1st AId

04 - Chapter 1 How to Succeed in the Psychiatry Clerksh

01 - Chapter 1 How to Succeed in the Psychiatry Cl
Chapter 1 How to Succeed in the Psychiatry Clerkship
Why Spend Time on Psychiatry?.................................................................................................2
How to Behave on the Wards......................................................................................................2
Respect the Patients..............................................................................................................2
Respect the Field of Psychiatry..............................................................................................2
Take Responsibility for Your Patients......................................................................................2
Respect Patients’ Rights.........................................................................................................3
Volunteer...............................................................................................................................3
Be a Team Player....................................................................................................................3
Keep Patient Information Handy...........................................................................................3
Present Patient Information in an Organized Manner............................................................3
How to Prepare for the Clerkship (Shelf) Exam...........................................................................4
Study with Friends.................................................................................................................4
Study in a Bright Room..........................................................................................................4
Eat Light, Balanced Meals......................................................................................................4
Utilize Question Banks and/or Take Practice Exams................................................................4
Pocket Cards..........................................................................................................................4
PSYCHIATRY CLERKSHIP
HOW TO SU CCE ED IN T H E
CHAPTER 1
2
HOW TO SUCCEED IN THE PSYCHIATRY CLERKSHIP
RESPECT THE PATIENTS
RESPECT THE FIELD OF PSYCHIATRY
■ Dress in a professional manner.
TAKE RESPONSIBILITY FOR YOUR PATIENTS
Your psychiatry clerkship will undoubtedly be very interesting and exciting.
A key to doing well in this clerkship is finding the balance between drawing a
firm boundary of professionalism with your patients while maintaining a relationship of trust and empathy.
Why Spend Time on Psychiatry?
For most, your medical school psychiatry clerkship will encompass the entirety
of your formal training in psychiatry during your career in medicine.
Being aware of and understanding the features of mental dysfunction in
psychiatric patients will serve you well in recognizing psychiatric symptoms
in your patients, regardless of your specialty choice.
While anxiety and depression can worsen the prognosis of patients’ other
medical conditions, medical illnesses can cause significant psychological stress,
often uncovering a previously subclinical psychiatric condition. The stress of
extended hospitalizations can strain normal mental and emotional functioning
beyond their adaptive reserve, resulting in transient psychiatric symptoms.
Psychotropic medications are frequently prescribed in the general population.
Many of these drugs have significant medical side effects and drug interactions.
You will become familiar with these during your clerkship and will encounter
them in clinical practice regardless of your field of medicine.
Because of the unique opportunity to spend a great deal of time interacting
with your patients, the psychiatry clerkship is an excellent time to practice your
interview skills and “bedside manner.”
How to Behave on the Wards
Always maintain professionalism and give respect to the patients. Be respectful
when discussing cases with your residents and attendings.
n Regardless of your interest in psychiatry, take the rotation seriously.
■ You may not agree with all the decisions that your residents and attendings
make, but it is important for everyone to be on the same page.
■ Because of the intense emotional suffering experienced by psychiatric
patients, working with them can be overwhelming. Keep yourself healthy.
■ Psychiatry is a multidisciplinary field. It would behoove you to continuously
communicate with nurses, social workers, and psychologists.
■ Address patients formally unless otherwise told.
Know as much as possible about your patients: their history, psychiatric and
medical problems, test results, treatment plan, and prognosis. Keep your intern
or resident informed of new developments that they might not be aware of,
and ask them for any updates you might not be aware of. Assist the team in
developing a plan; speak to consultants and family members. Never deliver bad
news to patients or family members without the assistance of your supervising
resident or attending.
RESPECT PATIENTS’ RIGHTS
All patients have the right to have their personal medical information kept
private. This means do not discuss the patient’s information with family
members without that patient’s consent, and do not discuss any patient in
public areas (e.g., hallways, elevators, cafeterias).
All patients have the right to refuse treatment. This means they can refuse
treatment by a specific individual (the medical student) or of a specific type
(electroconvulsive therapy). Patients can even refuse lifesaving treatment.
The only exceptions to this rule are if the patient is deemed to not have the
capacity to make decisions or if the patient is suicidal or homicidal.
All patients should be informed of the right to seek advance directives on
admission. Often, this is done by the admissions staff or by a social worker.
If your patient is chronically ill or has a life-threatening illness, address
the subject of advance directives with the assistance of your resident or
attending.
VOLUNTEER
Be enthusiastic and self-motivated. Volunteer to help with a procedure or a difficult task. Volunteer to give a 20-minute talk on a topic of your choice, to take
additional patients, and to stay late.
BE A TEAM PLAYER
Help other medical students with their tasks; teach them information you have
learned. Support your supervising intern or resident whenever possible. Never
steal the spotlight or make a fellow medical student look bad. If your work for
the day is completed, offer to help with tasks on other patients on your team,
even if they are not your primary patients; helping to get work done may free
up time for the resident or attending to spend more time teaching.
KEEP PATIENT INFORMATION HANDY
Use a clipboard, notebook, or index cards to keep patient information, including a history and physical, lab, and test results, at hand. However, make sure to
keep all confidential patient information secure.
PRESENT PATIENT INFORMATION IN AN ORGANIZED MANNER
Here is a template for the “bullet” presentation:
“This is a [age]-year-old [gender] with a history of [major history such as
bipolar disorder] who presented on [date] with [major symptoms, such
as auditory hallucinations] and was found to have [working diagnosis].
[Tests done] showed [results]. Yesterday, the patient [state important
changes, new plan, new tests, new medications]. This morning the patient feels [state the patient’s words], and the mental status and physical
exams are significant for [state major findings]. Plan is [state plan].”
HOW TO SUCCEED IN THE PSYCHIATRY CLERKSHIP
4
HOW TO SUCCEED IN THE PSYCHIATRY CLERKSHIP
STUDY WITH FRIENDS
STUDY IN A BRIGHT ROOM
EAT LIGHT, BALANCED MEALS
POCKET CARDS
The newly admitted patient generally deserves a longer presentation following
the complete history and physical format.
Many patients have extensive histories. The complete history should be present
in the admission note, but during ward presentations, the entire history is often
too much to absorb. In these cases, it will be very important that you generate a
good summary that is concise but maintains an accurate picture of the patient.
How to Prepare for the Clerkship (Shelf) Exam
If you have studied the core psychiatric symptoms and illnesses, you will know
a great deal about psychiatry. To specifically study for the clerkship or shelf
exam, we recommend:
2–3 weeks before exam: Read this entire review book, taking notes.
10 days before exam: Read the notes you took during the rotation and the
corresponding review book sections.
5 days before exam: Read this entire review book, concentrating on lists and
mnemonics.
2 days before exam: Exercise, eat well, skim the book, and go to bed early.
1 day before exam: Exercise, eat well, review your notes and the mnemonics,
and go to bed on time. Do not have any caffeine after 2 PM.
Other helpful studying strategies are discussed below.
Group studying can be very helpful. Other people may point out areas that you
have not studied enough and may help you focus more effectively. If you tend
to get distracted by other people in the room, limit this amount to less than half
of your study time.
Find the room in your home or library that has the brightest light. This will
help prevent you from falling asleep. If you don’t have a bright light, obtain a
halogen desk lamp or a light that simulates sunlight.
Make sure your meals are balanced, with lean protein, fruits and vegetables,
and fiber. A high-sugar, high-carbohydrate meal will give you an initial burst of
energy for 1–2 hours, but then your blood sugar will quickly drop.
UTILIZE QUESTION BANKS AND/OR TAKE PRACTICE EXAMS
The purpose of practice exams is not just for the content that is contained in
the questions, but the process of sitting for several hours and attempting to
choose the best answer for each and every question.
The “cards” on the following page contain information that is often helpful in
psychiatry practice. We advise that you make a photocopy of these cards, cut
them out, and carry them with you.
Mental Status Exam
Appearance/Behavior: Apparent age, attitude and cooperativeness, eye contact, posture, dress and hygiene, psychomotor status.
Speech: Rate, rhythm, volume, tone, articulation.
Mood: Patient’s subjective emotional state—depressed, anxious, sad, angry,
etc.
Affect: Objective emotional expression—euthymic, dysphoric, euphoric,
appropriate (to stated mood), labile, full, constricted, flat, etc.
Thought process: Logical/linear, circumstantial, tangential, flight of ideas,
looseness of association, thought blocking.
Thought content: Suicidal/homicidal ideation, delusions, ideas of reference,
paranoia, obsessions, preoccupations, hyperreligiosity.
Perceptual disturbances: Hallucinations, illusions, derealization,
depersonalization.
Cognition:
Level of consciousness: Alert, sleepy, lethargic.
Orientation: Person, place, date.
Attention/Concentration: Serial 7s, spell “world” backward.
Abstract thought: Interpretation of proverbs, analogies.
Memory:
Registration: Immediate recall of three objects.
Short term: Recall of objects after 5 minutes.
Long term: Ask about verifiable personal information.
Fund of knowledge: Current events.
Insight: Patient’s awareness of their illness and need for treatment.
Judgment: Patient’s ability to approach their problems in an appropriate
manner.
Delirium
Characteristics: Acute onset, waxing/waning sensorium (worse at night),
disorientation, inattention, impaired cognition, disorganized thinking, altered
sleep-wake cycle, perceptual disorders (hallucinations, illusions).
Etiology: Drugs (narcotics, benzodiazepines, anticholinergics [e.g., diphenhydramine], TCAs, steroids), EtOH withdrawal, metabolic (cardiac, respiratory, renal, hepatic, endocrine), infection, neurological causes (increased ICP,
encephalitis, postictal, stroke).
Investigations:
Routine: CBC, chemistry panel, glucose, LFTs, TFTs, thiamine, folate, UA,
urine toxicology screen, CXR, vital signs.
Medium-yield: ABG, ECG (silent MI), ionized Ca2+.
If above inconclusive: Head CT/MRI, EEG, LP.
Management: Identify/correct underlying cause, simplify Rx regimen, discontinue potentially offensive medications if possible, avoid benzodiazepines
(except in EtOH withdrawal), create safe environment, provide reassurance/
education, judiciously use antipsychotics for acute agitation.
HOW TO SUCCEED IN THE PSYCHIATRY CLERKSHIP
6
HOW TO SUCCEED IN THE PSYCHIATRY CLERKSHIP
Orientation (10):
Language (9):
Distractibility
Irritable mood/insomnia
Grandiosity
Flight of ideas
Agitation/increase in goal-directed activity
Speedy thoughts/speech
Sex—Male
Age >60 years
Depression
Previous attempt
Ethanol/drug abuse
Rational thinking loss
Suicide in family
Organized plan/access
No support
Sickness
Mini-Mental State Examination (MMSE)
What is the [year] [season] [date] [day] [month]? (1 pt. each)
Where are we [state] [county] [town] [hospital] [floor]?
Registration (3): Ask the patient to repeat three unrelated objects (1 pt. each
on first attempt). If incomplete on first attempt, repeat up to six times (record
number of trials).
Attention (5): Either serial 7s or spell “world” backward (1 pt. for each correct
letter or number).
Delayed recall (3): Ask patient to recall the three objects previously named
(1 pt. each).
■
■Name two common objects, e.g., watch, pen (1 pt. each).
■
■Repeat the following sentence: “No ifs, ands, or buts” (1 pt.).
■
■Give patient blank paper. “Take it in your right hand, use both hands to
fold it in half, and then put it on the floor” (1 pt. for each part correctly
executed).
■
■Have patient read and follow: “Close your eyes” (1 pt.).
■
■Ask patient to write a sentence. The sentence must contain a subject and a
verb; correct grammar and punctuation are not necessary (1 pt.).
■
■Ask the patient to copy the design. Each figure must have five sides, and
two of the angles must intersect (1 pt.).
Mania (“DIG FAST”)
Thoughtlessness: seek pleasure without regard to consequences
Suicide Risk (“SAD PERSONS”)
Major Depression (“SIG E. CAPS”)
Sleep
Interest
Guilt
Energy
Concentration
Appetite
Psychomotor ∆s
Suicidal ideation
■
■Hopelessness
■
■Helplessness
■
■Worthlessness
Drugs of Abuse
Drug
Intoxication
Withdrawal
Alcohol benzodiazepines
Disinhibition, mood lability, incoordination, slurred speech, ataxia,
blackouts (EtOH), respiratory
depression
Barbiturates
Respiratory depression
Anxiety, seizures, delirium,
life-threatening cardiovascular
collapse
Opioids
CNS depression, nausea, vomiting, sedation, decreased pain
perception, decreased GI motility,
pupil constriction, respiratory
depression
Euphoria, increased attention
span, aggressiveness, psychomotor agitation, pupil dilatation,
hypertension, tachycardia,
cardiac arrhythmias, psychosis,
formication with cocaine
Amphetamines
cocaine
PCP
Belligerence, impulsiveness, psychomotor agitation, vertical/horizontal nystagmus, hyperthermia,
tachycardia, ataxia, psychosis,
homicidality
LSD
Altered perceptual states (hallucinations, distortions of time and
space), elevation of mood, “bad
trips” (panic reaction), flashbacks
(reexperience of the sensations in
absence of drug use)
Cannabis
Euphoria, anxiety, paranoia, slowed
time, social withdrawal, increased
appetite, dry mouth, tachycardia,
amotivational syndrome
Nicotine/
Caffeine
Restlessness, insomnia, anxiety,
anorexia
Irritability, lethargy, headache,
increased appetite, weight gain
First Aid for the Psychiatry Clerkship, 4e; copyright © 2015 McGraw-Hill. All rights reserved.
HOW TO SUCCEED IN THE PSYCHIATRY CLERKSHIP
Tremulousness, hypertension,
tachycardia, anxiety, psychomotor agitation, nausea, seizures,
­hallucinations, DTs (EtOH)
Increased sympathetic activity,
N/V, diarrhea, diaphoresis, rhinorrhea, piloerection, yawning, stomach cramps, myalgias, arthralgias,
restlessness, anxiety, anorexia
Post-use “crash”: restlessness,
headache, hunger, severe
depression, irritability, insomnia/
hypersomnia, strong
psychological craving
May have recurrence of symptoms due to reabsorption in GI
tract
8
HOW TO SUCCEED IN THE PSYCHIATRY CLERKSHIP
Delirium Tremens (DTs):
■
■Idiosyncratic, time-limited reaction.
Serotonin Syndrome:
■
■May occur at any Li level (usually >1.5).
■
■Classic ECG finding is QRS >100 ms.
■
■Discontinue the medication.
Psychiatric Emergencies
■
■Typically within 2–4 days after cessation of EtOH but may occur later.
■
■Delirium, agitation, fever, autonomic hyperactivity, auditory and visual
hallucinations.
■
■Treat aggressively with benzodiazepines and hydration.
Neuroleptic Malignant Syndrome (NMS):
■
■Fever, rigidity, autonomic instability, clouding of consciousness, elevated
WBC/CPK.
■
■Withhold neuroleptics, hydrate, consider dantrolene, and/or bromocriptine.
■
■Precipitated by use of two drugs with serotonin-enhancing properties
(e.g., MAOI + SSRI).
■
■Altered mental status, fever, agitation, tremor, myoclonus, hyperreflexia,
ataxia, incoordination, diaphoresis, shivering, diarrhea.
■
■Discontinue offending agents, benzodiazepines, consider cyproheptadine.
Tyramine Reaction/Hypertensive Crisis:
■
■Precipitated by ingestion of tyramine-containing foods while on MAOIs.
■
■Hypertension, headache, neck stiffness, sweating, nausea, vomiting, visual
problems. Most serious consequences are stroke and possibly death.
■
■Treat with nitroprusside or phentolamine.
Acute Dystonia:
■
■Early, sudden onset of muscle spasm: eyes, tongue, jaw, neck; may lead to
laryngospasm requiring intubation.
■
■Treat with benztropine (Cogentin) or diphenhydramine (Benadryl).
■
■If clinically appropriate, reduce the dose, discontinue the medication, or
switch to another agent.
Lithium Toxicity:
■
■Nausea, vomiting, slurred speech, ataxia, incoordination, myoclonus,
­hyperreflexia, seizures, nephrogenic diabetes insipidus, delirium, coma.
■
■Discontinue Li, hydrate aggressively, consider hemodialysis.
Tricyclic Antidepressant (TCA) Toxicity:
■
■Primarily anticholinergic effects, cardiac conduction disturbances,
­hypotension, respiratory depression, agitation, hallucinations, seizures.
■
■Treatment includes sodium bicarbonate, activated charcoal, cathartics,
supportive treatment.

05 - Chapter 2 Examination and Diagnosis

01 - Chapter 2 Examination and Diagnosis
Chapter 2 Examination and Diagnosis
EXAMINATION AND
CHAPTER 2
DIAGNOSIS
History and Mental Status Examination....................................................................................10
Interviewing........................................................................................................................10
Taking the History................................................................................................................11
Mental Status Examination..................................................................................................12
Bedside Cognitive Testing....................................................................................................15
Sample Write-Up......................................................................................................................16
Interviewing Skills....................................................................................................................19
General Approaches to Types of Patients..............................................................................19
Diagnosis and Classification......................................................................................................19
Diagnosis as per DSM-5.......................................................................................................19
Diagnostic Testing.....................................................................................................................19
Intelligence Tests.................................................................................................................19
Objective Personality Assessment Tests...............................................................................20
Projective (Personality) Assessment Tests............................................................................20
10
EXAMINATION AND DIAGNOSIS
WARDS TIP
INTERVIEWING
The history of present illness (HPI)
should include information about
the current episode, including
symptoms, duration, context,
stressors, and impairment in
function.
WARDS TIP
If you are seeing the patient in
the ER, make sure to ask how they
got to the ER (police, bus, walk-in,
family member) and look to see
what time they were triaged. For
all initial evaluations, ask why the
patient is seeking treatment today
as opposed to any other day.
Date and Location:
Identifying Patient Data:
Chief Complaint:
WARDS TIP
History of Present Illness:
When taking a substance history,
remember to ask about caffeine
and nicotine use. If a heavy smoker
is hospitalized and does not have
access to nicotine replacement
therapy, nicotine withdrawal may
cause anxiety and agitation.
Past Psychiatric History:
First contact:
Diagnosis:
Prior hospitalizations:
Suicide attempts:
Outpatient treatment:
Med trials:
Substance History:
Smoking:
Family Psychiatric History:
Legal History:
FIGURE 2-1.  Psychiatric history outline.
History and Mental Status Examination
Making the Patient Comfortable
The initial interview is of utmost importance to the psychiatrist. With practice, you will develop your own style and learn how to adapt the interview to
the individual patient. In general, start the interview by asking open-ended
questions. Carefully note how the patient responds, as this is critical information for the mental status exam. Consider preparing for the interview by
writing down the subheadings of the exam (see Figure 2-1). Find a safe and
private area to conduct the interview. Use closed-ended questions to obtain the
remaining pertinent information. During the first interview, the psychiatrist
must establish a meaningful rapport with the patient in order to get accurate
and pertinent information. This requires that the questions be asked in a quiet,
comfortable setting so that the patient is at ease. The patient should feel that the
psychiatrist is interested, nonjudgmental, and compassionate. In psychiatry,
the history is the most important factor in formulating a diagnosis and
treatment plan.
Past Medical History:
Allergies:
Current Meds:
Developmental History:
Relationships (children/marital status):
Education:
Work History:
Military History:
Housing:
Income:
Religion:
TAKING THE HISTORY
The psychiatric history follows a similar format as the history for other types of
patients. It should include the following:
n Identifying data: The patient’s name, preferred gender, age, marital
status.
n Chief complaint (use the patient’s own words): If called as a consultant, list
reason for the consult.
n Sources of information.
n History of present illness (HPI):
• The 4 Ps: The patient’s psychosocial and environmental conditions
predisposing to, precipitating, perpetuating, and protecting against the
current episode.
• The patient’s support system (whom the patient lives with, distance and
level of contact with friends and relatives).
• Neurovegetative symptoms (quality of sleep, appetite, energy,
psychomotor retardation/activation, concentration).
• Suicidal ideation/homicidal ideation.
• How work and relationship have been affected (for most diagnoses in the
Diagnostic and Statistical Manual of Mental Disorders, 5th edition
[DSM-5] there is a criterion that specifies that symptoms must cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning).
• Psychotic symptoms (e.g., auditory and visual hallucinations, delusions).
• Establish a baseline of mental health:
Patient’s level of functioning when “well.”
Goals (outpatient setting).
n Past psychiatric history (include as applicable: history of suicide attempts,
history of self-harm [e.g., cutting, burning oneself], information about
previous episodes, other psychiatric disorders in remission, medication
trials, past psychiatric hospitalizations, current outpatient psychiatrist).
n Substance history (age of first use, amount and route of use, history of
withdrawal/delirium tremens (DTs), longest period of sobriety, history of
intravenous drug use, participation in outpatient or inpatient drug rehab
programs).
n Medical history (ask specifically about head trauma, seizures, pregnancy
status).
n Family psychiatric and medical history (include substance use, suicides, and
response to specific psychotropic agents as patient may respond similarly).
n Medications (ask about supplements and over-the-counter [OTC]
medications, as well as compliance).
n Allergies: Clarify if it was a true allergy or an adverse drug event (e.g.,
abdominal pain).
n Developmental/Social history: Achieved developmental milestones on time,
friends in school, history of trauma or abuse, performance academically.
Also include income source, employment, education, place of residence,
who they live with, number of children, support system, religious affiliation
and beliefs, legal history, and amount of exercise.
EXAMINATION AND DIAGNOSIS
WARDS
QUESTION
Q: What OTC medication would be
important to ask and document
in a patient with bipolar disorder
taking Lithium.
A: Nonsteroidal anti-­inflammatory
drugs (NSAIDs) as they can ↑
lithium concentrations.
12
EXAMINATION AND DIAGNOSIS
MENTAL STATUS EXAMINATION
WARDS TIP
Psychomotor retardation, which
refers to the slowness of voluntary
and involuntary movements, may
also be referred to as hypokinesia
or bradykinesia. The term akinesia
is used in extreme cases where
absence of movement is
observed.
n Appearance/Behavior
n Speech
n Mood/Affect
n Thought process
n Thought content
n Perceptual disturbances
n Cognition
n Insight
KEY FACT
Automatisms are spontaneous,
involuntary movements that
occur during an altered state of
consciousness and can range from
purposeful to disorganized.
Appearance/Behavior
WARDS
QUESTION
Q: What is pressured speech?
A: Speech that is usually
­uninterruptible with the patient
compelled to continue speaking.
WARDS TIP
To assess mood, ask, “How are
you feeling today?” It can also be
helpful to have patients rate their
stated mood on a scale of 1–10.
WARDS
QUESTION
Q: What is a flat affect?
A: A patient who remains expressionless and monotone even when
discussing extremely sad or happy
moments in their life.
This is analogous to performing a physical exam in other areas of medicine. It
is the nuts and bolts of the psychiatric exam. It should describe the patient in as
much detail as possible. The mental status exam assesses the following:
n Judgment/Impulse control
The mental status exam tells only about the mental status at that moment; it
can change every hour or every day, etc.
n Appearance: Gender, age (looks older/younger than stated age), type of
clothing, hygiene (including smelling of alcohol, urine, feces), posture,
grooming, physical abnormalities, tattoos, body piercings. Take specific
notice of the following, which may be clues for possible diagnoses:
• Pupil size: Drug intoxication/withdrawal.
• Bruises in hidden areas: ↑ suspicion for abuse.
• Needle marks/tracks: Drug use.
• Eroding of tooth enamel: Eating disorders (from vomiting).
• Superficial cuts on arms: Self-harm.
n Behavior: Attitude (cooperative, seductive, flattering, charming, eager to please,
entitled, controlling, uncooperative, hostile, guarded, critical, antagonistic,
childish), positioning (sitting, standing), mannerisms, tics, eye contact, activity
level, psychomotor retardation/activation, akathisia, automatisms, catatonia,
choreoathetoid movements, compulsions, dystonias, tremor.
Speech
Rate (pressured, slowed, regular), rhythm (i.e., prosody), articulation (dysarthria,
stuttering), accent/dialect, volume/modulation (loudness or softness), tone, long
or short latency of speech, quantity of speech (hyperverbal, paucity of speech).
Mood
Mood is the emotion that the patient tells you they feel, often in quotations.
Affect
Affect is an assessment of how the patient’s mood appears to the examiner,
including the amount and range of emotional expression. It is described with
the following dimensions:
n Type of affect: Euthymic, euphoric, neutral, dysphoric.
n Range describes the depth and range of the feelings shown. Parameters: flat
(none)—blunted (shallow)—constricted (limited)—full (average)—intense
(more than normal).
n Motility describes how quickly a person appears to shift emotional states.
Parameters: sluggish—supple—labile.
n Appropriateness to content describes whether the affect is congruent with
the subject of conversation or stated mood. Parameters: appropriate—not
appropriate.
Thought Process
The patient’s form of thinking—how they use language and put ideas together.
It describes whether the patient’s thoughts are logical, meaningful, and goal
directed. It does not comment on what the patient thinks, only how the patient
expresses their thoughts.
n Logical/Linear/Goal-directed: Answers to questions and conversation clear
and follows a logical sequence.
n Circumstantiality is when the point of the conversation is eventually
reached but with overinclusion of trivial or irrelevant details.
Examples of thought disorders include:
n Tangentiality: Can follow conversation but point never reached or question
never answered.
n Loosening of associations: No logical connection from one thought to
another.
n Flight of ideas: Thoughts change abruptly from one idea to another,
often based on understandable associations or distracting stimuli; usually
accompanied by rapid/pressured speech.
n Neologisms: Made-up words.
n Word salad: Incoherent collection of words.
n Clang associations: Word connections due to phonetics rather than actual
meaning. “My car is red. I’ve been in bed. It hurts my head.”
n Thought blocking: Abrupt cessation of communication before the idea is
finished.
Thought Content
Describes the types of ideas expressed by the patient. Examples of disorders:
n Poverty of thought versus overabundance: Too few versus too many ideas
expressed.
n Delusions: Fixed, false beliefs that are not shared by the person’s culture and
remain despite evidence to the contrary. Delusions are classified as bizarre
(impossible to be true) or nonbizarre (at least possible).
n Suicidal and homicidal ideation: Ask if the patient feels like harming
themself or others. Identify if the plan is well formulated. Ask if the patient
has an intent (i.e., if released right now, would they kill themself or harm
others?). Ask if the patient has means to kill themself (firearms in the house/
multiple prescription bottles).
n Phobias: Persistent, irrational fears.
n Obsessions: Repetitive, intrusive thoughts.
Perceptual Disturbances
n Hallucinations: Sensory perceptions that occur in the absence of an actual
stimulus.
• Describe the sensory modality: Auditory (most common), visual,
­gustatory, olfactory, or tactile.
• Describe the details (e.g., auditory hallucinations may be ringing,
­humming, whispers, or voices speaking clear words). Command auditory
hallucinations are voices that instruct the patient to do something.
EXAMINATION AND DIAGNOSIS
KEY FACT
An example of inappropriate affect
is a patient’s laughing when being
told they have a serious illness.
WARDS TIP
A patient who is laughing one
second and crying the next has a
labile affect.
