorders
is based on anomalous activity preferences. These disorders are subdivided into courtship
disorders, which resemble distorted components of human courtship behavior (voyeuristic
disorder, exhibitionistic disorder, and frotteuristic disorder), and algolagnic disorders, which
involve pain and suffering (sexual masochism disorder and sexual sadism disorder). The second
group of disorders is based on anomalous target preferences. These disorders include one
directed at other humans (pedophilic disorder) and two directed elsewhere (fetishistic disorder
and transvestic disorder).
The term paraphilia denotes any intense and persistent sexual interest other than sexual
interest in genital stimulation or preparatory fondling with phenotypically normal, physically
mature, consenting human partners. In some circumstances, the criteria “intense and persistent”
may be difficult to apply, such as in the assessment of persons who are very old or medically ill
and who may not have “intense” sexual interests of any kind. In such circumstances, the term
paraphilia may be defined as any sexual interest greater than or equal to nonparaphilic sexual
interests. There are also specific paraphilias that are generally better described as preferential
sexual interests than as intense sexual interests.
Some paraphilias primarily concern the individual’s erotic activities, and others primarily
concern the individual’s erotic targets. Examples of the former would include intense and
persistent interests in spanking, whipping, cutting, binding, or strangulating another person, or an
interest in these activities that equals or exceeds the individual’s interest in copulation or
equivalent interaction with another person. Examples of the latter would include intense or
preferential sexual interest in children, corpses, or amputees (as a class), as well as intense or

F65.3
preferential interest in nonhuman animals, such as horses or dogs, or in inanimate objects, such
as shoes or articles made of rubber. An individual’s pattern of paraphilic interests is often
reflected in his or her choice of pornography.
A paraphilic disorder is a paraphilia that is currently causing distress or impairment to the
individual or a paraphilia whose satisfaction has entailed personal harm, or risk of harm, to
others. A paraphilia is a necessary but not a sufficient condition for having a paraphilic disorder,
and a paraphilia by itself does not necessarily justify or require clinical intervention.
In the diagnostic criteria set for each of the listed paraphilic disorders, Criterion A specifies
the qualitative nature of the paraphilia (e.g., an erotic focus on children or on exposing the
genitals to strangers), and Criterion B specifies the negative consequences of the paraphilia (i.e.,
distress, impairment, or harm to others). In keeping with the distinction between paraphilias and
paraphilic disorders, the term diagnosis should be reserved for individuals whose paraphilic
interests or behaviors meet both Criteria A and B (i.e., individuals who have a paraphilic
disorder). If an individual’s paraphilic interests or behaviors meet Criterion A but not Criterion B
for a particular paraphilia—a circumstance that might arise when a benign paraphilia is
discovered during the clinical investigation of some other condition—then the individual may be
said to have that paraphilia but not a paraphilic disorder.
It is not rare for an individual to manifest two or more paraphilias. In some cases, the
paraphilic foci are closely related and the connection between the paraphilias is intuitively
comprehensible (e.g., foot fetishism and shoe fetishism). In other cases, the connection between
the paraphilias is not obvious, and the presence of multiple paraphilias may be coincidental or
else related to some generalized vulnerability to anomalies of psychosexual development. In any
event, comorbid diagnoses of separate paraphilic disorders may be warranted if more than one
paraphilia is causing suffering to the individual or harm to others.
Because of the two-pronged nature of diagnosing paraphilic disorders, clinician-rated or selfrated measures and severity assessments could address either the strength of the paraphilia itself
or the seriousness of its consequences. Although the distress and impairment stipulated in the
Criterion B are special in being the immediate or ultimate result of the paraphilia and not
primarily the result of some other factor, the phenomena of reactive depression, anxiety, guilt,
poor work history, impaired social relations, and so on are not unique in themselves and may be
quantified with multipurpose measures of psychosocial functioning or quality of life.
Voyeuristic Disorder
Diagnostic Criteria
A. Over a period of at least 6 months, recurrent and intense sexual arousal from
observing an unsuspecting person who is naked, in the process of disrobing, or
engaging in sexual activity, as manifested by fantasies, urges, or behaviors.
B. The individual has acted on these sexual urges with a nonconsenting person, or

the sexual urges or fantasies cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
C. The individual experiencing the arousal and/or acting on the urges is at least 18
years of age.
Specify if:
In a controlled environment: This specifier is primarily applicable to individuals
living in institutional or other settings where opportunities to engage in
voyeuristic behavior are restricted.
In full remission: The individual has not acted on the urges with a
nonconsenting person, and there has been no distress or impairment in social,
occupational, or other areas of functioning, for at least 5 years while in an
uncontrolled environment.
Specifiers
The “in full remission” specifier does not address the continued presence or absence of
voyeurism per se, which may still be present after behaviors and distress have remitted.
Diagnostic Features
The diagnostic criteria for voyeuristic disorder can apply both to individuals who more or less
freely disclose this paraphilic interest and to those who categorically deny any sexual arousal
from observing an unsuspecting person who is naked, disrobing, or engaged in sexual activity
despite substantial objective evidence to the contrary. If disclosing individuals also report
distress or psychosocial problems because of their voyeuristic sexual preferences, they could be
diagnosed with voyeuristic disorder. On the other hand, if they declare no distress, demonstrated
by lack of anxiety, obsessions, guilt, or shame, about these paraphilic impulses and are not
impaired in other important areas of functioning because of this sexual interest, and their
psychiatric or legal histories indicate that they do not act on it, they could be ascertained as
having voyeuristic sexual interest but should not be diagnosed with voyeuristic disorder.
Nondisclosing individuals include, for example, individuals known to have been spying
repeatedly on unsuspecting persons who are naked or engaging in sexual activity on separate
occasions but who deny any urges or fantasies concerning such sexual behavior, and who may
report that known episodes of watching unsuspecting naked or sexually active persons were all
accidental and nonsexual. Others may disclose past episodes of observing unsuspecting naked or
sexually active persons but contest any significant or sustained sexual interest in this behavior.
Since these individuals deny having fantasies or impulses about watching others nude or
involved in sexual activity, it follows that they would also reject feeling subjectively distressed
or socially impaired by such impulses. Despite their nondisclosing stance, such individuals may
be diagnosed with voyeuristic disorder. Recurrent voyeuristic behavior constitutes sufficient
support for voyeurism (by fulfilling Criterion A) and simultaneously demonstrates that this
paraphilically motivated behavior is causing harm to others (by fulfilling Criterion B).
“Recurrent” spying on unsuspecting persons who are naked or engaging in sexual activity

Temperamental.
Environmental.
may be interpreted as requiring multiple victims, each on a separate occasion; this requirement
for multiple victims on separate occasions is relevant because it increases the confidence in the
clinical inference that the individual is motivated by voyeuristic disorder. Fewer victims can be
interpreted as satisfying this criterion if there were multiple occasions of watching the same
victim or if there is corroborating evidence of a distinct or preferential interest in secret watching
of naked or sexually active unsuspecting persons. Note that multiple victims, as suggested
earlier, are a sufficient but not a necessary condition for diagnosis; the criteria may also be met if
the individual acknowledges intense voyeuristic sexual interest.
Adolescence and puberty generally increase sexual curiosity and activity. To reduce the risk
of pathologizing normative sexual interest and behavior during pubertal adolescence, the
minimum age for the diagnosis of voyeuristic disorder is 18 years (Criterion C).
Prevalence
The population prevalence of individuals whose presentations meet the full criteria for
voyeuristic disorder is unknown. Voyeuristic acts, however, are the most common of potentially
law-breaking sexual behaviors. For example, in a Quebec Internet and phone survey sample, the
lifetime prevalence of voyeuristic behaviors was reported to be as high as 34.5% (50.3% in men,
21.2% in women). Because this same study found that an “intense desire” and “persistent
behavior” occur with much less frequency (9.6% and 2.1%, respectively), the prevalence of
voyeuristic disorder is likely much lower. The ratio of voyeuristic behavior in men to women
was approximately 2:1 in the Quebec sample and 3:1 in a Swedish general population sample. In
a study determining which particular disorders were prevalent
in individuals incarcerated for sexual offenses, a study of 1,346 incarcerated sex offenders from
Austria found a prevalence of voyeuristic disorder of 3.7%.
Development and Course
Adult men with voyeuristic disorder often first become aware of their sexual interest in secretly
watching unsuspecting persons during adolescence. However, the minimum age for a diagnosis
of voyeuristic disorder is 18 years because there is substantial difficulty in differentiating it from
age-appropriate puberty-related sexual curiosity and activity. The persistence of voyeurism over
time is unclear. With or without treatment of voyeuristic disorder, the subjective distress (e.g.,
guilt, shame, intense sexual frustration, loneliness) or impairment from the disorder may change
over time, as may a number of factors that may potentially affect the course of the disorder, such
as psychiatric morbidity, hypersexuality, and sexual impulsivity. Thus, the severity and course
may vary over time. As with other sexual preferences, advancing age may be associated with
decreasing voyeuristic sexual preferences and behavior.
Risk and Prognostic Factors
Because voyeurism is a necessary precondition for voyeuristic disorder, risk
factors for voyeurism should also increase the risk of voyeuristic disorder.
Childhood 
sexual 
abuse, 
substance 
misuse, 
and 
sexual

Voyeurism.
Manic episode, major neurocognitive disorder, intellectual developmental disorder, personality
change due to another medical condition, substance intoxication, and schizophrenia.
Conduct disorder and antisocial personality disorder.
F65.2
preoccupation/hypersexuality have been suggested as risk factors, although the causal
relationship to voyeuristic behavior is uncertain and the specificity unclear.
Sex- and Gender-Related Diagnostic Issues
Voyeuristic disorder is very uncommon among women in clinical settings, whereas the ratio in
men to women for single sexually arousing voyeuristic acts is less extreme and may be 2:1–3:1.
Differential Diagnosis
Individuals with voyeurism experience recurrent, intense sexual arousal from the act
of observing an unsuspecting person who is naked, in the process of disrobing, or engaging in
sexual activity. Unless the individual acts on these urges with an unsuspecting person (e.g.,
surreptitiously peeping through a neighbor’s window) or unless there is accompanying clinically
significant distress or impairment in social, occupational, or other important areas of functioning,
a diagnosis of voyeuristic disorder is not warranted.
Individuals with a major neurocognitive disorder, intellectual developmental disorder,
personality change due to another medical condition, or schizophrenia, or who are in a manic
episode or experiencing substance intoxication, may become sexually disinhibited or have
impaired judgment or impulse control and engage in voyeuristic behavior. Unless that behavior
occurs at times other than in the context of one of these disorders, a diagnosis of voyeuristic
disorder should not be made.
Conduct disorder in adolescents and antisocial
personality disorder would be characterized by additional norm-breaking and antisocial
behaviors, and the specific sexual interest in secretly watching unsuspecting others who are
naked or engaging in sexual activity will usually be lacking.
Comorbidity
Known comorbidities in voyeuristic disorder are largely based on research with males suspected
of or convicted for acts involving the secret watching of unsuspecting nude or
sexually active persons. Hence, these comorbidities might not apply to all individuals with
voyeuristic disorder. Conditions that occur comorbidly with voyeuristic disorder include
hypersexuality and other paraphilic disorders, particularly exhibitionistic disorder. Depressive,
bipolar, anxiety, and substance use disorders; attention-deficit/hyperactivity disorder; and
conduct disorder and antisocial personality disorder are also frequent comorbid conditions.
Exhibitionistic Disorder
Diagnostic Criteria

A. Over a period of at least 6 months, recurrent and intense sexual arousal from the
exposure of one’s genitals to an unsuspecting person, as manifested by
fantasies, urges, or behaviors.
B. The individual has acted on these sexual urges with a nonconsenting person, or
the sexual urges or fantasies cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
Specify whether:
Sexually aroused by exposing genitals to prepubertal children
Sexually aroused by exposing genitals to physically mature individuals
Sexually aroused by exposing genitals to prepubertal children and to
physically mature individuals
Specify if:
In a controlled environment: This specifier is primarily applicable to individuals
living in institutional or other settings where opportunities to expose one’s
genitals are restricted.
In full remission: The individual has not acted on the urges with a
nonconsenting person, and there has been no distress or impairment in social,
occupational, or other areas of functioning, for at least 5 years while in an
uncontrolled environment.
Subtypes
The subtypes for exhibitionistic disorder are based on the age or physical maturity of the
nonconsenting persons to whom the individual prefers to expose his or her genitals. The
nonconsenting persons could be prepubescent children, adults, or both. This specifier should help
draw adequate attention to characteristics of victims of individuals with exhibitionistic disorder
to prevent co-occurring pedophilic disorder from being overlooked. However, indications that
the individual with exhibitionistic disorder is sexually attracted to exposing his or her genitals to
children should not preclude a diagnosis of pedophilic disorder.
Specifiers
The “in full remission” specifier does not address the continued presence or absence of
exhibitionism per se, which may still be present after behaviors and distress have remitted.
Diagnostic Features
The diagnostic criteria for exhibitionistic disorder can apply both to individuals who more or less
freely disclose this paraphilia and to those who categorically deny any sexual arousal from
exposing their genitals to unsuspecting persons despite substantial objective evidence to the
contrary. If disclosing individuals also report psychosocial difficulties because of their sexual
attractions or preferences for exposing, they may be diagnosed with exhibitionistic

disorder. In contrast, if they declare no distress (exemplified by absence of anxiety, obsessions,
and guilt or shame about these paraphilic impulses) and are not impaired by this sexual interest
in other important areas of functioning, and their self-reported, psychiatric, or legal histories
indicate that they do not act on them, they could be ascertained as having exhibitionistic sexual
interest but not be diagnosed with exhibitionistic disorder.
Examples of nondisclosing individuals include those who have exposed themselves
repeatedly to unsuspecting persons on separate occasions but who deny any urges or fantasies
about such sexual behavior and who report that known episodes of exposure were all accidental
and nonsexual. Others may disclose past episodes of sexual behavior involving genital exposure
but refute any significant or sustained sexual interest in such behavior. Since these individuals
deny having urges or fantasies involving genital exposure, it follows that they would also deny
feeling subjectively distressed or socially impaired by such impulses. Such individuals may be
diagnosed with exhibitionistic disorder despite their negative self-report. Recurrent
exhibitionistic behavior constitutes sufficient support for exhibitionism (Criterion A) and
simultaneously demonstrates that this paraphilically motivated behavior is causing harm to
others (Criterion B).
“Recurrent” genital exposure to unsuspecting others may be interpreted as requiring multiple
victims, each on a separate occasion; this requirement for multiple victims on separate occasions
is relevant because it increases the confidence in the clinical inference that the individual is
motivated by exhibitionistic disorder. Fewer victims can be interpreted as satisfying this criterion
if there were multiple occasions of exposure to the same victim, or if there is corroborating
evidence of a strong or preferential interest in genital exposure to unsuspecting persons. Note
that multiple victims, as suggested earlier, are a sufficient but not a necessary condition for
diagnosis, as criteria may be met by an individual’s acknowledging intense exhibitionistic sexual
interest with distress or impairment.
Prevalence
The population prevalence of individuals whose presentations meet the full criteria for
exhibitionistic disorder is unknown, although the disorder is highly unusual in women.
Exhibitionistic acts, however, are not uncommon, and single sexually arousing exhibitionistic
acts occur up to half as often among women compared with men. In a Quebec Internet and phone
survey sample, lifetime prevalence of exhibitionistic behaviors was reported to be 30.9% (32.6%
in men, 29.4% in women). Because this same study found that an “intense desire” and “persistent
behavior” occur with much less frequency (4.8% and 0.8%, respectively), the prevalence of
exhibitionistic disorder is likely much lower. For example, a Swedish study suggested that the
lifetime prevalence of exhibitionistic disorder in the general population was 4.1% in men and
2.1% in women.
Development and Course
Adult men with exhibitionistic disorder often report that they first became aware of sexual
interest in exposing their genitals to unsuspecting persons during adolescence, at a somewhat
later time than the typical development of normative sexual interest in women or men. Although
there is no minimum age requirement for the diagnosis of exhibitionistic disorder, it may be
difficult to differentiate exhibitionistic behaviors from age-appropriate sexual curiosity in

Temperamental.
Environmental.
Exhibitionism.
Manic episode, major neurocognitive disorder, intellectual developmental disorder, personality
change due to another medical condition, substance intoxication, and schizophrenia.
Conduct disorder and antisocial personality disorder.
adolescents. Whereas exhibitionistic impulses appear to emerge in adolescence or early
adulthood, very little is known about persistence over time. With or without treatment of
exhibitionistic disorder, the subjective distress (e.g., guilt, shame, intense sexual frustration,
loneliness) or impairment from the disorder may change over time, as may a number of factors
that may potentially affect the course of the disorder, such as psychiatric morbidity,
hypersexuality, and sexual impulsivity. Thus, the severity and course may vary over time. As
with other sexual preferences, advancing age may be associated with decreasing exhibitionistic
sexual preferences and behavior.
Risk and Prognostic Factors
Because exhibitionism is a necessary precondition for exhibitionistic disorder,
risk factors for exhibitionism should also increase the risk of exhibitionistic disorder. Antisocial
history, antisocial personality disorder, alcohol misuse, and pedophilic sexual preference might
increase risk of sexual recidivism in exhibitionistic offenders. Hence, antisocial personality
disorder, alcohol use disorder, and pedophilic interest may be considered risk factors for
exhibitionistic disorder in men with exhibitionistic sexual preferences.
Childhood sexual and emotional abuse and sexual preoccupation/hypersexuality
have been suggested as risk factors for exhibitionism, although the causal relationship to
exhibitionism is uncertain and the specificity unclear.
Differential Diagnosis
Individuals with exhibitionism experience recurrent, intense sexual arousal from
the act of exposing their genitals to an unsuspecting person. Unless the individual acts on these
urges with an unsuspecting person (e.g., exposing his genitals to riders on a train) or unless there
is accompanying clinically significant distress or impairment in social, occupational, or other
important areas of functioning, a diagnosis of exhibitionistic disorder is not warranted.
Individuals with a major neurocognitive disorder, intellectual developmental disorder,
personality change due to another medical condition, or schizophrenia, or who are in a manic
episode or experiencing substance intoxication, may become sexually disinhibited or have
impaired judgment or impulse control and engage in exhibitionistic behavior. Unless that
behavior occurs at times other than in the context of one of these disorders, a diagnosis of
exhibitionistic disorder should not be made.
Conduct disorder in adolescents and antisocial
personality disorder would be characterized by additional norm-breaking and antisocial
behaviors, and the specific sexual interest in exposing the genitals will usually be lacking.
Comorbidity
Known comorbidities in exhibitionistic disorder are largely based on research with individuals
(almost all men) convicted for criminal acts involving genital exposure to nonconsenting
persons. Hence, these comorbidities might not apply to all individuals who qualify for a