KEY FACT
Examples of delusions:
• Grandeur—Belief that one has
special powers or is someone
important (Jesus, President).
• Paranoid—Belief that one is
being persecuted.
• Reference—Belief that some
event is uniquely related
to ­patient (e.g., a TV show
­character is sending messages
to patient).
• Thought broadcasting—­Belief
that one’s thoughts can be
heard by others.
• Religious—Conventional
beliefs exaggerated (e.g., God
wants me to be the Messiah).
• Somatic—False belief
­concerning body image (e.g., I
have cancer).
WARDS TIP
The following question can help
screen for obsessions: Do you
think and/or worry about checking, cleaning, or counting on a
repetitive basis?
14
EXAMINATION AND DIAGNOSIS
WARDS
QUESTION
Q: What type of hallucinations are
an important risk factor for suicide
or homicide?
A: Command hallucinations (auditory hallucinations that instruct
a patient to harm themselves or
others).
Cognition
n Orientation: To person, place, and time.
n Calculation: Ability to add/subtract.
n Memory:
WARDS TIP
Alcoholic hallucinosis refers to
hallucinations (usually auditory,
although visual and tactile may
occur) that occur either during
or after a period of heavy alcohol
consumption. Patients usually are
aware that these hallucinations are
not real. In contrast to DTs, there is
no clouding of sensorium and vital
signs are normal.
KEY FACT
You can roughly assess a patient’s intellectual functioning by
utilizing the proverb interpretation and vocabulary strategies.
Proverb interpretation is helpful
in assessing whether a patient has
difficulty with abstraction. Being
able to define a particular vocabulary word correctly and appropriately use it in a sentence reflects a
person’s intellectual capacity.
• Ask if the hallucination is experienced only while falling asleep ­(hypnagogic
hallucination) or upon awakening (hypnopompic ­hallucination).
n Illusions: Inaccurate perception of existing sensory stimuli (e.g., wall appears
as if it’s moving).
n Derealization/Depersonalization: The experience of feeling detached from
one’s surroundings/mental processes.
n Consciousness: Patient’s level of awareness; possible range includes: alert—
drowsy—lethargic—stuporous—comatose.
• Immediate (registration)—Dependent on attention/concentration and
can be tested by asking a patient to repeat several digits or words.
• Recent (short-term memory)—Events within the past few minutes, hours,
or days.
• Remote memory (long-term memory).
n Fund of knowledge: Level of knowledge in the context of the patient’s
culture and education (e.g., Who is the president? Who was Picasso?).
n Attention/Concentration: Ability to subtract serial 7s from 100 or to spell
“world” backward.
n Reading/Writing: Simple sentences (must make sure the patient is literate
first).
n Abstract concepts: Ability to explain similarities between objects and
understand the meaning of simple proverbs.
Insight
Insight is the patient’s level of awareness and understanding of their problem.
Problems with insight include complete denial of illness or blaming it on something else. Insight can be described as full, partial/limited, or minimal.
Judgment
Judgment is the patient’s ability to understand the outcome of their actions and
use this awareness in decision making; it is best determined from information
from the HPI and recent behavior (e.g., how a patient was brought to treatment
or medication compliance). Judgment can be described as excellent, good, fair,
or poor.
Mrs. W is a 52-year-old female who arrives at the emergency room
reporting that her deceased husband of 25 years told her that he would
be waiting for her there. To meet him, she drove nonstop for 22 hours
from a nearby state. She claims that her husband is a famous preacher
and that she, too, has a mission from God. Although she does not specify
the details of her mission, she says that she was given the ability to stop
time until her mission is completed. She reports experiencing high levels
of energy despite not sleeping for 22 hours. She also reports that she has
a history of psychiatric hospitalizations but refuses to provide further
information.
While obtaining her history you perform a mental status exam. Her
appearance is that of a woman who looks older than her stated age.
She is obese and unkempt. There is no evidence of tattoos or piercings.
She has tousled hair and is dressed in a mismatched flowered skirt and
a red T-shirt. Upon her arrival at the emergency room, her behavior is
demanding, as she insists that you let her husband know that she has
arrived. She then becomes irate and proceeds to yell, banging her head
against the wall. She screams, “Stop hiding him from me!” She is uncooperative with redirection and is guarded during the remainder of the
interview. Her eye contact is poor as she is looking around the room. Her
psychomotor activity is agitated. Her speech is loud and pressured,
with a foreign accent.
She reports that her mood is “angry,” and her affect as observed during
the interview is labile and irritable.
Her thought process includes flight of ideas. Her thought content
is significant for delusions of grandeur and thought broadcasting, as
evidenced by her refusing to answer most questions claiming that you
are able to know what she is thinking. She denies suicidal or homicidal
ideation. She expresses disturbances in perception as she admits to
frequent auditory hallucinations without commands.
She is uncooperative with formal cognitive testing, but you notice
that she is oriented to place and person. However, she erroneously states that it is 2005. Her attention and concentration are notably
impaired, as she appears distracted and frequently needs questions
repeated. Her insight, judgment, and impulse control are determined
to be poor.
You decide to admit Mrs. W to the inpatient psychiatric unit in order to
allow for comprehensive diagnostic evaluation, the opportunity to obtain
collateral information from her prior hospitalizations, safety monitoring,
medical workup for possible reversible causes of her symptoms, and psychopharmacological treatment.
BEDSIDE COGNITIVE TESTING
The Montreal Cognitive Assessment (MoCA)
The MoCA is a simple, brief test used to assess gross cognitive functioning.
The test and its instructions are available online (Figure 2-2). The areas tested
include:
n Orientation (to person, place, and time).
• Memory (immediate—repeating five words; and recent—recalling the
words 5 minutes later).
• Attention (serial 7s, tapping hand with certain letters, repeating digits).
• Language (naming, repetition, fluency).
• Abstraction (e.g., saying how a “train” and “bicycle” are alike).
• Visuospatial ability/executive functioning (trail making task, cube
copying, clock drawing).
The Mini-Mental State Examination (MMSE)
The MMSE is another test of cognition that can be performed in a few minutes
at the bedside. Unlike the MoCA, the MMSE is copyright protected.
EXAMINATION AND DIAGNOSIS
WARDS TIP
To test ability to abstract, ask:
Similarities: How are an apple
and orange alike? (Normal answer: “They are fruits.” Concrete
answer: “They are round.”)
Proverb testing: What is meant
by the phrase, “You can’t judge
a book by its cover?” (Normal
answer: “You can’t judge people
just by how they look.” Concrete
answer: “Books have different
covers.”)
KEY FACT
A prior history of violence is the
most important predictor of future
violence.
16
EXAMINATION AND DIAGNOSIS
Sample Write-Up
FIGURE 2-2.  Montreal Cognitive Assessment Test (MoCA). Copyright © Z. Nasreddine MD.
Reproduced with permission. Copies are available at www.mocatest.org.
CHIEF COMPLAINT: “I’m in despair and hopeless”
HISTORY OF PRESENT ILLNESS:
A 58 year-old domiciled, recently unemployed, single female with a past psychiatric history of depression and no past medical history who presented to the
emergency room for depression and suicidal ideation with a plan to jump in
front of a train.
The patient explained that she was working as an Licensed Practical Nurse (LPN)
for a nursing home when the coronavirus pandemic began. She currently lives
with her mother and brother. Her mother is elderly with chronic medical conditions, so they serve as her caretakers. When patients and staff at the nursing
home began to test positive for COVID, the patient’s brother urged her to quit,
given her elevated risk of infection and potential spread to the rest of her family.
She therefore quit her job and has been staying at home with her mother in
quarantine for 4 months. For the past 2 months, she has noticed a decline in
her mood. She describes feeling “in despair and hopeless…I feel so useless
now.” She has also been experiencing hypersomnia with worsening fatigue,
poor appetite, anhedonia, anergia, and difficulty concentrating. She expressed
that for the past 2 weeks she has had suicidal ideation with a plan to jump in
front of the train near her home. She denies preparatory behaviors or prior
suicide attempts. She denies self-harm behaviors. She realized she needed help
now because the suicidal thoughts were becoming more persistent. She notes
that her family is what has prevented her from acting on these thoughts. She
denies any auditory/visual hallucinations, clustered manic symptoms, or homicidal ideation. She denies any illicit drug or alcohol use.
Of note, for the past week, she has been taking a friend’s sertraline to help with
her mood.
Patient was amenable to inpatient psychiatric admission. She was agreeable to
starting sertraline for her depression.
PAST PSYCHIATRIC HISTORY:
Diagnoses: Depression
Prior Hospitalizations: One time at age 38 for similar symptoms of depression.
She was treated with sertraline 50 mg with significant improvement in her
symptoms. She continued medications and outpatient therapy for 1 year, but
she discontinued both because her depressive symptoms resolved.
Prior Self-Injury: No history of suicide attempts or self-harm
SUBSTANCE USE:
Tobacco: Smokes 1/2 pack per day
Alcohol: None
Illicits: None
Rehabilitation: Denies
PAST MEDICAL HISTORY:
None. No history of seizures or head trauma.
MEDICATIONS: Sertraline 50 mg daily
ALLERGIES: No known drug allergies
FAMILY HISTORY: Mother with depression but not treated. No history of suicide attempts.
SOCIAL HISTORY
Lives with brother and mother in apartment
No history of physical or sexual abuse.
Development: Met all milestones on time
Employment: Was working as LPN at a nursing home, currently unemployed
Education: 2 years of college
Relationship: Single, never married, no children
Legal: No legal problems
EXAMINATION AND DIAGNOSIS
18
EXAMINATION AND DIAGNOSIS
MENTAL STATUS EXAM
Appearance: Medium-built female, dressed in hospital gown, good grooming
and hygiene, appears consistent with stated age
Behavior: Sitting comfortably, cooperative during interview, attentive, maintains appropriate eye contact; some psychomotor retardation, no abnormal
movements/tics
Speech: Increased speech latency, low tone, normal prosody
Mood: “Hopeless”
Affect: Dysphoric, constricted, congruent with stated mood, non-labile
Thought Process: Linear, logical, goal-directed
Thought Content: +Suicidal ideation with plan to jump in front of train,
denies homicidal ideation, paranoia, or delusions
Perceptions: Denies auditory or visual hallucinations and does not appear to
be responding to abnormal internal stimuli
Cognition: Alert and oriented to person, place, and time; memory intact to
recent/remote events, good attention (able to do serial 7s)
Insight: Good—realizes she is having similar symptoms to prior episode of
depression related to job loss and isolation.
Judgement: Fair—brought herself in when she was feeling more suicidal but
taking friend’s sertraline.
ASSESSMENT:
Patient is a 58 year-old, domiciled, recently unemployed, single female with a
past psychiatric history of depression and no past medical history who presented to the emergency room for depression and suicidal ideation with a plan
to jump in front of a train. Biologically, she has a first-degree parent (mother)
with a history of depression. She denies illicit drug use or alcohol use, therefore not a substance-induced mood disorder. She has a history of depression,
and currently has major neurovegetative signs and symptoms consistent with
another major depressive episode. She has suicidal ideation with a plan to jump
in front of a train and is therefore at high acute risk of harm to self. Psychosocially, her recent unemployment and home quarantine due to the coronavirus
was the catalyst for her current mood disturbance. She requires inpatient hospitalization for acute safety/stabilization as she poses a significant risk of harm
to herself.
Principal DSM-5 diagnosis:
Major depressive disorder, recurrent, severe
PLAN:
Admit to inpatient psychiatry
Vitals: Per ward routine
Labs: Chemistry panel, complete blood count, urine toxicology screen, blood
alcohol level, thyroid panel
Diet: General
Activity: Up ad lib
Depression
Start sertraline 50 mg daily given prior benefit and tolerability
Tobacco Use
Offer nicotine replacement (e.g., nicotine patch/gum)
#Social/disposition: Consider family meeting, refer to outpatient medication
management, consider psychotherapy
Interviewing Skills
GENERAL APPROACHES TO TYPES OF PATIENTS
Violent Patient
Do not interview a potentially violent patient alone. Inform staff of your
whereabouts. Know if there are accessible panic buttons. To assess violence or
homicidality, one can simply ask, “Do you feel like you want to hurt someone
or that you might hurt someone?” If the patient expresses imminent threats
against specific friends, family, or others, the doctor must notify potential
­victims and/or protection agencies (Tarasoff Rule).
Delusional Patient
Although you should not directly challenge a delusion or insist that it is untrue,
you should not imply you believe it either; you should simply acknowledge that
you understand that the patient believes the delusion is true.
Depressed Patient
A depressed patient may be skeptical that they can be helped. It is important to offer
reassurance that they can improve with appropriate therapy. Inquiring about suicidal
thoughts is crucial; a feeling of hopelessness, substance use, and/or a history of prior
suicide attempts reveal an ↑ risk for suicide. If the patient is actively planning or
contemplating suicide, they should be hospitalized or otherwise protected.
Diagnosis and Classification
DIAGNOSIS AS PER DSM-5
The American Psychiatric Association (APA) uses a criterion-based system for
diagnoses. Criteria and codes for each diagnosis are outlined in the DSM-5.
Diagnostic Testing
INTELLIGENCE TESTS
Aspects of intelligence include memory, logical reasoning, ability to assimilate
factual knowledge, and understanding of abstract concepts.
Intelligence Quotient (IQ)
IQ is a test of intelligence with a mean of 100 and a standard deviation of 15.
These scores are adjusted for age. An IQ of 100 signifies that mental age equals
chronological age and corresponds to the 50th percentile in intellectual ability
for the general population.
Intelligence tests assess cognitive function by evaluating comprehension, fund
of knowledge, math skills, vocabulary, picture assembly, and other verbal and
performance skills. Two common tests are:
Wechsler Adult Intelligence Scale (WAIS):
n Most common test for ages 16–90.
n Assesses overall intellectual functioning.
n Four index scores: Verbal comprehension, perceptual reasoning, working
memory, processing speed.
Wechsler Intelligence Scale for Children (WISC): Tests intellectual ability in
patients ages 6–16.
EXAMINATION AND DIAGNOSIS
WARDS TIP
In assessing suicidality, do not
simply ask, “Do you want to hurt
yourself?” because this does not
directly address suicidality (they
may plan on dying in a painless
way). Ask directly about killing
self or suicide. If contemplating
suicide, ask the patient if they have
a plan of how to do it and if they
have intent; a detailed plan, intent,
and the means to accomplish it
suggest a serious threat.
KEY FACT
The Minnesota Multiphasic Personality Inventory (MMPI) is an
objective psychological test that is
used to assess a person’s person­
ality and identify psychopathologies.
The mean score for each scale is 50
and the standard deviation is 10.
WARDS TIP
IQ Chart
Very superior: >130
Superior: 120–129
High average: 110–119
Average: 90–109
Low average: 80–89
Borderline: 70–79
Extremely low (intellectual
­disability): <70
20
EXAMINATION AND DIAGNOSIS
n Most commonly used.
Thematic Apperception Test (TAT)
Rorschach Test
n Interpretation of inkblots.
OBJECTIVE PERSONALITY ASSESSMENT TESTS
These tests are questions with standardized-answer format that are objectively
scored. The following is an example:
Minnesota Multiphasic Personality Inventory (MMPI-2)
n Tests personality for different pathologies and behavioral patterns.
PROJECTIVE (PERSONALITY) ASSESSMENT TESTS
Projective tests have no structured-response format. The tests often ask for
interpretation of ambiguous stimuli. Examples are:
n Test taker creates stories based on pictures of people in various situations.
n Used to evaluate motivations behind behaviors.
n Used to identify thought disorders and defense mechanisms.

06 - Chapter 3 Psychotic Disorders

01 - Chapter 3 Psychotic Disorders
Chapter 3 Psychotic Disorders
Psychosis..................................................................................................................................22
Delusions.............................................................................................................................22
Perceptual Disturbances......................................................................................................22
Differential Diagnosis of Psychosis.......................................................................................23
Psychotic Disorder Due to Another Medical Condition.........................................................23
Substance/Medication-Induced Psychotic Disorder.............................................................23
Schizophrenia...........................................................................................................................24
Positive, Negative, and Cognitive Symptoms.......................................................................24
Three Phases........................................................................................................................24
Diagnosis of Schizophrenia..................................................................................................24
Psychiatric Exam of Patients with Schizophrenia.................................................................25
Epidemiology......................................................................................................................26
Downward Drift...................................................................................................................26
Pathophysiology of Schizophrenia: The Dopamine Hypothesis............................................26
Other Neurotransmitter Abnormalities Implicated in Schizophrenia...................................27
Prognostic Factors...............................................................................................................27
Treatment............................................................................................................................28
Schizophreniform Disorder.......................................................................................................29
Schizoaffective Disorder............................................................................................................30
Brief Psychotic Disorder............................................................................................................30
Delusional Disorder...................................................................................................................30
Culture-Specific Psychoses........................................................................................................31
Comparing Time Courses and Prognoses of Psychotic Disorders................................................32
Quick and Easy Distinguishing Features...............................................................................32
PSYCHOTIC DISORDERS
CHAPTER 3
22
PSYCHOTIC DISORDERS
Psychosis
WARDS TIP
Psychosis is exemplified by delusions, hallucinations, or severe disorganization of thought/behavior.
DELUSIONS
Delusions can also be categorized by theme:
PERCEPTUAL DISTURBANCES
WARDS TIP
Auditory hallucinations that
directly tell the patient to perform
certain acts are called command
hallucinations.
Psychosis is a general term used to describe a distorted perception of reality.
Poor reality testing may be accompanied by delusions, perceptual disturbances (illusions or hallucinations), and/or disorganized thinking/behavior.
Psychosis can be a symptom of schizophrenia, mania, depression, delirium,
and major neurocognitive disorder (i.e., dementia), and it can be substance or
medication-induced.
Delusions are fixed, false beliefs that persist despite evidence to the contrary and
that do not make sense within the context of an individual’s cultural background.
They can be categorized as either bizarre or nonbizarre. A nonbizarre delusion is
a false belief that is plausible but is not true. Example: “The neighbors are spying
on me by reading my e-mail.” A bizarre delusion is a false belief that is impossible. Example: “Aliens are spying on me through a Wi-Fi connection in my brain.”
■ Delusions of persecution/paranoid delusions: Irrational belief that one
is being persecuted. Example: “The Central Intelligence Agency (CIA) is
monitoring me and tapped my cell phone.”
■ Delusions of reference: Belief that cues in the external environment
are uniquely related to the individual. Example: “The TV characters are
speaking directly to me.”
■ Delusions of control: Includes thought broadcasting (belief that one’s
thoughts can be heard by others) and thought insertion (belief that outside
thoughts are being placed in one’s head).
■ Delusions of grandeur: Belief that one has special powers beyond those of a
normal person. Example: “I am the all-powerful son of God and I shall bring
down my wrath on you if I don’t get my way.”
■ Delusions of guilt: Belief that one is guilty or responsible for something.
Example: “I am responsible for all the world’s wars.”
■ Somatic delusions: Belief that one has a certain illness or health condition.
Example: A patient believing she is pregnant despite negative pregnancy
tests and ultrasounds.
■ Illusion: Misinterpretation of an existing sensory stimulus (such as
mistaking a shadow for an evil spirit).
■ Hallucination: Sensory perception without an actual external stimulus.
●Auditory: The most common modality experienced by patients with
schizophrenia.
●Visual: Occurs in schizophrenia and other psychotic disorders, but
less common. May accompany drug intoxication, drug and alcohol
­withdrawal, or delirium.
●Olfactory: Usually an aura associated with epilepsy.
●Tactile: Usually secondary to drug intoxication (e.g., cocaine or
­psychostimulants) or alcohol withdrawal.
DIFFERENTIAL DIAGNOSIS OF PSYCHOSIS
■ Psychotic disorder due to another medical condition.
■ Substance/Medication-induced psychotic disorder.
■ Delirium/Major neurocognitive disorder (dementia).
■ Bipolar disorder, manic/mixed episode.
■ Major depressive disorder with psychotic features.
■ Brief psychotic disorder.
■ Schizophrenia.
■ Schizophreniform disorder.
■ Schizoaffective disorder.
■ Delusional disorder.
PSYCHOTIC DISORDER DUE TO ANOTHER MEDICAL CONDITION
Other Medical causes of psychosis include:
Central nervous system (CNS) disease (cerebrovascular disease, multiple sclerosis, neoplasm, Alzheimer disease, Parkinson disease, Huntington disease,
tertiary syphilis, epilepsy [often temporal lobe], encephalitis, prion disease,
neurosarcoidosis, AIDS).
Endocrinopathies (Addison/Cushing disease, hyper/hypothyroidism, hyper/
hypocalcemia, hypopituitarism).
Nutritional/Vitamin deficiency states (B12, folate, niacin).
Other (connective tissue disease [systemic lupus erythematosus, temporal
arteritis], porphyria).
DSM-5 criteria for psychotic disorder due to another medical condition
include:
■ Prominent hallucinations or delusions.
■ Symptoms do not occur only during an episode of delirium.
■ Evidence from history, physical, or lab data to support another medical
cause (i.e., not a primary psychiatric disorder).
SUBSTANCE/MEDICATION-INDUCED PSYCHOTIC DISORDER
Prescription medications that may cause psychosis in some patients include
anesthetics, antimicrobials, corticosteroids, antiparkinsonian agents, anticonvulsants, antihistamines, anticholinergics, antihypertensives, nonsteroidal
anti-inflammatory drugs (NSAIDs), digitalis, methylphenidate, and chemotherapeutic agents. Substances such as alcohol, cocaine, hallucinogens (LSD,
ecstasy), cannabis, benzodiazepines, barbiturates, inhalants, and phencyclidine
(PCP) can cause psychosis, either during intoxication or withdrawal.
DSM-5 Criteria
■ Hallucinations and/or delusions.
■ Symptoms do not occur only during episode of delirium.
■ Evidence from history, physical, or lab data to support a medication or
substance-induced cause.
■ Disturbance is not better accounted for by a psychotic disorder that is not
substance/medication-induced.
PSYCHOTIC DISORDERS
WARDS TIP
It’s important to be able to distinguish between a delusion, illusion,
and hallucination. A delusion is a
fixed, false belief, an illusion is a
misinterpretation of an external
stimulus, and a hallucination is
perception in the absence of an
external stimulus.
WARDS
QUESTION
Q: What is the most likely etiology
in an elderly, medically ill patient
presenting with the new onset of
psychotic symptoms?
A: Delirium.
WARDS TIP
To make the diagnosis of schizophrenia, a patient must have
symptoms of the disease for at
least 6 months.
24
PSYCHOTIC DISORDERS
Schizophrenia
KEY FACT
Think of positive symptoms as
things that are ADDED onto
normal behavior. Think of negative
symptoms as things that are SUBTRACTED or missing from normal
behavior.
WARDS TIP
Stereotyped movement, bizarre
posturing, and muscle rigidity are
examples of catatonia, a syndrome
which can be seen in schizophrenia, depression, bipolar disorder,
and other psychiatric conditions.
THREE PHASES
WARDS TIP
The 5 A’s of schizophrenia
(negative symptoms):
Anhedonia
Affect (flat)
Alogia (poverty of speech)
Avolition (apathy)
Attention (poor)
DIAGNOSIS OF SCHIZOPHRENIA
DSM-5 Criteria
A 24-year-old male graduate student without prior medical or psychiatric
history is reported by his mother to have been very anxious over the past
9 months, with increasing concern that people are watching him. He now
claims to “hear voices” telling him what must be done to “fix the country.”
Important workup? Comprehensive metabolic panel, urine drug screen,
thyroid-stimulating hormone (TSH), HIV testing. Consider brain ­imaging.
Likely diagnosis? If workup is unremarkable, schizophrenia. Next step?
­Antipsychotics.
Schizophrenia is a psychiatric disorder characterized by a constellation of
abnormalities in thinking, emotion, and behavior. There is no single symptom
that is pathognomonic, and there is a heterogeneous clinical presentation.
Schizophrenia is typically chronic, with significant psychosocial and medical
consequences to the patient.
POSITIVE, NEGATIVE, AND COGNITIVE SYMPTOMS
In general, the symptoms of schizophrenia are broken up into three categories:
■ Positive symptoms: Hallucinations, delusions, bizarre behavior,
disorganized speech. These tend to respond more robustly to antipsychotic
medications.
■ Negative symptoms: Flat or blunted affect, anhedonia, apathy, alogia, and
lack of interest in socialization. These symptoms are comparatively more
often treatment resistant and contribute significantly to the social isolation
and impaired function of schizophrenic patients.
■ Cognitive symptoms: Impairments in attention, executive function, and
working memory. These symptoms may lead to poor work and school
performance.
Symptoms of schizophrenia often present in the following three phases:
Prodromal: Decline in functioning that precedes the first psychotic episode.
The patient may become socially withdrawn and irritable. They may have
physical complaints, declining school/work performance, and/or newfound
interest in religion or the occult.
Psychotic: Perceptual disturbances, delusions, and disordered thought process/content.
Residual: Occurs following an episode of active psychosis. It is marked by
mild hallucinations or delusions, social withdrawal, and negative symptoms.
■ Two or more of the following must be present for at least 1 month:
Delusions.
Hallucinations.
Disorganized speech.
Grossly disorganized or catatonic behavior.
Negative symptoms.
Note: At least one must be 1, 2, or 3.
■ Must cause significant social, occupational, or functional (self-care)
deterioration.
■ Duration of illness for at least 6 months (including prodromal or residual
periods in which the above full criteria may not be met).
■ Symptoms not due to effects of a substance or another medical condition.
Mr. T is a 21-year-old man who is brought to the ER by his mother after he
began talking about “aliens” who were trying to steal his soul. He reports
that aliens leave messages for him by arranging sticks outside his home and
sometimes send thoughts into his mind. On exam, he is guarded and often
stops talking while in the middle of expressing a thought. Mr. T appears
anxious and frequently scans the room for aliens, which he thinks may have
followed him to the hospital. He denies any plan to harm himself, but admits
that the aliens sometimes want him to throw himself in front of a car, “as this
will change the systems that belong under us.”
The patient’s mother reports that he began expressing these ideas a few
months ago, but they have become more severe in the last few weeks. She
reports that during the past year, he has become isolated from his peers,
frequently talks to himself, and has stopped going to community college. He
has also spent most of his time reading science fiction books and creating
devices that will prevent aliens from hurting him. She reports that she is concerned because the patient’s father, who left while the patient was a child,
exhibited similar symptoms many years ago and has spent most of his life in
psychiatric hospitals.
What is the patient’s most likely diagnosis? What differential diagnoses
should be considered?
Mr. T’s most likely diagnosis is schizophrenia. He exhibits delusional ideas that
are bizarre and paranoid in nature. He also reports the presence of frequent
auditory hallucinations and disturbances in thought process that include
thought blocking. Although the patient’s mother reports that his psychotic
symptoms began “a few months ago,” the patient has exhibited social and occupational dysfunction during the last year. Mr. T quit school, became isolated,
and has been responding to internal stimuli since that time. In addition, his
father appears to also suffer from a psychotic disorder. In this case, it appears
that the disorder has been present for more than 6 months. However, if this is
unclear, the diagnosis of schizophreniform disorder should be made instead.