F65.81
diagnosis of exhibitionistic disorder. Conditions that occur comorbidly with exhibitionistic
disorder at high rates include depressive, bipolar, anxiety, and substance use disorders;
hypersexuality; attention-deficit/hyperactivity disorder; other paraphilic disorders; and antisocial
personality disorder.
Frotteuristic Disorder
Diagnostic Criteria
A. Over a period of at least 6 months, recurrent and intense sexual arousal from
touching or rubbing against a nonconsenting person, as manifested by fantasies,
urges, or behaviors.
B. The individual has acted on these sexual urges with a nonconsenting person, or
the sexual urges or fantasies cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
Specify if:
In a controlled environment: This specifier is primarily applicable to individuals
living in institutional or other settings where opportunities to touch or rub against
a nonconsenting person are restricted.
In full remission: The individual has not acted on the urges with a
nonconsenting person, and there has been no distress or impairment in social,
occupational, or other areas of functioning, for at least 5 years while in an
uncontrolled environment.
Specifiers
The “in remission” specifier does not address the continued presence or absence of frotteurism
per se, which may still be present after behaviors and distress have remitted.
Diagnostic Features
The diagnostic criteria for frotteuristic disorder can apply both to individuals who relatively
freely disclose this paraphilia and to those who firmly deny any sexual arousal from touching or
rubbing against a nonconsenting person regardless of considerable objective evidence to the
contrary. If disclosing individuals also report psychosocial impairment because of their sexual
preferences for touching or rubbing against a nonconsenting person, they could be diagnosed
with frotteuristic disorder. In contrast, if they declare no distress (demonstrated by lack of
anxiety, obsessions, guilt, or shame) about these paraphilic impulses and are not impaired in
other important areas of functioning because of this sexual interest, and their psychiatric or legal
histories indicate that they do not act on it, they could be ascertained as having frotteuristic

sexual interest but should not be diagnosed with frotteuristic disorder.
Nondisclosing individuals include, for instance, individuals known to have been touching or
rubbing against nonconsenting persons on separate occasions but who contest any urges or
fantasies concerning such sexual behavior. Such individuals may report that identified episodes
of touching or rubbing against an unwilling individual were all unintentional and nonsexual.
Others may disclose past episodes of touching or rubbing against nonconsenting persons but
contest any major or persistent sexual interest in this. Since these individuals deny having
fantasies or impulses about touching or rubbing, they would consequently reject feeling
distressed or psychosocially impaired by such impulses. Despite their nondisclosing position,
such individuals may be diagnosed with frotteuristic disorder. Recurrent frotteuristic behavior
constitutes satisfactory support for frotteurism (by fulfilling Criterion A) and concurrently
demonstrates that this paraphilically motivated behavior is causing harm to others (by fulfilling
Criterion B).
“Recurrent” touching or rubbing against a nonconsenting person may be interpreted as
requiring multiple victims, each on a separate occasion; this requirement for multiple victims on
separate occasions is relevant because it increases the confidence in the clinical inference that the
individual is motivated by frotteuristic disorder. Fewer victims can be interpreted as satisfying
this criterion if there were multiple occasions of touching or rubbing against the same unwilling
individual, or corroborating evidence of a strong or preferential interest in touching or rubbing
against nonconsenting persons. Note that multiple victims are a sufficient but not a necessary
condition for diagnosis; criteria may also be met if the individual acknowledges intense
frotteuristic sexual interest with clinically significant distress and/or impairment.
Prevalence
The population prevalence of individuals whose presentations meet the full criteria for
frotteuristic disorder is unknown, but frotteuristic acts, including the uninvited sexual touching of
or rubbing against another individual, may occur in up to 30% of adult men in the U.S. and
Canadian general population. Prevalence of frotteuristic disorder is certainly
much lower, considering the finding that “intense desire” and “persistent behavior” were
reported infrequently (3.8% and 0.7%, respectively). In outpatient settings for men with
paraphilic disorders and hypersexuality, approximately 10%–14% have a presentation that meets
diagnostic criteria for frotteuristic disorder. Prevalence among women is likely lower.
Development and Course
Adult men with frotteuristic disorder often report first becoming aware of their sexual interest in
surreptitiously touching unsuspecting persons during late adolescence or emerging adulthood.
However, children and adolescents may also touch or rub against unwilling others in the absence
of a diagnosis of frotteuristic disorder. Although there is no minimum age for the diagnosis,
frotteuristic disorder can be difficult to differentiate from conduct-disordered behavior without
sexual motivation in individuals at younger ages. The persistence of frotteurism over time is
unclear. With or without treatment of frotteuristic disorder, the subjective distress (e.g., guilt,

Temperamental.
Frotteurism.
Manic episode, major neurocognitive disorder, intellectual developmental disorder, personality
change due to another medical condition, substance intoxication, and schizophrenia.
Conduct disorder and antisocial personality disorder.
shame, intense sexual frustration, loneliness) or impairment from the disorder may change over
time, as may a number of factors that may potentially affect the course of the disorder, such as
psychiatric morbidity, hypersexuality, and sexual impulsivity. Thus, the severity and course may
vary over time. As with other sexual preferences, advancing age may be associated with
decreasing frotteuristic sexual preferences and behavior.
Risk and Prognostic Factors
Nonsexual antisocial behavior and sexual preoccupation/hypersexuality might be
nonspecific risk factors, although the causal relationship to frotteurism is uncertain and the
specificity unclear. However, because frotteurism is a necessary precondition for frotteuristic
disorder, risk factors for frotteurism should also increase the risk of frotteuristic disorder.
Differential Diagnosis
Individuals with frotteurism experience recurrent intense sexual arousal from the act
of touching or rubbing against a nonconsenting person. Unless the individual acts on these urges
with a nonconsenting person (e.g., rubbing his genitals against a passenger on a crowded subway
car) or unless there is accompanying clinically significant distress or impairment in social,
occupational, or other important areas of functioning, a diagnosis of frotteuristic disorder is not
warranted.
Individuals with a major neurocognitive disorder, intellectual developmental disorder,
personality change due to another medical condition, or schizophrenia, or who are in a manic
episode or experiencing substance intoxication, may become sexually disinhibited or have
impaired judgment or impulse control and engage in frotteuris-tic behavior. Unless that behavior
occurs at times other than in the context of one of these disorders, a diagnosis of frotteuristic
disorder should not be made.
Conduct disorder in adolescents and antisocial
personality disorder would be characterized by additional norm-breaking and antisocial
behaviors, and the specific sexual interest in touching or rubbing against a nonconsenting person
will usually be lacking.
Comorbidity
Known comorbidities in frotteuristic disorder are largely based on research with men suspected
of or convicted for criminal acts involving sexually motivated touching of or
rubbing against a nonconsenting person. Hence, these comorbidities might not apply to other
individuals with a diagnosis of frotteuristic disorder based on subjective distress over their sexual
interest. Conditions that occur comorbidly with frotteuristic disorder include hypersexuality and
other paraphilic disorders, particularly exhibitionistic disorder and voyeuristic disorder. Conduct
disorder, antisocial personality disorder, depressive disorders, bipolar disorders, anxiety
disorders, and substance use disorders also co-occur.

F65.51
Sexual Masochism Disorder
Diagnostic Criteria
A. Over a period of at least 6 months, recurrent and intense sexual arousal from the
act of being humiliated, beaten, bound, or otherwise made to suffer, as
manifested by fantasies, urges, or behaviors.
B. The fantasies, sexual urges, or behaviors cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
Specify if:
With asphyxiophilia: If the individual engages in the practice of achieving
sexual arousal related to restriction of breathing.
Specify if:
In a controlled environment: This specifier is primarily applicable to individuals
living in institutional or other settings where opportunities to engage in
masochistic sexual behaviors are restricted.
In full remission: There has been no distress or impairment in social,
occupational, or other areas of functioning for at least 5 years while in an
uncontrolled environment.
Diagnostic Features
The diagnostic criteria for sexual masochism disorder are intended to apply to individuals who
freely admit to having such paraphilic interests. Such individuals openly acknowledge intense
sexual arousal from the act of being humiliated, beaten, bound, or otherwise made to suffer, as
manifested by fantasies, urges, or behaviors. If these individuals also report psychosocial
difficulties because of their sexual attractions or preferences for being humiliated, beaten, bound,
or otherwise made to suffer, they may be diagnosed with sexual masochism disorder. In contrast,
if they declare no distress, exemplified by anxiety, obsessions, guilt, or shame, about these
paraphilic impulses, and are not hampered by them in pursuing other personal goals, they could
be ascertained as having masochistic sexual interest but should not be diagnosed with sexual
masochism disorder.
The term bondage-domination-sadism-masochism (BDSM) is broadly used to refer to a wide
range of behaviors that individuals with sexual masochism and/or sexual sadism (as well as other
individuals with similar sexual interests) engage in, such as restraints or restriction, discipline,
spanking, slapping, sensory deprivation (e.g., using blindfolds), and dominance-submission roleplay involving themes such as master/enslaved person, owner/pet, or kidnapper/victim.
Associated Features
The extensive use of pornography involving the act of being humiliated, beaten, bound, or
otherwise made to suffer is sometimes an associated feature of sexual masochism disorder.

Those who engage in sadomasochistic sexual behavior may experience a hyposensitivity to pain,
although it is unknown whether this finding applies to those with sexual masochism disorder.
Additionally, although it is often assumed that individuals with
masochistic sexual interest have a history of childhood sexual abuse experiences, there is
insufficient evidence to support this association.
Prevalence
The population prevalence of individuals whose presentations meet the full criteria for sexual
masochism disorder is unknown. In Australia, it has been estimated that 2.2% of men and 1.3%
of women had been involved in BDSM behavior in the past 12 months.
Development and Course
Individuals with paraphilias living in the community have reported a mean age at onset for
masochism of 19.3 years, although earlier ages, including puberty and childhood, have also been
reported for the onset of masochistic fantasies. Very little is known about persistence over time.
With or without treatment of sexual masochism disorder, the subjective distress (e.g., guilt,
shame, intense sexual frustration, loneliness) or impairment from the disorder may change over
time, as may a number of factors that may potentially affect the course of the disorder, such as
psychiatric morbidity, hypersexuality, and sexual impulsivity. Thus, the severity and course may
vary over time. As with other sexual preferences, advancing age may be associated with
decreasing sexual masochistic preferences and behavior.
Culture-Related Diagnostic Issues
It is important to distinguish self-harming behaviors that occur during collectively accepted
religious and spiritual practices from sadomasochistic behavior conducted for sexual arousal. For
example, collective rituals in various religions and societies include suspension from hooks, selfflagellation, self-mortification, and other painful ordeals. The role of sexual arousal or pleasure
in these practices remains unknown.
Association With Suicidal Thoughts or Behavior
Association of sexual masochism disorder with suicidal thoughts or behavior is unknown.
However, a study of 321 adults who endorsed BDSM involvement found an association of
stigma-related shame and guilt with suicidal ideation.
Functional Consequences of Sexual Masochism Disorder
The functional consequences of sexual masochism disorder are unknown. Individuals reporting
sexual interest in asphyxiophilia seem to experience more sexual distress and psychological
maladjustment than the general population. Individuals engaging in masochistic behavior are at
risk for accidental death while practicing asphyxiophilia or other autoerotic procedures.
However, the proportion of these decedents whose sexual interests and behavior fulfill diagnostic

Sexual masochism.
F65.52
criteria for sexual masochism is unknown.
Differential Diagnosis
Individuals with sexual masochism experience recurrent, intense sexual
arousal from the act of being humiliated, beaten, bound, or otherwise made to suffer. Unless the
sexual urges, fantasies, or behaviors involving being humiliated or made to suffer are
accompanied by clinically significant distress or impairment in social, occupational, or other
important areas of functioning, a diagnosis of sexual masochism disorder is not warranted.
Comorbidity
Known comorbidities with sexual masochism disorder are largely based on individuals in
treatment. Disorders that occur comorbidly with sexual masochism disorder typically
include other paraphilic disorders, such as transvestic fetishism. There is some indication of an
association of sexual masochism disorder with borderline personality disorder (based on data
from a small clinical sample of women with and without borderline personality disorder).
Sexual Sadism Disorder
Diagnostic Criteria
A. Over a period of at least 6 months, recurrent and intense sexual arousal from the
physical or psychological suffering of another person, as manifested by
fantasies, urges, or behaviors.
B. The individual has acted on these sexual urges with a nonconsenting person, or
the sexual urges or fantasies cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
Specify if:
In a controlled environment: This specifier is primarily applicable to individuals
living in institutional or other settings where opportunities to engage in sadistic
sexual behaviors are restricted.
In full remission: The individual has not acted on the urges with a
nonconsenting person, and there has been no distress or impairment in social,
occupational, or other areas of functioning, for at least 5 years while in an
uncontrolled environment.
Diagnostic Features
The diagnostic criteria for sexual sadism disorder are intended to apply both to individuals who
freely admit to having such paraphilic interests and to those who deny any sexual interest in the

physical or psychological suffering of another individual despite substantial objective evidence
to the contrary. Individuals who openly acknowledge intense sexual interest in the physical or
psychological suffering of others are referred to as “admitting individuals.” If these individuals
also report psychosocial difficulties because of their sexual attractions or preferences for the
physical or psychological suffering of another individual, they may be diagnosed with sexual
sadism disorder. In contrast, if admitting individuals declare no distress, exemplified by anxiety,
obsessions, guilt, or shame, about these paraphilic impulses, and are not hampered by them in
pursuing other goals, and their self-reported, psychiatric, or legal histories indicate that they do
not act on them with nonconsenting persons, then they could be ascertained as having sadistic
sexual interest but their presentation would not meet criteria for sexual sadism disorder.
Examples of individuals who deny any interest in the physical or psychological suffering of
another individual include individuals known to have inflicted pain or suffering on multiple
victims on separate occasions but who deny any urges or fantasies about such sexual behavior
and who may further claim that known episodes of sexual assault were either unintentional or
nonsexual. Others may admit past episodes of sexual behavior involving the infliction of pain or
suffering on a nonconsenting person but do not report any significant or sustained sexual interest
in the physical or psychological suffering of another person. Since these individuals deny having
urges or fantasies involving sexual arousal to pain and suffering, it follows that they would also
deny feeling subjectively distressed or socially impaired by such impulses. Such individuals may
be diagnosed with sexual sadism disorder despite their negative self-report. Their recurrent
behavior constitutes clinical support for the presence of the paraphilia of sexual sadism (by
satisfying Criterion A) and simultaneously demonstrates that their paraphilically motivated
behavior is causing clinically significant distress, harm, or risk of harm to others (satisfying
Criterion B).
“Recurrent” sexual sadism involving nonconsenting others may be interpreted as requiring
multiple victims, each on a separate occasion; this requirement for multiple victims on separate
occasions is relevant because it increases the confidence in the clinical inference that the
individual is motivated by sexual sadism disorder. Fewer victims can be interpreted as satisfying
this criterion, if there are multiple instances of infliction of pain and suffering to the same victim,
or if there is corroborating evidence of a strong or preferential interest in pain and suffering
involving multiple victims. Note that multiple victims, as suggested earlier, are a sufficient but
not a necessary condition for diagnosis, as the criteria may be met if the individual acknowledges
intense sadistic sexual interest.
The term bondage-domination-sadism-masochism (BDSM) is broadly used to refer to a wide
range of behaviors that individuals with sexual masochism and/or sexual sadism (as well as other
individuals with similar sexual interests) engage in, such as restraints or restriction, discipline,
spanking, slapping, sensory deprivation (e.g., using blindfolds), and dominance-submission roleplay involving themes such as master/enslaved person, owner/pet, or kidnapper/victim.
Associated Features
The extensive use of pornography involving the infliction of pain and suffering is sometimes an

Sexual sadism.
associated feature of sexual sadism disorder.
Prevalence
The population prevalence of individuals whose presentations meet the full criteria for sexual
sadism disorder is unknown and is largely based on individuals in forensic settings. Among
civilly committed sexual offenders in the United States, less than 10% have sexual sadism
disorder. Among individuals who have committed sexually motivated homicides, the proportion
of sexually sadistic behavior is about one-third.
Individuals with sexual sadism disorder in forensic samples are almost exclusively men, but a
representative sample of the population in Australia reported that 2.2% of men and 1.3% of
women said that they had been involved in BDSM behavior in the previous year. In a
population-based sample in Finland, the lifetime prevalence for sexually sadistic behavior was
2.7% among men and 2.3% among women.
Development and Course
Information on the development and course of sexual sadism disorder is extremely limited.
Whereas sexually sadistic preferences per se are probably a lifelong characteristic, sexual sadism
disorder may fluctuate according to the individual’s subjective distress or his or her propensity to
harm nonconsenting others. As with other sexual preferences, advancing age may be associated
with decreasing sexually sadistic preferences and behavior. Regarding sexually sadistic
preference, many individuals who engage in BDSM behavior became aware of their
corresponding interest in their teenage years.
Culture-Related Diagnostic Issues
The legal status of sexually sadistic behavior ranges across countries and societies, suggesting
the potential for variation in distress (because of variation in cultural acceptance) and functional
impairment (because of legal status).
Association With Suicidal Thoughts or Behavior
Association of sexual sadism disorder with suicidal thoughts or behavior is unknown. However,
a study of 321 adults who endorsed BDSM involvement found an association of stigma-related
shame and guilt with suicidal ideation.
Differential Diagnosis
Individuals with sexual sadism experience recurrent, intense sexual arousal from
the physical or psychological suffering of another person. Unless the sexual urges to make
another person suffer physically or psychologically are acted on with a non-consenting person, or
unless there is accompanying clinically significant distress or impairment in social, occupational,
or other important areas of functioning, a diagnosis of sexual sadism disorder is not warranted.
The majority of individuals who are active in community networks that practice sadistic and
masochistic behaviors do not express any dissatisfaction with their sexual interests, and their

Infliction of physical or psychological suffering during the commission of a sex crime.
Conduct disorder and antisocial personality disorder.
F65.4
behavior would not meet DSM-5 criteria for sexual sadism disorder.
Individuals 
who
commit rape or other sexual assaults might inflict pain on their victims as a result of the act of
rape, or in the course of subduing victims or restraining them to commit the sexual assault. Such
instrumental infliction of pain should not be considered to be indicative of sexual sadism
disorder unless there is evidence that the individual is deriving pleasure from the infliction of
pain and the resulting suffering of the victim (e.g., admission of specifically being aroused by the
pain, evidence of a preference for pornography involving themes of sexual sadism, excessive use
of pain-inducing violence that goes beyond what might be necessary in the course of committing
the sexual assault).
Individuals 
with 
conduct 
disorder 
and
antisocial personality disorder may be physically cruel to people and force others to engage in
sexual activity. Coercive or sadistic sexual behaviors that occur in the context of conduct
disorder or antisocial personality disorder but that do not reflect an underlying pattern of sexual
arousal from the physical or psychological suffering of another person should not be used as a
basis for diagnosing sexual sadism disorder. In cases in which the diagnostic criteria are met for
both sexual sadism disorder and conduct disorder/antisocial personality disorder, both disorders
may be diagnosed.
Comorbidity
Known comorbidities with sexual sadism disorder are largely based on individuals (almost all
men) convicted for criminal acts involving sadistic acts against nonconsenting victims. Hence,
these comorbidities might not apply to all individuals who never engaged in sadistic activity with
a nonconsenting victim but who qualify for a diagnosis of sexual sadism disorder based on
subjective distress over their sexual interest. Disorders that are commonly comorbid with sexual
sadism disorder include other paraphilic disorders. According to a population-based study in
Finland, individuals who had engaged in sexually sadistic behavior had also engaged in other
types of paraphilic behavior, namely (in descending order of co-occurrence) masochism (68.8%),
voyeurism (33.3%), transvestic fetishism (9.2%), and exhibitionism (6.4%).
Pedophilic Disorder
Diagnostic Criteria
A. Over a period of at least 6 months, recurrent, intense sexually arousing
fantasies, sexual urges, or behaviors involving sexual activity with a
prepubescent child or children (generally age 13 years or younger).
B. The individual has acted on these sexual urges, or the sexual urges or fantasies
cause marked distress or interpersonal difficulty.

C. The individual is at least age 16 years and at least 5 years older than the child or
children in Criterion A.
Note: Do not include an individual in late adolescence involved in an ongoing
sexual relationship with a 12- or 13-year-old.
Specify whether:
Exclusive type (attracted only to children)
Nonexclusive type
Specify if:
Sexually attracted to males
Sexually attracted to females
Sexually attracted to both
Specify if:
Limited to incest
Diagnostic Features
The diagnostic criteria for pedophilic disorder are intended to apply both to individuals who
freely disclose this paraphilia and to individuals who deny any sexual attraction to prepubertal
children (generally age 13 years or younger), despite substantial objective evidence to the
contrary. The age guideline of 13 or younger is approximate only, because the onset of puberty
varies from person to person, and there is good evidence the average age at onset of puberty has
been declining over time and differs across ethnicities and cultures. Examples of disclosing this
paraphilia include candidly acknowledging an intense sexual interest in children and indicating
that sexual interest in children is greater than or equal to sexual interest in physically mature
persons. If individuals also complain that their sexual attractions or preferences for children are
causing marked distress or psychosocial difficulties, they may be diagnosed with pedophilic
disorder. However, if they report an absence of feelings of guilt, shame, or anxiety about these
impulses and are not functionally limited by their paraphilic impulses (according to self-report,
objective assessment, or both), and their self-reported and legally recorded histories indicate that
they have never acted on their impulses, then these individuals have a pedophilic sexual interest
but not pedophilic disorder. When trying to differentiate child offenders with pedophilic disorder
from child offenders without pedophilic disorder, factors that suggest a diagnosis of pedophilic
disorder in the offender include self-reported interest in children, use of child pornography, a
history of multiple child victims, boy victims, and unrelated child victims.
Examples of individuals who deny attraction to children include individuals who are known
to have sexually approached multiple children on separate occasions but who deny any urges or
fantasies about sexual behavior involving children, and who may further claim that the known
episodes of physical contact were all unintentional and nonsexual. Other individuals may
acknowledge past episodes of sexual behavior involving children but deny any significant or
sustained sexual interest in children. Because these individuals may deny experiences, impulses,
or fantasies involving children, they may also deny feeling subjectively distressed. Such
individuals may still be diagnosed with pedophilic disorder despite the absence of self-reported

distress, provided that there is evidence of recurrent behaviors persisting for 6 months (Criterion
A) and evidence that the individual has acted on sexual urges or experienced interpersonal
difficulties as a consequence of the disorder (Criterion B). Behaviors include sexual interactions
with children, whether or not they involve physical contact (e.g., some pedophilic individuals
expose themselves to children). Although the use of sexually explicit content depicting
prepubescent children is typical of individuals with pedophilic sexual interests and thus might
contribute important information relevant to the evaluation of Criterion A, such behavior in the
absence of the individual’s sexual interactions with children (i.e., acting on these sexual urges in
person) is insufficient to conclude that Criterion B is met.
Presence of multiple victims, as discussed above, is sufficient but not necessary for
diagnosis; that is, the individual can still meet Criterion A by merely acknowledging intense or
preferential sexual interest in children.
Associated Features
Individuals with pedophilic disorder may experience an emotional and cognitive affinity with
children, sometimes referred to as emotional congruence with children. Emotional congruence
with children can manifest in different ways, including preferring social interactions with
children over adults, feeling like one has more in common with children than with adults, and
choosing occupations or volunteer roles in order to be around children more often. Studies show
that emotional congruence with children is related to both pedophilic sexual interest and the
likelihood of sexually reoffending among individuals who have sexually offended.
Prevalence
The population prevalence of individuals whose presentations meet the full criteria for
pedophilic disorder is unknown but is likely less than 3% among men in international studies.
The population prevalence of pedophilic disorder in women is even more uncertain, but it is
likely a small fraction of the prevalence in men.
Development and Course
Adult men with pedophilic disorder may indicate that they became aware of strong or
preferential sexual interest in children around the time of puberty—the same time frame in which
men who later prefer physically mature partners became aware of their sexual interest in women
or men. Attempting to diagnose pedophilic disorder at the age at which it first manifests is
problematic because of the difficulty during adolescent development in differentiating it from
age-appropriate sexual interest in peers or from sexual curiosity. Hence, Criterion C requires for
diagnosis a minimum age of 16 years and at least 5 years older than the child or children in
Criterion A.
Pedophilia per se appears to be a lifelong condition. Pedophilic disorder, however,
necessarily includes other elements that may change over time with or without treatment:
subjective distress (e.g., guilt, shame, intense sexual frustration, or feelings of isolation) or
psychosocial impairment, or the propensity to act out sexually with children, or both. Therefore,

Temperamental.
Environmental.
Genetic and physiological.
the course of pedophilic disorder may fluctuate, or the intensity might increase or decrease with
age.
Adults with pedophilic disorder may report an awareness of sexual interest in children that
preceded engaging in sexual behavior involving children or self-identification as an individual
with pedophilia. Advanced age is as likely to similarly diminish the frequency of sexual behavior
involving children as it does other paraphilically motivated and nonparaphilic sexual behavior.
Risk and Prognostic Factors
There appears to be an interaction between pedophilia and antisocial personality
traits such as callousness, impulsivity, and a willingness to take risks without adequate regard for
the consequences. Men with pedophilic interest and antisocial personality traits are more likely
to act out sexually with children and thus qualify for a diagnosis of pedophilic disorder. Thus,
antisocial personality disorder may be considered a risk factor for pedophilic disorder in males
with pedophilia.
Adult men with pedophilia sometimes report that they were sexually abused as
children. It is unclear, however, whether this correlation reflects a causal influence of childhood
sexual abuse on adult pedophilia.
Since pedophilia is a necessary condition for pedophilic disorder, any
factor that increases the probability of pedophilia also increases the risk of pedophilic disorder.
There is some evidence that neurodevelopmental perturbation in utero increases the probability
of development of a pedophilic interest.
Sex- and Gender-Related Diagnostic Issues
Laboratory measures of sexual interest, in terms of psychophysiological responses to sexual
stimuli depicting children, which are sometimes useful in diagnosing pedophilic disorder in men,
are not necessarily useful in diagnosing this disorder in women because there has been very
limited research on the assessment of pedophilic sexual interest in women.
Diagnostic Markers
Psychophysiological measures of sexual interest may sometimes be useful when an individual’s
history suggests the possible presence of pedophilic disorder but the individual denies strong or
preferential attraction to children. The most thoroughly researched and longest used of such
measures is penile plethysmography, although the sensitivity and specificity of diagnosis may
vary across sites, which frequently use different stimuli, procedures, and scoring. Viewing time,
using photographs of nude or minimally clothed persons as visual stimuli, is also used to
diagnose pedophilic disorder, especially in combination with self-report measures. U.S.
clinicians, however, should be aware that possession of visual sexual stimuli depicting children,
even for diagnostic purposes, may violate American law regarding possession of child
pornography and leave the clinician susceptible to criminal prosecution. The option exists to use
audio 
stimuli 
describing 
sexual 
interactions 
in 
penile 
plethysmography. 
Across
psychophysiological methods, the diagnostic marker is relative sexual response to stimuli

Pedophilia.
Other paraphilic disorders.
Antisocial personality disorder.
Substance intoxication.
Obsessive-compulsive disorder.
depicting children compared with stimuli depicting adults, rather than absolute response to child
stimuli.
Differential Diagnosis
Individuals with pedophilia experience recurrent, intense, sexually arousing fantasies
or sexual urges involving sexual activity with a prepubescent child or children. Unless the
individual has acted on these sexual urges with a prepubescent child or unless the sexual urges or
fantasies cause marked distress or interpersonal difficulty, a diagnosis of pedophilic disorder is
not warranted.
Sometimes individuals present with a different paraphilic disorder but
are referred for an evaluation regarding possible pedophilic disorder (e.g., when an individual
with a diagnosis of exhibitionistic disorder exposes himself to children as well as adults). In
some cases, both diagnoses may apply, whereas in others, it may be the case that one paraphilic
disorder diagnosis is sufficient. For example, an individual who exposes himself exclusively to
prepubescent children may have both exhibitionistic disorder and pedophilic disorder, whereas
another individual who exposes himself to victims, irrespective of the victims’ age, may be
considered to have only exhibitionistic disorder.
Some individuals with antisocial personality disorder sexually
abuse children, reflecting the fact that the presence of antisocial personality disorder increases
the likelihood that an individual who is primarily attracted to mature persons will approach a
child sexually, on the basis of relative access to the child. An additional diagnosis of pedophilic
disorder should only be considered if there is evidence that over a period of at least 6 months, the
individual has also had recurrent, intense, sexually arousing fantasies, sexual urges, or behaviors
involving sexual activity with a prepubescent child.
The disinhibiting effects of substance intoxication may also increase the
likelihood that an individual who is primarily attracted to mature persons will sexually approach
a child.
There are occasional individuals who complain about egodystonic thoughts and worries about possible attraction to children. Clinical interviewing usually
reveals an absence of positive feelings about these thoughts, no connection between these
thoughts and sexual behavior (e.g., masturbating to these thoughts), and sometimes additional
ego-dystonic, intrusive sexual ideas (e.g., concerns about homosexuality).
Comorbidity
Psychiatric comorbidity of pedophilic disorder includes substance use disorders; depressive,
bipolar, and anxiety disorders; antisocial personality disorder; and other paraphilic disorders.
However, findings on comorbid disorders are largely among individuals convicted for sexual
offenses involving children (almost all males) and may not be generalizable to other individuals
with pedophilic disorder (e.g., individuals who have never approached a child sexually but who
qualify for the diagnosis of pedophilic disorder on the basis of subjective distress).

F65.0
Fetishistic Disorder
Diagnostic Criteria
A. Over a period of at least 6 months, recurrent and intense sexual arousal from
either the use of nonliving objects or a highly specific focus on nongenital body
part(s), as manifested by fantasies, urges, or behaviors.
B. The fantasies, sexual urges, or behaviors cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
C. The fetish objects are not limited to articles of clothing used in cross-dressing (as
in transvestic disorder) or devices specifically designed for the purpose of tactile
genital stimulation (e.g., vibrator).
Specify:
Body part(s)
Nonliving object(s)
Other
Specify if:
In a controlled environment: This specifier is primarily applicable to individuals
living in institutional or other settings where opportunities to engage in fetishistic
behaviors are restricted.
In full remission: There has been no distress or impairment in social,
occupational, or other areas of functioning for at least 5 years while in an
uncontrolled environment.
Specifiers
Although individuals with fetishistic disorder may report intense and recurrent sexual arousal to
inanimate objects or a specific body part, it is not unusual for non–mutually exclusive
combinations of fetishistic sexual interests to occur. Thus, an individual may have fetishistic
disorder associated with an inanimate object (e.g., female undergarments) or an exclusive focus
on an intensely eroticized body part (e.g., feet, hair), or his or her fetishistic interest may meet
criteria for various combinations of these specifiers (e.g., socks, shoes, and feet).
Diagnostic Features
The paraphilic focus of fetishistic disorder involves the persistent and repetitive use of or
dependence on nonliving objects or a highly specific focus on a (typically nongenital) body part
as a primary element associated with sexual arousal (Criterion A). A diagnosis of fetishistic
disorder must include clinically significant personal distress or impairment in social,
occupational, or other important areas of functioning (Criterion B). Common fetish objects

include women’s undergarments, men’s or women’s footwear, rubber articles, leather clothing,
diapers, or other wearing apparel. Highly eroticized body parts associated with fetishistic
disorder include feet, toes, and hair. It is not uncommon for sexualized fetishes to include both
inanimate objects and body parts (e.g., dirty socks and feet), and for this reason the definition of
fetishistic disorder now re-incorporates partialism (i.e., an exclusive focus on a body part) into
its boundaries. Partialism, previously considered in DSM-IV-TR to be a paraphilia not otherwise
specified, had historically been subsumed in fetishism prior to DSM-III.
Many individuals who self-identify as fetishist practitioners do not necessarily report clinical
impairment in association with their fetish-associated behaviors. Such individuals could be
considered as having a fetishistic sexual interest (i.e., a recurrent and intense sexual arousal from
either the use of nonliving objects or a highly specific focus on a nongenital body part, as
manifested by fantasies, urges, or behaviors), but not fetishistic disorder. A diagnosis of
fetishistic disorder requires concurrent fulfillment of both the behaviors in Criterion A and the
clinically significant distress or impairment in functioning noted in Criterion B.
Associated Features
Fetishistic disorder can be a multisensory experience, including holding, tasting, rubbing,
inserting, or smelling the fetish object while masturbating, or preferring that a sexual partner
wear or utilize a fetish object during sexual encounters. It should be noted that many individuals
with fetishistic sexual interests also enjoy sexual experiences with their partner(s) without using
their fetish object. However, it should also be noted that individuals with a fetishistic sexual
interest often find that sexual experiences that involve their fetish object are more sexually
satisfying than sexual experience without it. And for a minority of people with a fetishistic
sexual interest, their fetish object is obligatory to becoming sexually aroused and/or satisfied.
Some individuals may acquire extensive collections of highly desired fetish objects.
Development and Course
Usually paraphilias have an onset during puberty, but fetishistic sexual interests can develop
prior to adolescence. Once established, fetishistic disorder tends to have a continuous course that
fluctuates in intensity and frequency of urges or behavior.
Culture-Related Diagnostic Issues
Knowledge of and appropriate consideration for normative aspects of sexual behavior are
important factors to explore to establish a clinical diagnosis of fetishistic disorder and to
distinguish a clinical diagnosis from a socially acceptable sexual behavior.
Sex- and Gender-Related Diagnostic Issues
Fetishistic behaviors have been reported more in men, but also occur in women. This gender
difference is smaller for fetishistic fantasy than for actual fetishistic behavior. In clinical samples,
fetishistic disorder is nearly exclusively reported in men.
Functional Consequences of Fetishistic Disorder
Typical impairments associated with fetishistic disorder include sexual dysfunction during

Transvestic disorder.
Sexual masochism disorder or other paraphilic disorders.
Fetishism.
F65.1
romantic reciprocal relationships when the preferred fetish object or body part is
unavailable during foreplay or coitus. Some individuals with fetishistic disorder may prefer
solitary sexual activity associated with their fetishistic preference(s) even while involved in a
meaningful reciprocal and affectionate relationship.
Differential Diagnosis
The nearest diagnostic neighbor of fetishistic disorder is transvestic
disorder. As noted in the diagnostic criteria, fetishistic disorder is not diagnosed when fetish
objects are limited to articles of clothing exclusively worn during cross-dressing (as in
transvestic disorder), or when the object is genitally stimulating because it has been designed for
that purpose (e.g., a vibrator).
Fetishistic disorder can co-occur with other
paraphilic disorders, especially sadomasochistic behavior or interests and transvestic disorder.
When an individual fantasizes about or engages in “forced cross-dressing” and is primarily
sexually aroused by the domination or humiliation associated with such fantasy or repetitive
activity, and experiences distress or functional impairment, the diagnosis of sexual masochism
disorder should be made.
Use of a fetish object for sexual arousal (fetishism) without any associated distress or
psychosocial role impairment or other adverse consequence would not meet criteria for fetishistic
disorder, as the threshold required by Criterion B would not be met. For example, an individual
whose sexual partner either shares or can successfully incorporate his interest in caressing,
smelling, or licking feet or toes as an important element of foreplay would not be diagnosed with
fetishistic disorder; nor would an individual who prefers, and is not distressed or impaired by,
solitary sexual behavior associated with wearing rubber garments or leather boots.
Comorbidity
Fetishistic disorder may co-occur with other paraphilic disorders as well as hypersexuality.
Rarely, fetishistic disorder may be associated with neurological conditions.
Transvestic Disorder
Diagnostic Criteria
A. Over a period of at least 6 months, recurrent and intense sexual arousal from
cross-dressing, as manifested by fantasies, urges, or behaviors.
B. The fantasies, sexual urges, or behaviors cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
Specify if:

With fetishism: If sexually aroused by fabrics, materials, or garments.
With autogynephilia: If sexually aroused by thoughts or images of self as a
woman.
Specify if:
In a controlled environment: This specifier is primarily applicable to individuals
living in institutional or other settings where opportunities to cross-dress are
restricted.
In full remission: There has been no distress or impairment in social,
occupational, or other areas of functioning for at least 5 years while in an
uncontrolled environment.
Specifiers
The presence of fetishism decreases the likelihood of gender dysphoria in men with transvestic
disorder. The presence of autogynephilia increases the likelihood of gender dysphoria in men
with transvestic disorder.
Diagnostic Features
The diagnosis of transvestic disorder does not apply to all individuals who dress as the opposite
sex, even those who do so habitually. It applies to individuals whose cross-dressing or thoughts
of cross-dressing are always or often accompanied by sexual excitement (Criterion A) and who
are emotionally distressed by this pattern or for whom it impairs their social or interpersonal
functioning (Criterion B). The cross-dressing may involve only one or two articles of clothing
(e.g., for men, it may pertain only to women’s undergarments), or it may involve dressing
completely in the inner and outer garments of the other sex and (in men) may include the use of
women’s wigs and makeup. Sexual arousal, in its most obvious form of penile erection, may cooccur with cross-dressing in various ways. In younger men, cross-dressing often leads to
masturbation, following which any women’s clothing is removed. Older men often learn to avoid
masturbating or doing anything to stimulate the penis so that the avoidance of ejaculation allows
them to prolong their cross-dressing session. Men and women sometimes complete a crossdressing session by having intercourse with their partners, and some have difficulty maintaining
sufficient sexual arousal for sexual activity without cross-dressing (or having private fantasies of
cross-dressing).
Clinical assessment of distress or impairment, like clinical assessment of transvestic sexual
arousal, is usually dependent on the individual’s self-report. The pattern of behavior “purging
and acquisition” often signifies the presence of distress in individuals with transvestic disorder.
During this behavioral pattern, an individual (usually a man) who has spent a great deal of
money on women’s clothes and other apparel (e.g., shoes, wigs) discards the items (i.e., purges
them) in an effort to overcome urges to cross-dress, and then begins acquiring a woman’s
wardrobe all over again.