The differential diagnosis should also include schizoaffective disorder,
medication/substance-induced psychotic disorder, psychotic disorder due to
another medical condition, and mood disorder with psychotic features.
What would be appropriate steps in the acute management of this
patient?
Treatment should include inpatient hospitalization in order to provide a safe
environment, with monitoring of suicidal ideation secondary to his psychosis. Routine laboratory tests, including a urine or serum drug screen, should
be undertaken. The patient should begin treatment with antipsychotic
­medication while closely being monitored for potential side effects.
PSYCHIATRIC EXAM OF PATIENTS WITH SCHIZOPHRENIA
The typical findings in patients with schizophrenia include:
■ Disheveled appearance.
■ Flat affect.
PSYCHOTIC DISORDERS
WARDS TIP
• Echolalia—Repeats words or
phrases
• EchoPRAxia—Mimics behavior
(PRActices behavior)
KEY FACT
Brief psychotic disorder lasts for
<1 month. Schizophreniform
­disorder can last between 1 and
6 months. Schizophrenia lasts for
6 months.
26
■ Disorganized thought process.
PSYCHOTIC DISORDERS
■ Intact procedural memory and orientation.
■ Auditory hallucinations.
■ Paranoid delusions.
■ Ideas of reference.
■ Lack of insight into their disease.
EPIDEMIOLOGY
●Women present in late 20s.
­compared to women.
■ There is a strong genetic predisposition:
KEY FACT
Schizophrenia is more prevalent
in lower socioeconomic groups
likely due to “downward drift”
(many patients face barriers
to higher education, regular
­employment, and other resources,
so they tend to drift downward
socioeconomically).
DOWNWARD DRIFT
Keep in mind that schizophrenia can have a very heterogeneous presentation—
patients may have schizophrenia without a disheveled appearance or clear
negative symptoms.
■ Schizophrenia affects approximately 0.3–0.7% of people over their lifetime.
■ Men and women are equally affected but have different presentations and
outcomes:
●Men tend to present in early to mid-20s.
●Men tend to have more negative symptoms and poorer outcome
■ Schizophrenia rarely presents before age 15 or after age 55.
●Fifty percent concordance rate among monozygotic twins.
●Forty percent risk of inheritance if both parents have schizophrenia.
●Twelve percent risk if one first-degree relative is affected.
■ Substance use is comorbid in many patients with schizophrenia. The most
commonly abused substance is nicotine (>50%), followed by alcohol,
cannabis, and cocaine.
■ Post-psychotic depression is the phenomenon of schizophrenic patients
developing a major depressive episode after resolution of their psychotic
symptoms.
Lower socioeconomic groups have higher rates of schizophrenia. This may be
due to the downward drift hypothesis, which postulates that people suffering
from schizophrenia are unable to function well in society and hence end up in
lower socioeconomic groups. Many homeless people in urban areas suffer from
schizophrenia.
PATHOPHYSIOLOGY OF SCHIZOPHRENIA: THE DOPAMINE HYPOTHESIS
Though the exact cause of schizophrenia is not known, it appears to be partly
related to increased dopamine activity in certain neuronal tracts. Evidence to
support this hypothesis is that most antipsychotics successful in treating schizophrenia are dopamine receptor antagonists. In addition, cocaine and amphetamines increase dopamine activity and can cause schizophrenia-like symptoms.
Theorized Dopamine Pathways Affected in Schizophrenia
■ Prefrontal cortical: Inadequate dopaminergic activity; responsible for
negative symptoms.
■ Mesolimbic: Excessive dopaminergic activity; responsible for positive
symptoms.
Other Important Dopamine Pathways Affected by Antipsychotics
■ Tuberoinfundibular: Blocked by antipsychotics, causing hyperprolactinemia,
which may lead to gynecomastia, galactorrhea, sexual dysfunction, and
menstrual irregularities.
■ Nigrostriatal: Blocked by antipsychotics, causing Parkinsonism/
extrapyramidal side effects such as tremor, rigidity, slurred speech, akathisia,
dystonia, and other abnormal movements.
OTHER NEUROTRANSMITTER ABNORMALITIES IMPLICATED
IN SCHIZOPHRENIA
■ Elevated serotonin: Some of the second-generation (atypical) antipsychotics
(e.g., risperidone and clozapine) antagonize serotonin and weakly
antagonize dopamine.
■ Elevated norepinephrine: Long-term use of antipsychotics has been shown
to decrease activity of noradrenergic neurons.
■ Low gamma-aminobutyric acid (GABA): There is lower expression of
the enzyme necessary to create GABA in the hippocampus of patients with
schizophrenia.
■ Low levels of glutamate receptors: Patients with schizophrenia have fewer
NMDA receptors; this corresponds to the psychotic symptoms observed
with NMDA antagonists like ketamine.
PROGNOSTIC FACTORS
Even with medication, 40–60% of patients remain significantly impaired after
their diagnosis, while only 20–30% function fairly well in society. About 20% of
patients with schizophrenia attempt suicide and many more experience ­suicidal
ideation. Several factors are associated with a better or worse prognosis:
Associated with Better Prognosis
■ Later onset.
■ Good social support.
■ Positive symptoms.
■ Mood symptoms.
■ Acute onset.
■ Female gender.
■ Few relapses.
■ Good premorbid functioning.
Associated with Worse Prognosis
■ Early onset.
■ Poor social support.
■ Negative symptoms.
■ Family history.
■ Gradual onset.
■ Male gender.
■ Many relapses.
PSYCHOTIC DISORDERS
KEY FACT
Akathisia is an unpleasant, subjective sense of restlessness and need
to move, often manifested by the
inability to sit still. Severe akathisia
can be a risk factor for suicide.
WARDS
QUESTION
Q: What are the most appropriate
treatments for akathisia?
A: Tapering down antipsychotic
medication, beta-blockers such as
propranolol, or benzodiazepines.
KEY FACT
The lifetime prevalence of schizophrenia is 0.3–0.7%.
KEY FACT
Schizophrenia has a large genetic
component. If one identical twin
has schizophrenia, the risk of
the other identical twin having
schizophrenia is 50%. A biological child of a schizophrenic
person has a higher chance of
developing schizophrenia, even
if adopted into a family without
­schizophrenia.
28
PSYCHOTIC DISORDERS
KEY FACT
■ Comorbid substance use.
TREATMENT
Computed tomography (CT) and
magnetic resonance imaging (MRI)
scans of patients with schizophrenia may show enlargement of the
ventricles, diffuse cortical atrophy,
and reduced brain volume.
KEY FACT
Schizophrenia often involves neologisms. A neologism is a newly
coined word or expression that
has meaning only to the person
who uses it.
WARDS
QUESTION
Q: What is the typical age of onset
for schizophrenia?
A: For men, 15–25. For women,
15–30, with a second (smaller)
peak incidence in the late 40s.
WARDS TIP
First-generation antipsychotic
medications are referred to as
typical or conventional antipsychotics (often called neuroleptics).
Second-generation antipsychotic
medications are referred to as
atypical antipsychotics.
■ Poor premorbid functioning (social isolation, etc.).
A multimodal approach is the most effective, and therapy must be tailored
to the needs of the specific patient. Pharmacologic treatment consists
­primarily of antipsychotic medications. (For more detail, see Chapter 18,
“­Psychopharmacology.”)
■ First-generation (or typical) antipsychotic medications
(e.g., chlorpromazine, fluphenazine, haloperidol, perphenazine):
●Primarily dopamine (mostly D2) antagonists.
●Treat positive symptoms with minimal impact on negative symptoms.
●Side effects include extrapyramidal symptoms, neuroleptic malignant
syndrome, and tardive dyskinesia (see below).
■ Second-generation (or atypical) antipsychotic medications
(e.g., aripiprazole, asenapine, clozapine, iloperidone, lurasidone, olanzapine,
quetiapine, risperidone, ziprasidone):
●These antagonize serotonin receptors (5-HT2) as well as dopamine
(D4>D2) receptors.
●Research has not shown a significant difference between first- and
second-generation antipsychotics in efficacy. The selection requires the
weighing of benefits and risks in individual clinical cases.
●Lower incidence of extrapyramidal side effects, but higher risk of metabolic syndrome.
●Medications should be taken for at least 4 weeks before efficacy is determined.
●Clozapine is reserved for patients who have failed multiple antipsychotic
trials due to its risk of agranulocytosis.
Behavioral therapy attempts to improve patients’ ability to function in society.
Patients are helped through a variety of methods to improve their social skills,
become self-sufficient, and minimize disruptive behaviors. Family therapy and
group therapy are also useful adjuncts.
Important Side Effects and Sequelae of Antipsychotic Medications
Side effects of antipsychotic medications include:
Extrapyramidal symptoms (especially with the use of high-potency
first-generation antipsychotics):
• Dystonia (spasms) of face, neck, and tongue.
• Parkinsonism (resting tremor, rigidity, bradykinesia).
• Akathisia (feeling of restlessness).
• Treatment: Anticholinergics (benztropine, diphenhydramine),
­benzodiazepines/beta-blockers (specifically for akathisia).
Anticholinergic symptoms (especially low-potency first-generation antipsychotics and atypical antipsychotics): Dry mouth, constipation, blurred
vision, hyperthermia.
Treatment: As per symptom (eye drops, stool softeners, etc.).
Metabolic syndrome (second-generation antipsychotics): A constellation of
conditions— elevated blood pressure, elevated blood sugar levels, excess
body fat around the waist, abnormal cholesterol levels—that occur together,
increasing the risk for cardiovascular disease, stroke, and type 2 diabetes.
Treatment: Consider switching to a first-generation antipsychotic or a more
“weight-neutral” second-generation antipsychotic such as aripiprazole or
ziprasidone. Consider metformin if the patient is not already on it. Monitor lipids and blood glucose measurements. Refer the patient to primary
care for appropriate treatment of hyperlipidemia, diabetes, etc. Encourage
appropriate diet, exercise, and smoking cessation.
4. Tardive dyskinesia (more likely with first-generation antipsychotics):
Choreoathetoid movements, usually seen in the face, tongue, and head.
Treatment: Discontinue or reduce the medication and consider substituting
an atypical antipsychotic (if appropriate). VMAT-2 inhibitors such as
valbenazine, benzodiazepines, Botox, and vitamin E may be used. The
movements may persist despite withdrawal of the drug. Although less
common, atypical antipsychotics can also cause tardive dyskinesia.
5. Neuroleptic malignant syndrome (NMS) (typically high-potency
first-generation antipsychotics):
●Change in mental status, autonomic instability (high fever, labile blood
pressure, tachycardia, tachypnea, diaphoresis), “lead pipe” rigidity, elevated creatine kinase (CK) levels, leukocytosis, and metabolic acidosis.
Reflexes are decreased.
●NMS is a medical emergency that requires prompt withdrawal of all antipsychotic medications and immediate medical assessment and treatment.
●May be observed in any patient being treated with any antipsychotic (including second generation) medications at any time, but is more
frequently associated with the initiation of treatment and at higher IV/IM
dosing of high-potency neuroleptics.
●Patients with a history of prior neuroleptic malignant syndrome are at
increased risk of recurrent episodes when retrialed with antipsychotic
agents.
6. Prolonged QTc interval and other electrocardiogram changes, hyperprolactinemia (gynecomastia, galactorrhea, amenorrhea, diminished libido, and
impotence), hematologic effects (agranulocytosis may occur with clozapine,
requiring frequent blood draws when this medication is used), ophthalmologic conditions (thioridazine may cause irreversible retinal pigmentation
at high doses; deposits in lens and cornea may occur with chlorpromazine),
dermatologic conditions (such as rashes and photosensitivity).
Schizophreniform Disorder
Diagnosis and DSM-5 Criteria
The diagnosis of schizophreniform disorder is made using the same DSM-5 criteria as schizophrenia. The only difference is that in schizophreniform disorder
the symptoms have lasted between 1 and 6 months, whereas in schizophrenia
the symptoms must be present for >6 months.
Prognosis
One-third of patients recover completely; two-thirds progress to schizoaffective
disorder or schizophrenia.
Treatment
Hospitalization (if necessary), 6-month course of antipsychotics, and supportive psychotherapy.
PSYCHOTIC DISORDERS
WARDS TIP
Patients who are treated with
first-generation (typical) antipsychotic medication need to be
closely monitored for extrapyramidal symptoms, such as acute
dystonia and tardive dyskinesia.
WARDS TIP
Patients with schizophrenia who
are treated with second-generation
(atypical) antipsychotic medications need a careful medical evaluation for metabolic syndrome. This
includes checking weight, body
mass index (BMI), fasting blood
glucose or HbA1c, lipid assessment, and blood pressure.
KEY FACT
High-potency antipsychotics (such
as haloperidol and fluphenazine)
have a higher incidence of extrapyramidal side effects, while
low-potency antipsychotics (such
as chlorpromazine) have primarily
anticholinergic and antiadrenergic
side effects.
WARDS
QUESTION
Q: What antipsychotic medications are available as long-acting
injectables?
A: First generation: haloperidol,
fluphenazine. Second generation:
risperidone, paliperidone, aripiprazole, olanzapine.
30
PSYCHOTIC DISORDERS
Schizoaffective Disorder
WARDS TIP
Tardive dyskinesia occurs most
often in older women after at least
6 months of medication. A small
percentage of patients will experience spontaneous remission,
so discontinuation of the agent
should be considered if clinically
appropriate.
WARDS TIP
The cumulative risk of developing
tardive dyskinesia from antipsychotics (particularly first generation) is 5% per year.
Treatment
WARDS
QUESTION
Brief Psychotic Disorder
Q: Which antipsychotic has been
shown to reduce suicidality in
patients with schizophrenia?
A: Clozapine.
WARDS TIP
Clozapine is typically considered
for treating schizophrenia when
a patient fails both typical and
other atypical antipsychotics. It is a
very effective medication, but can
cause agranulocytosis; therefore,
patients’ white blood cell and
absolute neutrophil counts must
be monitored regularly. Clozapine
also has black box warnings for
orthostatic hypotension, seizures,
and cardiomyopathy. Other common side effects include sedation,
excessive drooling, and severe
constipation.
Delusional Disorder
■ One or more delusions for at least 1 month.
■ Does not meet criteria for schizophrenia.
Diagnosis and DSM-5 Criteria
The diagnosis of schizoaffective disorder is made in patients who:
■ Meet criteria for either a major depressive or manic episode during which
psychotic symptoms consistent with schizophrenia are also met.
■ Have delusions or hallucinations for 2 weeks in the absence of mood
disorder symptoms (this criterion is necessary to differentiate schizoaffective
disorder from a mood disorder with psychotic features).
■ Have mood symptoms for a majority of the psychotic illness.
■ Have symptoms not due to the effects of a substance (drug or medication) or
another medical condition.
Prognosis
Worse with poor premorbid adjustment, slow onset, early onset, predominance
of psychotic symptoms, long course, and family history of schizophrenia.
■ Hospitalization (if necessary) and supportive psychotherapy.
■ Medical therapy: Antipsychotics (second-generation medications may target
both psychotic and mood symptoms); mood stabilizers, antidepressants, or
electroconvulsive therapy (ECT) may be indicated for treatment of mood
symptoms.
Diagnosis and DSM-5 Criteria
Patient with psychotic symptoms as in schizophrenia; however, the symptoms
last from 1 day to 1 month, and there must be eventual full return to premorbid
level of functioning. Symptoms must not be due to the effects of a substance
(drug or medication) or another medical condition. This is a rare diagnosis,
much less common than schizophrenia. It may be seen in reaction to extreme
stress such as bereavement and sexual assault.
Prognosis
High rates of relapse, but almost all completely recover.
Treatment
Brief hospitalization (usually required for workup, safety, and stabilization),
supportive therapy, course of antipsychotics for psychosis, and/or benzodiazepines for agitation.
Delusional disorder occurs more often in middle-aged or older patients (after
age 40). Immigrants, the hearing impaired, and those with a family history of
schizophrenia are at increased risk.
Diagnosis and DSM-5 Criteria
To be diagnosed with delusional disorder, the following criteria must be met:
TABLE 3-1. Schizophrenia versus Delusional Disorder
Schizophrenia
Delusional Disorder
■ Bizarre or nonbizarre delusions
■ Usually nonbizarre delusions
■ Daily functioning significantly impaired
■ Daily functioning not significantly
­impaired
■ Must have two or more of the
following:
■ Does not meet the criteria for
■ Delusions
■ Hallucinations
■ Disorganized speech
■ Disorganized behavior
■ Negative symptoms
■ Functioning in life not significantly impaired, and behavior not obviously
bizarre.
■ While delusions may be present in both delusional disorder and
schizophrenia, there are important differences (see Table 3-1).
Types of Delusions
Patients are further categorized based on the types of delusions they
­experience:
■ Erotomanic type: Delusion that another person is in love with the
individual.
■ Grandiose type: Delusions of having great talent.
■ Somatic type: Physical delusions.
■ Persecutory type: Delusions of being persecuted.
■ Jealous type: Delusions of unfaithfulness.
■ Mixed type: More than one of the above.
■ Unspecified type: Not a specific type as described above.
Prognosis
Better than schizophrenia with treatment:
■ >50%: Full recovery.
■ >20%: Decrease in symptoms.
■ <20%: No change.
Treatment
Difficult to treat, especially given the lack of insight and impairment. Antipsychotic medications are recommended despite somewhat limited evidence.
Supportive therapy is often helpful.
Culture-Specific Psychoses
The following are examples of psychotic disorders seen within certain cultures:
Psychotic Manifestation
Culture
Koro
Intense anxiety that the penis will recede into the
body, possibly leading to death.
Southeast Asia
(e.g., Singapore)
Amok
Sudden unprovoked outbursts of violence, often
followed by suicide.
Malaysia
Brain fag
Headache, fatigue, eye pain, cognitive ­difficulties, and
other somatic disturbances in male students.
Africa
PSYCHOTIC DISORDERS
WARDS TIP
If a schizophrenia presentation has
not been present for 6 months,
think schizophreniform disorder.
­schizophre­nia, as described in the left
column
KEY FACT
Patients with borderline personality disorder may have transient,
stress-related psychotic experiences. These are considered part
of their underlying personality
disorder and are not diagnosed as
a brief psychotic disorder.
32
PSYCHOTIC DISORDERS
Time Course
■ <1 month—Brief psychotic disorder.
■ 1–6 months—Schizophreniform disorder.
■ >6 months—Schizophrenia.
KEY FACT
SchizophreniFORM = the FORMation of a schizophrenic, but not
quite there (i.e., <6 months).
Comparing Time Courses and Prognoses
of Psychotic Disorders
Prognosis from Best to Worst
Mood disorder with psychotic features > schizoaffective disorder >
­schizophreniform disorder > schizophrenia.
QUICK AND EASY DISTINGUISHING FEATURES
■ Schizophrenia: Lifelong psychotic disorder.
■ Schizophreniform: Schizophrenia for >1 and <6 months.
■ Schizoaffective: Distinct mood episodes with psychosis persisting between
mood episodes.
■ Schizotypal (personality disorder): Paranoid, odd or magical beliefs,
eccentric, lack of friends, social anxiety. Criteria for overt psychosis are
not met.
[
■ Schizoid (personality disorder): Solitary activities, lack of enjoyment from
social interactions, no psychosis.

07 - Chapter 4 Mood Disorders

01 - Chapter 4 Mood Disorders
Chapter 4 Mood Disorders
Concepts in Mood Disorders......................................................................................................34
Mood Disorders versus Mood Episodes......................................................................................34
Mood Episodes..........................................................................................................................34
Major Depressive Episode (MDE)..........................................................................................34
Manic Episode.....................................................................................................................34
Hypomanic Episode.............................................................................................................35
Differences between Manic and Hypomanic Episodes.........................................................35
Mixed Features....................................................................................................................35
Mood Disorders.........................................................................................................................35
Differential Diagnosis of Mood Disorders Due to Other Medical Conditions.........................35
Substance/Medication-Induced Mood Disorders.................................................................36
Major Depressive Disorder (MDD)........................................................................................37
Specifiers for Depressive Disorders.......................................................................................40
Bereavement.......................................................................................................................40
Bipolar I Disorder.................................................................................................................40
Bipolar II Disorder................................................................................................................42
Specifiers for Bipolar Disorders............................................................................................42
Persistent Depressive Disorder (Dysthymia).........................................................................43
Cyclothymic Disorder...........................................................................................................44
Premenstrual Dysphoric Disorder........................................................................................44
Disruptive Mood Dysregulation Disorder (DMDD)................................................................45
Other Disorders of Mood in DSM-5.......................................................................................46
MOOD DISORDERS
CHAPTER 4
34
MOOD DISORDERS
WARDS TIP
Major depressive episodes can be
present in major depressive disorder, persistent depressive disorder
(dysthymia), bipolar I/II disorder,
and schizoaffective disorder.
WARDS TIP
When patients have delusions
and hallucinations due to underlying mood disorders, they
are usually mood congruent.
For example, depression causes
psychotic themes of paranoia and
worthlessness, and mania causes
psychotic themes of grandiosity
and ­invincibility.
Mood Episodes
MAJOR DEPRESSIVE EPISODE (MDE)
KEY FACT
Symptoms of major depression—
SIG E. CAPS (Prescribe Energy
Capsules)
Sleep
Interest
Guilt
Energy
Concentration
Appetite
Psychomotor activity
Suicidal ideation
MANIC EPISODE
Concepts in Mood Disorders
A mood is a description of one’s internal emotional state. Both external and
internal stimuli can trigger moods, which may be labeled as sad, happy, angry,
irritable, and so on. It is normal to have a wide range of moods and to have a
sense of control over one’s moods.
Patients with mood disorders (also called affective disorders) experience an abnormal range of moods and lose some level of control over them. Distress may
be caused by the severity of their moods and the resulting impairment in social
and occupational functioning.
Mood Disorders versus Mood Episodes
■ Mood episodes are distinct periods of time in which some abnormal mood
is present. They include depression, mania, and hypomania.
■ Mood disorders are defined by their patterns of mood episodes. They
include major depressive disorder (MDD), bipolar I disorder, bipolar II
disorder, persistent depressive disorder, and cyclothymic disorder. Some
may have psychotic features (delusions or hallucinations).
Must have at least five of the following symptoms (must include either number
1 or 2) for at least a 2-week period:
Depressed mood most of the time.
Anhedonia (loss of interest in pleasurable activities).
Change in appetite or weight (↑ or ↓).
Feelings of worthlessness or excessive guilt.
Insomnia or hypersomnia.
Diminished concentration.
Psychomotor agitation or retardation (i.e., restlessness or slowness).
Fatigue or loss of energy.
Recurrent thoughts of death or suicide.
Symptoms must not be attributable to the effects of a substance (drug or
­medication) or another medical condition, and they must cause clinically
­significant distress or social/occupational impairment.
A distinct period of abnormally and persistently elevated, expansive, or ­irritable
mood, and abnormally and persistently increased goal-directed ­activity or energy, lasting at least 1 week (or any duration if hospitalization is necessary), and
including at least three of the following (four if the mood is only irritable):
Distractibility.
Inflated self-esteem or grandiosity.
↑ in goal-directed activity (socially, at work, or sexually) or psychomotor
agitation.
↓ need for sleep.
Flight of ideas or racing thoughts.
More talkative than usual or pressured speech (rapid and uninterruptible).
Excessive involvement in pleasurable activities that have a high risk of negative consequences (e.g., shopping sprees, sexual indiscretions).
Symptoms must not be attributable to the effects of a substance (drug or medication) or another medical condition, and they must cause clinically significant
distress or social/occupational impairment. Greater than 50% of patients with
manic episodes have psychotic symptoms.
HYPOMANIC EPISODE
A hypomanic episode is a distinct period of abnormally and persistently elevated, expansive, or irritable mood, and abnormally and persistently increased
goal-directed activity or energy, lasting at least 4 consecutive days, that includes at least three of the symptoms listed for the manic episode criteria (four
if mood is only irritable). There are significant differences between mania and
hypomania (see below).
DIFFERENCES BETWEEN MANIC AND HYPOMANIC EPISODES
Hypomania
Lasts at least 4 days
No marked impairment in social or
occupational functioning
Does not require hospitalization
No psychotic features
Mania
Lasts at least 7 days
Causes severe impairment in social or
occupational functioning
May necessitate hospitalization to prevent
harm to self or others
May have psychotic features
MIXED FEATURES
Criteria are met for a manic or hypomanic episode and at least three symptoms
of a MDE are present for the majority of the time. These criteria must be present nearly every day for at least 1 week.
Mood Disorders
Mood disorders often have chronic courses that are marked by relapses with
relatively normal functioning between episodes, which is a key factor in distinguishing a mood disorder from other chronic psychiatric disorders such as
schizophrenia. Like most psychiatric diagnoses, mood episodes may be caused
by another medical condition or drug (prescribed or illicit). Therefore, always
investigate medical or substance-induced causes (see below) before diagnosing
a primary mood disorder.
DIFFERENTIAL DIAGNOSIS OF MOOD DISORDERS DUE
TO OTHER MEDICAL CONDITIONS
Medical Causes of a Depressive Episode
Cerebrovascular disease (stroke, myocardial
infarction)
Endocrinopathies (diabetes mellitus,
Cushing syndrome, Addison disease,
hypoglycemia, hyper/hypothyroidism,
hyper/hypocalcemia)
MOOD DISORDERS
WARDS TIP
A suicide risk assessment should
include evaluating current or
recent suicidal ideation (including wishing to be dead, thinking
of methods, planning, or having
intent) and should assess frequency, duration, and intensity of these
thoughts.
Suicide Risk Factors:
SAD PERSONS
S: Male sex
A: <19 or >45 years
D: Depression
P: Previous attempt
E: Excess alcohol or substance use
R: Rational thinking loss
S: Social supports lacking
O: Organized plan
N: No spouse
S: Sickness
KEY FACT
Symptoms of mania—DIG FAST
Distractibility
Insomnia/Impulsive behavior
Grandiosity
Flight of ideas/Racing thoughts
Activity/Agitation
Speech (pressured)
Thoughtlessness
WARDS TIP
A manic episode is a psychiatric
emergency; severely impaired
judgment and impulsivity can
make a patient dangerous to self
and others.
Medical Causes of a Manic Episode
Metabolic (hyperthyroidism)
Neurological disorders (temporal lobe
seizures, multiple sclerosis)
36
MOOD DISORDERS
Parkinson disease
Viral illnesses (e.g., mononucleosis)
Carcinoid syndrome
Cancer (especially lymphoma and
pancreatic carcinoma)
Collagen vascular disease (e.g., systemic
lupus erythematosus)
WARDS TIP
Irritability is often the predominant mood state in mood disorders with mixed features. Patients
with mixed features have a poorer
response to lithium. Anticonvulsants such as valproic acid may be
more helpful.
Substance/Medication-Induced
Depressive Disorder
EtOH
Antihypertensives
Barbiturates
Corticosteroids
Levodopa
Sedative-hypnotics
Anticonvulsants
Antipsychotics
Diuretics
Sulfonamides
Opiates
Withdrawal from stimulants (e.g., cocaine,
amphetamines)
KEY FACT
Patients with cardiovascular disease or strokes are at a significant
risk for developing depression,
and this is associated with a poorer outcome overall.
KEY FACT
Depression is common in patients
with pancreatic cancer.
Neoplasms
HIV infection
SUBSTANCE/MEDICATION-INDUCED MOOD DISORDERS
Substance/Medication-Induced Bipolar
Disorder
Antidepressants
Sympathomimetics
Dopamine
Corticosteroids
Levodopa
Bronchodilators
Cocaine
Amphetamines
Ms. Cruz is a 28-year-old sales clerk who arrives at your outpatient clinic complaining of sadness after her boyfriend of 6 months ended their relationship
1 month ago. She describes a history of failed romantic relationships, and
says, “I don’t do well with breakups.” Ms. Cruz reports that, although she has
no prior psychiatric treatment, she was urged by her employer to seek therapy. Ms. Cruz has arrived late to work on several occasions because of oversleeping. She also has difficulty in getting out of bed stating, “It’s difficult to
walk; it’s like my legs weigh a ton.” She feels fatigued during the day despite
spending over 12 hours in bed, and is concerned that she might be suffering from a serious medical condition. She denies any significant changes in
appetite or weight since these symptoms began.
Ms. Cruz reports that, although she has not missed workdays, she has
difficulty concentrating and has become tearful in front of clients while worrying about not finding a significant other. She feels tremendous guilt over
“not being good enough to get married,” and says that her close friends are
concerned because she has been spending her weekends in bed and not answering their calls. Although during your evaluation Ms. Cruz appears tearful,
she brightens up when talking about her newborn nephew and her plans to
visit a college friend next summer. Ms. Cruz denies suicidal ideation.
What is Ms. Cruz’s diagnosis?
Ms. Cruz’s diagnosis is MDD with atypical features. She complains of sadness,
fatigue, poor concentration, hypersomnia, feelings of guilt, anhedonia, and
impairment in her social and occupational functioning. The atypical features specifier is given in this case as she exhibited mood reactivity (mood
brightens in response to positive events) when talking about her nephew
and visiting her friend, and complained of a heavy feeling in her legs (leaden
paralysis) and hypersomnia. It is also important to explore Ms. Cruz’s history
of “not doing well with breakups,” as this could be indicative of a long pattern
of interpersonal rejection sensitivity. Although it is common for patients who
suffer from atypical depression to report an ↑ in appetite, Ms. Cruz exhibits
enough symptoms to fulfill atypical features criteria. Adjustment disorder
should also be considered in the differential diagnosis.
What would be your pharmacological recommendation?
Ms. Cruz should be treated with an antidepressant medication. While
monoamine oxidase inhibitors (MAOIs) such as phenelzine had traditionally
been superior to tricyclic antidepressants (TCAs) in the treatment of MDD
with atypical features, selective serotonin reuptake inhibitors (SSRIs) would
be the first-line treatment given more favorable safety and side-effect
profile. The combination of pharmacotherapy and psychotherapy has been
shown to be more effective for treating mild-to-moderate MDD than either
treatment alone.
MAJOR DEPRESSIVE DISORDER (MDD)
MDD is marked by episodes of depressed mood associated with loss of interest
in daily activities. Patients may not acknowledge their depressed mood or may
express vague, somatic complaints (fatigue, headache, abdominal pain, muscle
tension, etc.).
Diagnosis and DSM-5 Criteria
■ At least one MDE (see above).
■ No history of manic or hypomanic episode.
Epidemiology
■ Lifetime prevalence: 12% worldwide.
■ Onset at any age, but the age of onset peaks in the 20s.
■ 1.5–2 times as prevalent in women than men during reproductive years.
■ No ethnic or socioeconomic differences.
■ Lifetime prevalence in the elderly: <10%.
■ Depression can ↑ mortality for patients with other comorbidities such as
diabetes, stroke, and cardiovascular disease.
Sleep Problems Associated with MDD
■ Multiple awakenings.
■ Initial and terminal insomnia (hard to fall asleep and early morning
awakenings).
■ Hypersomnia (excessive sleepiness) is less common.
■ Rapid eye movement (REM) sleep shifted earlier in the night and for a
greater duration, with reduced stages 3 and 4 (slow wave) sleep.
■ Caution: Other medical conditions like obstructive sleep apnea (OSA) can
cause sleep disturbances with associated changes in energy or mood that can
mimic symptoms of depression.
Etiology
The precise cause of depression is unknown, but MDD is believed to be
a ­heterogeneous disease, with biological, genetic, environmental, and
­psychosocial factors contributing.
■ MDD is likely caused by neurotransmitter abnormalities in the brain.
Evidence for this is the following: antidepressants exert their therapeutic
effect by increasing catecholamines; ↓ cerebrospinal fluid (CSF) levels of
MOOD DISORDERS
KEY FACT
Anhedonia is the inability to
experience pleasure, and apathy
is the inability to feel interested
or motivated; both are a common
finding in depression.
WARDS
QUESTION
Q: What are the most common
psychiatric disorders among those
who commit suicide?
A: MDD and bipolar I disorder.
WARDS TIP
The two most common types of
sleep disturbances associated with
MDD are difficulty falling asleep
and early morning awakenings.
38
MOOD DISORDERS
KEY FACT
The Hamilton Depression Rating Scale (HAM-D) measures the
severity of depression and is used
in research to assess the effectiveness of therapies. PHQ-9 is a
depression screening form often
used in the primary care setting.
KEY FACT
Loss of a parent before age 11 is
associated with the later development of major depression.
Course and Prognosis
KEY FACT
Most adults with depression do
not see a mental health professional, but they often first present
to a primary care physician for
other reasons.
Treatment
Hospitalization
n Antidepressant medications:
KEY FACT
Unfortunately only half of patients
with MDD receive treatment.
5-hydroxyindolacetic acid (5-HIAA), the main metabolite of serotonin, have
been found in depressed patients with impulsive and suicidal behavior.
■ Increased sensitivity of beta-adrenergic receptors in the brain has also been
postulated in the pathogenesis of MDD.
■ High cortisol: Hyperactivity of hypothalamic-pituitary-adrenal axis,
as shown by failure to suppress cortisol levels in the dexamethasone
suppression test.
■ Abnormal thyroid axis: Thyroid disorders are associated with depressive
symptoms.
■ Gamma-aminobutyric acid (GABA), glutamate, and endogenous opiates
may additionally have a role.
■ Psychosocial/Life events: Multiple adverse childhood experiences (ACEs)
are a risk factor for later developing MDD.
■ Genetics: First-degree relatives are two to four times more likely to have
MDD. Concordance rate for monozygotic twins is <40%, and for dizygotic
twins is 10–20%.
■ Untreated, depressive episodes are self-limiting but last from 6 to 12 months.
Generally, episodes occur more frequently as the disorder progresses. The
risk of a subsequent MDE is 50–60% within the first 2 years after the first
episode. Up to 15% of patients with MDD eventually commit suicide.
■ Approximately 60–70% of patients show a significant response to
antidepressants. The gold standard for treatment of MDD is the combined
use of both an antidepressant and psychotherapy, which produces a
significantly ↑ response.
n Indicated if the patient is at risk for suicide, homicide, or is unable to care
for themselves.
Pharmacotherapy
• Selective serotonin reuptake inhibitors (SSRIs): Inhibit the reuptake of
serotonin, thus increasing the amount of serotonin in the brain. Safer and
better tolerated than other classes of antidepressants; side effects are mild
but include headache, gastrointestinal disturbance, sexual dysfunction,
and rebound anxiety. Examples are fluoxetine (Prozac®), escitalopram
(Lexapro®), and sertraline (Zoloft®).
• Serotonin-norepinephrine reuptake inhibitors (SNRIs): Inhibit the ­reuptake
of both serotonin and norepinephrine, thus increasing the level of both
neurotransmitters in the brain. Includes venlafaxine (Effexor®) and
­duloxetine (Cymbalta®).
• Other antidepressants: Other agents commonly used to treat depression
include the a2-adrenergic receptor antagonist mirtazapine (Remeron®),
and the dopamine-norepinephrine reuptake inhibitor bupropion
(Wellbutrin®).
• Tricyclic antidepressants (TCAs): Most lethal in overdose due to cardiac arrhythmias; side effects include sedation, weight gain, orthostatic
hypotension, and anticholinergic effects. Can aggravate prolonged QTc
syndrome.
• Monoamine oxidase inhibitors (MAOIs): Older medications rarely used for
refractory depression; risk of hypertensive crisis when used with sympathomimetics or ingestion of tyramine-rich foods, such as wine, beer, aged
cheeses, liver, and smoked meats (tyramine is an intermediate in the conversion of tyrosine to norepinephrine); risk of serotonin syndrome when
used in combination with SSRIs. Most common side effect is orthostatic
hypotension.
• Novel agents: Newer agents acting with unique mechanisms are available
such as vilazodone (Viibryd) which has serotonin partial agonism, or vortioxetine (Trintilix) which interacts with additional serotonin receptors.
Note: new medications can be prohibitively expensive until the generic
form is available
n Adjunct medications:
• Atypical (second-generation) antipsychotics along with antidepressants
are first-line treatment in patients with MDD with psychotic features. In
addition, they may also be prescribed in patients with treatment resistant/
refractory MDD without psychotic features.
• Triiodothyronine (T3), levothyroxine (T4), and lithium have demonstrated some benefit when augmenting antidepressants in treatment refractory MDD.
• While stimulants (such as methylphenidate) may be used in certain patients (e.g., geriatric and terminally ill patients), the efficacy is limited and
trials are small.
Psychotherapy
n Cognitive-behavioral therapy (CBT), interpersonal psychotherapy,
supportive therapy, psychodynamic psychotherapy, problem-solving therapy,
and family/couples therapy have all demonstrated benefit in treating MDD.
• Among the major kinds of psychotherapy, there is no compelling evidence that one is superior to the rest. The choice is usually based on
availability and patient preference.
• CBT and interpersonal psychotherapy are often selected as initial treatment because they have been the most widely studied.
n May be used alone or in conjunction with pharmacotherapy.
n Early dropout is common (as with pharmacotherapy). It is important to
track patient adherence over time.
Electroconvulsive Therapy (ECT)
n Indicated if the patient is unresponsive to pharmacotherapy, if patient
cannot tolerate pharmacotherapy (pregnancy, etc.), or if rapid reduction
of symptoms is desired (e.g., immediate suicide risk, refusal to eat/drink,
catatonia).
n ECT is extremely safe (primary risk is from anesthesia) and may be used
alone or in combination with pharmacotherapy.
n ECT is often performed by premedication with atropine, followed by general
anesthesia (e.g., methohexital) and administration of a muscle relaxant
(typically succinylcholine). A generalized seizure is then induced by passing
a current of electricity across the brain (either bilateral or unilateral); the
seizure should last between 30 and 60 seconds, and no longer than
90 seconds.
n 6–12 treatments are administered over a 2- to 3-week period, but significant
improvement is sometimes noted after the first several treatments. Some
MOOD DISORDERS
WARDS TIP
MAOIs were considered particularly useful in the treatment of
“atypical” depression; however,
SSRIs remain first-line treatment
for MDEs with atypical features.
WARDS
QUESTION
Q: What is the most effective antidepressant medication and how
quickly does it work?
A: All antidepressant medications
are equally effective but differ in
side-effect profiles. Medications
take 4–6 weeks to reach peak
efficacy.
WARDS
QUESTION
Q: What are the hallmark symptoms of serotonin syndrome?
A: Autonomic instability, hyperthermia, hyperreflexia (including
myoclonus), and seizures. Coma or
death may result.
40
MOOD DISORDERS
WARDS TIP
Adjunctive treatment is usually
performed after multiple first-line
treatment failures.
SPECIFIERS FOR DEPRESSIVE DISORDERS
KEY FACT
The postpartum period conveys
an elevated risk of depression in
women.
WARDS TIP
Triad for seasonal affective
disorder:
• Irritability
• Carbohydrate craving
• Hypersomnia
BEREAVEMENT
KEY FACT
Bereavement is NOT a DSM-5
­diagnosis—if a patient meets
­criteria for MDD following the
loss of a loved one, the diagnosis would be major depressive
disorder.
BIPOLAR I DISORDER
patients require weekly or monthly maintenance ECT, though there is
limited data on the efficacy of this.
n Retrograde and anterograde amnesia are common side effects, which usually
resolve within 6 months.
n Other common but transient side effects: headache, nausea, muscle soreness.
■ Melancholic features: Present in approximately 25–30% of patients with
a MDE and more likely in severely ill inpatients, including those with
psychotic features. Characterized by anhedonia, early morning awakenings,
depression worse in the morning, psychomotor disturbance, excessive
guilt, and anorexia. For example, you would list the diagnosis as MDD with
melancholic features.
■ Atypical features: Characterized by hypersomnia, hyperphagia, reactive
mood, leaden paralysis, and hypersensitivity to interpersonal rejection.
■ Mixed features: Manic/hypomanic symptoms present during the majority
of days during a MDE: elevated mood, grandiosity, talkativeness/pressured
speech, flight of ideas/racing thoughts, increased energy/goal-directed
activity, excessive involvement in dangerous activities, and decreased need
for sleep.
■ Catatonia: Features include catalepsy (immobility), purposeless motor
activity, extreme negativism (resistance to instructions), staring, mutism,
bizarre postures, and echolalia. Treatment is lorazepam (Ativan) though
catatonia is especially responsive to ECT. (May also be applied to bipolar
disorder.)
■ Psychotic features: Characterized by the presence of delusions and/or
hallucinations. Present in 24–53% of older, hospitalized patients with MDD.
■ Anxious distress: Defined by feeling keyed up/tense, restless, difficulty
concentrating, fears of something bad happening, and feelings of loss of
control.
■ Peripartum onset: Onset of MDD symptoms occurs during pregnancy or 4
weeks following delivery.
■ Seasonal pattern: Temporal relationship between the onset of a MDE and
particular time of the year (most commonly the winter but may occur in any
season). Patients with fall-onset SAD (seasonal affective disorder or “winter
depression”) often respond to light therapy (a 10,000 lux white light for 30
minutes in the early morning).
Bereavement, also known as simple grief, is a normal reaction to a major loss,
usually of a loved one, and it is not a mental illness. While symptoms are usually
self-limited and only last for several months, if an individual meets criteria for a
depressive episode, they would be diagnosed with MDD. Normal bereavement
should not include gross psychotic symptoms, disorganization, or active suicidality.
Bipolar I disorder involves episodes of mania and of major depression; however, episodes of major depression are not required for the diagnosis. It is also
known as manic-depression.
Diagnosis and DSM-5 Criteria
The only requirement for this diagnosis is the occurrence of a manic episode
(5% of patients experience only manic episodes). Between manic episodes,
there may be interspersed euthymia, MDEs, or hypomanic episodes, but none
of these are required for the diagnosis. There is usually a return to baseline
functioning in between mood episodes.
Epidemiology
■ Lifetime prevalence: 1–2%.
■ Women and men are equally affected.
■ No ethnic differences seen; however, high-income countries have twice the
rate of low-income countries (1.4% versus 0.7%).
■ Onset usually before age 30, mean age of first mood episode is 18.
■ Frequently misdiagnosed as unipolar depression and thereby inappropriately
or inadequately treated.
Etiology
■ Biological, environmental, psychosocial, and genetic factors are all
important.
■ First-degree relatives of patients with bipolar disorder are 10 times more
likely to develop the illness.
■ Concordance rates for monozygotic twins are 40–70%, and rates for
dizygotic twins range from 5% to 25%.
■ Bipolar I has the highest genetic link of all major psychiatric disorders.
Course and Prognosis
■ Untreated manic episodes generally last several months.
■ The course is usually chronic with relapses; as the disease progresses,
episodes may occur more frequently.
■ Ninety percent of individuals after one manic episode will have a repeat
mood episode within 5 years.
■ Bipolar disorder has a poorer prognosis than MDD: treatment refusal
frequently occurs in patients with mania who enjoy their increased creativity
and energy, and lack insight into the dangerousness of the illness.
■ Maintenance treatment with mood stabilizing medications between episodes
helps to ↓ the risk of relapse.
■ 25–50% of people with bipolar disorder attempt suicide, and 10–15% die by
suicide.
Treatment
■ Pharmacotherapy:
●Lithium remains the gold standard as a mood stabilizer; 50–70% treated
with lithium show partial reduction of mania. The mechanism is unclear,
but long-term use reduces suicide risk. Acute overdose can be fatal due
to its narrow therapeutic index.
●The anticonvulsants carbamazepine and valproic acid are also mood
stabilizers. They are particularly useful for rapid cycling bipolar disorder
and those with mixed features.
●Atypical antipsychotics (e.g., risperidone, olanzapine, quetiapine,
ziprasidone) are effective as both monotherapy and adjunct therapy for
acute mania. In fact, many patients (especially with severe mania and/
MOOD DISORDERS
WARDS
QUESTION
Q: What is the most effective treatment for major depression with
psychotic features?
A: Combination of an antidepressant and antipsychotic, or ECT.
WARDS
QUESTION
Q: How is bipolar I disorder different from major depressive disorder?
A: Bipolar I disorder requires a
manic episode.
WARDS
QUESTION
Q: What is the first-line treatment
for bipolar disorder?
A: Lithium, valproic acid, and
­carbamazepine, or secondgeneration antipsychotics.
KEY FACT
Side effects of lithium include:
• Weight gain
• Tremor
• Gastrointestinal disturbances
• Fatigue
• Cardiac arrhythmias
• Seizures
• Goiter/Hypothyroidism
• Leukocytosis (benign)
• Coma (in toxic doses)
• Polyuria (nephrogenic diabetes
insipidus)
• Polydipsia
• Alopecia
• Metallic taste
Note: Lithium’s toxidrome has a
similar presentation though it is
more severe.
42
MOOD DISORDERS
WARDS TIP
The following mood stabilizers
require monitoring of blood
concentrations to guide dose adjustments. The therapeutic range
is simple to remember with the 8
and 12 rule:
■ ECT:
Lithium: 0.8–1.2 mEq/L
Carbamazapine: 8–12 mcg/mL
Valproic acid: 80–120 mcg/mL
BIPOLAR II DISORDER
KEY FACT
ECT is the best treatment for a
pregnant woman who is having a
manic episode. It provides a good
alternative to antipsychotics and
can be used with relative safety in
all trimesters.
Epidemiology
■ May be slightly more common in women.
■ Onset usually before age 30.
KEY FACT
■ No ethnic differences seen.
A patient with a history of postpartum mania has a high risk of
relapse with future deliveries and
should be treated with mood
stabilizing agents as prophylaxis.
However, some of these medications may be contraindicated in
breastfeeding.
Etiology
Same as bipolar I disorder (see above).
KEY FACT
SPECIFIERS FOR BIPOLAR DISORDERS
Rapid cycling is defined by the
occurrence of four or more mood
episodes (major depressive, hypomanic, or manic) in 1 year.
or with psychotic features) are treated with a combination of a mood
stabilizer and antipsychotic; studies have shown a greater and faster
response with combination therapy.
●Antidepressants are discouraged as monotherapy due to concerns of
activating mania or hypomania. They are occasionally used to treat
depressive episodes when patients concurrently take mood stabilizers.
■ Psychotherapy: Supportive psychotherapy, family therapy, group therapy
(may prolong remission once the acute manic episode has been controlled).
●Works quickly in treatment of manic episodes.
●Some patients require more treatments (up to 20) than for depression.
●Especially effective for refractory or life-threatening acute mania or
depression.
●Like lithium, ECT reduces suicide risk.
Alternatively thought of as recurrent MDEs with hypomania.
Diagnosis and DSM-5 Criteria
History of one or more MDEs and at least one hypomanic episode. Remember:
If there has been a full manic episode, even in the past, or if the patient ever has
a history of psychosis, then the diagnosis is bipolar I, not bipolar II disorder.
■ Prevalence is unclear, with some studies showing greater and others less
prevalence than bipolar I.
■ Frequently misdiagnosed as unipolar depression and thereby inappropriately
treated.
Course and Prognosis
Tends to be chronic, requiring long-term treatment. Likely better prognosis
than bipolar I given the lack of overt manic episodes.
Treatment
Fewer studies focus on the treatment for bipolar II. Currently, treatment is the
same as bipolar I disorder (see above).
■ Anxious distress: Defined by feeling keyed up/tense, restless, difficulty
concentrating, fears of something bad happening, and feelings of loss of
control.
■ Mixed features: Depressive symptoms present during the majority of
days during mania/hypomania: dysphoria/depressed mood, anhedonia,
psychomotor retardation, fatigue/loss of energy, feelings of worthlessness or
inappropriate guilt, thoughts of death or suicidal ideation.
■ Rapid cycling: At least four mood episodes (manic, hypomanic, depressed)
within 12 months.
■ Melancholic features (during depressed episode): Characterized by
anhedonia, early morning awakenings, depression worse in the morning,
psychomotor disturbance, excessive guilt, and anorexia.
■ Atypical features (during depressed episode): Characterized by hypersomnia,
hyperphagia, reactive mood, leaden paralysis, and hypersensitivity to
interpersonal rejection.
■ Psychotic features: Characterized by the presence of delusions and/or
hallucinations.
■ Catatonia: Catalepsy, purposeless motor activity, extreme negativism or
mutism, bizarre postures, and echolalia. Especially responsive to ECT.
■ Peripartum onset: Onset of manic or hypomanic symptoms occurs during
pregnancy or 4 weeks following delivery.
■ Seasonal pattern: Temporal relationship between onset of mania/
hypomania and particular time of the year.
PERSISTENT DEPRESSIVE DISORDER (DYSTHYMIA)
Patients with persistent depressive disorder (dysthymia) have chronic depression most of the time, and they may have discrete MDEs.
Diagnosis and DSM-5 Criteria
Depressed mood for the majority of time most days for at least 2 years (in
children or adolescents for at least 1 year).
At least two of the following:
●Poor concentration or difficulty making decisions.
●Feelings of hopelessness.
●Poor appetite or overeating.
●Insomnia or hypersomnia.
l Low energy or fatigue.
l Low self-esteem.
During the 2-year period:
●The person has not been without the above symptoms for >2 months at
a time.
●May have MDE(s) or meet criteria for major depression continuously.
●The patient must never have had a manic or hypomanic episode (this
would make the diagnosis bipolar disorder or cyclothymic disorder,
respectively).
Epidemiology
■ Twelve-month prevalence: 2%.
■ More common in women.
■ Onset often in childhood, adolescence, and early adulthood.
Course and Prognosis
Early and insidious onset, with a chronic course. Depressive symptoms much
less likely to resolve than in MDD.
MOOD DISORDERS
WARDS TIP
Bipolar I disorder may have
psychotic features (delusions or
hallucinations); these can occur
during major depressive or manic
episodes, but not in between.
­Remember to always include
bipolar disorder in the differential
diagnoses of a psychotic patient.
WARDS TIP
Schizoaffective disorder is characterized by psychosis with mood
symptoms that are only present
during psychotic episodes, while
major depression with psychotic
features is characterized by depression with psychosis only during
depressive episodes. Remember
this by looking at the word order:
schizoaffective is psychosis as the
main symptom, and depression
with psychotic features has depression as the main symptom.
WARDS TIP
Persistent Depressive Disorder
(DD) = 2 Ds
2 years of depression
2 listed criteria
Never asymptomatic for >2 months
44
MOOD DISORDERS
Treatment
WARDS TIP
Symptoms of persistent depressive disorder (dysthymia)—two or
more of:
CHASES
Poor Concentration or difficulty
making decisions
Feelings of Hopelessness
Poor Appetite or overeating
InSomnia or hypersomnia
Low Energy or fatigue
Low Self-esteem
CYCLOTHYMIC DISORDER
Diagnosis and DSM-5 Criteria
WARDS
QUESTION
Q: What is the difference between
bipolar I and bipolar II disorder?
A: Bipolar I disorder requires
at least one manic episode but
not necessarily a MDE, whereas
bipolar II disorder requires both a
hypomanic episode plus at least
one MDE.
Epidemiology
■ Lifetime prevalence: <1%.
■ Onset usually between ages 15 and 25.
■ Occurs equally in males and females.
PREMENSTRUAL DYSPHORIC DISORDER
Diagnosis and DSM-5 Criteria
■ Combination treatment with psychotherapy and pharmacotherapy is more
efficacious than either alone.
■ Cognitive therapy, interpersonal therapy, and insight-oriented
psychotherapy are the most effective.
■ Antidepressants found to be beneficial include SSRIs, SNRIs, novel
antidepressants (e.g., bupropion, mirtazapine), TCAs, and MAOIs.
Alternating periods of hypomania and periods with mild-to-moderate depressive symptoms.
■ Numerous periods with hypomanic symptoms (but not a full hypomanic
episode) and periods with depressive symptoms (but not full MDE) for at
least 2 years.
■ The person must never have been symptom free for >2 months during those
2 years.
■ No history of MDE, hypomania, or manic episode.
■ May coexist with borderline personality disorder.
Course and Prognosis
Chronic course; approximately one-third of patients eventually develop bipolar
I/II disorder.
Treatment
Antimanic agents (mood stabilizers or second-generation antipsychotics) are
used to treat bipolar disorder (see above).
Mood lability, irritability, dysphoria, and anxiety that occur repeatedly during
the premenstrual phase of the cycle.
■ In most menstrual cycles, at least five symptoms (below) are present in the
final week before menses, improve within a few days after menses, and are
minimal/absent in the week postmenses (should be confirmed by daily
ratings for at least two menstrual cycles).
■ At least one of the following symptoms is present: affective lability,
irritability/anger, depressed mood, anxiety/tension.
■ At least one of the following symptoms is present (for total of at least five
symptoms when combined with above): anhedonia, problems concentrating,
anergia, appetite changes/food cravings, hypersomnia/insomnia, feeling
overwhelmed/out of control, physical symptoms (e.g., breast tenderness/
swelling, joint/muscle pain, bloating, weight gain).
■ Symptoms cause clinically significant distress or impairment in functioning.
■ Symptoms are not only exacerbation of another disorder (e.g., MDD, panic
disorder, persistent depressive disorder).
■ Symptoms are not due to a substance (medication or drug) or another
medical condition.
Epidemiology/Etiology
■ Prevalence: 1.8%.
■ Onset can occur at any time after menarche.
■ Has been observed worldwide.
■ Environmental and genetic factors contribute.
Course and Prognosis
Symptoms may worsen prior to menopause but cease after menopause.
Treatment
SSRIs are first-line treatment, either as daily therapy or luteal phase-only treatment (starting on cycle day 14 and stopping upon menses or shortly thereafter). Oral contraceptives may reduce symptoms. Gonadotropin-releasing hormone (GnRH) agonists have also been used, and, in rare, severe cases, bilateral
oophorectomy with hysterectomy will resolve symptoms.
DISRUPTIVE MOOD DYSREGULATION DISORDER (DMDD)
Chronic, severe, persistent irritability occurring in childhood and adolescence.
Diagnosis and DSM-5 Criteria
■ Severe recurrent verbal and/or physical outbursts out of proportion to
situation.
■ Outbursts ≥3 per week and inconsistent with developmental level.
■ Mood between outbursts is persistently angry/irritable most of the day
nearly every day, and is observed by others.