Associated Features
Transvestic disorder in men is often accompanied by autogynephilia (i.e., a man’s paraphilic
tendency to be sexually aroused by the thought or image of himself as a woman). Autogynephilic
fantasies and behaviors may focus on the idea of exhibiting female physiological functions (e.g.,
lactation, menstruation), engaging in stereotypically feminine behavior (e.g., knitting), or
possessing female anatomy (e.g., breasts).
Prevalence
The prevalence of transvestic disorder is unknown; however, it appears to be much more
prevalent in men than in women. Fewer than 3% of Swedish men report having ever been
sexually aroused by dressing in women’s attire. The percentage of individuals who have crossdressed with sexual arousal more than once or a few times in their lifetimes would be even
lower.
Development and Course
In men, the first signs of transvestic disorder may begin in childhood, in the form of strong
fascination with a particular item of women’s attire. Prior to puberty, cross-dressing produces
generalized feelings of pleasurable excitement. With the arrival of puberty, dressing in women’s
clothes begins to elicit penile erection and, in some cases, leads directly to first ejaculation. In
many cases, cross-dressing elicits less and less sexual excitement as the individual grows older;
eventually it may produce no discernible penile response at all. The desire to cross-dress, at the
same time, remains the same or grows even stronger.
Individuals who report such a diminution of sexual response typically report that the sexual
excitement of cross-dressing has been replaced by feelings of comfort or well-being.
In some cases, the course of transvestic disorder is continuous, and in others it is episodic. It
is not rare for men with transvestic disorder to lose interest in cross-dressing when they first fall
in love with a woman and begin a relationship, but such abatement usually proves temporary.
When the desire to cross-dress returns, so does the associated distress.
Some cases of transvestic disorder progress to gender dysphoria. The men in these cases,
who may be indistinguishable from others with transvestic disorder in adolescence or early
childhood, gradually develop desires to remain in the woman’s role for longer periods and to
feminize their anatomy. The development of gender dysphoria is usually accompanied by a (selfreported) reduction or elimination of sexual arousal in association with cross-dressing.
The manifestation of transvestism in penile erection and stimulation, like the manifestation of
other paraphilic as well as nonparaphilic sexual interests, is most intense in adolescence and
early adulthood. The severity of transvestic disorder is highest in adulthood, when the transvestic
drives are most likely to conflict with performance in heterosexual intercourse and desires to
marry and start a family. Middle-age and older men with a history of transvestism are less likely
to present with transvestic disorder than with gender dysphoria.
Functional Consequences of Transvestic Disorder

Transvestism.
Fetishistic disorder.
Gender dysphoria.
Engaging in transvestic behaviors can interfere with, or detract from, heterosexual relationships.
This can be a source of distress to men who wish to maintain conventional marriages or romantic
partnerships with women.
Differential Diagnosis
Individuals with transvestism experience recurrent and intense sexual arousal from
cross-dressing. Unless the fantasies, sexual urges, or behaviors involving cross-dressing are
accompanied by clinically significant distress or impairment in social, occupational, or other
important areas of functioning, a diagnosis of transvestic disorder is not warranted.
This disorder may resemble transvestic disorder, in particular, in men with
fetishism who put on women’s undergarments while masturbating with them. Distinguishing
transvestic disorder depends on the individual’s specific thoughts during such activity (e.g., are
there any ideas of being a woman, being like a woman, or being dressed as a woman?) and on
the presence of other fetishes (e.g., soft, silky fabrics, whether these are used for garments or for
something else).
Individuals with transvestic disorder do not report an incongruence between
their experienced gender and their assigned gender or a desire to be of the other gender; and they
typically do not have a history of childhood cross-gender behaviors, which would be present in
individuals with gender dysphoria. Individuals with a presentation that meets full criteria for
transvestic disorder as well as gender dysphoria should be given both diagnoses.
Comorbidity
Transvestic disorder is often found in association with other paraphilias. The most frequently cooccurring paraphilias are fetishistic sexual interests or behavior and masochistic sexual interests
or behavior. One particularly dangerous form of masochistic sexual interests or behavior,
autoerotic asphyxia, is associated with transvestic sexual interests or behavior in a substantial
proportion of fatal cases.
Other Specified Paraphilic Disorder
F65.89
This category applies to presentations in which symptoms characteristic of a
paraphilic disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the paraphilic disorders diagnostic class.
The other specified paraphilic disorder category is used in situations in which the
clinician chooses to communicate the specific reason that the presentation does not
meet the criteria for any specific paraphilic disorder. This is done by recording “other
specified paraphilic disorder” followed by the specific reason (e.g., “zoophilia”).

Examples of presentations that can be specified using the “other specified” designation
include, but are not limited to, recurrent and intense sexual arousal involving telephone
scatologia (obscene phone calls), necrophilia (corpses), zoophilia (animals), coprophilia
(feces), klismaphilia (enemas), or urophilia (urine) that has been present for at least 6 months
and causes marked distress or impairment in social, occupational, or other important areas of
functioning. Other specified paraphilic disorder can be specified as in remission and/or as
occurring in a controlled environment.
Unspecified Paraphilic Disorder
F65.9
This category applies to presentations in which symptoms characteristic of a
paraphilic disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the paraphilic disorders diagnostic class.
The unspecified paraphilic disorder category is used in situations in which the
clinician chooses not to specify the reason that the criteria are not met for a specific
paraphilic disorder, and includes presentations in which there is insufficient
information to make a more specific diagnosis.

# 20 - Other Mental Disorders and Additional Codes

# Other Mental Disorders and Additional Codes

803

Other Mental Disorders and Additional Codes
This chapter provides diagnostic codes for psychiatric presentations that are mental
disorders (i.e., symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning) but that do not meet diagnostic
requirements for any of the mental disorders in the prior Section II chapters. These codes allow
for the documentation and coding of these otherwise unclassified mental disorders. This chapter
also includes an additional code, “No diagnosis or condition,” for situations in which the
individual has been evaluated and it is determined that no mental disorder or condition is present.
The categories 1) other specified mental disorder due to another medical condition and 2)
unspecified mental disorder due to another medical condition are for presentations for which it
has been determined that the psychiatric symptoms (e.g., dissociative symptoms) are a direct
physiological consequence of another medical condition but do not otherwise meet diagnostic
criteria for any of the prior Section II mental disorders due to another medical condition. For the
diagnosis of other specified or unspecified mental disorder due to another medical condition, it is
necessary to code and list the medical condition first (e.g., B20 HIV disease), followed by the
applicable code for either other specified or unspecified mental disorder due to another medical
condition.
The categories 1) other specified mental disorder and 2) unspecified mental disorder are
residual categories used when all of the following considerations are met: the psychiatric
presentation is a mental disorder (i.e., the symptoms cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning); the presentation
does not meet diagnostic criteria for any of the specific mental disorders in Section II; neither
does the presentation meet the definitional requirements of any of the other specified and
unspecified mental disorder categories presented in Section II; and no other mental disorder
diagnosis applies.
As is the case with other specified and unspecified categories throughout DSM-5, the other
specified category is used when the clinician chooses to specify the specific reason that the
presentation does not meet the criteria for any of the existing categories (e.g., other specified
mental disorder due to complex partial seizures, with dissociative symptoms), and the
unspecified category is used when the clinician chooses not to specify the reason.
Other Specified Mental Disorder Due to Another Medical
Condition
F06.8
This category applies to presentations in which symptoms characteristic of a mental

disorder due to another medical condition that cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning
predominate but do not meet the full criteria for any specific mental disorder
attributable to another medical
condition. The other specified mental disorder due to another medical condition
category is used in situations in which the clinician chooses to communicate the
specific reason that the presentation does not meet the criteria for any specific
mental disorder attributable to another medical condition. This is done by recording
the name of the disorder, with the specific etiological medical condition inserted in
place of “another medical condition,” followed by the specific symptomatic
manifestation that does not meet the criteria for any specific mental disorder due to
another medical condition. Furthermore, the diagnostic code for the specific medical
condition must be listed immediately before the code for the other specified mental
disorder due to another medical condition. For example, dissociative symptoms due
to complex partial seizures would be coded and recorded as G40.209 complex
partial seizures, F06.8 other specified mental disorder due to complex partial
seizures, dissociative symptoms.
An example of a presentation that can be specified using the “other specified”
designation is the following:
Dissociative symptoms: This includes symptoms occurring, for example, in the
context of complex partial seizures.
Unspecified Mental Disorder Due to Another Medical
Condition
F09
This category applies to presentations in which symptoms characteristic of a mental
disorder due to another medical condition that cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning
predominate but do not meet the full criteria for any specific mental disorder due to
another medical condition. The unspecified mental disorder due to another medical
condition category is used in situations in which the clinician chooses not to specify
the reason that the criteria are not met for a specific mental disorder due to another
medical condition, and includes presentations for which there is insufficient
information to make a more specific diagnosis (e.g., in emergency room settings).
This is done by recording the name of the disorder, with the specific etiological
medical condition inserted in place of “another medical condition.” Furthermore, the

diagnostic code for the specific medical condition must be listed immediately before
the code for the unspecified mental disorder due to another medical condition. For
example, dissociative symptoms due to complex partial seizures would be coded
and recorded as G40.209 complex partial seizures, F09 unspecified mental disorder
due to complex partial seizures.
Other Specified Mental Disorder
F99
This category applies to presentations in which symptoms characteristic of a mental
disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any specific mental disorder. The other specified mental disorder
category is used in situations in which the clinician chooses to communicate the
specific reason that the presentation does not meet the criteria for any specific
mental disorder. This is done by recording “other specified mental disorder” followed
by the specific reason.
Unspecified Mental Disorder
F99
This category applies to presentations in which symptoms characteristic of a mental
disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet
the full criteria for any mental disorder. The unspecified mental disorder category is
used in situations in which the clinician chooses not to specify the reason that the
criteria are not met for a specific mental disorder, and includes presentations for
which there is insufficient information to make a more specific diagnosis (e.g., in
emergency room settings).
Additional Codes
Z03.89 No Diagnosis or Condition
This code applies to situations in which the person has been evaluated and it is determined that
no mental disorder or condition is present.

# 21 - Medication Induced Movement Disorders and Oth

# Medication-Induced Movement Disorders and Other Adverse Effects of Medication

807

Medication-Induced Movement Disorders and
Other Adverse Effects of Medication
Medication-induced movement disorders are included in Section II because
of their frequent importance in 1) the management by medication of mental disorders or other
medical conditions and 2) the differential diagnosis of mental disorders (e.g., anxiety disorder vs.
medication-induced akathisia; malignant catatonia [a particularly severe and potentially lifethreatening form of catatonia] vs. neuroleptic malignant syndrome; tardive dyskinesia vs.
chorea). Although these movement disorders are labeled “medication induced,” it is often
difficult to establish the causal relationship between medication exposure and the development of
the movement disorder, especially because some of these movement disorders also occur in the
absence of medication exposure. The conditions and problems listed in this chapter are not
mental disorders.
The term neuroleptic is becoming outdated because it highlights the propensity of
antipsychotic medications to cause abnormal movements, and it is being replaced with the term
antipsychotic medications and other dopamine receptor blocking agents in many contexts.
Although newer antipsychotic medications may be less likely to cause some medication-induced
movement disorders, those disorders still occur. Antipsychotic medications and other dopamine
receptor blocking agents include so-called conventional, “typical,” or first-generation
antipsychotic agents (e.g., chlorpromazine, haloperidol, fluphenazine); “atypical” or secondgeneration antipsychotic agents (e.g., clozapine, risperidone, olanzapine, quetiapine); certain
dopamine receptor blocking drugs used in the treatment of symptoms such as nausea and
gastroparesis (e.g., prochlorperazine, promethazine, trimethobenzamide, thiethylperazine,
metoclopramide); and amoxapine, which is indicated for the treatment of depression.
Medication-Induced Parkinsonism
G21.11 Antipsychotic Medication– and Other Dopamine Receptor
Blocking Agent–Induced Parkinsonism
G21.19 Other Medication-Induced Parkinsonism
Medication-induced parkinsonism (MIP), the second most common cause of parkinsonism after
Parkinson’s disease, is associated with significant morbidity, disability, and treatment
nonadherence, particularly in individuals with psychiatric disorders. Because early recognition is
important, any new case of parkinsonism should prompt a thorough medication history, which is
essential for diagnosis of MIP. A temporal relationship between medication initiation and onset
of parkinsonism should be evident. A host of agents that may be prescribed in individuals with
psychiatric disorders may also induce parkinsonism, but MIP is most often seen upon exposure

to antipsychotic medications that block dopamine D2 receptors. MIP occurs at higher rates with
antipsychotics that have higher potency for the dopamine D2 receptor, such as haloperidol,
fluphenazine, and risperidone, but there are no
differences in the clinical features of parkinsonism between first- and second-generation
antipsychotics.
Other medications that can cause MIP include calcium channel antagonists (e.g., flunarizine,
cinnarizine), dopamine depleters (e.g., reserpine, tetrabenazine), antiepileptics (e.g., phenytoin,
valproate, levetiracetam), antidepressants (e.g., selective serotonin reuptake inhibitors,
monoamine oxidase inhibitors), lithium, chemotherapeutic drugs (e.g., cystosine arabinoside,
cyclophosphamide, vincristine, doxorubicin, paclitaxel, etoposide), and immunosuppressants
(e.g., cyclosporine, tacrolimus). Toxins (e.g., 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
[MPTP], organophosphate pesticides, manganese, methanol, cyanide, carbon monoxide, and
carbon disulfide) may also cause MIP.
The time course for development of MIP varies. Usually, MIP develops a few weeks after
starting or raising the dose of a medication known to cause parkinsonism or after reducing an
antiparkinsonian medication (e.g., an anticholinergic agent) that is being used to treat or prevent
medication-induced dystonia or parkinsonian symptoms. However, MIP may also develop
rapidly after starting or raising the dose of a medication or have an insidious onset after many
months of exposure. With antipsychotic medications or other dopamine receptor blocking agents,
MIP typically develops 2–4 weeks after starting the medication and usually by 3 months. Mainly
with calcium channel blockers, a second peak of symptom onset is reported after about 1 year.
Reported rates of MIP are affected by absence of standard diagnostic criteria, incorrect
diagnosis or misattribution of MIP signs to Lewy body disease (e.g., Parkinson’s disease), or a
psychiatric condition, and overall lack of recognition, especially in milder cases. It is estimated
that at least 50% of outpatients receiving long-term antipsychotic treatment with typical agents
develop parkinsonian signs or symptoms at some point in their course of treatment.
There are no clinical characteristics that distinguish MIP reliably from Parkinson’s disease.
Because motor signs and symptoms in Parkinson’s disease begin unilaterally and progress
asymmetrically, the subacute onset of bilateral parkinsonism within weeks of starting an
antipsychotic or other MIP-causing agent is highly suggestive for MIP. Parkinsonian signs are
often symmetric in MIP, but asymmetric patterns are not uncommon and should not exclude a
diagnosis of MIP. In addition, the course and presentation of parkinsonism should not be better
accounted for by psychiatric phenomena, such as catatonia, negative symptoms of schizophrenia,
or psychomotor retardation in a major depressive episode; other nonparkinsonian medicationinduced movement disorders; another neurological or medical condition (e.g., Parkinson’s
disease, Wilson’s disease); or antipsychotic-exacerbated Parkinson’s disease.
In MIP, rigidity and bradykinesia are more often present, whereas tremor is somewhat less
common and may be absent. Parkinsonian tremor, also referred to as a “pill-rolling tremor,” is a
steady, rhythmic oscillatory movement (3–6 cycles per second) that is apparent at rest and is
typically slower than other tremors. It may be intermittent, unilateral or bilateral, or dependent on
limb position (i.e., positional tremor). The tremor may involve the limbs, head, jaw, mouth, lip
(“rabbit syndrome”), or tongue. As it is present at rest, the tremor can be suppressed, especially

when the individual attempts to perform a task with the tremulous limb. Individuals may
describe the tremor as “shaking” and report that it may worsen with anxiety, stress, or fatigue.
Parkinsonian rigidity is experienced as an involuntary stiffness and inflexibility of the
muscles of the limbs, shoulders, neck, or trunk. Rigidity is evaluated by assessing muscle tone,
or the amount of resistance present when the examiner moves a limb (and stretches the muscles)
passively around a joint. In lead-pipe rigidity, increased tone is constant throughout range of
motion (in contrast to the clasp-knife rigidity spasticity). Cogwheel rigidity is thought to
represent a tremor superimposed on rigidity. Most common in the wrists and elbows, it is
experienced as a rhythmic, ratchet-like resistance (cogwheeling) when the muscles are passively
moved around a joint. Individuals with parkinsonian rigidity may
complain of generalized muscle tenderness or stiffness, tightness in their limbs, muscle or
joint pain, body aching, or lack of coordination.
Bradykinesia and akinesia are observable states of decreased or absent spontaneous motor
activity, respectively. There is global slowing as well as slowness in initiating and executing
movements. Everyday behaviors (e.g., grooming) can be difficult to perform normally and may
be reduced. Individuals may complain of listlessness, lack of spontaneity and drive, or fatigue.
Parkinsonian rigidity and bradykinesia manifest as gait abnormalities, including decreased stride
length, arm swing, or overall spontaneity of walking. Other signs include a hunched posture with
bent-over neck and stooped shoulders, a staring facial expression, and small shuffling steps.
Drooling can arise as a result of reduced pharyngeal motor activity and swallowing, but because
of anticholinergic properties of these medications, it may be less common in antipsychoticinduced parkinsonism as compared with other medications that cause MIP.
MIP is associated with increased gait dysfunction, falls, and nursing home placement. As
such, MIP is a serious iatrogenic movement disorder in older individuals that warrants
recognition and early diagnosis. Associated behavioral symptoms may include depression and
worsening of negative signs of schizophrenia. Other parkinsonian signs and symptoms include
small handwriting (micrographia), reduced motor dexterity, hypophonia, decreased gag reflex,
dysphagia, postural instability, reduced facial expression and blinking, and seborrhea. When
parkinsonism is associated with severe decreased motor activity, medical complications of
parkinsonism include contractures, bedsores, pulmonary emboli, urinary incontinence, aspiration
pneumonia, weight loss, and hip fractures.
Consistent risk factors are female gender, older age, cognitive impairment, other concurrent
neurological conditions, HIV infection, family history of Parkinson’s disease, and severe
psychiatric disease. MIP secondary to antipsychotic use is also reported in children. The risk of
MIP is reduced if individuals are taking anticholinergic medications.
Differential Diagnosis
Parkinson’s disease and Parkinson’s-plus conditions such as multiple system atrophy,
progressive supranuclear palsy, and Wilson’s disease are distinguished from MIP by their other
signs and symptoms that accompany parkinsonism. For example, Parkinson’s disease is
suggested by evidence of three or more cardinal features of Parkinson’s disease (e.g., resting

tremor, rigidity, bradykinesia, postural instability), hyposmia, sleep disturbances such as rapid
eye movement (REM) sleep behavior disorder, and urinary and other autonomic symptoms
common to Parkinson’s disease. These features are less likely to be present in MIP. Individuals
with primary neurological causes of parkinsonism are also susceptible to worsening symptoms if
treated with medications causing MIP.
Nonparkinsonian tremors tend to be finer (e.g., smaller amplitude) and faster (10 cycles per
second) and worsen on intention (e.g., when reaching out to grab an object). With substance
withdrawal, there is usually associated hyperreflexia and increased autonomic signs. In cerebellar
disease, tremor worsens on intention and may be associated with nystagmus, ataxia, or scanning
speech. Choreiform movements associated with tardive dyskinesia lack the steady rhythmicity of
a parkinsonian tremor. Strokes and other central nervous system lesions can cause focal
neurological signs or immobility from flaccid or spastic paralysis, which is characterized by
decreased muscle strength and increased tone on passive movement that gives way with further
pressure (i.e., clasp-knife rigidity). This contrasts with the lead-pipe rigidity and normal muscle
strength in MIP.
Diagnostic alternatives to MIP are also suggested by a family history of an inherited
neurological condition, rapidly progressive parkinsonism not accounted for by recent
psychopharmacological changes, or presence of focal neurological signs (e.g., frontal release
signs, cranial nerve abnormalities, a positive Babinski sign). Neuroleptic malignant syndrome
involves severe akinesia and rigidity, but also characteristic physical and laboratory findings
(e.g., fever, increased creatine phosphokinase).
Psychomotor slowing, inactivity, and apathy seen in major depressive disorder can be
indistinguishable from the motor slowness or akinesia of MIP, but major depressive disorder is
more likely to include vegetative signs (e.g., early-morning awakening), hopelessness, and
despair. Negative symptoms of schizophrenia, catatonia associated with schizophrenia, or mood
disorders with catatonic features may also be difficult to distinguish from medication-induced
akinesia. Rigidity may also manifest in psychotic disorders, delirium, major neurocognitive
disorder, anxiety disorders, and functional neurological symptom disorder (conversion disorder).
In parkinsonian rigidity, resistance to passive motion is constant through the full range of
motion, whereas it is inconsistent in psychiatric disorders or other neurological conditions
presenting with rigidity. In general, the constellation of associated physical signs on examination
and symptoms associated with the tremor, rigidity, and bradykinesia of parkinsonism helps
distinguish MIP-related rigidity and bradykinesia from other primary psychiatric causes of
rigidity and decreased movement.
Neuroleptic Malignant Syndrome
G21.0 Neuroleptic Malignant Syndrome
Individuals with neuroleptic malignant syndrome have generally been exposed to a dopamine
antagonist within 72 hours prior to symptom development. Hyperthermia (>100.4°F or >38.0°C
on at least two occasions, measured orally), associated with profuse diaphoresis, is a

distinguishing feature of neuroleptic malignant syndrome, setting it apart from other neurological
side effects of antipsychotic medications and other dopamine receptor blocking agents. Extreme
elevations in temperature, reflecting a breakdown in central thermoregulation, are more likely to
support the diagnosis of neuroleptic malignant syndrome. Generalized rigidity, described as
“lead pipe” in its most severe form and usually unresponsive to antiparkinsonian agents, is a
cardinal feature of the disorder and may be associated with other neurological symptoms (e.g.,
tremor, 
sialorrhea, 
akinesia, 
dystonia, 
trismus, 
myoclonus, 
dysarthria, 
dysphagia,
rhabdomyolysis). Creatine kinase elevation of at least four times the upper limit of normal is
commonly seen. Changes in mental status, characterized by delirium or altered consciousness
ranging from stupor to coma, are often an early sign of neuroleptic malignant syndrome.
Affected individuals may appear alert but dazed and unresponsive, consistent with catatonic
stupor. Autonomic activation and instability—manifested by tachycardia (rate > 25% above
baseline), diaphoresis, blood pressure elevation (systolic or diastolic ≥ 25% above baseline) or
fluctuation (≥ 20 mmHg diastolic change or ≥25 mmHg systolic change within 24 hours), urinary
incontinence, and pallor—may be seen at any time but provide an early clue to the diagnosis.
Tachypnea (rate > 50% above baseline) is common, and respiratory distress—resulting from
metabolic acidosis, hypermetabolism, chest wall restriction, aspiration pneumonia, or pulmonary
emboli—can occur and lead to sudden respiratory arrest.
Although several laboratory abnormalities are associated with neuroleptic malignant
syndrome, no single abnormality is specific to the diagnosis. Individuals with neuroleptic
malignant syndrome may have leukocytosis, metabolic acidosis, hypoxia, decreased serum iron
concentrations, and elevations in serum muscle enzymes and catecholamines. Findings from
cerebrospinal fluid analysis and neuroimaging studies are generally normal, whereas
electroencephalography shows generalized slowing. Autopsy findings in fatal cases have been
nonspecific and variable, depending on complications.
Evidence from database studies suggests incidence rates for neuroleptic malignant syndrome
of 0.01%–0.02% among individuals treated with antipsychotics. A population-based study
conducted in Hong Kong found an incidence risk of 0.11% in individuals treated with
antipsychotic medication.
The temporal progression of signs and symptoms provides important clues to the diagnosis
and prognosis of neuroleptic malignant syndrome. Alteration in mental status and other
neurological signs typically precede systemic signs. The onset of symptoms varies from hours to
days after drug initiation. Some cases develop within 24 hours after drug initiation, most within
the first week, and virtually all cases within 30 days. Once the syndrome is diagnosed and oral
antipsychotic drugs and other dopamine receptor blocking agents are discontinued, neuroleptic
malignant syndrome is self-limited in most cases. The mean recovery time after drug
discontinuation is 7–10 days, with most individuals recovering within 1 week and nearly all
within 30 days. The duration may be prolonged when long-acting antipsychotic medications are
implicated. There have been reports of individuals in whom residual neurological signs persisted
for weeks after the acute hypermetabolic symptoms resolved. Total resolution of symptoms can
be obtained in most cases of neuroleptic malignant syndrome; however, fatality rates of 10%–
20% have been reported when the disorder is not recognized. Although many individuals do not

experience a recurrence of neuroleptic malignant syndrome when rechallenged with
antipsychotic medication, some do, especially when antipsychotic medications are reinstituted
soon after an episode.
Neuroleptic malignant syndrome is a potential risk in any individual after administration of
an antipsychotic medication or other dopamine receptor blocking agent. It is not specific to any
neuropsychiatric diagnosis and may occur in persons without a diagnosable mental disorder who
receive dopamine antagonists. Clinical, systemic, and metabolic factors associated with a
heightened risk of neuroleptic malignant syndrome include agitation, exhaustion, dehydration,
and iron deficiency. A prior episode associated with antipsychotic medication and other
dopamine receptor blocking agents has been described in 15%–20% of index cases, suggesting
underlying vulnerability in some individuals; however, genetic findings based on
neurotransmitter receptor polymorphisms have not been replicated consistently.
Nearly all antipsychotic medication and other dopamine receptor blocking agents have been
associated with neuroleptic malignant syndrome, although high-potency antipsychotics pose a
greater risk compared with low-potency agents and atypical antipsychotics. Partial or milder
forms may be associated with newer antipsychotics, but neuroleptic malignant syndrome varies
in severity even with older drugs. Dopamine receptor blocking agents used in medical settings
(e.g., metoclopramide, prochlorperazine) have also been implicated. Parenteral administration
routes, rapid titration rates, and higher total drug dosages have been associated with increased
risk; however, neuroleptic malignant syndrome usually occurs within the therapeutic dosage
range of antipsychotic medications and other dopamine receptor blocking agents.
Differential Diagnosis
Neuroleptic malignant syndrome should be distinguished from other serious neurological or
medical conditions, including central nervous system infections, inflammatory or autoimmune
conditions, status epilepticus, subcortical structural lesions, and systemic conditions (e.g.,
pheochromocytoma, thyrotoxicosis, tetanus, heat stroke).
Neuroleptic malignant syndrome also should be distinguished from similar syndromes
resulting from the use of other substances or medications, such as serotonin syndrome;
parkinsonian hyperthermia syndrome following abrupt discontinuation of dopamine agonists;
alcohol or sedative withdrawal; malignant hyperthermia occurring during anesthesia;
hyperthermia associated with misuse of stimulants and hallucinogens; and atropine poisoning
from anticholinergics.
In rare instances, individuals with schizophrenia or a mood disorder may present with
malignant catatonia, which may be indistinguishable from neuroleptic malignant syndrome.
Some investigators consider neuroleptic malignant syndrome to be a drug-induced form of
malignant catatonia.
Medication-Induced Acute Dystonia
G24.02 Medication-Induced Acute Dystonia
The essential feature of medication-induced acute dystonia is sustained abnormal muscle

contractions (increased muscle tone) and postures that develop in association with use of a
medication known to cause acute dystonia. Any medication that blocks dopamine D2-like
receptors can induce an acute dystonic reaction (ADR). Most commonly, ADRs occur after
exposure to antipsychotics and antiemetic and promotility agents. A variety of other medication
classes are also reported to have induced ADRs, including selective serotonin reuptake
inhibitors, cholinesterase inhibitors, opioids, and methylphenidate.
Dystonic reactions vary greatly in severity and location and can be focal, segmented, or
generalized. They most often affect head and neck muscles, but can extend to upper and lower
limbs or trunk. A common presentation is acute oro-mandibular (jaw) dystonia involving the
tongue and mouth with tongue protrusion, or gaping or grimacing postures that can impair
speech (dysarthria) and swallowing (dysphagia) and may evolve into frank trismus (lockjaw).
Involvement of ocular muscles (oculogyric crisis) manifests as involuntary forced and sustained
conjugate deviations of eyes upward, downward, or sideways that can last minutes to hours.
Blepharospasm can also occur. Cervical (neck) dystonia presents as abnormal forward,
backward, lateral, or twisting positions of the head and neck in relation to the body (e.g.,
antecollis, retrocollis, laterocollis, and torticollis). Focal limb dystonia, generally more distal
than proximal, Pisa syndrome (lateral bending of the trunk with a tendency to lean to one side),
and back arching that may evolve into opisthotonos (backward arching of head, neck, and spine)
can also occur. Acute laryngeal dystonia is life-threatening, causing airway obstruction, and
manifests as a “clutching of the throat,” stridor, dysphonia, dysphagia, dyspnea, and respiratory
distress from the medication effects on vocal cords and laryngeal muscles.
At least 50% of individuals develop ADR signs or symptoms within 24–48 hours of starting
or rapidly raising the dose of antipsychotic medication or other dopamine receptor blocking
agent or of reducing a medication being used to treat or prevent acute extrapyramidal symptoms
(e.g., anticholinergic agents). Approximately 90% of affected individuals have onset of ADRs
within 5 days. The symptoms must not be better accounted for by a mental disorder (e.g.,
catatonia) and must not be due to a primary neurological or other medical condition, or a tardive
medication-induced movement disorder.
Fear and anxiety often accompany ADRs given their intense nature, inability of the
individual to control or stop the movements, and, when present, difficulty breathing, speaking, or
swallowing. Some individuals experience pain or cramps in affected muscles. Individuals who
are unaware of the possibility of developing a medication-induced dystonia can be especially
distressed, increasing the likelihood of subsequent medication nonadherence. Thought disorder,
delusions, or mannerisms in an individual with psychosis may cause the affected individual or
others to mistakenly regard his or her dystonic symptoms as a feature of the psychiatric
condition, which could lead to increased doses of the causative medication. The risk of
developing ADRs is greatest in children and in adults younger than age 40 with psychosis, with a
greater incidence in males than females in both children and adults. Other risk factors for
developing ADRs include prior dystonic reactions to antipsychotic medications or other
dopamine receptor blocking agents and use of high-potency typical antipsychotic medications.
Differential Diagnosis
It is important to distinguish between medication-induced ADRs and other causes of dystonia,
especially in individuals being treated with antipsychotic or other dopamine receptor blocking

medications. A primary neurological or other medical condition is evident
based on the time course and evolution of the dystonic phenomena (e.g., dystonia precedes
exposure to the antipsychotic medication or progresses in the absence of change in medication)
and, possibly, other evidence of focal neurological signs. Idiopathic focal or segmental dystonias
usually persist for several days or weeks independent of medication. A family history of dystonia
may also be present. Tardive dystonia secondary to medication exposure, including antipsychotic
medication or other dopamine receptor blocking agents, does not have acute onset and may
become evident when the dose of an antipsychotic medication is lowered. Other neurological
conditions (e.g., epileptic seizures, viral and bacterial infections, trauma, space-occupying
lesions in the peripheral or central nervous system) and endocrinopathies (e.g.,
hypoparathyroidism) can also produce symptoms (e.g., tetany) that resemble a medicationinduced acute dystonia. Other diagnoses that mimic an acute medication-induced dystonia
include anaphylaxis, tardive laryngeal dystonia, and respiratory dyskinesia. Neuroleptic
malignant syndrome can produce dystonia but differs in that it is also accompanied by fever and
generalized rigidity.
Catatonia associated with a mood disorder or schizophrenia can be distinguished by the
temporal relationship between the symptoms and the exposure to antipsychotic treatment (e.g.,
dystonia preceding exposure to antipsychotic medication) and response to pharmacological
intervention (e.g., no improvement after lowering of dose of the antipsychotic medication or in
response to anticholinergic administration). Furthermore, individuals with medication-induced
acute dystonia are generally distressed about the dystonic reaction and usually seek intervention.
In contrast, individuals with the retarded type of catatonia are typically mute and withdrawn and
do not express subjective distress about their condition.
Medication-Induced Acute Akathisia
G25.71 Medication-Induced Acute Akathisia
The essential features of medication-induced acute akathisia are subjective complaints of
restlessness and at least one of the following observed movements: fidgety movements or
swinging of the legs while seated, rocking from foot to foot or “walking on the spot” while
standing, pacing to relieve the restlessness, or an inability to sit or stand still for at least several
minutes. Individuals experiencing the most severe form of medication-induced acute akathisia
may be unable to maintain any position for more than a few seconds. The subjective complaints
include a sense of inner restlessness, most often in the legs; a compulsion to move one’s legs;
distress if one is asked not to move one’s legs; and dysphoria and anxiety. The symptoms
typically occur within 4 weeks of initiating or increasing the dose of a medication that can cause
akathisia, which includes antipsychotic medications and other dopamine receptor blocking
agents, tricyclic antidepressants, selective serotonin reuptake inhibitors, dopamine agonists, and
calcium channel blockers, and can occasionally follow the reduction of medication used to treat
or prevent acute extrapyramidal symptoms (e.g., anticholinergic agents). The symptoms are not
better explained by a mental disorder (e.g., schizophrenia, substance withdrawal, agitation from a