■ Symptoms for at least 1 year, and no more than 3 months without
symptoms.
■ Symptoms in at least two settings (e.g., home, school, peers).
■ Symptoms must have started before age 10, but diagnosis can be made from
ages 6 to 18.
■ No episodes meeting full criteria for manic/hypomanic episode lasting
longer than 1 day.
■ Behaviors do not occur during MDD and not better explained by another
mental disorder (this disorder cannot coexist with oppositional defiant
disorder, intermittent explosive disorder, or bipolar disorder).
■ Symptoms not due to a substance (medication or drug) or another medical
condition.
Epidemiology/Etiology
■ Prevalence is unclear as this is a newer diagnosis.
■ 6–12-month prevalence rates of chronic/severe persistent irritability in
children: 2–5%.
■ Rates likely greater in males than females.
MOOD DISORDERS
46
MOOD DISORDERS
Course and Prognosis
Treatment
OTHER DISORDERS OF MOOD IN DSM-5
■ Unspecified depressive/bipolar disorder.
■ By definition, DMDD must occur prior to 10 years of age.
■ Approximately 50% of those with DMDD continue to meet criteria after
1 year.
■ Rates of conversion to bipolar disorder are very low.
■ Very high rates of comorbidity, especially with ADHD, MDD, and substance
use disorders.
■ Given the newer nature of this diagnosis, there are no consensus
evidenced-based treatments. Psychotherapy (such as parent management
training) for the patient and family is generally first line.
■ Medications should be used to treat comorbid disorders.
■ Stimulants, SSRIs, mood stabilizers, and second-generation antipsychotics
have all been used to treat the primary symptoms of DMDD.
■ Mood disorder due to another medical condition.
■ Substance/Medication-induced mood disorder.
■ Specified depressive/bipolar disorder (meets criteria for MDE or bipolar
except shorter duration or too few symptoms)

08 - Chapter 5 Anxiety, Obsessive Compulsive, Trauma, a

01 - Chapter 5 Anxiety, Obsessive Compulsive, Trau
Chapter 5 Anxiety, Obsessive-Compulsive, Trauma, and Stressor-Related Disorders
Anxiety Disorders......................................................................................................................48
Treatment Guidelines................................................................................................................49
Pharmacotherapy.....................................................................................................................49
Psychotherapy..........................................................................................................................49
Panic Attacks.......................................................................................................................49
Panic Disorder......................................................................................................................50
Agoraphobia........................................................................................................................51
Specific Phobias...................................................................................................................51
Social Anxiety Disorder (Social Phobia)................................................................................52
Selective Mutism.................................................................................................................52
Separation Anxiety Disorder................................................................................................53
Generalized Anxiety Disorder (GAD).....................................................................................54
Obsessive-Compulsive and Related Disorders...........................................................................55
Obsessive-Compulsive Disorder (OCD).................................................................................55
Body Dysmorphic Disorder...................................................................................................56
Hoarding Disorder...............................................................................................................56
Trichotillomania (Hair-Pulling Disorder)..............................................................................57
Excoriation (Skin-Picking) Disorder......................................................................................58
Posttraumatic Stress Disorder (PTSD) and Acute Stress Disorder..........................................58
Adjustment Disorders..........................................................................................................60
STRESSOR-RELATED DISORDERS
A N X I E T Y, OBSES S IV E - CO M P U L S I V E, T R AU MA, A ND
CHAPTER 5
48
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
Anxiety Disorders
WARDS TIP
Assess for psychopathology if an
individual’s symptoms are causing
Social and/or Occupational Dysfunction (use mnemonic SOD).
WARDS TIP
Late-onset anxiety symptoms
without a prior history or family
psychiatric history should increase
suspicion of anxiety caused by
another medical condition or
substance use.
TABLE 5-1. Signs and Symptoms of Anxiety
WARDS
QUESTION
Constitutional
Fatigue, diaphoresis, shivering
Q: In a patient with comorbid
anxiety and depression, would
treatment with a benzodiazepine
be a first-line treatment?
A: No. Avoid use of benzodiazepines because they may worsen
depression.
TABLE 5-3. Medical Conditions That Cause Anxiety
Anxiety disorders are characterized by excessive or inappropriate fear or anxiety. Fear is manifested by a transient increase in sympathetic activity (“fight
or flight” physiologic response, thoughts, feelings, behaviors) in a situation
perceived as dangerous or threatening. By contrast, anxiety involves apprehension regarding the possibility of a negative future event. The criteria for most
anxiety disorders involve symptoms that cause clinically significant distress
or impairment in social and/or occupational functioning (see Table 5-1).
DSM-5 anxiety disorders include generalized anxiety disorder, panic disorder,
agoraphobia, social anxiety disorder, selective mutism, and specific phobias.
■ Anxiety disorders are caused by a combination of genetic, biological,
environmental, and psychosocial factors.
■ Primary anxiety disorders are diagnosed after determining that symptoms
are NOT due to the physiological effects of a substance, medication (see
Table 5-2), or another medical condition (see Table 5-3).
■ Major neurotransmitter systems implicated: norepinephrine (NE), serotonin
(5-HT), and gamma-aminobutyric acid (GABA).
Cardiac
Chest pain, palpitations, tachycardia, hypertension
Pulmonary
Shortness of breath, hyperventilation
Neurologic/
musculoskeletal
Vertigo, light-headedness, paresthesias, tremors, insomnia, muscle
tension
Gastrointestinal
Abdominal discomfort, anorexia, nausea, emesis, diarrhea,
constipation
TABLE 5-2. Medications and Substances That Cause Anxiety
Alcohol
Intoxication/withdrawal
Sedatives, hypnotics, or anxiolytics
Withdrawal
Cannabis
Intoxication
Hallucinogens (PCP, LSD, MDMA)
Intoxication
Stimulants (amphetamines, cocaine)
Intoxication/withdrawal
Caffeine
Intoxication/withdrawal
Tobacco
Intoxication/withdrawal
Opioids
Withdrawal
LSD, lysergic acid diethylamide; MDMA, 3,4-methylenedioxy methamphetamine; PCP, phencyclidine.
Neurologic
Epilepsy, migraines, brain tumors, multiple sclerosis, Huntington
disease
Endocrine
Hyperthyroidism, hypoglycemia, pheochromocytoma, carcinoid
syndrome
Metabolic
Vitamin B12 deficiency, electrolyte abnormalities, porphyria
Respiratory
Asthma, chronic obstructive pulmonary disease (COPD), hypoxia,
pulmonary embolism (PE), pneumonia, pneumothorax
Cardiovascular
Congestive heart failure (CHF), angina, arrhythmia, myocardial
infarction (MI)
■ Most common form of psychopathology.
■ More frequently seen in women compared to men, approximately 2:1 ratio.
Treatment Guidelines
■ Determine treatment course based on the severity of symptoms.
■ Initiate psychotherapy for mild anxiety.
■ Consider a combination of therapy and medication for moderate to severe
anxiety.
Pharmacotherapy
■ Selective serotonin reuptake inhibitors (SSRIs) (e.g., sertraline) and
serotonin-norepinephrine reuptake inhibitors (SNRIs) (e.g., venlafaxine)
are first-line medications.
■ Benzodiazepines can be used as an adjunctive short-term treatment to
achieve acute reduction of severe anxiety symptoms (e.g., while getting
stabilized on an SSRI), but regular use can result in dependence. Therefore,
minimize the use, duration, and dose, and avoid in patients with a history of
substance use disorders, particularly alcohol.
■ Mechanism of action: Enhance activity of GABA at GABA-A receptor.
■ In patients with comorbid substance use consider nonaddictive anxiolytic
alternatives for PRN use, such as gabapentin and antihistamines with
anxiolytic properties (e.g., diphenhydramine or hydroxyzine).
■ Buspirone is a non-benzodiazepine anxiolytic which has partial agonist
activity at the 5-HT1A receptor. Due to minimal efficacy as monotherapy,
buspirone is typically prescribed only as augmentation.
■ Beta-blockers (e.g., propranolol) may be used to help control autonomic
symptoms (e.g., palpitations, tachycardia, sweating) of panic attacks or
performance anxiety.
■ Tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors
(MAOIs) may be considered if first-line agents are not effective. Their sideeffect profile, especially cardiovascular effects, makes them less tolerable and
more dangerous.
Psychotherapy
■ Many modalities of psychotherapy are helpful for patients suffering from
anxiety disorders.
●Cognitive-behavioral therapy (CBT) has proven effective for anxiety disorders. CBT examines the relationship between anxiety-driven
­cognitions (thoughts), emotions, and behavior.
●Psychodynamic psychotherapy facilitates insight into the development of anxiety symptoms, leading to more adaptive coping styles and
­subsequent improvement over time.
PANIC ATTACKS
A panic attack is a fear response involving a sudden onset of intense anxiety
which may either be triggered or occur spontaneously. Panic attacks peak
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
WARDS TIP
Use benzodiazepines to temporarily bridge patients until long-term
medication becomes effective.
WARDS
QUESTION
Q: How long does it take for SSRIs
to typically become fully effective?
A: About 4–6 weeks.
WARDS TIP
The goal of medication treatment
is to achieve symptomatic relief
and continue treatment for at least
6 months before attempting to
titrate off medications.
WARDS TIP
Medications can reduce symptoms
sufficiently so that a patient can
participate and learn the skills
offered in therapy. Therapy can additionally be used as maintenance
treatment to prevent relapse.
50
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
KEY FACT
Symptoms of panic attacks
Da PANICS
Dizziness, disconnectedness,
derealization (unreality), depersonalization (detached from self)
Palpitations, paresthesias
Abdominal distress
Numbness, nausea
Intense fear of dying, losing
­control or “going crazy”
Chills, chest pain
Sweating, shaking, shortness of
breath
PANIC DISORDER
Diagnosis and DSM-5 Criteria
WARDS TIP
Use the Bs to Block the Ps:
Beta-Blockers for Panic attacks and
Performance anxiety.
Etiology
WARDS TIP
Epidemiology
Smoking is a risk factor for panic
attacks.
■ Lifetime prevalence: 4%.
■ Median age of onset: 20–24 years old.
WARDS
QUESTION
Course and Prognosis
Q: When a patient presents with
the new onset of a panic attack,
what potentially life-threatening
medical conditions should be
ruled out?
A: Heart attack, cardiac arrhythmia, electrolyte dysfunction,
hypoglycemia, thyrotoxicosis, and
pulmonary embolism.
within minutes and usually resolve within half an hour. Patients may continue
to feel anxious for hours afterwards and believe they are experiencing a prolonged panic attack. Although classically associated with panic disorder, panic
attacks can also be experienced with other psychiatric disorders and medical
conditions.
Panic disorder is diagnosed in patients who experience spontaneous, recurrent
panic attacks and who are fearful of reoccurring attacks. These attacks most
often occur suddenly, out of the blue, although they may sometimes have a clear
trigger. The frequency of attacks ranges from multiple times per day to a few
times per month. The keystone feature of panic disorder is that patients develop debilitating anticipatory anxiety about having future attacks—“fear of the
fear.”
■ Recurrent, unexpected panic attacks without an identifiable trigger.
■ One or more of panic attacks followed by ≥1 month of continuous worry
about experiencing subsequent attacks or their consequences, and/or a
maladaptive change in behaviors (e.g., avoidance of possible triggers).
■ Not due to the physiological effects of a substance, another medical or
neurological condition (e.g., traumatic brain injury), or another mental
disorder.
■ Genetic factors: Greater risk of panic disorder if a first-degree relative is
affected.
■ Psychosocial factors: Increased incidence of stressors (especially loss) prior
to onset of disorder; history of childhood physical or sexual abuse.
■ Higher rates in woman compared to men, approximately 2:1.
■ Panic disorder has a chronic course with waxing and waning symptoms.
■ Relapses are common with discontinuation of medication.
■ Only a minority of patients have full remission of symptoms.
■ Up to 65% of patients with panic disorder also have major depression.
■ Additional comorbid syndromes include other anxiety disorders
(e.g., agoraphobia), bipolar disorder, and alcohol use disorder.
Treatment
Combination of CBT and Pharmacotherapy = most effective.
■ First-line: SSRIs (e.g., sertraline, citalopram, escitalopram).
■ SNRIs (e.g., venlafaxine, desvenlafaxine, duloxetine) are also efficacious.
■ If the above options are not effective, can consider TCAs
(e.g., clomipramine, imipramine).
■ Can use benzodiazepines (e.g., clonazepam, lorazepam) as scheduled or
PRN, until other medications reach therapeutic efficacy.
AGORAPHOBIA
Agoraphobia is an intense fear of being in public places where escape or obtaining help may be difficult. It often develops with panic disorder. The course
of the disorder is usually chronic. Avoidance behaviors may become as extreme
as complete confinement to the home.
Diagnosis and DSM-5 Criteria
■ Intense fear/anxiety about at least two situations due to concerns of
difficulty escaping or obtaining help in case of panic or other humiliating
symptoms:
●Outside of the home alone.
●Open spaces (e.g., bridges).
●Enclosed places (e.g., stores).
●Public transportation (e.g., trains).
●Crowds/lines.
■ The triggering situations cause fear/anxiety that is out of proportion to the
potential danger posed, leading to endurance of intense anxiety, avoidance,
or need for a companion. This holds true even if the patient suffers from
another medical condition such as inflammatory bowel disease (IBS), which
may lead to embarrassing public scenarios.
■ Symptoms cause significant social or occupational dysfunction.
■ Symptoms last ≥6 months.
■ Symptoms not better explained by another mental disorder.
Etiology
■ Strong genetic factor: Heritability about 60%.
■ Psychosocial factor: Onset frequently follows a traumatic event.
Course/Prognosis
■ More than 50% of patients experience a panic attack prior to developing
agoraphobia.
■ Onset is usually before age 35.
■ Course is persistent and chronic, with rare full remission.
■ Comorbid diagnoses include other anxiety disorders, depressive disorders,
and substance use disorders.
Treatment
■ CBT and SSRIs
SPECIFIC PHOBIAS
A phobia is defined as an irrational fear that leads to endurance of the anxiety and/or avoidance of the feared object or situation. A specific phobia is an
intense fear of a specific object or situation (i.e., the phobic stimulus).
Diagnosis and DSM-5 Criteria
■ Persistent, excessive fear elicited by a specific situation or object which is out
of proportion to any actual danger/threat.
■ Exposure to the situation triggers an immediate fear response.
■ Situation or object is avoided when possible or tolerated with intense anxiety.
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
WARDS TIP
A classic panic disorder case
involves a woman who repeatedly
visits the ER because she is afraid
of dying when she experiences
episodes of palpitations, diaphoresis, and shortness of breath.
The patient has no prior medical
history and the medical workup is
negative.
WARDS TIP
Carefully screen patients with
panic attacks for suicidality. They
are at an increased risk for suicide
attempts.
WARDS TIP
Start SSRIs or SNRIs at low doses
and ↑ slowly because side effects
may initially worsen anxiety,
­especially in panic disorder.
KEY FACT
Characteristic situations avoided
in agoraphobia include bridges,
crowds, buses, trains, or any open
areas outside the home.
KEY FACT
Common Domains of Social
­Anxiety Disorder (Social Phobia):
• Speaking in public.
• Eating in public.
• Using public restrooms.
52
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
KEY FACT
■ Duration ≥6 months.
Common Specific Phobias:
Animal—spiders, insects, dogs,
snakes, and mice.
Natural environment—heights,
storms, and water.
Situational—elevators, airplanes,
buses, and enclosed spaces.
Blood-injection-injury—needles,
injections, blood, injuries, and
invasive medical procedures.
Epidemiology
Treatment
■ Treatment of choice: CBT with exposure.
WARDS TIP
Patients with blood-injury- injection-specific phobia (fear of
needles, etc.) may experience
­bradycardia and hypotension
­leading to vasovagal syncope.
KEY FACT
Substance use and depressive
disorders frequently co-occur
with phobias.
Epidemiology
WARDS
QUESTION
Treatment
■ Treatment of choice: CBT.
Q: What medication often successfully treats performance anxiety?
A: Beta-blockers.
SELECTIVE MUTISM
■ Symptoms cause significant social or occupational dysfunction.
■ Not due to the physiological effects of a substance, another medical or
neurological condition (e.g., traumatic brain injury), or another mental
disorder.
■ Phobias are the most common psychiatric disorder in women and second
most common in men (substance-related is first).
■ Lifetime prevalence of specific phobia: >10%.
■ Mean age of onset for specific phobia is 10 years.
■ Specific phobia rates are higher in women compared to men (2:1) but vary
depending on the type of stimulus.
SOCIAL ANXIETY DISORDER (SOCIAL PHOBIA)
Social anxiety disorder (social phobia) is the fear of scrutiny by others or fear
of acting in a humiliating or embarrassing way. The phobia may develop in
the wake of negative or traumatic encounters with the stimulus. Social situations causing significant anxiety may be avoided altogether, resulting in social
and academic/occupational impairment.
The diagnostic criteria for social anxiety disorder (social phobia) are similar
to specific phobia except the phobic stimulus is related to social scrutiny and
negative evaluation. The patients fear embarrassment, humiliation, and rejection. This fear may be limited to performance or public speaking, which may
be routinely encountered in the patient’s occupation or academic pursuit.
■ Median age of onset for social anxiety disorder is 13 years.
■ Social anxiety disorder occurs equally across genders.
■ First-line medication, if needed: SSRIs (e.g., sertraline, fluoxetine) or SNRIs
(e.g., venlafaxine) for debilitating symptoms.
■ Benzodiazepines (e.g., clonazepam, lorazepam) can be used as scheduled or
PRN.
■ Beta-blockers (e.g., atenolol, propranolol) PRN for performance anxiety/
public speaking.
Selective mutism is a rare condition characterized by a failure to speak in
specific situations for at least 1 month, despite the intact ability to comprehend and use language. Symptom onset typically starts during childhood. The
majority of these patients suffer from anxiety, particularly social anxiety, as the
mutism manifests in social settings. The patients may remain completely silent
or just whisper. They may use nonverbal means of communication, such as
writing or gesturing.
Diagnosis and DSM-5 Criteria
■ Consistent failure to speak in select social situations (e.g., school) despite
speech ability in other scenarios.
■ Mutism is not due to a language difficulty or a communication disorder.
■ Symptoms cause significant impairment in academic, occupational, or social
functioning.
■ Symptoms last >1 month (extending beyond first month of school).
Treatment
■ Psychotherapy: CBT, family therapy.
■ Medications: SSRIs (especially with comorbid social anxiety disorder).
SEPARATION ANXIETY DISORDER
As part of normal human development, infants become distressed when they
are separated from their primary caregiver. Stranger anxiety begins around
6 months and peaks around 9 months, while separation anxiety typically
emerges by 1 year of age and peaks by 18 months. However, when the anxiety
due to separation becomes extreme or developmentally inappropriate, it is
considered pathologic. Separation anxiety disorder may be preceded by a
stressful life event.
Diagnosis and DSM-5 Criteria
Excessive and developmentally inappropriate fear/anxiety regarding separation from attachment figures, with at least three of the following:
■ Separation from attachment figures leads to extreme distress.
■ Excessive worry about loss of or harm to attachment figures.
■ Excessive worry about experiencing an event that leads to separation from
attachment figures.
■ Reluctance to leave home or attend school or work.
■ Reluctance to be alone.
■ Reluctance to sleep alone or away from home.
■ Complaints of physical symptoms when separated from major attachment
figures.
■ Nightmares of separation and refusal to sleep without proximity to
attachment figure.
■ Lasts for ≥4 weeks in children/adolescents and ≥6 months in adults.
■ Symptoms cause significant social, academic, or occupational dysfunction.
■ Symptoms not due to another mental disorder.
Treatment
■ Psychotherapy: CBT, family therapy.
■ Medications: SSRIs can be effective as an adjunct to therapy.
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
WARDS TIP
Separation anxiety may lead to
complaints of somatic symptoms
to avoid school/work.
54
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
WARDS TIP
GAD Mnemonic
Worry WARTS
Wound up, worn-out
Absent-minded
Restless
Tense
Sleepless
GENERALIZED ANXIETY DISORDER (GAD)
WARDS TIP
For patients with anxiety,
­evaluate for caffeine use and
­recommend significant reduction
or ­elimination.
Diagnosis and DSM-5 Criteria
■ Difficulty controlling worry.
WARDS TIP
Exercise can significantly reduce
anxiety.
Epidemiology/Etiology
■ Lifetime prevalence: 5–9%.
WARDS TIP
Course/Prognosis
■ Symptoms of worry begin in childhood.
The worries associated with GAD
are free-floating across various
areas, as opposed to being fixed
on a specific trigger.
■ Median age of onset of GAD: 30 years.
■ Rates of full remission are low.
A 24-year-old law student presents to an outpatient psychiatry clinic with a
chief complaint that she is “so stressed out, worrying about everything.” She
is overwhelmed with her academic workload and upcoming exams. She has
had trouble falling asleep and feels chronically fatigued. The patient also suffers from frequent headaches and muscle tightness in her neck and shoulders.
The patient’s husband describes her as “a worrier. She’s always concerned
about me getting into an accident, her flunking out of school, not finding a
job—the list goes on.”
The patient reports that she has always had some degree of anxiety, but
previously found it motivating. Over the last year since law school began, her
symptoms have become debilitating.
What is the most likely diagnosis?
With the patient’s history of excessive worrying about everything, the most
likely diagnosis is generalized anxiety disorder (GAD). Like many patients
with GAD, she is described as a worrier. She reports typical associated symptoms: insomnia, fatigue, and impaired concentration. Her symptoms have
been present for over 6 months.
What is the next step?
A complete physical exam and medical workup should be performed to rule
out other medical conditions or substance use contributing to or causing her
anxiety symptoms.
What are treatment options?
Treatment options for GAD include psychotherapy (usually CBT) and pharmacotherapy (typically SSRIs). A combination of both modalities may achieve
better remission rates than either treatment alone.
Patients with GAD have persistent, excessive anxiety about many aspects of
their daily lives. Commonly associated physical symptoms include fatigue and
muscle tension, which often lead to an initial presentation to primary care.
■ Excessive anxiety/worry about various daily events/activities ≥6 months.
■ Associated ≥3 symptoms: restlessness, fatigue, impaired concentration,
irritability, muscle tension, insomnia.
■ Not due to the physiological effects of a substance, another medical or
neurological condition (e.g., traumatic brain injury), or another mental disorder.
■ Symptoms cause significant social or occupational dysfunction.
■ GAD rates higher in women compared to men (2:1).
■ One-third of risk for developing GAD is genetic.
■ Course is chronic, with waxing and waning symptoms.
■ GAD is highly comorbid with other anxiety and depressive disorders.
Treatment
The most effective treatment approach combines psychotherapy and
­pharmacotherapy:
■ CBT.
■ SSRIs (e.g., sertraline, citalopram) or SNRIs (e.g., venlafaxine, duloxetine).
■ Can also consider a short-term course of benzodiazepines or augmentation
with buspirone.
■ Much less commonly used medications are TCAs and MAOIs.
Obsessive-Compulsive and Related Disorders
OBSESSIVE-COMPULSIVE DISORDER (OCD)
OCD is characterized by obsessions and/or compulsions that are time-consuming, distressing, and impairing. Obsessions are recurrent, intrusive, and undesired thoughts that increase anxiety. Patients may attempt to relieve the anxiety
by performing compulsions, which are repetitive behaviors or mental rituals.
Anxiety may increase when a patient resists acting out a ­compulsion. Patients
with OCD have varying degrees of insight.
Diagnosis and DSM-5 Criteria
■ Experiencing obsessions and/or compulsions that are time-consuming (e.g.,
1 hr/day) and cause significant distress or dysfunction.
●Obsessions: Recurrent, intrusive, anxiety-provoking thoughts, images, or
urges that the patient attempts to suppress, ignore, or neutralize by some
other thought or action (i.e., by performing a compulsion).
●Compulsions: Repetitive behaviors or mental acts the patient feels driven
to perform in response to an obsession, or a rule aimed at stress reduction
or disaster prevention. The behaviors are excessive and/or not realistically
connected to what they are meant to prevent.
■ Not due to the physiological effects of a substance, another medical or
neurological condition (e.g., traumatic brain injury), or another mental
disorder.
Epidemiology
■ Lifetime prevalence: 2–3%.
■ No gender difference in prevalence overall.
Etiology
■ Significant genetic component: Higher rates of OCD in first-degree relatives
and monozygotic twins than in the general population. Higher rate of OCD
in first-degree relatives with Tourette’s disorder.
Course/Prognosis
■ Chronic, with waxing and waning symptoms.
■ Less than 20% remission rate without treatment.
■ Suicidal ideation in 50% and suicide attempts in 25% of patients with OCD.
■ High comorbidity with other anxiety disorders, depressive or bipolar
disorder, obsessive-compulsive personality disorder, and tic disorder.
Treatment
Utilize a combination of psychopharmacology and CBT.
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
KEY FACT
Compulsions can often take the
form of repeated checking or
counting.
KEY FACT
Patients with OCD often initially
seek help from primary care and
other nonpsychiatric providers
for help with the consequences
of compulsions (e.g., excessive
washing).
KEY FACT
The triad of “uncontrollable
urges”—OCD, ADHD, and tic
disorder—are usually first seen in
children or adolescents.
KEY FACTS
Common Patterns of Obsessions
and Compulsions
Obsessions
Compulsions
Contamination
Cleaning or avoidance of contaminant
Doubt or
harm
Checking multiple
times to avoid potential danger
Symmetry
Ordering or counting
Intrusive,
taboo
thoughts
With or without
related compulsion
56
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
KEY FACT
Differentiating OCD and obsessive-compulsive personality
disorder (OCPD):
• Individuals with OCPD are
­obsessed with details, control,
and perfectionism without
­experiencing unwanted preoccupations or compulsions.
• OCD patients are distressed by
their symptoms (ego-dystonic).
BODY DYSMORPHIC DISORDER
Diagnosis and DSM-5 Criteria
Epidemiology
■ Mean age of onset: 15 years.
Course/Prognosis
■ High rate of suicidal ideation and attempts.
Treatment
HOARDING DISORDER
Diagnosis and DSM-5 Criteria
CBT focuses on exposure and response prevention: prolonged, graded exposure
to ritual-eliciting stimulus and prevention of the relieving compulsion.
■ First-line medication: SSRIs (e.g., sertraline, fluoxetine), typically at higher doses.
■ Second-line agents: SNRIs (e.g., venlafaxine) or the most serotonin selective
TCA, clomipramine.
■ Can augment with atypical antipsychotics in severe cases.
■ In debilitating, treatment-resistant cases, consider psychosurgery
(cingulotomy) or electroconvulsive therapy (ECT).
■ Patients with body dysmorphic disorder are preoccupied with nonexistent or
minor physical defects that they regard as severe, grotesque, and repulsive.
■ These individuals spend significant time trying to correct perceived flaws
with makeup, dermatological procedures, or plastic surgery.
■ Preoccupation with one or more perceived defects or flaws in physical
appearance that are not observable by or appear slight to others.
■ In response to the appearance concerns, repetitive behaviors (e.g., skin
picking, excessive grooming) or mental acts (e.g., comparing appearance to
others) are performed.
■ Preoccupation causes significant distress or impairment in functioning.
■ Appearance preoccupation is not better accounted for by concerns with
body fat/weight in an eating disorder.
■ Slightly more common in women than men.
■ Prevalence elevated in those with high rates of childhood abuse and neglect.
■ Increased risk in first-degree relatives of patients with OCD.
■ Higher prevalence in dermatologic and cosmetic surgery patients.
■ The onset is usually gradual, beginning in early adolescence. Symptoms tend
to be chronic.
■ Surgical or dermatological procedures are routinely unsuccessful in
satisfying the patient.
■ Comorbidity with major depression, social anxiety disorder (social phobia),
and OCD.
■ SSRIs and/or CBT may reduce the obsessive and compulsive symptoms in
many patients.
■ Persistent difficulty discarding possessions, regardless of value.
■ Difficulty is due to need to save the items and distress associated with
discarding them.
■ Results in accumulation of possessions that congest/clutter living areas and
compromise use.
■ Hoarding causes clinically significant distress or impairment in social,
occupational, or other areas of functioning.
■ Hoarding is not attributable to another medical condition or another mental
disorder.
Epidemiology/Etiology
■ Point prevalence of significant hoarding is 2–6%.
■ Hoarding is three times more prevalent in the elderly population.
■ Onset often preceded by stressful and traumatic events.
■ 50% of individuals with hoarding have at least one hoarding relative.
Course/Prognosis
■ Hoarding behavior begins in early teens and tends to worsen over time.
■ Usually chronic course.
■ 75% of individuals have comorbid mood (MDD) or anxiety disorder (social
anxiety disorder).
■ 20% of individuals have comorbid OCD.
Treatment
■ Very difficult to treat.
■ Specialized CBT for hoarding.
■ SSRIs can be used.
TRICHOTILLOMANIA (HAIR-PULLING DISORDER)
Diagnosis and DSM-5 Criteria
■ Recurrent pulling out of one’s hair, resulting in hair loss.
■ Repeated attempts to decrease or stop hair pulling.
■ Causes significant distress or impairment in daily functioning.
■ Hair pulling or hair loss is not due to another medical condition or
psychiatric disorder.
■ Usually involves the scalp, eyebrows, or eyelashes. May include facial,
axillary, or pubic hair.
Epidemiology/Etiology
■ Lifetime prevalence: 1–2% of the adult population.
■ More common in women than in men (10:1 ratio).
■ Onset usually at puberty and frequently associated with a stressful event.
■ Etiology may involve biological, genetic, and environmental factors.
■ Increased incidence of comorbid OCD, major depressive disorder, and
excoriation (skin-picking) disorder.
■ Course may be chronic with waxing and waning periods. Adult onset is
generally more difficult to treat.
Treatment
■ Recommended: Specialized types of cognitive-behavior therapy (e.g., habit
reversal training).
■ Pharmacologic treatment includes SSRIs, second-generation antipsychotics,
lithium, or N-acetylcysteine (NAC).
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
58
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
EXCORIATION (SKIN-PICKING) DISORDER
Diagnosis and DSM-5 Criteria
■ Recurrent skin picking resulting in lesions.
Epidemiology/Etiology
■ More than 75% of cases are women.
Course/Prognosis
■ Skin picking begins in adolescence.
Treatment
■ SSRIs have shown some benefit.
Trauma and Stressor-Related Disorders
■ Repeated attempts to decrease or stop skin picking.
■ Causes significant distress or impairment in daily functioning.
■ Not due to the physiological effects of a substance, another medical or
neurological condition (e.g., traumatic brain injury), or another mental
disorder.
■ Lifetime prevalence: 1.4% of the adult population.
■ More common in individuals with OCD and first-degree family members.
■ Course is chronic with waxing and waning periods if untreated.
■ Comorbidity with OCD, trichotillomania, and MDD.
■ Specialized types of cognitive-behavior therapy (e.g., habit reversal training).
A 19-year-old freshman is brought to the ER by her college roommate due
to her concerns that she “really needs to get some help—she hasn’t been
herself since a party we went to together.” The freshman has been hypervigilant, tearful, and crying out so loudly in her sleep that she wakes up her
peers. The roommate discloses concern that a traumatic incident occurred at
a party last month. The patient is guarded and reluctant to talk about details.
She reports that since the party, she has experienced intrusive thoughts and
nightmares. The patient is afraid to leave her room, and feels on edge most of
the time.
What is the most likely diagnosis?
The patient has been suffering from symptoms of posttraumatic stress disorder (PTSD) for the last month after a traumatic incident with associated low
mood, avoidance, hypervigilance, intrusive thoughts, and nightmares.
POSTTRAUMATIC STRESS DISORDER (PTSD) AND ACUTE STRESS DISORDER
PTSD is characterized by the development of multiple symptoms after exposure
to one or more traumatic events: intrusive symptoms (e.g., nightmares, flashbacks), avoidance, negative alterations in thoughts and mood, and increased
arousal. The symptoms last for at least a month and may occur immediately
after the trauma or with delayed ­expression.
Acute stress disorder is diagnosed in patients who experience a major traumatic event and suffer from similar symptoms as PTSD (see Table 5-4) but for a
shorter duration. The onset of symptoms occurs within 1 month of the trauma
and symptoms last for less than 1 month.
TABLE 5-4. Posttraumatic Stress Disorder and Acute Stress Disorder
Posttraumatic Stress Disorder
Acute Stress Disorder
Trauma occurred at any time in past
Trauma occurred <1 month ago
Symptoms last >1 month
Symptoms last <1 month
Diagnosis and DSM-5 Criteria
■ Exposure to actual or threatened death, serious injury, or sexual violence by
directly experiencing or witnessing the trauma.
■ Recurrent intrusions of reexperiencing the event via memories, nightmares,
or dissociative reactions (e.g., flashbacks); intense distress at exposure to cues
relating to the trauma; or physiological reactions to cues relating to the trauma.
■ Active avoidance of triggering stimuli (e.g., memories, feelings, people,
places, objects) associated with the trauma.
■ At least two of the following negative cognitions/mood: dissociative
amnesia, negative feelings of self/others/world, self-blame, negative
emotions (e.g., fear, horror, anger, guilt), anhedonia, feelings of detachment/
estrangement, inability to experience positive emotions.
■ At least two of the following symptoms of increased arousal/reactivity:
hypervigilance, exaggerated startle response, irritability, angry outbursts,
impaired concentration, insomnia.
■ Symptoms not caused by the direct effects of a substance or another medical
condition.
■ Symptoms result in significant impairment in social or occupational
functioning.
■ The presentation differs in children <7 years of age.
Epidemiology/Etiology
■ Lifetime prevalence of PTSD: >8%.
■ Higher prevalence in women, most likely due to greater risk of exposure
to traumatic events, particularly rape and other forms of interpersonal
violence.
■ Exposure to prior trauma, especially during childhood, is a risk factor for
developing PTSD.
Course/Prognosis
■ PTSD usually begins within 3 months after the trauma.
■ Symptoms may manifest after a delayed expression.
■ Fifty percent of patients with PTSD have complete recovery within
3 months.
■ Symptoms tend to diminish with older age.
■ Eighty percent of patients with PTSD have a comorbid mental disorder
(e.g., MDD, bipolar disorder, anxiety disorder, substance use disorder).
Treatment
■ Pharmacological
●First-line antidepressants: SSRIs (e.g., sertraline) or SNRIs (e.g., venlafaxine).
●Prazosin, a1-receptor antagonist, targets nightmares and hypervigilance.
●Consider augmentation with a second-generation antipsychotic in severe
or treatment-resistant cases.
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
WARDS TIP
Q: What medication has shown
some efficacy as an adjunct treatment for nightmares in patients
with PTSD?
A: Prazosin.
WARDS TIP
Criteria of PTSD: TRAUMA
Traumatic event
Reexperience
Avoidance
Unable to function
Month or more of symptoms
Arousal increased
60
■ Psychotherapy
ANXIETY, OBSESSIVE-COMPULSIVE, TRAUMA, AND STRESSOR-RELATED DISORDERS
WARDS TIP
Cognitive processing therapy is
a modified form of CBT in which
thoughts, feelings, and meanings
of the event are revisited and
questioned.
●Couples/family therapy.
ADJUSTMENT DISORDERS
WARDS TIP
Addictive medications such as
benzodiazepines should be avoided in the treatment of PTSD because of the high rate of ­comorbid
substance use disorders and the
lack of efficacy.
Epidemiology
KEY FACT
■ May occur at any age.
PTSD stressor = life threatening.
Etiology
Adjustment disorder stressor ≠
life threatening.
■ Triggered by psychosocial factors.
Treatment
■ Supportive psychotherapy.
■ Group therapy.
●Specialized forms of CBT (e.g., exposure therapy, cognitive processing
therapy).
●Supportive and psychodynamic therapy.
Adjustment disorders occur when behavioral or emotional symptoms develop
after a non-life-threatening, stressful life event (e.g., divorce, death of a loved
one, or loss of a job).
Diagnosis and DSM-5 Criteria
Development of emotional or behavioral symptoms within 3 months in response to an identifiable stressful life event. These symptoms produce either:
• Excessive distress in relation to the event.
• Significant impairment in daily functioning.
The symptoms are not those of normal bereavement.
Symptoms resolve within 6 months after the stressor has terminated.
The stress-related disturbance does not meet criteria for another mental
disorder.
Subtypes: Based on a predominance of either depressed mood, anxiety, mixed
anxiety and depression, disturbance of conduct (such as aggression), or mixed
disturbance of emotions and conduct.
■ 5–20% of patients in outpatient mental health clinics have an adjustment
disorder.
Prognosis
May be chronic if the stressor is chronic or recurrent.
■ If clinically indicated, pharmacotherapy can target associated impairing
symptoms (insomnia, anxiety, or depression).

09 - Chapter 6 Personality Disorders

01 - Chapter 6 Personality Disorders
Chapter 6 Personality Disorders
CHAPTER 6
PER SON AL I T Y
DISORDERS
Definition.................................................................................................................................62
Diagnosis and DSM-5 Criteria...............................................................................................62
Clusters.....................................................................................................................................62
Etiology...............................................................................................................................63
Treatment............................................................................................................................63
Cluster A...................................................................................................................................63
Paranoid Personality Disorder (PPD)....................................................................................63
Schizoid Personality Disorder...............................................................................................64
Schizotypal Personality Disorder..........................................................................................65
Cluster B...................................................................................................................................66
Antisocial Personality Disorder............................................................................................67
Borderline Personality Disorder (BPD).................................................................................68
Histrionic Personality Disorder (HPD)...................................................................................69
Narcissistic Personality Disorder (NPD)................................................................................70
Cluster C....................................................................................................................................70
Avoidant Personality Disorder..............................................................................................70
Dependent Personality Disorder (DPD)................................................................................72
Obsessive-Compulsive Personality Disorder (OCPD).............................................................73
Personality Change Due to Another Medical Condition........................................................74
Other Specified Personality Disorder....................................................................................74
Unspecified Personality Disorder.........................................................................................74
62
PERSONALITY DISORDERS
Definition
WARDS TIP
Many people have odd ­tendencies
and quirks. These are not
­pathological unless they cause
significant distress or impairment
in daily functioning.
DIAGNOSIS AND DSM-5 CRITERIA
KEY FACT
Ego-syntonic refers to feelings,
thoughts, and/or behaviors that
are acceptable to the self; that are
consistent with one’s fundamental
personality. Ego-dystonic refers to
feelings, thoughts, and/or behaviors that are distressing, unacceptable, or inconsistent with one’s
self-concept.
Clusters
WARDS TIP
Personality disorder
­criteria—CAPRI
Cognition
Affect
Personal Relations
Impulse control
● Patients seem anxious or fearful.
Personality is one’s set of stable, predictable, emotional, and behavioral traits.
Personality disorders involve enduring patterns of inner experience and behavior that deviate markedly from expectations of an individual’s culture. They
are pervasive, maladaptive, and cause significant impairment in social or
occupational functioning. Patients with personality disorders often lack insight
about their problems; their symptoms are either ego-syntonic or viewed as
immutable. In addition, individuals with personality disorders have significant
comorbidity with other mental disorders.
Enduring pattern of behavior/inner experience that deviates from the
­person’s culture and is manifested in two or more of the following ways:
• Cognition
• Affect
• Interpersonal functioning
• Impulse control
The pattern:
l Is pervasive and inflexible in a broad range of situations.
l Is stable and has an onset no later than adolescence or early adulthood.
l Leads to significant distress in functioning.
l Is not accounted for by another mental/medical illness or by use of a ­substance.
The international prevalence of personality disorders is approximately 7–12%.
Personality disorders vary by gender. Many patients with personality disorders
will meet the criteria for more than one disorder; they should be classified as
having all of the disorders for which they qualify.
Personality disorders are divided into the following three clusters:
■ Cluster A—Schizoid, schizotypal, and paranoid:
● Patients seem eccentric, peculiar, or withdrawn.
● Familial association with psychotic disorders.
■ Cluster B—Antisocial, borderline, histrionic, and narcissistic:
● Patients seem emotional, dramatic, or inconsistent.
● Familial association with mood disorders.
■ Cluster C—Avoidant, dependent, and obsessive-compulsive:
● Familial association with anxiety disorders.
Other specified/unspecified personality disorder includes characteristics of a
personality disorder that do not meet full criteria for any of the other personality disorders.
ETIOLOGY
■ Biological, genetic, and psychosocial factors during childhood and
adolescence contribute to the development of personality disorders.
■ The prevalence of some personality disorders in monozygotic twins is
several times higher than in dizygotic twins.
TREATMENT
■ Personality disorders are generally very difficult to treat, especially since few
patients are aware that they need help. The disorders tend to be chronic and
lifelong.
■ In general, pharmacologic treatment has limited usefulness (see individual
exceptions below) except in treating comorbid mental conditions
(e.g., major depressive disorder).
■ Psychotherapy is usually the most helpful.
Cluster A
These patients are perceived as eccentric or odd by others and can have
­psychotic symptoms (see Table 6-1).
PARANOID PERSONALITY DISORDER (PPD)
Patients with PPD have a pervasive distrust and suspiciousness of others and
often interpret motives as malevolent. They tend to blame their own problems
on others and seem angry and hostile. They are often characterized as being
pathologically jealous, which leads them to think that their sexual partners or
spouses are cheating on them.
Diagnosis and DSM-5 Criteria
■ Diagnosis requires a general distrust of others, beginning by early adulthood
and present in a variety of contexts.
TABLE 6-1. Cluster A Personality Disorders and Classic Clinical Examples
Personality
Disorder
Clinical Example
Paranoid
personality
disorder
A 30-year-old man says his wife has been cheating on him because he does
not have a good enough job to provide for her needs. He also claims that
on his previous job, his boss laid him off because he did a better job than
his boss. He has initiated several lawsuits. He believes the neighbors are
critical of him. He refuses couples therapy because he is certain the therapist will side with his wife.
Schizoid
personality
disorder
A 45-year-old scientist works in the lab most of the day and, according to
his coworkers, has no friends. He is at risk of losing this job because of a
failure to collaborate with others. He expresses no desire to make friends
and is content with his single life. He has no evidence of a thought disorder.
Schizotypal
personality
disorder
A 35-year-old man dresses in a wizard costume every weekend with friends
as part of a live action role-playing community. He spends a great deal
of time on his computers set up in his basement for video games and to
“detect the presence of extraterrestrial communications in space.” He has
no auditory or visual hallucinations. He is lonely and sad, feels ostracized by
others, and desires an intimate relationship.
PERSONALITY DISORDERS
64
PERSONALITY DISORDERS
Epidemiology
■ Prevalence: 1–4%.
Differential Diagnosis
Course and Prognosis
Treatment
WARDS
QUESTION
Q: What is the key difference
between schizoid and avoidant
personality disorders?
A: Patients with schizoid personality disorder prefer to be alone
whereas those with avoidant
personality disorder prefer to be in
a relationship.
SCHIZOID PERSONALITY DISORDER
Diagnosis and DSM-5 Criteria
■ At least four of the following must also be present:
Suspicion (without evidence) that others are exploiting or ­deceiving them.
Preoccupation with doubts of loyalty or trustworthiness of friends or
acquaintances.
Reluctance to confide in others.
Interpretation of benign remarks as threatening or demeaning.
Persistence of grudges.
Perception of attacks on their character that is not apparent to others;
quick to counterattack.
Suspicions regarding fidelity of spouse or partner.
■ More commonly diagnosed in men than in women.
■ Higher incidence in family members of schizophrenics.
■ This personality disorder may be misdiagnosed in minority groups,
immigrants, and deaf individuals.
■ Schizophrenia: Unlike patients with schizophrenia, patients with PPD do not
have any fixed delusions and are not frankly psychotic, although they may
have transient psychosis under stressful situations.
■ Social disenfranchisement and social isolation: Without a social support
system, individuals can react with suspicion to others. The differential in
favor of PPD can be assisted by collateral history from others in close contact
with the person, who may identify what they consider as excess suspicion.
■ The disorder usually has a chronic course, causing lifelong marital and
job-related problems.
■ Psychotherapy is the treatment of choice, although, as stated above, patients
rarely initiate treatment.
■ Group psychotherapy should be avoided due to mistrust and
misinterpretation of others’ statements.
■ Patients may also benefit from a short course of antipsychotics for transient
psychosis.
Patients with schizoid personality disorder have a lifelong pattern of social
withdrawal. They are often perceived as eccentric and reclusive. They are quiet,
unsociable, and have a constricted affect. They have no desire for close relationships and prefer to be alone.
■ A pattern of voluntary social withdrawal and restricted range of emotional
expression, beginning by early adulthood and present in a variety of contexts.
■ Four or more of the following must also be present:
Neither enjoying nor desiring close relationships (including family).
Generally choosing solitary activities.
Little (if any) interest in sexual activity with another person.
Taking pleasure in few activities (if any).
Few close friends or confidants (if any).
Indifference to praise or criticism.
Emotional coldness, detachment, or flattened affect.
Epidemiology
■ Prevalence: 3–5%.
■ Diagnosed more often in men than women.
■ May be increased prevalence of schizoid personality disorder in relatives of
individuals with schizophrenia.
Differential Diagnosis
■ Schizophrenia: Unlike patients with schizophrenia, patients with schizoid
personality disorder do not have overt psychotic symptoms such as
delusions or hallucinations.
■ Schizotypal personality disorder: Patients with schizoid personality disorder
do not have the same eccentric behavior or magical thinking seen in patients
with schizotypal personality disorder. Schizotypal patients are more similar
to schizophrenic patients in terms of odd perceptions, thought, and behavior.
Course
Usually chronic course.
Treatment
■ Lack insight for individual psychotherapy, and may find group therapy
threatening; may benefit from day programs or drop-in centers.
■ Antidepressants if comorbid major depression is diagnosed.
SCHIZOTYPAL PERSONALITY DISORDER
Patients with schizotypal personality disorder have a pervasive pattern of eccentric behavior and peculiar thought patterns. They are often perceived as strange
and odd. The disorder was developed out of the observation that certain family
traits predominate in first-degree relatives of those with schizophrenia.
Diagnosis and DSM-5 Criteria
■ A pattern of social deficits marked by eccentric behavior, cognitive or
perceptual distortions, and discomfort with close relationships, beginning by
early adulthood and present in a variety of contexts.
■ Five or more of the following must be present:
Ideas of reference (excluding delusions of reference).
Odd beliefs or magical thinking, inconsistent with cultural norms.
Unusual perceptual experiences (such as bodily illusions).
Suspiciousness.
Inappropriate or restricted affect.
Odd or eccentric appearance or behavior.
Few close friends or confidants.
Odd thinking or speech (vague, stereotyped, etc.).
Excessive social anxiety.
■ Magical thinking may include:
• Belief in clairvoyance or telepathy.
• Bizarre fantasies or preoccupations.
• Belief in superstitions.
■ Odd behaviors may include involvement in cults or strange religious practices.
PERSONALITY DISORDERS
66
PERSONALITY DISORDERS
Epidemiology
Prevalence: 4%.
Differential Diagnosis
WARDS TIP
Course
Q: What is the premorbid personality seen in schizophrenia?
A: Schizotypal personality
disorder.
Treatment
Cluster B
■ Schizophrenia: Unlike patients with schizophrenia, patients with schizotypal
personality disorder are not frankly psychotic (though they can become
transiently so under stress), nor do they have delusions.
■ Schizoid personality disorder: Patients with schizoid personality disorder
do not have the same eccentric behavior seen in patients with schizotypal
personality disorder.
■ Course is chronic, with a small minority developing schizophrenia.
■ Premorbid personality type for a patient with schizophrenia.
■ Psychotherapy is the treatment of choice to help develop social skills training.
■ A short course of low-dose second-generation antipsychotic may help with
the cognitive-perceptual disturbances.
Includes antisocial, borderline, histrionic, and narcissistic personality disorders. These patients are often emotional, impulsive, and dramatic (Table 6-2).
Mr. Harris is a 35-year-old man with no prior psychiatric history who was
arrested for assaulting his pregnant girlfriend. While in jail, he reports feeling
depressed, and you are called in for a psychiatric evaluation. Mr. Harris is
cooperative during the evaluation and presents as friendly and likeable.
He reports that he is innocent of his charges and expresses feeling sad and
tearful since his incarceration 2 days ago. He requests that you transfer him
to the mental health unit at the correctional facility. However, you perform a
thorough evaluation, and you do not find symptoms suggestive of a mood
or psychotic disorder. When asked if he has been incarcerated before, he
reports a history of multiple arrests and convictions for robbery and gun
possession. He reports that he is unemployed because he has been “in and
out of jail” during the past 5 years. He provides rationalizations for his limited
involvement in these past crimes and does not appear remorseful.
Mr. Harris reveals a pattern of repeated fights since childhood and says
that he quit school while in the ninth grade after being suspended for
smoking pot on school grounds. Mr. Harris reports that throughout his
childhood he bullied others, and laughs when recounting an episode
during which he threw his cat against the wall to see if it would bounce
back. He denies any family history of psychiatric illnesses, but reports that
his father is currently incarcerated for drug trafficking.
What is his diagnosis?
Mr. Harris’s diagnosis is antisocial personality disorder. His history shows a pervasive pattern of disregard for and violation of the rights of others since age 15, and
there is evidence of conduct disorder with onset before age 15 years. Remember
that, although it is common, not all criminals have antisocial personality disorder.
What are some associated findings?
Antisocial personality disorder is more prevalent in males, is associated with low
socioeconomic background, and has a genetic predisposition. It has been found
that the children of parents with antisocial personality disorder have an increased
risk for this disorder, somatic symptom disorder, and substance use disorders.
TABLE 6-2. Cluster B Personality Disorders and Classic Clinical Examples
Personality
Disorder
Clinical Example
Antisocial
personality
disorder
A 30-year-old unemployed man has been accused of killing three senior
citizens after robbing them. He is surprisingly charming in the interview.
In his adolescence, he was arrested several times for stealing cars and
assaulting other kids.
Borderline
personality
disorder
A 23-year-old medical student attempted to cut her wrist because things
did not work out with a man she had been dating over the past 3 weeks.
She states that guys are jerks and “not worth her time.” She often feels
that she is “alone in this world.”
Histrionic
personality
disorder
A 33-year-old provocatively dressed woman comes to your office
complaining that her fever feels like “she is burning in hell.” She vividly
describes how the fever has affected her work as a teacher but displays
superficial expressions of emotion.
Narcissistic
personality
disorder
A 48-year-old company CEO is rushed to the ED after an automobile
accident. He does not let the residents operate on him and requests the
Chief of trauma surgery as he is “vital to the company.” He makes several
business phone calls in the ED to stay on “top of his game.”
ANTISOCIAL PERSONALITY DISORDER
Patients diagnosed with antisocial personality disorder often exploit and violate
the rights of others, and break rules to meet their own needs. They lack empathy, compassion, and remorse for their actions. They are impulsive, deceitful,
and often violate the law. They are frequently skilled at reading social cues and
can appear charming and normal to others who meet them for the first time
and do not know their history.
Diagnosis and DSM-5 Criteria
■ Pattern of disregard for and violation of the rights of others since age 15.
■ Patients must be at least 18 years old for this diagnosis; history of behavior
as a child/adolescent must be consistent with conduct disorder (see
Chapter 10, “Psychiatric Disorders in Children”).
■ Three or more of the following should be present:
Failure to conform to social norms by committing unlawful acts.
Deceitfulness/repeated lying/manipulating others for personal gain.
Impulsivity/failure to plan ahead.
Irritability and aggressiveness/repeated fights or assaults.
Recklessness and disregard for safety of self or others.
Irresponsibility/failure to sustain work or honor financial obligations.
Lack of remorse for actions.
Epidemiology
■ Prevalence: 1–4% of the general population.
■ Males are three to five times as likely to be diagnosed as women.
■ Males with alcoholic parents are at increased risk.
■ There is a higher incidence in poor urban areas and in prisoners but no
racial difference.
■ Genetic component: Increased risk among first-degree relatives.
Differential Diagnosis
Substance use disorder: It is necessary to ascertain which came first. Patients
who began abusing drugs before their antisocial behavior started may have
behavior attributable to the effects of their addiction.
PERSONALITY DISORDERS
WARDS TIP
Symptoms of antisocial ­
personality disorder—CORRUPT
Cannot follow law
Obligations ignored
Remorselessness
Reckless disregard for safety
Underhanded (deceitful)
Planning deficit (impulsive)
Temper (irritable, aggressive)
68
PERSONALITY DISORDERS
Course
KEY FACT
Antisocial personality disorder
begins in childhood as conduct
disorder. Patient may have a history of being abused (physically or
sexually) as a child or a history of
hurting animals or starting fires. It
is often associated with violations
of the law.
Treatment
■ Psychotherapy is generally ineffective.
WARDS
QUESTION
Q: What is the most commonly
diagnosed personality disorder in
psychiatric inpatients?
A: Borderline personality disorder.
Diagnosis and DSM-5 Criteria
WARDS TIP
Symptoms of BPD—IMPULSIVE
Impulsive
Moody
Paranoid under stress
Unstable self-image
Labile, intense relationships
Suicidal
Inappropriate anger
Vulnerable to abandonment
Emptiness
Epidemiology
■ Lifetime prevalence: 6%.
■ Suicide rate: 10%.
WARDS
QUESTION
Differential Diagnosis
Q: What is a common defense
mechanism used by patients
with BPD?
A: Splitting—They view others and
themselves as all good or all bad.
■ Usually has a chronic course, but some improvement of symptoms may
occur as the patient ages.
■ Many patients have multiple somatic complaints, and coexistence of
substance use disorders and/or major depression is common.
■ There is increased morbidity from substance use, trauma, suicide, or
homicide.
■ Pharmacotherapy may be used to treat symptoms of anxiety, depression, or
aggression, but use caution given the high comorbidity with substance use
disorders in these patients.
BORDERLINE PERSONALITY DISORDER (BPD)
Patients with BPD have unstable moods, behaviors, and interpersonal relationships. They fear abandonment and have poorly formed identity. Relationships
begin with intense attachments and end with the slightest conflict. Aggression
is common. They are impulsive and may have a history of repeated suicide
attempts/gestures or episodes of self-mutilation. They have higher rates of
childhood physical, emotional, and sexual abuse than the general population.