major depressive or manic episode, hyperactivity in attention-deficit/hyperactivity disorder) and
are not due to a neurological or other medical condition (e.g., Parkinson’s disease, irondeficiency anemia).
The subjective distress resulting from akathisia is significant and can lead to noncompliance
with antipsychotic or antidepressant treatment. Akathisia may be associated with dysphoria,
irritability, aggression, or suicide attempts. Worsening of psychotic symptoms or behavioral
dyscontrol may lead to an increase in medication dose, which may exacerbate the problem.
Akathisia can develop very rapidly after initiating or increasing the causative medication. The
development of akathisia appears to be dose dependent and to be more frequently associated with
particular high-potency antipsychotic medications or drugs with higher affinity for central
dopamine receptors. Acute akathisia tends to persist for
as long as the causative medication is continued, although the intensity may fluctuate over
time. The reported prevalence of akathisia among individuals receiving antipsychotic medication
or other dopamine receptor blocking agents has varied widely (20%–75%). Variations in
reported prevalence may be attributable to a lack of consistency in the definition, antipsychotic
prescribing practices, study design, and the demographics of the population being studied.
Differential Diagnosis
Medication-induced acute akathisia may be clinically indistinguishable from syndromes of
restlessness due to certain neurological or other medical conditions, and to agitation presenting
as part of a mental disorder (e.g., a manic episode). The akathisia of Parkinson’s disease and
iron-deficiency anemia is phenomenologically similar to medication-induced acute akathisia.
The frequently abrupt appearance of restlessness soon after initiation or increase in medication
usually distinguishes medication-induced acute akathisia.
Serotonin-specific reuptake inhibitor antidepressant medications may produce akathisia that
appears to be identical in phenomenology and treatment response to akathisia induced by
antipsychotic medication or other dopamine receptor blocking agents. Tardive dyskinesia also
often has a component of generalized restlessness that may coexist with akathisia in an
individual receiving antipsychotic medications or other dopamine blocking agents. Antipsychotic
medication and other dopamine blocking agent–induced acute akathisia is differentiated from
antipsychotic medication and other dopamine blocking agent–induced tardive dyskinesia by the
nature of the movements and their relationship to the initiation of medication. The time course of
symptomatic presentation relative to medication dose changes may aid in this distinction. An
increase in antipsychotic medication will often exacerbate akathisia, whereas it often temporarily
relieves the symptoms of tardive dyskinesia.
Medication-induced acute akathisia should be distinguished from symptoms that are better
accounted for by a mental disorder. Individuals with depressive episodes, manic episodes,
generalized anxiety disorder, schizophrenia spectrum and other psychotic disorders, attentiondeficit/hyperactivity disorder, major neurocognitive disorder, delirium, substance intoxication
(e.g., with cocaine), or substance withdrawal (e.g., from an opioid) may also display agitation
that is difficult to distinguish from akathisia. Some of these individuals are able to differentiate

akathisia from the anxiety, restlessness, and agitation characteristic of a mental disorder by their
experience of akathisia as being different from previously experienced feelings. Other evidence
that restlessness or agitation may be better accounted for by a mental disorder includes the onset
of agitation prior to exposure to the causative medication, absence of increasing restlessness with
increasing doses of the causative medication, and absence of relief with pharmacological
interventions (e.g., no improvement after decreasing the dose of the causative medication or
treatment with another medication intended to treat the akathisia).
Tardive Dyskinesia
G24.01 Tardive Dyskinesia
The essential features of tardive dyskinesia are abnormal, involuntary movements of the tongue,
jaw, trunk, or extremities that develop in association with the use of medications that block
postsynaptic dopamine receptors, such as first- and second-generation antipsychotic medications
and other medications such as metoclopramide for gastrointestinal disorders. The movements are
present over a period of at least 4 weeks and may be choreiform (rapid, jerky, nonrepetitive),
athetoid (slow, sinuous, continual), or semirhythmic (e.g., stereotypies) in nature; however, the
movements are distinctly different from the rhythmic
(3-6 Hz) tremors commonly seen in medication-induced parkinsonism. Signs or symptoms of
tardive dyskinesia develop during exposure to the antipsychotic medication or other dopamine
blocking agent, or within 4 weeks of withdrawal from an oral agent (or within 8 weeks of
withdrawal from a long-acting injectable agent). There must be a history of the use of the
offending agent for at least 3 months (or 1 month in individuals age 60 years or older). Although
a large number of epidemiological studies have established the etiological relationship between
dopamine blocking drug use and tardive dyskinesia, any dyskinesia in an individual who is
receiving antipsychotic medication is not necessarily tardive dyskinesia.
Abnormal orofacial movements are the most obvious manifestations of tardive dyskinesia
and have been observed in most individuals afflicted with tardive dyskinesia; however,
approximately one-half can have limb involvement, and up to one-quarter can have axial
dyskinesia of the neck, shoulders, or trunk. Involvement of other muscle groups (e.g.,
pharyngeal, diaphragm, abdominal) may occur but is uncommon, especially in the absence of
dyskinesia of the orofacial region, limbs, or trunk. Limb or truncal dyskinesia without orofacial
involvement may be more common in younger individuals, whereas orofacial dyskinesias are
typical in older individuals.
The symptoms of tardive dyskinesia tend to be worsened by stimulants, antipsychotic
medication withdrawal, and anticholinergic medications (such as benztropine, commonly used to
manage medication-induced parkinsonism) and may be transiently worsened by emotional
arousal, stress, and distraction during voluntary movements in unaffected parts of the body. The
abnormal movements of dyskinesia are transiently reduced by relaxation and by voluntary
movements in affected parts of the body. They are generally absent during sleep. Dyskinesia may
be suppressed, at least temporarily, by increased doses of antipsychotic medication.

The overall prevalence of tardive dyskinesia in individuals who have received long-term
antipsychotic medication treatment ranges from 20% to 30%. The overall incidence among
younger individuals ranges from 3% to 5% per year. Middle-age and elderly individuals appear
to develop tardive dyskinesia more often, with prevalence figures reported up to 50% and an
incidence of 25%–30% after an average of 1 year’s cumulative exposure to antipsychotic
medication. Prevalence also varies depending on setting, with tardive dyskinesia tending to be
more common among chronically institutionalized individuals. Variations in reported prevalence
may be attributable to a lack of consistency in the definition of tardive dyskinesia, antipsychotic
prescribing practices, study design, and the demographics of the population being studied.
There is no obvious gender difference in the susceptibility to tardive dyskinesia, although the
risk may be somewhat greater in postmenopausal women. Greater cumulative amounts of
antipsychotic medications and early development of acute extrapyramidal side effects (such as
medication-induced parkinsonism) are two of the most consistent risk factors for tardive
dyskinesia. Mood disorders (especially major depressive disorder), neurological conditions, and
alcohol use disorder have also been found to be risk factors in some groups of individuals.
Second-generation antipsychotics are associated with a somewhat lower incidence of tardive
dyskinesia compared with first-generation antipsychotics, but the difference is not as large as
once thought, especially when the dose of the first-generation antipsychotic is taken into account;
the most important risk factors are age and cumulative exposure.
Onset of tardive dyskinesia may occur at any age and is almost always insidious. The signs
are typically minimal to mild at onset and escape notice except by a keen observer. In many
cases, tardive dyskinesia is objectively mild but, although it has been thought of as a cosmetic
problem, can be associated with significant distress and social avoidance. In severe cases, it may
be associated with medical complications (e.g., ulcers in cheeks and tongue; loss of teeth;
macroglossia; difficulty in walking, swallowing, or breathing; muffled speech; weight loss;
depression; suicidal ideation). In older individuals there is a greater
likelihood that tardive dyskinesia may become more severe or more generalized with
continued antipsychotic medication use. When antipsychotic medications are discontinued, some
individuals experience symptom improvement over time; however, for others tardive dyskinesia
can be enduring.
Differential Diagnosis
It is imperative to distinguish medication-induced parkinsonism from tardive dyskinesia because
the treatments commonly used to manage medication-induced parkinsonism (i.e., anticholinergic
medications) may worsen the abnormal motor movements associated with tardive dyskinesia.
Moreover, treatments used to manage tardive dyskinesia (i.e., VMAT2 inhibitors) may worsen
the symptoms of medication-induced parkinsonism.
Dyskinesia that emerges during withdrawal from an antipsychotic medication or other
dopamine receptor blocking agent may remit with continued withdrawal from the medication. If
the dyskinesia persists for at least 4 weeks, a diagnosis of tardive dyskinesia may be warranted.
Tardive dyskinesia must be distinguished from other causes of orofacial and body dyskinesia.

These conditions include Huntington’s disease, Wilson’s disease, Sydenham’s (rheumatic)
chorea, systemic lupus erythematosus, thyrotoxicosis, heavy metal poisoning, ill-fitting dentures,
dyskinesia due to other medications such as L-dopa or bromocriptine, and spontaneous
dyskinesias. Factors that may be helpful in making the distinction are evidence that the
symptoms preceded the exposure to the antipsychotic medication or other dopamine receptor
blocking agent or that other focal neurological signs are present. It should be noted that other
movement disorders may coexist with tardive dyskinesia. Because spontaneous dyskinesia can
occur in more than 5% of individuals and is also more common in elderly persons, it may be
difficult to prove that antipsychotic medications produced tardive dyskinesia in a given
individual. Tardive dyskinesia must be distinguished from symptoms that are due to a
medication-induced acute movement disorder (e.g., medication-induced parkinsonism, acute
dystonia, acute akathisia). Acute dystonia and acute akathisia can develop quickly within hours
to days, and medication-induced parkinsonism develops within weeks of initiating or increasing
the dose of an antipsychotic medication or other dopamine receptor blocking agent (or reducing
the dose of a medication used to treat the acute extrapyramidal symptoms). Tardive dyskinesia,
on the other hand, generally develops after more prolonged exposure to antipsychotic medication
(months to years) and can appear after the withdrawal of antipsychotic medication; the minimum
exposure history required for the diagnosis of tardive dyskinesia is antipsychotic medication use
for at least 3 months (or 1 month in middle-age and elderly individuals).
Tardive Dystonia Tardive Akathisia
G24.09 Tardive Dystonia
G25.71 Tardive Akathisia
This category is for tardive syndromes involving other types of movement problems, such as
dystonia or akathisia, which are distinguished by their late emergence in the course of treatment
and their potential persistence for months to years, even in the face of discontinuation of an
antipsychotic medication or other dopamine receptor blocking agent or dosage reduction.
Medication-Induced Postural Tremor
G25.1 Medication-Induced Postural Tremor
The essential feature of this condition is a fine tremor occurring during attempts to maintain a
posture, which develops in association with the use of medication. Medications with which such
a tremor may be associated include lithium, β-adrenergic medications (e.g., isoproterenol),
stimulants (e.g., amphetamine), dopaminergic medications, anticonvulsant medications (e.g.,
valproic acid), antidepressant medications, and methylxanthines (e.g., caffeine, theophylline).
The tremor is a regular, rhythmic oscillation of the limbs (most commonly hands and fingers),
head, mouth, or tongue, most commonly with a frequency of between 8 and 12 cycles per
second. It is most easily observed when the affected body part is held in a sustained posture (e.g.,
hands outstretched, mouth held open). The tremor may worsen in severity when the affected

body part is moved intentionally (kinetic or action tremor). When an individual describes a
tremor that is consistent with postural tremor but the clinician does not directly observe the
tremor, it may be helpful to try to re-create the situation in which the tremor occurred (e.g.,
drinking from a cup and saucer).
Most available information concerns lithium-induced tremor. Lithium tremor is a common,
usually benign, and well-tolerated side effect of therapeutic doses. However, it may cause social
embarrassment, occupational difficulties, and noncompliance in some individuals. As serum
lithium levels approach toxic levels, the tremor may become coarser and be accompanied by
muscle twitching, fasciculations, or ataxia. Nontoxic lithium tremor may improve spontaneously
over time. A variety of factors may increase the risk of lithium tremor (e.g., increasing age, high
serum lithium levels, concurrent antidepressant or antipsychotic medication or another dopamine
receptor blocking agent, excessive caffeine intake, personal or family history of tremor, presence
of alcohol use disorder, and associated anxiety). The frequency of complaints about tremor
appears to decrease with duration of lithium treatment. Factors that may exacerbate the tremor
include anxiety, stress, fatigue, hypoglycemia, thyrotoxicosis, pheochromocytoma, hypothermia,
and alcohol withdrawal. Tremor can also be an early feature of serotonin syndrome.
Differential Diagnosis
Medication-induced postural tremor should be distinguished from a preexisting tremor that is not
caused by the effects of a medication. Factors that help to establish that the tremor was
preexisting include its temporal relationship to the initiation of medication, lack of correlation
with serum levels of the medication, and persistence after the medication is discontinued. If a
preexisting, nonpharmacologically induced tremor is present (e.g., essential tremor) that worsens
with medication, such a tremor would not be considered to be medication-induced postural
tremor. The factors described above that may contribute to the severity of a medication-induced
postural tremor (e.g., anxiety, stress, fatigue, hypoglycemia, thyrotoxicosis, pheochromocytoma,
hypothermia, alcohol withdrawal) may also be a cause of tremor independent of the medication.
Medication-induced postural tremor is not diagnosed if the tremor is better accounted for by
medication-induced parkinsonism. A medication-induced postural tremor is usually absent at rest
and intensifies when the affected part is brought into action or held in a sustained position. In
contrast, the tremor related to medication-induced parkinsonism is usually lower in frequency
(3–6 Hz), worse at rest, and suppressed during intentional movement and usually occurs in
association with other symptoms of medication-induced parkinsonism (e.g., akinesia, rigidity).
Other Medication-Induced Movement Disorder
G25.79 Other Medication-Induced Movement Disorder
This category is for medication-induced movement disorders not captured by any of the specific
disorders listed earlier. Examples include 1) presentations resembling neuroleptic malignant
syndrome that are associated with medications other than antipsychotic medications and other
dopamine receptor blocking agents and 2) other medication-induced tardive conditions.

Antidepressant Discontinuation Syndrome
T43.205A Initial encounter
T43.205D Subsequent encounter
T43.205S Sequelae
Discontinuation symptoms may occur following treatment with all types of antidepressants. The
incidence of this syndrome depends on the dosage and half-life of the medication being taken, as
well as the rate at which the medication is tapered. Short half-life medications that are abruptly
discontinued (or when the dose is significantly reduced) rather than tapered gradually may pose
the greatest risk. The short-acting antidepressants paroxetine and venlafaxine are the agents most
commonly associated with discontinuation symptoms. Antidepressant discontinuation syndrome
may occur in the context of intermittent non-adherence to treatment and therefore may be
irregularly present in some individuals who have not actually stopped taking the medication.
This is especially true for very short half-life medications (e.g., venlafaxine). By contrast, long
half-life medications like fluoxetine seldom produce significant discontinuation effects.
Unlike withdrawal syndromes associated with opioids, alcohol, and other substances,
antidepressant discontinuation syndrome has no pathognomonic symptoms. Instead, the
symptoms tend to be vague and variable. Symptoms typically begin 2–4 days after the last dose
of the antidepressant. For selective serotonin reuptake inhibitors, symptoms such as dizziness,
tinnitus, “electric shock”–like sensations, insomnia, and acute anxiety are described. The
antidepressant use before discontinuation must not have incurred hypomania or mixed state (i.e.,
there should be confidence that the discontinuation syndrome is not the result of fluctuations in
mood stability associated with the previous treatment). For the tricyclic antidepressants, sudden
discontinuation has been associated with gastrointestinal symptoms (cramping—reflecting
cholinergic overactivity after stopping an anticholinergic tricyclic antidepressant) as well as
rebound hypomania.
The antidepressant discontinuation syndrome is based solely on pharmacological factors and
is not related to the reinforcing effects of an antidepressant. Unlike the discontinuation of
substances with reinforcing effects like opioids, drug craving does not occur. Also, when a
stimulant is used to augment an antidepressant, abrupt cessation may result in stimulant
withdrawal symptoms (see “Stimulant Withdrawal” in the chapter “Substance-Related and
Addictive Disorders”) rather than the antidepressant discontinuation syndrome described here.
The prevalence of antidepressant discontinuation syndrome is unknown but is thought to vary
according to any of the following factors: the dosage before discontinuation, the half-life (i.e.,
occurring more commonly with short half-life medications) and receptor-binding affinity of the
medication (e.g., more likely to occur with serotonin reuptake inhibitors), and possibly the
individual’s genetically influenced rate of metabolism for this
medication. Therefore, discontinuation reactions occur more frequently with short half-life
medications, but may also be influenced by rapid or ultrarapid metabolizer status of cytochrome
enzymes that metabolize the antidepressant.

Because longitudinal studies are lacking, little is known about the clinical course of
antidepressant discontinuation syndrome. Symptoms appear to abate over time with very gradual
dosage reductions. Symptoms are usually short-lived, lasting no more than 2 weeks, and are
seldom present more than 3 weeks after discontinuation.
Differential Diagnosis
The differential diagnosis of antidepressant discontinuation syndrome includes a relapse of the
disorder for which the medication was prescribed (e.g., depression or panic disorder), somatic
symptom disorder, bipolar I or bipolar II disorder with mixed features, substance use disorders,
migraine, or cerebrovascular accident. Discontinuation symptoms often resemble symptoms of a
persistent anxiety disorder or a return of somatic symptoms of depression for which the
medication was initially given. It is important not to confuse discontinuation syndrome with a
relapse of the original depressive or anxiety disorder for which the medication was being
prescribed. Antidepressant discontinuation syndrome differs from substance withdrawal in that
antidepressants themselves have no reinforcing or euphoric effects. Individuals typically do not
escalate the dose of medications on their own, and they generally do not engage in drug-seeking
behavior to obtain additional medication. Criteria for a substance use disorder are not met.
Other Adverse Effect of Medication
T50.905A Initial encounter
T50.905D Subsequent encounter
T50.905S Sequelae
This category is available for optional use by clinicians to code side effects of medication (other
than movement symptoms) when these adverse effects become a main focus of clinical attention.
Examples include severe hypotension, cardiac arrhythmias, and priapism.