■ Pervasive pattern of impulsivity and unstable relationships, affects,
self-image, and behaviors, present by early adulthood and in a variety of
contexts.
■ At least five of the following must be present:
Frantic efforts to avoid real or imagined abandonment.
Unstable, intense interpersonal relationships (e.g., extreme love–hate
relationships).
Unstable self-image.
Impulsivity in at least two potentially harmful ways (spending, sexual
activity, substance use, binge eating, etc.).
Recurrent suicidal threats or attempts or self-mutilation.
Unstable mood/affect.
Chronic feelings of emptiness.
Difficulty controlling anger.
Transient, stress-related paranoid ideation or dissociative symptoms.
■ Diagnosed three times more often in women than men in clinical settings.
■ Schizophrenia: Unlike patients with schizophrenia, patients with BPD do
not have frank psychosis (may have transient psychosis, however, if they
decompensate under stress or substances of abuse).
■ Bipolar I/II: Mood swings experienced in BPD are rapid, brief,
moment-to-moment reactions to perceived environmental or psychological
triggers.
Course
■ Variable, but many develop stability in middle age.
■ High incidence of coexisting major depression and/or substance use
disorders.
■ Increased risk of suicide.
Treatment
■ Dialectical behavior therapy (DBT) is the treatment of choice—includes
cognitive-behavioral therapy, mindfulness skills, and group therapy.
■ Other psychotherapies found to be beneficial include mentalization-based
therapy, transference-focused therapy, and schema-focused therapy.
■ Pharmacotherapy should be considered an adjunct to psychotherapy. Mood
stabilizers and low-dose antipsychotic medications have been found to be
more effective than antidepressants in the treatment of mood swings/lability.
HISTRIONIC PERSONALITY DISORDER (HPD)
Patients with HPD exhibit attention-seeking behavior and excessive emotionality. They are dramatic, flamboyant, and extroverted, but are unable to form
long-lasting, meaningful relationships. They are often sexually inappropriate
and provocative.
Diagnosis and DSM-5 Criteria
■ Pattern of excessive emotionality and attention seeking, present by early
adulthood and in a variety of contexts.
■ At least five of the following must be present:
Uncomfortable when not the center of attention.
Inappropriately seductive or provocative behavior.
Rapidly shifting but shallow expression of emotion.
Uses physical appearance to draw attention to self.
Speech that is impressionistic and lacking in detail.
Theatrical and exaggerated expression of emotion.
Easily influenced by others or situation.
Perceives relationships as more intimate than they actually are.
Epidemiology
■ Prevalence in the general population: <2%.
■ Women are more likely to have HPD than men.
Differential Diagnosis
BPD: Patients with BPD are more likely to suffer from depression, brief psychotic episodes, and to attempt suicide. HPD patients are generally more
functional.
Course
Usually chronic, with some improvement of symptoms with age.
Treatment
■ Psychotherapy (e.g., supportive, problem-solving, interpersonal, group) is
the treatment of choice.
■ Pharmacotherapy to treat associated depressive or anxious symptoms as
necessary.
PERSONALITY DISORDERS
WARDS TIP
Pharmacotherapy has been shown
to be more useful in BPD than in
any other personality disorder.
WARDS TIP
Histrionic patients often use
the defense mechanism of
­regression—they revert to childlike
behaviors.
70
PERSONALITY DISORDERS
Diagnosis and DSM-5 Criteria
WARDS TIP
Narcissism is characterized by
an inflated sense of entitlement.
People with narcissistic personality
are often “fishing for compliments”
and become irritated and anxious when they are not treated as
important.
Epidemiology
Prevalence: Approximately 6%.
WARDS
QUESTION
Q: Which personality disorder
has an overlap with social anxiety
disorder (social phobia)?
A: Avoidant personality disorder (may be same syndrome/
spectrum).
Treatment
■ Psychotherapy is the treatment of choice.
WARDS TIP
Symptoms of avoidant personality
disorder—AFRAID
Avoids occupation with others
Fear of embarrassment and
criticism
Reserved unless they are certain
that they are liked
Always thinking rejection
Isolates from relationships
Distances self unless certain that
they are liked
Cluster C
AVOIDANT PERSONALITY DISORDER
NARCISSISTIC PERSONALITY DISORDER (NPD)
Patients with NPD have a sense of superiority, a need for admiration, and a
lack of empathy. They consider themselves “special” and will exploit others for
their own gain. Despite their grandiosity, however, these patients often have
fragile self-esteem.
■ Pattern of grandiosity, need for admiration, and lack of empathy beginning
by early adulthood and present in a variety of contexts.
■ Five or more of the following must be present:
Exaggerated sense of self-importance.
Preoccupation with fantasies of unlimited money, success, brilliance, etc.
Believe that they are “special” or unique and can associate only with other
high-status individuals.
Requires excessive admiration.
Has sense of entitlement.
Takes advantage of others for self-gain.
Lacks empathy.
Envious of others or believes others are envious of them.
Arrogant or haughty.
Differential Diagnosis
Antisocial personality disorder: Both types of patients exploit others, but NPD
patients want status and recognition, while antisocial patients want material
gain or simply the subjugation of others. Narcissistic patients become depressed when they don’t get the recognition they think they deserve.
Course
Usually has a chronic course; higher incidence of depression and midlife crises
since these patients put such a high value on youth and power.
■ Psychotropics may be used if a comorbid psychiatric disorder is also
diagnosed.
Includes avoidant, dependent, and obsessive-compulsive personality disorders.
These patients appear anxious and fearful (see Table 6-3).
Patients with avoidant personality disorder have a pervasive pattern of social
inhibition and an intense fear of rejection. They will avoid situations in which
they may be rejected. Their fear of rejection is so overwhelming that it affects
all aspects of their lives. They avoid social interactions and may seek jobs in
which there is little interpersonal contact. These patients desire companionship
but are extremely shy and easily injured.
TABLE 6-3. Cluster C Personality Disorders and Classic Clinical Examples
Personality Disorder
Clinical Example
Avoidant personality
disorder
A 30-year-old postal worker rarely goes out with her coworkers
and often makes excuses when they ask her to join them because
she is afraid they will not like her. She wishes to go out and meet
new people but, according to her, she is too “shy.”
Dependent
personality disorder
A 40-year-old man who lives with his parents has trouble deciding how to get his car fixed. He calls his father at work several
times to ask very trivial things. He has been unemployed over
the past 3 years. He has been in several long-term but abusive
relationships.
Obsessive-compulsive
personality disorder
A 40-year-old secretary has been recently fired because of her
inability to prepare some work projects in time. According to her,
they were not in the right format and she had to revise them six
times, which led to the delay. This has happened before but she
feels that she is not given enough time to “get it perfect.”
Diagnosis and DSM-5 Criteria
■ A pattern of social inhibition, hypersensitivity, and feelings of inadequacy
since early adulthood.
■ At least four of the following must be present:
Avoids occupation that involves interpersonal contact due to a fear of
criticism and rejection.
Unwilling to interact unless certain of being liked.
Cautious of interpersonal relationships.
Preoccupied with being criticized or rejected in social situations.
Inhibited in new social situations because he or she feels inadequate.
Believes they are socially inept and inferior.
Reluctant to engage in new activities for fear of embarrassment.
Epidemiology
■ Prevalence: Approximately 2%.
Differential Diagnosis
■ Schizoid personality disorder: Patients with avoidant personality disorder
desire companionship but are extremely shy, whereas patients with schizoid
personality disorder have little or no desire for companionship.
■ Social anxiety disorder (social phobia): See Chapter 5, “Anxiety
Obsessive-Compulsive, Trauma, and Stressor-Related Disorders.” Both
involve fear and avoidance of social situations. If the symptoms are an
integral part of the patient’s personality and have been evident since
adolescence, personality disorder is the more likely diagnosis. Social anxiety
disorder involves a fear of embarrassment in a particular setting (speaking
in public, urinating in public, etc.), whereas avoidant personality disorder is
an overall fear of rejection and a sense of inadequacy. However, a patient can
have both disorders concurrently and should carry both diagnoses if criteria
for each are met.
■ Dependent personality disorder: Avoidant personality disorder patients cling
to relationships, similar to dependent personality disorder patients; however,
avoidant patients are slow to get involved, whereas dependent patients
actively and aggressively seek relationships.
PERSONALITY DISORDERS
KEY FACT
Schizoid patients prefer to be
alone. Avoidant patients want to
be with others but are too scared
of rejection.
72
PERSONALITY DISORDERS
Course
WARDS TIP
Symptoms of dependent personality disorder—OBEDIENT
Obsessive about approval
Bound by other’s decisions
Enterprises are rarely initiated due
to their lack of self-confidence
Difficult to make own decisions
Invalid feelings while alone
Engrossed with fears of
self-reliance
Needs to be in a relationship
Tentative about decisions
Treatment
■ Group therapy may also be beneficial.
DEPENDENT PERSONALITY DISORDER (DPD)
KEY FACT
Diagnosis and DSM-5 Criteria
Regression is often seen in people
with DPD. This is defined as going
back to a younger age of maturity.
WARDS
QUESTION
Q: What childhood conditions
predispose to later development
of DPD?
A: Medical illness and separation
anxiety disorders.
Epidemiology
■ Prevalence: Approximately 2%.
Differential Diagnosis
Course
■ Usually has a chronic course.
■ Course is usually chronic, although may remit with age.
■ Particularly difficult during adolescence, when attractiveness and
socialization are important.
■ Increased incidence of associated anxiety and depressive disorders.
■ If support system fails, patient is left very susceptible to depression, anxiety,
and anger.
■ Psychotherapy, including assertiveness and social skills training, is most effective.
■ Selective serotonin reuptake inhibitors (SSRIs) may be prescribed for
comorbid social anxiety disorder or major depression.
Patients with DPD have poor self-confidence and fear of separation. They have
an excessive need to be taken care of and allow others to make decisions for
them. They feel helpless when left alone.
■ A pattern of excessive need to be taken care of that leads to submissive and
clinging behavior.
■ At least five of the following must be present:
Difficulty making everyday decisions without reassurance from others.
Need others to assume responsibilities for most areas of their life.
Difficulty expressing disagreement because of fear of loss of approval.
Difficulty initiating projects because of lack of self-confidence.
Goes to excessive lengths to obtain support from others.
Feels helpless when alone.
Urgently seeks another relationship when one ends.
Preoccupied with fears of being left to take care of self.
■ Women are more likely to be diagnosed with DPD than men.
■ Childhood medical illness or separation anxiety disorder may increase the
likelihood of developing DPD.
■ Avoidant personality disorder: See discussion above.
■ BPD and HPD: Patients with DPD usually have a long-lasting relationship
with one person on whom they are dependent. While patients with
borderline and histrionic personality disorders are often dependent on other
people, they are unable to maintain long-lasting relationships.
■ Patients are prone to depression, particularly after loss of person on whom
they are dependent.
■ Difficulties with employment since they cannot act independently or
without close supervision.
Treatment
■ Psychotherapy, particularly cognitive-behavioral, assertiveness, and social
skills training, is the treatment of choice.
■ Pharmacotherapy may be used to treat associated symptoms of anxiety or
depression.
OBSESSIVE-COMPULSIVE PERSONALITY DISORDER (OCPD)
Patients with OCPD have a pervasive pattern of perfectionism, inflexibility,
and orderliness. They become so preoccupied with unimportant details that
they are often unable to complete simple tasks in a timely fashion. They appear stiff, serious, and formal, with constricted affect. They are often successful
­professionally but have poor interpersonal skills.
Diagnosis and DSM-5 Criteria
■ Pattern of preoccupation with orderliness, control, and perfectionism at
the expense of efficiency and flexibility, present by early adulthood and in a
variety of contexts.
■ At least four of the following must be present:
Preoccupation with details, rules, lists, and organization such that the
major point of the activity is lost.
Perfectionism that is detrimental to completion of task.
Excessive devotion to work.
Excessive conscientiousness and scrupulousness about morals and ethics.
Will not delegate tasks.
Unable to discard worthless objects.
Miserly spending style.
Rigid and stubborn.
Epidemiology
■ Prevalence: 2–7%.
■ Men are two times more likely to be diagnosed with OCPD than women.
Differential Diagnosis
■ Obsessive-compulsive disorder (OCD): Patients with OCPD do not have the
recurrent obsessions or compulsions that are present in OCD. In addition,
the symptoms of OCPD are ego-syntonic rather than ego-dystonic (as in
OCD); OCD patients are aware that they have a problem and wish that their
thoughts and behaviors would go away.
■ NPD: Both disorders entail assertiveness and achievement, but NPD
patients are motivated by status, whereas OCPD patients are motivated by
perfectionism and the work itself.
Course
■ Unpredictable course.
■ A significant number have comorbid OCD (most do not, however).
Treatment
■ Psychotherapy is the treatment of choice. Cognitive-behavior therapy may
be particularly useful.
■ Pharmacotherapy may be used to treat associated symptoms as necessary.
PERSONALITY DISORDERS
74
PERSONALITY DISORDERS
OTHER SPECIFIED PERSONALITY DISORDER
UNSPECIFIED PERSONALITY DISORDER
PERSONALITY CHANGE DUE TO ANOTHER MEDICAL CONDITION
This refers to a persistent personality change from a previous pattern due to
the direct pathophysiological result of a medical condition (e.g., head trauma,
stroke, epilepsy, central nervous system infection, or neoplasm). Subtypes
include labile, disinhibited, aggressive, apathetic, or paranoid.
This diagnosis is reserved for a personality disorder that does not meet the full
criteria for any of the disorders, but where the clinician chooses to communicate the specific reason that the presentation does not meet the criteria for any
specific personality disorder (e.g., “mixed personality disorder”).
This diagnosis is used for a personality disorder that does not meet the full
criteria for any of the disorders, but where the clinician chooses not to specify
the reason that the criteria are not met for any specific personality disorder
(e.g., not enough information to make a more specific diagnosis).

10 - Chapter 7 Substance Related and Addictive Disorder

01 - Chapter 7 Substance Related and Addictive Dis
Chapter 7 Substance-Related and Addictive Disorders
Substance Use Disorders...........................................................................................................77
Diagnosis and DSM-5 Criteria...............................................................................................77
Epidemiology......................................................................................................................77
Psychiatric Symptoms..........................................................................................................77
Acute Intoxication and Withdrawal......................................................................................78
Detection of Substance Use.................................................................................................78
Treatment of Substance Use Disorders.................................................................................78
Alcohol (EtOH)..........................................................................................................................79
Intoxication.........................................................................................................................79
Withdrawal..........................................................................................................................80
Alcohol Use Disorder............................................................................................................83
Cocaine.....................................................................................................................................84
Intoxication.........................................................................................................................84
Cocaine Use Disorder...........................................................................................................85
Withdrawal..........................................................................................................................85
Amphetamines.........................................................................................................................85
Intoxication.........................................................................................................................86
Phencyclidine (PCP)..................................................................................................................86
Intoxication.........................................................................................................................86
Withdrawal..........................................................................................................................86
Sedative-Hypnotics...................................................................................................................87
Intoxication.........................................................................................................................87
Withdrawal..........................................................................................................................87
Clinical Presentation............................................................................................................87
Opioids.....................................................................................................................................88
Intoxication.........................................................................................................................88
Opiate Use Disorder.............................................................................................................88
Withdrawal..........................................................................................................................88
Hallucinogens...........................................................................................................................89
Intoxication.........................................................................................................................89
Withdrawal..........................................................................................................................90
S U BSTAN CE- R E LAT E D A ND
CHAPTER 7
ADDICTIVE DISORDERS
76
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
Marijuana.................................................................................................................................90
Intoxication.........................................................................................................................90
Withdrawal..........................................................................................................................90
Inhalants..................................................................................................................................90
Intoxication.........................................................................................................................91
Withdrawal..........................................................................................................................91
Caffeine....................................................................................................................................91
Overdose.............................................................................................................................91
Withdrawal..........................................................................................................................91
Nicotine....................................................................................................................................92
Treatment of Nicotine Dependence......................................................................................92
Gambling Disorder....................................................................................................................92
Diagnosis and DSM-5 Criteria...............................................................................................92
Epidemiology/Etiology........................................................................................................93
Treatment............................................................................................................................93
Substance Use Disorders
Substance use disorders are characterized by a problematic pattern of substance
use that leads to some form of functional impairment or distress. Keep in mind
that frequent use of a substance does not necessarily indicate a substance use
disorder unless it is causing problems for the patient.
DIAGNOSIS AND DSM-5 CRITERIA
Substance use disorders are characterized by a problematic pattern of substance
use causing impairment or distress, as manifested by at least two of the following within a 12-month period:
■ Using substance more than originally intended.
■ Persistent desire or unsuccessful efforts to cut down on use.
■ Significant time spent in obtaining, using, or recovering from substance.
■ Craving to use substance.
■ Failure to fulfill obligations at work, school, or home.
■ Continued use despite social or interpersonal problems due to the
substance use.
■ Limiting social, occupational, or recreational activities because of
substance use.
■ Use in dangerous situations (e.g., driving a car).
■ Continued use despite subsequent physical or psychological problem
(e.g., drinking alcohol despite worsening liver problems).
■ Tolerance (needing higher amounts of the substance to achieve the desired
effect or experiencing diminished effects when repeating the same dose).
■ Withdrawal (a substance-specific syndrome occurring when a patient stops
or reduces heavy/prolonged substance use).
Note that these criteria remain the same regardless of what substance(s) the
patient is using. The disorder may be classified as mild, moderate, or severe
depending on the number of criteria met.
EPIDEMIOLOGY
■ One-year prevalence of any substance use disorder in the United States is
approximately 8%.
■ More common in men than women.
■ Alcohol and nicotine are the most commonly used substances.
PSYCHIATRIC SYMPTOMS
■ Mood symptoms are common among persons with substance use disorders.
■ Psychotic symptoms may occur with some substances.
■ Personality disorders and psychiatric comorbidities (e.g., major depression,
anxiety disorders) are common among persons with substance use disorders.
■ It is often challenging to decide whether psychiatric symptoms are primary
or substance-induced. Many patients may use substances to self-medicate
for undertreated psychiatric symptoms.
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
WARDS TIP
It is possible to have a substance
use disorder without having physiological dependence (i.e., without
having withdrawal or tolerance).
WARDS TIP
Substance-induced mood symptoms improve during prolonged
abstinence, whereas primary
mood symptoms persist.
78
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
ACUTE INTOXICATION AND WITHDRAWAL
KEY FACT
Withdrawal symptoms of a drug
are usually the opposite of its
intoxication effects. For example,
alcohol is sedating, but alcohol
withdrawal can cause brain excitation and seizures.
DETECTION OF SUBSTANCE USE
See Table 7-1.
TREATMENT OF SUBSTANCE USE DISORDERS
TABLE 7-1. Direct Testing for Substance Use
Phencyclidine
(PCP)
Marijuana
Urine detection:
Both the intoxicated and withdrawing patient can present difficulties in diagnosis and treatment. Since it is common for persons to abuse several ­substances
at once, the clinical presentation is often confusing, and signs/symptoms may
be atypical. Always be on the lookout for use of multiple substances.
■ Behavioral counseling should be part of every substance use disorder
treatment.
See Table 7-2.
■ Psychosocial treatments are effective and include motivational intervention
(MI), cognitive-behavioral therapy (CBT), contingency management, and
individual and group therapy.
■ For severe substance use disorders, residential (usually 28-day) “rehab”
programs are common; some patients may choose to do partial
hospitalization or intensive outpatient programming.
Alcohol
■ Stays in system for only a few hours.
■ Breathalyzer test, commonly used by law enforcement.
■ Blood/urine testing more accurate.
■ Urine screening for metabolite (ethyl glucuronide) — not useful for
assessing acute intoxication, but can indicate alcohol use over the
preceding 2–5 days.
Cocaine
■ Urine drug screen positive for 2–4 days (up to 8 days for heavy
users).
Amphetamines
■ Urine drug screen positive for 1–3 days.
■ Most assays have poor sensitivity and/or specificity.
■ Urine drug screen positive for 4–7 days.
■ OTC cold medications may yield false positive.
■ Creatine kinase (CK) and aspartate aminotransferase (AST) are often
elevated.
Sedativehypnotics
In urine and blood for variable amounts of time.
Barbiturates:
■ Short-acting (pentobarbital): 24 hours
■ Long-acting (phenobarbital): 3 weeks
Benzodiazepines:
■ Short-acting (e.g., lorazepam): up to 5 days
■ Long-acting (diazepam): up to 30 days
Opioids
■ Urine drug test remains positive for 1–3 days, depending on opioid
used.
■ Routine screening tests detect morphine, which is the eventual
metabolite of all natural opioids.
■ Buprenorphine, synthetic opioids (methadone, fentanyl, tramadol)
and semi-synthetic opioids (oxycodone, hydrocodone) will not be
detected on routine screening (order separate assay).
■ After a single use, about 3 days. In heavy users, up to 4 weeks (THC
is released from adipose stores).
79
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
■ Community-based groups such as SMART Recovery, Alcoholics
Anonymous (AA), and Narcotics Anonymous (NA) should also be
encouraged as part of the treatment.
■ Pharmacotherapy is available for some drugs of abuse, and will be discussed
later in this chapter as relevant to a particular substance.
Alcohol (EtOH)
■ Alcohol activates gamma-aminobutyric acid (GABA), dopamine, and
serotonin receptors in the central nervous system (CNS). It inhibits
glutamate receptor activity and voltage-gated calcium channels. GABA
receptors are inhibitory, and glutamate receptors are excitatory; thus, alcohol
is a potent CNS depressant.
■ Lifetime prevalence of alcohol use disorder in the United States is 5% of
women and 12% of men.
■ Alcohol is metabolized in the following manner:
Alcohol → acetaldehyde (enzyme: alcohol dehydrogenase).
Acetaldehyde → acetic acid (enzyme: aldehyde dehydrogenase).
These enzymes are upregulated in heavy drinkers. Some populations produce
less aldehyde dehydrogenase due to genetic variation, resulting in flushing and
nausea with alcohol use.
INTOXICATION
Clinical Presentation
■ The absorption and elimination rates of alcohol are variable and depend
on many factors, including age, sex, body weight, chronic nature of use,
TABLE 7-2. Stages of Change
Stage
Definition
Example
Precontemplation
Patients do not view their addiction as a problem. They
may see substance use as helpful and/or enjoyable.
A college student who drinks heavily feels that
they need alcohol to overcome social anxiety and
enjoy parties. They do not identify any negative
consequences from their use.
Contemplation
The patient begins to think about cutting down or
stopping altogether. They recognize potential benefits
of making a change, but may be ambivalent or feel
unable to do so.
The student misses several deadlines due to hangovers
from drinking the night before. They think cutting down
on alcohol might improve their grades, but aren’t sure
they want to stop.
Preparation
The patient plans for the process of change. They collect
information, and may experiment with very small
changes.
The student begins researching self-help strategies for
reducing alcohol intake. They look up campus resources
for individual and group therapy.
Action
The patient takes direct steps toward reducing or
stopping substance use.
The student begins attending substance-use-focused
groups on campus, and talks with their primary care
doctor about starting naltrexone.
Maintenance
The patient has successfully made significant behavior
change, and works to avoid relapse.
The student continues to drink, but limits themself
to 1–2 drinks per day, and only consumes alcohol on
weekends.
Relapse
After a successful period of remission, patients resume
substance use (or fall back into unhealthy patterns
of use).
After graduating, the student is unemployed.
They begin drinking again to cope with stress and
unstructured time, and quickly escalates to near
daily use.
Alcohol is the most common
co-ingestant in drug overdoses.
WARDS TIP
Most adults will show some signs
of intoxication with BAL >100
and obvious signs with BAL
150 mg/dL.
KEY FACT
80
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
WARDS
QUESTION
Q: What is the average rate of
alcohol metabolism?
A: Between15 and 35 mg/dL
per hour.
KEY FACT
Ethanol, along with methanol and
ethylene glycol, can be a cause of
anion gap metabolic acidosis.
Treatment
KEY FACT
Males with substance use disorders, especially alcohol, have higher rates of perpetrating domestic
violence.
WARDS
QUESTION
Q: What are the typical features of
Wernicke’s encephalopathy?
A: The classic triad is confusion
(altered mental status), ataxic gait,
and oculomotor findings (typically
nystagmus or gaze palsies).
WITHDRAWAL
TABLE 7-3. Clinical Presentation of Alcohol Intoxication
Effects
BAL
Impaired fine motor control
20–50 mg/dL
Impaired judgment and coordination
50–100 mg/dL
Ataxic gait and poor balance
100–150 mg/dL
Lethargy, difficulty sitting upright, difficulty with memory,
nausea/vomiting
150–250 mg/dL
Coma (in the novice drinker)
300 mg/dL
Respiratory depression, death possible
400 mg/dL
duration of consumption, food in the stomach, and the state of nutrition and
liver health.
■ In addition to the above factors, the effects of EtOH also depend on the
blood alcohol level (BAL). Serum EtOH level or an expired air breathalyzer
can determine the extent of intoxication. As shown in Table 7-3, patients
with high tolerance may show diminished effects at a given BAL.
■ Monitor: Airway, breathing, circulation, glucose, electrolytes, acid–base
status.
■ Give parenteral thiamine (to prevent or treat Wernicke’s encephalopathy)
and folate. Remember thiamine must be given before glucose, as it’s a
necessary cofactor for glucose metabolism.
■ Naloxone may be necessary to reverse effects of co-ingested opioids.
■ A computed tomography (CT) scan of the head may be necessary to rule out
subdural hematoma or other brain injury.
■ The liver will eventually metabolize alcohol without any other interventions.
■ Severely intoxicated patients may require mechanical ventilation with
attention to acid–base balance, temperature, and electrolytes while they are
recovering.
■ Gastrointestinal evacuation (e.g., gastric lavage, induction of emesis,
and charcoal) is not indicated in the treatment of EtOH overdose unless
a significant amount of EtOH was ingested within the preceding 30–60
minutes.
A 42-year-old man has routine surgery for a knee injury. After 72 hours in
the hospital he becomes anxious, flushed, diaphoretic, hypertensive, and
tachycardic. What most likely accounts for this patient’s symptoms? Alcohol
withdrawal. Treatment? Benzodiazepines (chlordiazepoxide [Librium] or
lorazepam [Ativan] are considered the drugs of choice). What are you most
concerned about? Seizures, delirium tremens, autonomic instability, and cardiac arrhythmias. Remember that alcohol withdrawal can be fatal.
Chronic alcohol use has a depressant effect on the CNS, and cessation of use
causes a compensatory hyperactivity with glutamate excitotoxicity. Alcohol
withdrawal is potentially lethal!
Clinical Presentation
■ Signs and symptoms of alcohol withdrawal syndrome include insomnia,
anxiety, hand tremor, irritability, anorexia, nausea, vomiting, autonomic
hyperactivity (diaphoresis, tachycardia, hypertension), psychomotor
agitation, fever, seizures, hallucinations, and delirium tremens (see Table 7-4).
■ The earliest symptoms of EtOH withdrawal begin between 6 and 24 hours
after the patient’s last drink and depend on the duration and quantity of
EtOH consumption, liver size, and body mass.