# 22 - Other Conditions That May Be a Focus of Clini

# Other Conditions That May Be a Focus of Clinical Attention

821

Other Conditions That May Be a Focus of
Clinical Attention
This chapter includes conditions and psychosocial or environmental problems that may be
a focus of clinical attention or otherwise affect the diagnosis, course, prognosis, or treatment of
an individual’s mental disorder. These conditions are presented with their corresponding codes
from ICD-10-CM (usually Z codes). A condition or problem in this chapter may be coded 1) if it
is a reason for the current visit; 2) if it helps to explain the need for a test, procedure, or
treatment; 3) if it plays a role in the initiation or exacerbation of a mental disorder; or 4) if it
constitutes a problem that should be considered in the overall management plan.
The conditions and problems listed in this chapter are not mental disorders. Their inclusion in
DSM-5-TR is meant to draw attention to the scope of additional issues that may be encountered
in routine clinical practice and to provide a systematic listing that may be useful to clinicians in
documenting these issues.
For quick reference to all codes in this section, see the DSM-5-TR Classification. Conditions
and problems that may be a focus of clinical attention are listed in the subsequent text as follows:
1. Suicidal behavior (potentially self-injurious behavior with at least some intent to die) and
nonsuicidal self-injury (intentional self-inflicted damage to the body in the absence of
suicidal intent).
2. Abuse and neglect (e.g., child and adult maltreatment and neglect problems, including
physical abuse, sexual abuse, neglect, and psychological abuse).
3. Relational problems (e.g., parent-child relational problem, sibling relational problem,
relationship distress with spouse or intimate partner, disruption by separation or divorce).
4. Educational problems (e.g., illiteracy or low-level literacy, schooling unavailable or
unattainable, failed school examinations, underachievement in school).
5. Occupational problems (e.g., unemployment, change of job, threat of job loss, stressful
work schedule, discord with boss and workmates).
6. Housing problems (e.g., homelessness; inadequate housing; discord with neighbor, lodger,
or landlord).
7. Economic problems (e.g., lack of adequate food or safe drinking water, extreme poverty,
low income).
8. Problems related to the social environment (e.g., problem related to living alone,
acculturation difficulty, social exclusion or rejection).
9. Problems related to interaction with the legal system (e.g., conviction in criminal
proceedings, imprisonment or other incarceration, problems related to release from prison,
problems related to other legal circumstances).
0. Problems related to other psychosocial, personal, and environmental circumstances
(e.g., problems related to unwanted pregnancy, victim of crime, victim of terrorism).

1. 
Problems related to access to medical and other health care (e.g., unavailability or
inaccessibility of health care facilities).
2. 
Circumstances of personal history (e.g., personal history of psychological trauma, military
deployment).
3. 
Other health service encounters for counseling and medical advice (e.g., sex counseling,
other counseling or consultation).
4. 
Additional conditions or problems that may be a focus of clinical attention (e.g.,
wandering associated with a mental disorder, uncomplicated bereavement, phase of life
problem).
Suicidal Behavior and Nonsuicidal Self-Injury
Coding Note for ICD-10-CM Suicidal Behavior
For T codes only, the 6th character should be coded as follows:
A (initial encounter)—Use while the individual is receiving active treatment for the
condition (e.g., emergency department encounter, evaluation and treatment by a new
clinician); or
D (subsequent encounter)—Use for encounters after the individual has received active
treatment for the condition and when he or she is receiving routine care for the condition
during the healing or recovery phase (e.g., medication adjustment, other aftercare and
follow-up visits).
Suicidal Behavior
This category may be used for individuals who have engaged in potentially self-injurious
behavior with at least some intent to die as a result of the act. Evidence of intent to end one’s life
can be explicit or inferred from the behavior or circumstances. A suicide attempt may or may not
result in actual self-injury. If the individual is dissuaded by another person or changes his or her
mind before initiating the behavior, this category does not apply.
Current Suicidal Behavior
T14.91A Initial encounter: If suicidal behavior is part of the initial encounter with the clinical
presentation
T14.91D Subsequent encounter: If suicidal behavior is part of subsequent encounters with the
clinical presentation
Z91.51
History of Suicidal Behavior
If suicidal behavior has occurred during the individual’s lifetime
Nonsuicidal Self-Injury
This category may be used for individuals who have engaged in intentional self-inflicted damage

to their body of a sort likely to induce bleeding, bruising, or pain (e.g., cutting, burning, stabbing,
hitting, excessive rubbing) in the absence of suicidal intent.
R45.88
Current Nonsuicidal Self-Injury
If nonsuicidal self-injurious behavior is part of the clinical presentation
Z91.52
History of Nonsuicidal Self-Injury
If nonsuicidal self-injurious behavior has occurred during the individual’s lifetime
Abuse and Neglect
Maltreatment by a family member (e.g., caregiver, intimate adult partner) or by a nonrelative can
be the area of current clinical focus, or such maltreatment can be an important factor in the
assessment and treatment of individuals with mental disorders or other medical conditions.
Because of the legal implications of abuse and neglect, care should be used in assessing these
conditions and assigning these codes. Having a past history of abuse or
neglect can influence diagnosis and treatment response in a number of mental disorders, and may
also be noted along with the diagnosis.
For the following categories, in addition to listings of the confirmed or suspected event of
abuse or neglect, other codes are provided for use if the current clinical encounter is to provide
mental health services to either the victim or the perpetrator of the abuse or neglect. A separate
code is also provided for designating a past history of abuse or neglect.
Coding Note for ICD-10-CM Abuse and Neglect Conditions
For T codes only, the 7th character should be coded as follows:
A (initial encounter)—Use while the individual is receiving active treatment for the
condition (e.g., surgical treatment, emergency department encounter, evaluation and
treatment by a new clinician); or
D (subsequent encounter)—Use for encounters after the individual has received active
treatment for the condition and when he or she is receiving routine care for the condition
during the healing or recovery phase (e.g., cast change or removal, removal of external or
internal fixation device, medication adjustment, other aftercare and follow-up visits).
Child Maltreatment and Neglect Problems
Child Physical Abuse
This category may be used when physical abuse of a child is a focus of clinical attention. Child
physical abuse is nonaccidental physical injury to a child—ranging from minor bruises to severe
fractures or death—occurring as a result of punching, beating, kicking, biting, shaking, throwing,
stabbing, choking, hitting (with a hand, stick, strap, or other object), burning, or any other
method that is inflicted by a parent, caregiver, or other individual who has responsibility for the
child. Such injury is considered abuse regardless of whether the caregiver intended to hurt the
child. Physical discipline, such as spanking or paddling, is not considered abuse as long as it is

reasonable and causes no bodily injury to the child.
Child Physical Abuse, Confirmed
T74.12XA Initial encounter
T74.12XD Subsequent encounter
Child Physical Abuse, Suspected
T76.12XA Initial encounter
T76.12XD Subsequent encounter
Other Circumstances Related to Child Physical Abuse
Z69.010 Encounter for mental health services for victim of child physical abuse by parent
Z69.020 Encounter for mental health services for victim of nonparental child physical abuse
Z62.810 Personal history (past history) of physical abuse in childhood
Z69.011 Encounter for mental health services for perpetrator of parental child physical abuse
Z69.021  Encounter for mental health services for perpetrator of nonparental child physical
abuse
Child Sexual Abuse
This category may be used when sexual abuse of a child is a focus of clinical attention. Child
sexual abuse encompasses any sexual act involving a child that is intended to provide sexual
gratification to a parent, caregiver, or other individual who has responsibility
for the child. Sexual abuse includes activities such as fondling a child’s genitals, penetration,
incest, rape, sodomy, and indecent exposure. Sexual abuse also includes noncontact exploitation
of a child by a parent or caregiver—for example, forcing, tricking, enticing, threatening, or
pressuring a child to participate in acts for the sexual gratification of others, without direct
physical contact between child and abuser.
Child Sexual Abuse, Confirmed
T74.22XA Initial encounter
T74.22XD Subsequent encounter
Child Sexual Abuse, Suspected
T76.22XA Initial encounter
T76.22XD Subsequent encounter
Other Circumstances Related to Child Sexual Abuse

Z69.010 Encounter for mental health services for victim of child sexual abuse by parent
Z69.020 Encounter for mental health services for victim of nonparental child sexual abuse
Z62.810 Personal history (past history) of sexual abuse in childhood
Z69.011 Encounter for mental health services for perpetrator of parental child sexual abuse
Z69.021 Encounter for mental health services for perpetrator of nonparental child sexual abuse
Child Neglect
This category may be used when child neglect is a focus of clinical attention. Child neglect is
defined as any confirmed or suspected egregious act or omission by a child’s parent or other
caregiver that deprives the child of basic age-appropriate needs and thereby results, or has
reasonable potential to result, in physical or psychological harm to the child. Child neglect
encompasses abandonment; lack of appropriate supervision; failure to attend to necessary
emotional or psychological needs; and failure to provide necessary education, medical care,
nourishment, shelter, and/or clothing.
Child Neglect, Confirmed
T74.02XA Initial encounter
T74.02XD Subsequent encounter
Child Neglect, Suspected
T76.02XA Initial encounter
T76.02XD Subsequent encounter
Other Circumstances Related to Child Neglect
Z69.010 Encounter for mental health services for victim of child neglect by parent
Z69.020 Encounter for mental health services for victim of nonparental child neglect
Z62.812 Personal history (past history) of neglect in childhood
Z69.011 Encounter for mental health services for perpetrator of parental child neglect
Z69.021 Encounter for mental health services for perpetrator of nonparental child neglect
Child Psychological Abuse
This category may be used when psychological abuse of a child is a focus of clinical attention.
Child psychological abuse is nonaccidental verbal or symbolic acts by a child’s parent or
caregiver that result, or have reasonable potential to result, in significant psychological harm to
the child. (Physical and sexual abusive acts are not included in this category.) Examples of
psychological abuse of a child include berating, disparaging, or humiliating the child; threatening
the child; harming/abandoning—or indicating that the alleged offender will harm/abandon—
people or things that the child cares about; confining the child (as by tying a child’s arms or legs

together or binding a child to furniture or another object, or confining a child to a small enclosed
area [e.g., a closet]); egregious scapegoating of the child; coercing the child to inflict pain on
himself or herself; and disciplining the child excessively (i.e., at an extremely high frequency or
duration, even if not at a level of physical abuse) through physical or nonphysical means.
Child Psychological Abuse, Confirmed
T74.32XA Initial encounter
T74.32XD Subsequent encounter
Child Psychological Abuse, Suspected
T76.32XA Initial encounter
T76.32XD Subsequent encounter
Other Circumstances Related to Child Psychological Abuse
Z69.010 Encounter for mental health services for victim of child psychological abuse by parent
Z69.020 Encounter for mental health services for victim of nonparental child psychological
abuse
Z62.811 Personal history (past history) of psychological abuse in childhood
Z69.011 Encounter for mental health services for perpetrator of parental child psychological
abuse
Z69.021 Encounter for mental health services for perpetrator of nonparental child
psychological abuse
Adult Maltreatment and Neglect Problems
Spouse or Partner Violence, Physical
This category may be used when spouse or partner physical violence is a focus of clinical
attention. Spouse or partner physical violence is nonaccidental acts of physical force that result,
or have reasonable potential to result, in physical harm to an intimate partner or that evoke
significant fear in the partner. Nonaccidental acts of physical force include shoving, slapping,
hair pulling, pinching, restraining, shaking, throwing, biting, kicking, hitting with the fist or an
object, burning, poisoning, applying force to the throat, cutting off the air supply, holding the
head under water, and using a weapon. Acts for the purpose of physically protecting oneself or
one’s partner are excluded.
Spouse or Partner Violence, Physical, Confirmed
T74.11XA Initial encounter
T74.11XD Subsequent encounter

Spouse or Partner Violence, Physical, Suspected
T76.11XA Initial encounter
T76.11XD Subsequent encounter
Other Circumstances Related to Spouse or Partner Violence, Physical
Z69.11
Encounter for mental health services for victim of spouse or partner violence, physical
Z91.410 Personal history (past history) of spouse or partner violence, physical
Z69.12
Encounter for mental health services for perpetrator of spouse or partner violence,
physical
Spouse or Partner Violence, Sexual
This category may be used when spouse or partner sexual violence is a focus of clinical
attention. Spouse or partner sexual violence involves the use of physical force or psychological
coercion to compel the partner to engage in a sexual act against his or her will, whether or not the
act is completed. Also included in this category are sexual acts with an intimate partner who is
unable to consent.
Spouse or Partner Violence, Sexual, Confirmed
T74.21XA Initial encounter
T74.21XD Subsequent encounter
Spouse or Partner Violence, Sexual, Suspected
T76.21XA Initial encounter
T76.21XD Subsequent encounter
Other Circumstances Related to Spouse or Partner Violence, Sexual
Z69.81
Encounter for mental health services for victim of spouse or partner violence, sexual
Z91.410 Personal history (past history) of spouse or partner violence, sexual
Z69.12
Encounter for mental health services for perpetrator of spouse or partner violence,
sexual
Spouse or Partner Neglect
This category may be used when spouse or partner neglect is a focus of clinical attention. Spouse
or partner neglect is any egregious act or omission by one partner that deprives a dependent
partner of basic needs and thereby results, or has reasonable potential to result, in physical or
psychological harm to the dependent partner. This category may be used in the context of
relationships in which one partner is extremely dependent on the other partner for care or for
assistance in navigating ordinary daily activities—for example, a partner who is incapable of
self-care because of substantial physical, psychological/intellectual, or cultural limitations (e.g.,
inability to communicate with others and manage everyday activities as a result of living in a
foreign culture).

Spouse or Partner Neglect, Confirmed
T74.01XA Initial encounter
T74.01XD Subsequent encounter
Spouse or Partner Neglect, Suspected
T76.01XA Initial encounter
T76.01XD Subsequent encounter
Other Circumstances Related to Spouse or Partner Neglect
Z69.11
Encounter for mental health services for victim of spouse or partner neglect
Z91.412 Personal history (past history) of spouse or partner neglect
Z69.12
Encounter for mental health services for perpetrator of spouse or partner neglect
Spouse or Partner Abuse, Psychological
This category may be used when spouse or partner psychological abuse is a focus of clinical
attention. Spouse or partner psychological abuse encompasses nonaccidental verbal or symbolic
acts by one partner that result, or have reasonable potential to result, in significant harm to the
other partner. Acts of psychological abuse include berating or humiliating the victim;
interrogating the victim; restricting the victim’s ability to come and go freely; obstructing the
victim’s access to assistance (e.g., law enforcement; legal, protective, or medical resources);
threatening the victim with physical harm or sexual assault; harming, or threatening to harm,
people or things that the victim cares about; unwarranted restriction of the victim’s access to or
use of economic resources; isolating the victim from family, friends, or social support resources;
stalking the victim; and trying to make the victim question his or her sanity (“gaslighting”).
Spouse or Partner Abuse, Psychological, Confirmed
T74.31XA Initial encounter
T74.31XD Subsequent encounter
Spouse or Partner Abuse, Psychological, Suspected
T76.31XA Initial encounter
T76.31XD Subsequent encounter
Other Circumstances Related to Spouse or Partner Abuse, Psychological
Z69.11
Encounter for mental health services for victim of spouse or partner psychological
abuse
Z91.411 Personal history (past history) of spouse or partner psychological abuse

Z69.12
Encounter for mental health services for perpetrator of spouse or partner
psychological abuse
Adult Abuse by Nonspouse or Nonpartner
This category may be used when the abuse of an adult by another adult who is not an intimate
partner is a focus of clinical attention. Such maltreatment may involve acts of physical, sexual, or
emotional abuse. Examples of adult abuse include nonaccidental acts of physical force (e.g.,
pushing/shoving, scratching, slapping, throwing something that could hurt, punching, biting) that
have resulted—or have reasonable potential to result—in physical harm or have caused
significant fear; forced or coerced sexual acts; and verbal or symbolic acts with the potential to
cause psychological harm (e.g., berating or humiliating the person; interrogating the person;
restricting the person’s ability to come and go freely; obstructing the person’s access to
assistance; threatening the person; harming or threatening to harm people or things that the
person cares about; restricting the person’s
access to or use of economic resources; isolating the person from family, friends, or social
support resources; stalking the person; trying to make the person think that he or she is crazy).
Acts for the purpose of physically protecting oneself or the other person are excluded.
Adult Physical Abuse by Nonspouse or Nonpartner, Confirmed
T74.11XA Initial encounter
T74.11XD Subsequent encounter
Adult Physical Abuse by Nonspouse or Nonpartner, Suspected
T76.11XA Initial encounter
T76.11XD Subsequent encounter
Adult Sexual Abuse by Nonspouse or Nonpartner, Confirmed
T74.21XA Initial encounter
T74.21XD Subsequent encounter
Adult Sexual Abuse by Nonspouse or Nonpartner, Suspected
T76.21XA Initial encounter
T76.21XD Subsequent encounter
Adult Psychological Abuse by Nonspouse or Nonpartner, Confirmed
T74.31XA Initial encounter
T74.31XD Subsequent encounter
Adult Psychological Abuse by Nonspouse or Nonpartner, Suspected

T76.31XA Initial encounter
T76.31XD Subsequent encounter
Other Circumstances Related to Adult Abuse by Nonspouse or Nonpartner
Z69.81
Encounter for mental health services for victim of nonspousal or nonpartner adult
abuse
Z69.82
Encounter for mental health services for perpetrator of nonspousal or nonpartner adult
abuse
Relational Problems
Key relationships, especially intimate adult partner relationships and parent/caregiver-child
relationships, have a significant impact on the health of the individuals in these relationships.
These relationships can be health promoting and protective, neutral, or detrimental to health
outcomes. In the extreme, these close relationships can be associated with maltreatment or
neglect, which has significant medical and psychological consequences for the affected
individual. A relational problem may come to clinical attention either as the reason that the
individual seeks health care or as a problem that affects the course, prognosis, or treatment of the
individual’s mental disorder or other medical condition.
Parent-Child Relational Problem
Z62.820 Parent–Biological Child
Z62.821 Parent–Adopted Child
Z62.822 Parent–Foster Child
Z62.898 Other Caregiver–Child
For this category, the term parent is used to refer to one of the child’s primary caregivers, who
may be a biological, adoptive, or foster parent or may be another relative (such as a grandparent)
who fulfills a parental role for the child. This category may be used when the main focus of
clinical attention is to address the quality of the parent-child relationship or when the quality of
the parent-child relationship is affecting the course, prognosis, or treatment of a mental disorder
or other medical condition. Typically, the parent-child relational problem is associated with
impaired functioning in behavioral, cognitive, or affective domains. Examples of behavioral
problems include inadequate parental control, supervision, and involvement with the child;
parental overprotection; excessive parental pressure; arguments that escalate to threats of
physical violence; and avoidance without resolution of problems. Cognitive problems may
include negative attributions of the other’s intentions, hostility toward or scapegoating of the
other, and unwarranted feelings of estrangement. Affective problems may include feelings of
sadness, apathy, or anger about the other individual in the relationship. Clinicians should take
into account the developmental needs of the child and the cultural context.
Z62.891 Sibling Relational Problem

This category may be used when the focus of clinical attention is a pattern of interaction among
siblings that is associated with significant impairment in individual or family functioning or with
development of symptoms in one or more of the siblings, or when a sibling relational problem is
affecting the course, prognosis, or treatment of a sibling’s mental disorder or other medical
condition. This category may be used for either children or adults if the focus is on the sibling
relationship. Siblings in this context include full, half-, step-, foster, and adopted siblings.
Z63.0
Relationship Distress With Spouse or Intimate Partner
This category may be used when the major focus of the clinical contact is to address the quality
of the intimate (spouse or partner) relationship or when the quality of that relationship is
affecting the course, prognosis, or treatment of a mental disorder or other medical condition.
Partners can be of the same or different genders. Typically, the relationship distress is associated
with impaired functioning in behavioral, cognitive, or affective domains. Examples of behavioral
problems include conflict resolution difficulty, withdrawal, and overinvolvement. Cognitive
problems can manifest as chronic negative attributions of the other’s intentions or dismissals of
the partner’s positive behaviors. Affective problems would include chronic sadness, apathy,
and/or anger about the other partner.
Problems Related to the Family Environment
Z62.29
Upbringing Away From Parents
This category may be used when the main focus of clinical attention pertains to issues regarding
a child being raised away from the parents or when this separate upbringing affects the course,
prognosis, or treatment of a mental disorder or other medical condition. The child could be one
who is under state custody and placed in kin care or foster care. The child could also be one who
is living in a nonparental relative’s home, or with friends, but whose out-of-home placement is
not mandated or sanctioned by the courts. Problems related to a child living in a group home or
orphanage are also included. This category excludes issues related to Z59.3 Problem Related to
Living in a Residential Institution.
Z62.898 Child Affected by Parental Relationship Distress
This category may be used when the focus of clinical attention is the negative effects of parental
relationship discord (e.g., high levels of conflict, distress, or disparagement) on a child in the
family, including effects on the child’s mental disorder or other medical condition.
Z63.5
Disruption of Family by Separation or Divorce
This category may be used when partners in an intimate adult couple are living apart because of
relationship problems or are in the process of divorce.
Z63.8
High Expressed Emotion Level Within Family
Expressed emotion is a construct used as a qualitative measure of the “amount” of emotion—in
particular, hostility, emotional overinvolvement, and criticism directed toward a family member
who is an identified patient—displayed in the family environment. This category may be used
when a family’s high level of expressed emotion is the focus of clinical attention or is affecting
the course, prognosis, or treatment of a family member’s mental disorder or other medical

condition.
Educational Problems
These categories may be used when an academic or educational problem is the focus of clinical
attention or has an impact on the individual’s diagnosis, treatment, or prognosis. Problems to be
considered include illiteracy or low-level literacy; lack of access to schooling owing to
unavailability or unattainability; problems with academic performance (e.g., failing school
examinations, receiving failing marks or grades) or underachievement (below what would be
expected given the individual’s intellectual capacity); discord with teachers, school staff, or other
students; problems related to inadequate teaching; and any other problems related to education
and/or literacy.
Z55.0
Illiteracy and Low-Level Literacy
Z55.1
Schooling Unavailable and Unattainable
Z55.2
Failed School Examinations
Z55.3
Underachievement in School
Z55.4
Educational Maladjustment and Discord With Teachers and Classmates
Z55.8
Problems Related to Inadequate Teaching
Z55.9
Other Problems Related to Education and Literacy
Occupational Problems
These categories may be used when an occupational problem is the focus of clinical attention or
has an impact on the individual’s treatment or prognosis. Areas to be considered include
problems with employment or in the work environment, including problems related to current
military deployment status; unemployment; recent change of job; threat of job loss; stressful
work schedule; uncertainty about career choices; sexual harassment on the job; other discord
with boss, supervisor, co-workers, or others in the work environment; uncongenial or hostile
work environments; other physical or mental strain related to work; sexual harassment on the
job; and any other problems related to employment and/or occupation.
Z56.82
Problem Related to Current Military Deployment Status
This category may be used when an occupational problem directly related to an individual’s
military deployment status is the focus of clinical attention or has an impact on the individual’s
diagnosis, treatment, or prognosis. Psychological reactions to deployment are not included in this
category; such reactions would be better captured as an adjustment disorder or another mental
disorder.
Z56.0
Unemployment
Z56.1
Change of Job

Z56.2
Threat of Job Loss
Z56.3
Stressful Work Schedule
Z56.4
Discord With Boss and Workmates
Z56.5
Uncongenial Work Environment
Z56.6
Other Physical and Mental Strain Related to Work
Z56.81
Sexual Harassment on the Job
Z56.9
Other Problem Related to Employment
Housing Problems
Z59.01
Sheltered Homelessness
This category may be used when sheltered homelessness has an impact on an individual’s
treatment or prognosis. An individual is considered to be experiencing sheltered homelessness if
the primary nighttime residence is a homeless shelter, a warming shelter, a domestic violence
shelter, a motel, or in a temporary or transitional living situation.
Z59.02
Unsheltered Homelessness
This category may be used when unsheltered homelessness has an impact on an individual’s
treatment or prognosis. An individual is considered to be experiencing unsheltered homelessness
if residing in a place not meant for human habitation, such as a public space (e.g., tunnel,
transportation station, mall), a building not intended for residential use (e.g., abandoned
structure, unused factory), a car, a cave, a cardboard box, or some other ad hoc housing situation.
Z59.1
Inadequate Housing
This category may be used when lack of adequate housing has an impact on an individual’s
treatment or prognosis. Examples of inadequate housing conditions include lack of heat (in cold
temperatures) or electricity, infestation by insects or rodents, inadequate plumbing and toilet
facilities, overcrowding, lack of adequate sleeping space, and excessive noise. It is important to
consider cultural norms before assigning this category.
Z59.2
Discord With Neighbor, Lodger, or Landlord
This category may be used when discord with neighbors, lodgers, or a landlord is a focus of
clinical attention or has an impact on the individual’s treatment or prognosis.
Z59.3
Problem Related to Living in a Residential Institution
This category may be used when a problem (or problems) related to living in a residential
institution is a focus of clinical attention or has an impact on the individual’s treatment or
prognosis. Psychological reactions to a change in living situation are not included in this
category; such reactions would be better captured as an adjustment disorder.
Z59.9
Other Housing Problem
This category may be used when there is a problem related to housing circumstances other than
as specified above.

Economic Problems
These categories may be used when an economic problem is the focus of clinical attention or has
an impact on the individual’s treatment or prognosis. Areas to be considered include lack of
adequate food (food insecurity) or safe drinking water, extreme poverty, low income, insufficient
social or health insurance or welfare support, or any other economic problems.
Z59.41
Food Insecurity
Z58.6
Lack of Safe Drinking Water
Z59.5
Extreme Poverty
Z59.6
Low Income
Z59.7
Insufficient Social or Health Insurance or Welfare Support
This category may be used for individuals who meet eligibility criteria for social or welfare
support but are not receiving such support, who receive support that is insufficient to address
their needs, or who otherwise lack access to needed insurance or support programs. Examples
include inability to qualify for welfare support because of lack of proper documentation or
evidence of address, inability to obtain adequate health insurance because of age or a preexisting
condition, and denial of support owing to excessively stringent income or other requirements.
Z59.9
Other Economic Problem
This category may be used when there is a problem related to economic circumstances other than
as specified above.
Problems Related to the Social Environment
Z60.2
Problem Related to Living Alone
This category may be used when a problem associated with living alone is the focus of clinical
attention or has an impact on the individual’s treatment or prognosis. Examples of such problems
include chronic feelings of loneliness, isolation, and lack of structure in carrying out activities of
daily living (e.g., irregular meal and sleep schedules, inconsistent performance of home
maintenance chores).
Z60.3
Acculturation Difficulty
This category may be used when difficulty in adjusting to a new culture (e.g., following
migration) is the focus of clinical attention or has an impact on the individual’s treatment or
prognosis.
Z60.4
Social Exclusion or Rejection
This category may be used when there is an imbalance of social power such that there is
recurrent social exclusion or rejection by others. Examples of social rejection include bullying,
teasing, and intimidation by others; being targeted by others for verbal abuse and humiliation;
and being purposefully excluded from the activities of peers, workmates, or others in one’s social
environment.

Z60.5
Target of (Perceived) Adverse Discrimination or Persecution
This category may be used when there is perceived or experienced discrimination against or
persecution of the individual based on his or her membership (or perceived membership) in a
specific category. Typically, such categories include gender or gender identity, race, ethnicity,
religion, sexual orientation, country of origin, political beliefs, disability status, caste, social
status, weight, and physical appearance.
Z60.9
Other Problem Related to Social Environment
This category may be used when there is a problem related to the individual’s social environment
other than as specified above.
Problems Related to Interaction With the Legal System
These categories may be used when a problem related to interaction with the legal system is the
focus of clinical attention or has an impact on the individual’s treatment or prognosis. Areas to
be considered include conviction in criminal proceedings, imprisonment or other incarceration,
problems related to release from prison, and problems related to other legal circumstances (e.g.,
civil litigation, child custody or support proceedings).
Z65.0
Conviction in Criminal Proceedings Without Imprisonment
Z65.1
Imprisonment or Other Incarceration
Z65.2
Problems Related to Release From Prison
Z65.3
Problems Related to Other Legal Circumstances (e.g., civil litigation, child
custody or support proceedings)
Problems Related to Other Psychosocial, Personal, and
Environmental Circumstances
Z72.9
Problem Related to Lifestyle
This category may be used when a lifestyle problem is a specific focus of treatment or directly
affects the course, prognosis, or treatment of a mental disorder or other medical condition.
Examples of lifestyle problems include lack of physical exercise, inappropriate diet, high-risk
sexual behavior, and poor sleep hygiene. A problem that is attributable to a symptom of a mental
disorder should not be coded unless that problem is a specific focus of treatment or directly
affects the course, prognosis, or treatment of the individual. In such cases, both the mental
disorder and the lifestyle problem should be coded.
Z64.0
Problems Related to Unwanted Pregnancy
Z64.1
Problems Related to Multiparity
Z64.4
Discord With Social Service Provider, Including Probation Officer, Case
Manager, or Social Services Worker

Z65.4
Victim of Crime
Z65.4
Victim of Terrorism or Torture
Z65.5
Exposure to Disaster, War, or Other Hostilities
Problems Related to Access to Medical and Other Health Care
These categories may be used when a problem related to access to medical or other health care is
the focus of clinical attention or has an impact on the individual’s treatment or prognosis.
Z75.3
Unavailability or Inaccessibility of Health Care Facilities
Z75.4
Unavailability or Inaccessibility of Other Helping Agencies
Circumstances of Personal History
Z91.49
Personal History of Psychological Trauma
Z91.82
Personal History of Military Deployment
Other Health Service Encounters for Counseling and Medical
Advice
Z31.5
Genetic Counseling
This category may be used for individuals seeking genetic counseling to understand the risks of
developing a mental disorder with a significant genetic component (e.g., bipolar disorder) for
themselves and other family members, including their existing children, as well as the risks for
their future children.
Z70.9
Sex Counseling
This category may be used when the individual seeks counseling related to sex education, sexual
behavior, sexual orientation, sexual attitudes (embarrassment, timidity), others’ sexual behavior
or orientation (e.g., spouse, partner, child), sexual enjoyment, or any other sex-related issue.
Z71.3
Dietary Counseling
This category may be used when the individual seeks counseling related to dietary issues like
weight management.
Z71.9
Other Counseling or Consultation
This category may be used when counseling is provided or advice/consultation is sought for a
problem that is not specified above or elsewhere in this chapter (e.g., counseling regarding drug
abuse prevention in an adolescent).
Additional Conditions or Problems That May Be a Focus of

Clinical Attention
Z91.83
Wandering Associated With a Mental Disorder
This category may be used for individuals with a mental disorder whose desire to walk about
leads to significant clinical management or safety concerns. For example, individuals with major
neurocognitive or neurodevelopmental disorders may experience a restless urge to wander that
places them at risk for falls and causes them to leave supervised settings without needed
accompaniment. This category excludes individuals whose intent is to escape an unwanted
housing situation (e.g., children who are running away from home, individuals who no longer
wish to remain in the hospital) or those who walk or pace as a result of medication-induced
akathisia.
Coding note: First code associated mental disorder (e.g., major neurocognitive disorder,
autism spectrum disorder), then code Z91.83 wandering associated with [specific mental
disorder].
Z63.4
Uncomplicated Bereavement
This category may be used when the focus of clinical attention is a normal reaction to the death
of a loved one. As part of their reaction to such a loss, some grieving individuals present with
symptoms characteristic of a major depressive episode—for example, feelings of sadness and
associated symptoms such as insomnia, poor appetite, and weight loss. The bereaved individual
typically regards the depressed mood as “normal,” although the individual may seek professional
help for relief of associated symptoms such as insomnia or anorexia. The duration and
expression of “normal” bereavement vary considerably among different cultural groups. Further
guidance in distinguishing grief from a major depressive episode and from prolonged grief
disorder is provided in their respective texts.
Z60.0
Phase of Life Problem
This category may be used when a problem adjusting to a life-cycle transition (a particular
developmental phase) is the focus of clinical attention or has an impact on the individual’s
treatment or prognosis. Examples of such transitions include entering or completing school,
leaving parental control, getting married, starting a new career, becoming a parent, adjusting to
an “empty nest” after children leave home, and retiring.
Z65.8
Religious or Spiritual Problem
This category may be used when the focus of clinical attention is a religious or spiritual problem.
Examples include distressing experiences that involve loss or questioning of faith, problems
associated with conversion to a new faith, or questioning of spiritual values that may not
necessarily be related to an organized church or religious institution.
Z72.811 Adult Antisocial Behavior
This category may be used when the focus of clinical attention is adult antisocial behavior that is
not attributable to a mental disorder (e.g., conduct disorder, antisocial personality disorder).
Examples include the behavior of some professional thieves, racketeers, or dealers in illegal
substances.

Z72.810 Child or Adolescent Antisocial Behavior
This category may be used when the focus of clinical attention is antisocial behavior in a child or
adolescent that is not attributable to a mental disorder (e.g., intermittent explosive disorder,
conduct disorder). Examples include isolated antisocial acts by children or adolescents (not a
pattern of antisocial behavior).
Z91.19
Nonadherence to Medical Treatment
This category may be used when the focus of clinical attention is nonadherence to an important
aspect of treatment for a mental disorder or another medical condition. Reasons for such
nonadherence may include discomfort resulting from treatment (e.g., medication side effects),
expense of treatment, personal value judgments or religious or cultural beliefs about the
proposed treatment, age-related debility, and the presence of a mental disorder (e.g.,
schizophrenia, personality disorder). This category may be used only when the problem is
sufficiently severe to warrant independent clinical attention and does not meet diagnostic criteria
for psychological factors affecting other medical conditions.
E66.9
Overweight or Obesity
This category may be used when overweight or obesity is a focus of clinical attention.
Z76.5
Malingering
The essential feature of malingering is the intentional production of false or grossly exaggerated
physical or psychological symptoms, motivated by external incentives such as avoiding military
duty, avoiding work, obtaining financial compensation, evading criminal prosecution, or
obtaining drugs. Under some circumstances, malingering may represent adaptive behavior—for
example, feigning illness while a captive of the enemy during wartime. Malingering should be
strongly considered if any combination of the following is noted:
1. 
Medicolegal context of presentation (e.g., the individual is referred by an attorney to the
clinician for examination, or the individual self-refers while litigation or criminal charges are
pending).
2. 
Marked discrepancy between the individual’s claimed stress or disability and the objective
findings and observations.
3. 
Lack of cooperation during the diagnostic evaluation and in complying with the prescribed
treatment regimen.
4. 
The presence of antisocial personality disorder.
Malingering differs from factitious disorder in that the motivation for the symptom
production in malingering is an external incentive, whereas in factitious disorder external
incentives are absent. Malingering is differentiated from functional neurological symptom
disorder (conversion disorder) and other somatic symptom–related mental disorders by the
intentional production of symptoms and by the obvious external incentives associated with it.
Definite evidence of feigning (such as clear evidence that loss of function is present during the
examination but not at home) would suggest a diagnosis of factitious disorder if the individual’s
apparent aim is to assume the sick role, or malingering if it is to obtain an incentive, such as
money.
R41.81
Age-Related Cognitive Decline
This category may be used when the focus of clinical attention is an objectively identified

decline in cognitive functioning consequent to the aging process that is within normal limits
given the individual’s age. Individuals with this condition may report problems remembering
names or appointments or may experience difficulty in solving complex problems. This category
should be considered only after it has been determined that the cognitive impairment is not better
explained by a specific mental disorder or attributable to a neurological condition.
R41.83
Borderline Intellectual Functioning
This category may be used when an individual’s borderline intellectual functioning is the focus
of clinical attention or has an impact on the individual’s treatment or prognosis. Differentiating
borderline intellectual functioning and mild intellectual developmental disorder (intellectual
disability) requires careful assessment of intellectual and adaptive functions and their
discrepancies, particularly in the presence of co-occurring mental disorders that may affect
patient compliance with standardized testing procedures (e.g., schizophrenia or attentiondeficit/hyperactivity disorder, with severe impulsivity).