■ Generalized tonic-clonic seizures usually occur between 12 and 48 hours
after cessation of drinking, with a peak around 12–24 hours.
■ About a third of persons with seizures develop delirium tremens (DTs).
■ Hypomagnesemia may predispose to seizures; thus, it should be corrected
promptly.
■ Seizures are treated with benzodiazepines. Long-term treatment with
anticonvulsants is not recommended for alcohol withdrawal seizures.
Delirium Tremens
■ The most serious form of EtOH withdrawal.
■ Usually begins 48–96 hours after the last drink but may occur later.
■ While only 5% of patients who experience EtOH withdrawal develop DTs,
there is a roughly 5% mortality rate (up to 35% if left untreated).
■ Physical illness predisposes to the condition.
■ Age >30 and prior DTs increase the risk.
■ In addition to delirium, symptoms of DTs may include hallucinations
(most commonly visual), agitation, gross tremor, autonomic instability, and
fluctuating levels of psychomotor activity.
■ It is a medical emergency and should be treated with adequate doses of
benzodiazepines.
Treatment
■ Benzodiazepines (lorazepam, diazepam, or chlordiazepoxide) should be given
in sufficient doses to keep the patient calm and lightly sedated, then tapered
down slowly. Carbamazepine or valproic acid can be used in mild withdrawal.
TABLE 7-4. Timing of Alcohol Withdrawal Symptoms
Syndrome
Clinical Findings
Onset After
Last Drink
Minor
withdrawal
Tremulousness, mild anxiety, headache, diaphoresis,
palpitations, anorexia, gastrointestinal upset; normal
mental status
Seizures
Single or brief flurry of generalized tonic-clonic seizures,
short postictal period, status epilepticus rare
6 to 48 hours
Alcoholic
hallucinosis
Visual, auditory, and/or tactile hallucinations with intact
orientation and normal vital signs
12 to 48 hours
Delirium
tremens
Delirium, agitation, tachycardia, hypertension, fever,
diaphoresis
48 to 96 hours
Source: Used, with permission, from Hoffman RS, Weinhouse GL. Management of moderate and
severe alcohol withdrawal syndromes. https://www.uptodate.com/contents/management-of-moderat
e-and-severe-alcohol-withdrawal-syndromes. © 2021 UpToDate, Inc. and/or its affiliates. All Rights
Reserved.
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
KEY FACT
Risk of suicide attempts is higher
among those with psychiatric disorders and concurrent substance
use (especially alcohol).
KEY FACT
Delirium tremens is a dangerous
form of alcohol withdrawal involving mental status and neurological changes. Symptoms include
disorientation, agitation, visual
and tactile hallucinations, and
autonomic instability (increase in
respiratory rate, heart rate, and
blood pressure). It carries a 5%
mortality rate but occurs in only
5% of patients that experience
EtOH withdrawal. Patients often
require ICU level of care; treatment
includes supportive care and
­benzodiazepines.
6 to 36 hours
82
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
KEY FACT
Confabulation—inventing stories
of events that never occurred—is
often associated with Korsakoff’s
“psychosis,” or alcohol-induced
neurocognitive disorder. Patients
are unaware that they are “making
things up.”
Alcoholic Ketoacidosis
■ Parenteral thiamine, folic acid, and a multivitamin to treat nutritional
deficiencies (“banana bag”).
■ Electrolyte and fluid abnormalities must be corrected.
■ Monitor withdrawal signs and symptoms with the Clinical Institute
Withdrawal Assessment (CIWA) scale.
■ Providers must pay careful attention to the level of consciousness, and
consider the possibility of traumatic injuries.
■ Check for signs of hepatic failure (e.g., ascites, jaundice, caput medusae,
coagulopathy).
■ Frequently seen in the setting of alcohol cessation after an alcohol binge
secondary to protracted vomiting and lack of oral intake.
■ Hallmark is ketosis without hyperglycemia and a negative alcohol level.
■ Laboratory studies reveal a high anion gap metabolic acidosis, ketonemia,
and low levels of potassium, magnesium, and phosphorus.
■ Treatment consists of hydration with D5NS, and replacing electrolytes.
Mr. Smith is a 42-year-old divorced man who arrives to the ED requesting
treatment for alcohol detoxification. He began drinking at the age of 17.
Although he initially drank only on the weekends, his alcohol use gradually
progressed to drinking half a pint of whiskey daily by the age of 35. At that
time, he arrived to his workplace intoxicated on several occasions and was
referred to a 45-day inpatient alcohol addiction program. After completing the
program, he was able to maintain sobriety for 7 years. However, 2 years ago he
got divorced, was laid off from work, and ultimately relapsed into alcohol use.
Mr. Smith is currently living with his older sister and states that his drinking
is “out of control.” He had a DUI recently and has a court date in 2 weeks. He
has tried to quit alcohol on his own on several occasions. However, when
he stops drinking he feels “shaky, sweaty, anxious, and irritable” and thus
resumes his alcohol intake. He also reports a history of a seizure 10 years ago,
after he abruptly discontinued his alcohol use for a few days.
Mr. Smith’s last drink was about 8 hours prior to his arrival at the ED.
During the last month he has been feeling sad, with low energy, difficulty
falling and staying asleep, low appetite, and difficulty concentrating. He
denies suicidal ideation but has significant guilt over not being able to stop
drinking. He denies a history of depression or anxiety, and has not received
any other psychiatric treatment in the past.
Upon presentation to ER the patient’s blood alcohol level was 110, he did
not have symptoms of intoxication, and his urine drug screen was negative.
Vital signs were significant for blood pressure of 150/90 and pulse of 110
bpm. Complete blood count and electrolytes were within normal limits.
What is Mr. Smith’s most likely diagnosis?
The patient has a diagnosis of alcohol use disorder, with current signs of
withdrawal. It is clear that he has exhibited symptoms of tolerance and
withdrawal, has been using more alcohol than intended, and has made
unsuccessful efforts to cut down. He also describes symptoms suggestive
of a depressive disorder. The fact that his depressive symptoms began while
abusing alcohol warrants a diagnosis of alcohol-induced depressive disorder.
However, major depressive disorder should be ruled out once he remits his
alcohol use. If his depressive symptoms are indeed substance-induced, they
will improve and resolve with continuing sobriety.
What would be the next step in management?
Given the Mr. Smith’s heavy chronic alcohol use and history of complicated
withdrawal (i.e., seizure), he should be admitted to an inpatient unit for close
monitoring. Outpatient detoxification is not appropriate in this case. He will
likely require a standing and PRN benzodiazepine (the particular benzodiazepine sometimes varies depending on hospital’s protocol), as well as close
monitoring for signs of withdrawal.
ALCOHOL USE DISORDER
■ The AUDIT-C (Table 7-5) is used to screen for alcohol use disorder.
■ Biochemical markers are useful in detecting recent prolonged drinking;
ongoing monitoring of biomarkers can also help detect a relapse. Most
commonly used biomarkers are BAL, liver function tests ([LFTs]—aspartate
aminotransferase [AST], alanine aminotransferase [ALT]), gamma-glutamyl
transpeptidase (GGT), and mean corpuscular volume (MCV). Urine screening
for ethyl glucuronide can indicate alcohol use in the 2–5 days prior to testing.
Medications for Alcohol Use Disorder
See Table 7-6.
Long-Term Complications of Alcohol Intake
■ Wernicke’s encephalopathy:
●Caused by thiamine (vitamin B1) deficiency resulting from poor
nutrition.
TABLE 7-5. AUDIT-C
Question #1: How often did you have a drink containing alcohol in the past year?
■ Never
(0 points)
■ Monthly or less
(1 point)
■ Two to four times a month
(2 points)
■ Two to three times per week
(3 points)
■ Four or more times a week
(4 points)
Question #2: How many drinks did you have on a typical day when you were drinking in
the past year?
■ 1 or 2
(0 points)
■ 3 or 4
(1 point)
■ 5 or 6
(2 points)
■ 7 to 9
(3 points)
■ 10 or more
(4 points)
Question #3: How often did you have six or more drinks on one occasion in the
past year?
■ Never
(0 points)
■ Less than monthly
(1 point)
■ Monthly
(2 points)
■ Weekly
(3 points)
■ Daily or almost daily
(4 points)
The AUDIT-C is scored on a scale of 0–12 (scores of 0 reflect no alcohol use). In men, a score of 4 or
more is considered positive; in women, a score of 3 or more is considered positive.
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
WARDS TIP
At-risk or heavy drinking for men
is more than 4 drinks per day or
more than 14 drinks per week. For
women, it is more than 3 drinks
per day or more than 7 drinks
per week.
KEY FACT
AST:ALT ratio ≥2:1 and elevated GGT
suggest excessive long-term alcohol
use; they take a few weeks to return
to normal during abstinence.
84
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
●Acute and can be reversed with thiamine therapy.
●Features: Ataxia (broad-based), confusion, ocular abnormalities
(nystagmus, gaze palsies).
■ If left untreated, Wernicke’s encephalopathy may progress to Korsakoff
syndrome:
●Chronic amnestic syndrome.
●Reversible in only about 20% of patients.
●Features: Impaired recent memory, anterograde amnesia, compensatory
confabulation (unconsciously making up answers when memory has
failed).
Cocaine
Cocaine blocks the reuptake of dopamine, epinephrine, and norepinephrine
from the synaptic cleft, causing a stimulant effect. Dopamine plays a role in the
behavioral reinforcement (“reward”) system of the brain.
INTOXICATION
■ General: Euphoria, heightened self-esteem, increase or decrease in blood
pressure, tachycardia or bradycardia, nausea, dilated pupils, weight loss,
psychomotor agitation or depression, chills, and sweating.
■ Dangerous: Seizures, cardiac arrhythmias, hyperthermia, paranoia,
and hallucinations (especially tactile). Since cocaine is an indirect
sympathomimetic, intoxication mimics the fight-or-flight response.
■ Deadly: Cocaine’s vasoconstrictive effect may result in myocardial infarction
(MI), intracranial hemorrhage, or stroke.
WARDS
QUESTION
Q: What is the treatment for Wernicke’s encephalopathy?
A: High dose parenteral (IV or IM)
thiamine should be given for 2–7
days, followed by daily oral thiamine.
Give all patients with altered mental status thiamine before glucose,
to avoid precipitating Wernicke–
Korsakoff syndrome. Thiamine is
a coenzyme used in carbohydrate
metabolism.
WARDS TIP
TABLE 7-6. Pharmacological Treatment of Alcohol Use Disorder
Medication
Mechanism
Pros
Cons
Naltrexone
Opioid receptor antagonist; reduces
cravings and the “high” associated
with alcohol intoxication.
First-line treatment.
Will precipitate withdrawal in patients
with physical opioid dependence.
Can interfere with anesthesia (e.g., for
acute injury or planned surgeries).
Risk of LFT elevation.
Available as an oral tablet (can be
taken daily, or as-needed on drinking
days), or monthly injection. Can allow
some patients to engage in moderate
alcohol use without escalating to
binge drinking.
Acamprosate
Likely modulates glutamate
transmission.
First-line treatment.
Contraindicated in severe renal
disease.
Can be used for patients with liver
disease. Typically used for relapse
prevention in patients who have
already stopped drinking.
Disulfiram
Blocks aldehyde dehydrogenase,
causing buildup of acetaldehyde
and aversive symptoms (flushing,
headache, nausea/vomiting,
palpitations, shortness of breath).
Second-line. Can be effective for
highly motivated patients.
Medication adherence can be an
issue. Contraindicated in severe
cardiac disease, pregnancy, psychosis.
Must monitor LFTs.
Topiramate
Anticonvulsant; potentiates GABA
and inhibits glutamate receptors.
Second-line treatment. Reduces
cravings for alcohol, and decreases
alcohol use.
Common adverse effects: impaired
cognition (“DOPE-a-max”), nausea /
weight loss, metabolic acidosis.
Management
■ For mild-to-moderate agitation and anxiety: Reassurance of the patient and
benzodiazepines.
■ For severe agitation or psychosis: Antipsychotics (e.g., haloperidol).
■ Symptomatic support (i.e., control hypertension, arrhythmias).
■ Temperature of >102°F should be treated aggressively with an ice bath,
cooling blanket, and other supportive measures.
COCAINE USE DISORDER
Treatment of cocaine use disorder:
■ There is no Food and Drug Administration (FDA)-approved
pharmacotherapy for cocaine use disorder.
■ Off-label medications are sometimes used (naltrexone, modafinil,
topiramate).
■ Psychological interventions (contingency management, relapse prevention,
NA, etc.) are the mainstay of treatment.
WITHDRAWAL
■ Abrupt abstinence is not life threatening.
■ Produces post-intoxication depression (“crash”): Malaise, fatigue,
hypersomnolence, depression, anhedonia, hunger, constricted pupils, vivid
dreams, psychomotor agitation, or retardation. Occasionally, these patients
can become suicidal.
■ With mild-to-moderate cocaine use, withdrawal symptoms resolve within
72 hours; with heavy, chronic use, they may last for 1–2 weeks.
■ Treatment is supportive, but severe psychiatric symptoms may warrant
hospitalization.
Amphetamines
■ Classic amphetamines:
●Block reuptake and facilitate release of dopamine and norepinephrine
from nerve endings, causing a stimulant effect.
●Examples: Dextroamphetamine (Dexedrine), methylphenidate (Ritalin),
methamphetamine (Desoxyn, “ice,” “speed,” “crystal meth,” “crank”).
●Methamphetamines are easily manufactured in home laboratories using
over-the-counter medications (e.g., pseudoephedrine).
●Methamphetamines are used medically in the treatment of narcolepsy,
attention deficit/hyperactivity disorder (ADHD), binge eating, and
occasionally depressive disorders.
■ Substituted (“designer,” “club drugs”) amphetamines:
●Release dopamine, norepinephrine, and serotonin from nerve endings.
●Examples: MDMA (“ecstasy”), MDEA (“eve”).
●Often used in dance clubs and raves.
●Have both stimulant and hallucinogenic properties.
●Serotonin syndrome is possible if designer amphetamines are combined
with selective serotonin reuptake inhibitors (SSRIs).
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
WARDS
QUESTION
Q: Why should beta-blockers be
avoided for patients who regularly
use cocaine?
A: Cocaine has both alphaand beta-adrenergic effects.
If a beta-blocker is given
­simultaneously, unopposed
alpha-adrenergic activity can
cause coronary vasoconstriction
and induce myocardial infarction.
KEY FACT
Cocaine or amphetamines can
both cause formication, a tactile
hallucination of something crawling on or under the skin.
KEY FACT
Symptoms of amphetamine intoxication include euphoria, dilated
pupils, increased libido, tachycardia, perspiration, grinding teeth,
and chest pain.
86
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
INTOXICATION
WARDS TIP
Clinical Presentation
Chronic amphetamine use leads
to accelerated tooth decay (“meth
mouth”).
WARDS TIP
Both amphetamine and PCP use
can cause rhabdomyolysis. Look
for elevated creatine kinase (CK)
and monitor closely for acute
kidney injury. Treatment is mostly
supportive and emphasizes
­hydration.
Phencyclidine (PCP)
KEY FACT
Ketamine (“special K”) can produce
tachycardia, tachypnea, hallucinations, and amnesia.
INTOXICATION
Clinical Presentation
KEY FACT
PCP intoxication ­symptoms—
RED DANES
Rage
Erythema (redness of skin)
Dilated pupils
Delusions
Amnesia
Nystagmus
Excitation
Skin dryness
Treatment
WITHDRAWAL
KEY FACT
Nystagmus (especially rotary) is
very common in PCP intoxication.
■ Amphetamine intoxication causes symptoms similar to those of cocaine (see
above).
■ MDMA and MDEA may induce sense of closeness to others.
■ Overdose can cause hyperthermia, dehydration (especially after a prolonged
period of dancing in a club), rhabdomyolysis, and renal failure.
■ Complications of their long half-life can cause ongoing psychosis, even
during abstinence.
■ Amphetamine withdrawal can cause prolonged depression.
Treatment
Rehydrate, correct electrolyte balance, and treat hyperthermia.
PCP, or “angel dust,” is a dissociative, hallucinogenic drug that antagonizes
N-methyl-d-aspartate (NMDA) glutamate receptors and activates dopaminergic
­neurons. It can have stimulant or CNS depressant effects, depending on the dose taken.
■ PCP can be smoked as “wet” (sprinkled on cigarette) or as a “joint”
(sprinkled on marijuana).
■ Ketamine is similar to PCP, but is less potent. Ketamine is sometimes used
as a “date rape” drug, as it is odorless and tasteless.
■ Effects include agitation, depersonalization, hallucinations, synesthesia
(one sensory stimulation evokes another—e.g., hearing a sound causes one
to see a color), impaired judgment, memory impairment, combativeness,
nystagmus (rotary, horizontal, or vertical), ataxia, dysarthria, hypertension,
tachycardia, muscle rigidity, and high tolerance to pain.
■ Overdose can cause seizures, delirium, coma, and even death.
■ Monitor vitals, temperature, and electrolytes, and minimize sensory
stimulation.
■ Use benzodiazepines (lorazepam) to treat agitation, anxiety, muscle spasms,
and seizures.
■ Use antipsychotics (haloperidol) to control severe agitation or psychotic
symptoms.
No withdrawal syndrome, but “flashbacks” (recurrence of intoxication
­symptoms due to release of the drug from body lipid stores) may occur.
Sedative-Hypnotics
Agents in the sedative-hypnotics category include benzodiazepines, barbiturates,
zolpidem, zaleplon, gamma-hydroxybutyrate (GHB), meprobamate, and others.
These medications, especially benzodiazepines, are highly abused in the United
States, as they are more readily available than other drugs such as cocaine.
■ Benzodiazepines (BZDs):
●Commonly used in the treatment of anxiety disorders.
●Easily obtained via prescription from physicians’ offices and emergency
departments.
●Potentiate the effects of GABA by modulating the receptor, thereby
increasing frequency of chloride channel opening.
■ Barbiturates:
●Used in the treatment of epilepsy and as anesthetics.
●Potentiate the effects of GABA by binding to the receptor and increasing
duration of chloride channel opening.
●At high doses, barbiturates act as direct GABA agonists, and therefore
have a lower margin of safety relative to BZDs. Overdose can be lethal.
●They are synergistic in combination with BZDs (as well as other CNS
depressants such as alcohol); respiratory depression can occur.
INTOXICATION
Clinical Presentation
■ Intoxication with sedatives produces drowsiness, confusion, hypotension,
slurred speech, incoordination, ataxia, mood lability, impaired judgment,
nystagmus, respiratory depression, and coma or death in overdose.
■ Symptoms are synergistic when combined with EtOH or opioids/narcotics.
■ Long-term sedative use may lead to dependence and may cause depressive
symptoms.
Treatment
■ Maintain airway, breathing, and circulation. Monitor vital signs.
■ Activated charcoal and gastric lavage to prevent further gastrointestinal
absorption (if drug was ingested in the prior 4–6 hours).
■ For barbiturates only: Alkalinize urine with sodium bicarbonate to promote
renal excretion.
■ For benzodiazepines only: Flumazenil in overdose.
■ Supportive care—Improve respiratory status, control hypotension.
WITHDRAWAL
Abrupt abstinence after chronic use can be life threatening. While physiological dependence is more likely with short-acting agents, longer-acting agents
can also cause dependence and withdrawal symptoms.
CLINICAL PRESENTATION
Signs and symptoms of withdrawal are the same as these of EtOH withdrawal.
Tonic-clonic seizures may occur and can be life threatening.
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
KEY FACT
PCP intoxication is associated
with violence, more so than other
drugs.
KEY FACT
Gamma-hydroxybutyrate (GHB) is
a CNS depressant that produces
confusion, dizziness, drowsiness,
memory loss, respiratory distress,
and coma. It is commonly used as
a date-rape drug.
WARDS
QUESTION
Q: Which substances of abuse
have potentially fatal withdrawal
syndromes?
A: Alcohol, benzodiazepines, and
barbiturates.
WARDS TIP
Flumazenil is a very short-acting
BZD antagonist used for treating
BZD overdose. Use with caution
when treating overdose, as it may
precipitate seizures.
KEY FACT
The opioid dextromethorphan is
a common ingredient in cough
syrup.
88
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
Treatment
KEY FACT
Infection secondary to needle
sharing is a common cause of
morbidity from street heroin
usage.
Opioids
KEY FACT
Opioid intoxication: Nausea, vomiting, sedation, decrease in pain
perception, decrease in gastrointestinal motility, pupil constriction,
and respiratory depression (which
can be fatal).
INTOXICATION
Clinical Presentation
KEY FACT
Meperidine is the exception to
opioids producing miosis.
“Demerol Dilates pupils.”
Treatment
KEY FACT
■ Ventilatory support may be required.
Naloxone is the treatment of
choice for opiate overdose.
OPIATE USE DISORDER
WARDS TIP
WITHDRAWAL
Classic triad of opioid overdose—Rebels Admire Morphine
Respiratory depression
Altered mental status
Miosis
■ Benzodiazepines (stabilize patient, then taper gradually).
■ Carbamazepine or valproic acid taper not as beneficial.
■ Opioid medications and drugs of abuse stimulate mu, kappa, and delta
opiate receptors (normally stimulated by endogenous opiates), and are
involved in analgesia, sedation, and dependence. Examples include heroin,
oxycodone, codeine, dextromethorphan, morphine, methadone, and
meperidine (Demerol).
■ Opioids also have effects on the dopaminergic system, which mediates their
addictive and rewarding properties.
■ Prescription opioids (OxyContin [oxycodone], Vicodin [hydrocodone/
acetaminophen], and Percocet [oxycodone/acetaminophen])—not heroin—
are the most commonly used opioids.
■ Behaviors such as losing medication, “doctor shopping,” and running out of
medication early should alert clinicians of possible misuse.
■ Opioids are associated with more deaths (usually due to unintentional
overdose) than any other drug.
■ Opioid intoxication causes drowsiness, nausea/vomiting, constipation,
slurred speech, constricted pupils, seizures, and respiratory depression,
which may progress to coma or death in overdose.
■ Meperidine and monoamine oxidase inhibitors taken in combination may
cause serotonin syndrome: hyperthermia, confusion, hypertension or
hypotension, and hyperreflexia.
■ Ensure adequate airway, breathing, and circulation.
■ In overdose, administration of naloxone (an opioid antagonist) will
improve respiratory depression but may cause severe withdrawal in an
opioid-dependent patient.
■ Patients at risk of opioid overdose should be prescribed a naloxone (Narcan)
kit to keep at home for emergencies.
See Table 7-7 for treatment of opioid use disorder.
■ While not life threatening, abstinence in the opioid-dependent individual
leads to an unpleasant withdrawal syndrome characterized by dysphoria,
insomnia, lacrimation, rhinorrhea, yawning, weakness, sweating,
piloerection, nausea/vomiting, fever, dilated pupils, abdominal cramps,
arthralgia/myalgia, hypertension, tachycardia, and craving.
89
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
■ Treatment includes:
●Moderate symptoms: Symptomatic treatment with clonidine (for
autonomic signs and symptoms of withdrawal), nonsteroidal
anti-inflammatory drugs (NSAIDs) for pain, loperamide for diarrhea,
dicyclomine for abdominal cramps, promethazine for nausea, etc.
●Severe symptoms: Detox with buprenorphine or methadone.
●Monitor degree of withdrawal with COWS (Clinical Opioid Withdrawal
Scale), which uses objective measures (i.e., pulse, pupil size, tremor) to
assess withdrawal severity.
Hallucinogens
Hallucinogenic drugs of abuse include psilocybin (mushrooms), mescaline
(peyote cactus), and lysergic acid diethylamide (LSD). Pharmacological effects
vary, but LSD is believed to act on the serotonergic system. Hallucinogens do
not cause physical dependence or withdrawal, though users can rarely develop
psychological dependence.
INTOXICATION
■ Effects include perceptual changes (illusions, hallucinations, body image
distortions, synesthesia), labile affect, dilated pupils, tachycardia, hypertension,
hyperthermia, tremors, incoordination, sweating, and palpitations.
TABLE 7-7. Pharmacological Treatment of Opioid Use Disorder
Medication
Mechanism
Pros
Cons
Methadone
Full agonist at mu-opioid
receptor.
Administered once daily. Long half life.
Restricted to federally licensed substance
abuse treatment programs. Can cause
QTc interval prolongation: screening
electrocardiogram is indicated, particularly in
patients with high risk of cardiac disease.
Presenting to the methadone clinic
for regular pickups can be helpful
for patients who benefit from daily
structure and access to group therapy
or case management.
Patients can still use other opioids on top of
methadone.
Buprenorphine
Partial opioid receptor
agonist—can precipitate
withdrawal if used too
soon after full opioid
agonists.
Sublingual preparation that is safer
than methadone, as its effects reach a
plateau and make overdose unlikely.
In the outpatient setting, can only be
prescribed by a physician with a special
waiver on their controlled substances license.
Combined formulation
(buprenorphine-naloxone, or
Suboxone) prevents intoxication from
intravenous or intranasal use.
Naltrexone
Competitive opioid
antagonist, precipitates
withdrawal if used within 7
days of heroin use
Available as daily oral medication or
monthly depot injection. It is a good
choice for highly motivated patients
such as health care professionals.
Adherence is an issue for oral formulation.
Risk of LFT elevation. Can interfere with
anesthesia (e.g., for acute injuries or surgical
procedures).
Naloxone
Competitive opioid
antagonist, used in
treatment of overdose.
Can be life-saving for patients or
their peers, and should routinely be
prescribed for all patients with opioid
use disorder (especially for those who
are receiving medication-assisted
treatment).
Does not reduce opioid use or treat
symptoms of opioid use disorder.
Very short half-life; patients must be educated
about need to call EMS or present to ED
after it’s administered (even if the overdose
appears to be reversed).
Rapid recovery of consciousness
following the administration of intravenous (IV) naloxone (a potent
opioid antagonist) is consistent
with opioid overdose.
WARDS TIP
Eating large amounts of poppy
seed bagels or muffins can result
in a urine drug screen that is positive for opioids.
KEY FACT
90
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
KEY FACT
Remember the withdrawal symptoms of opiates: flu-like symptoms
(body aches, anorexia, rhinorrhea,
fever), diarrhea, anxiety, insomnia,
and piloerection. These are not life
threatening.
WITHDRAWAL
Marijuana
KEY FACT
An LSD flashback is a spontaneous
recurrence of symptoms mimicking a prior LSD “trip” that may last
for minutes to hours.
INTOXICATION
KEY FACT
Dronabinol is a pill form of THC
that is FDA-approved for certain
indications.
WITHDRAWAL
■ Treatment: Supportive and symptomatic.
Inhalants
■ Usually lasts 6–12 hours, but may last for several days.
■ May have a “bad trip” that consists of marked anxiety, panic, and psychotic
symptoms (paranoia, hallucinations).
■ Treatment: Monitor for dangerous behavior and reassure patient. Use
benzodiazepines as first-line for agitation (can use antipsychotics if needed).
No withdrawal syndrome is produced, but with long-term LSD use, patients
may experience flashbacks later in life.
■ Cannabis (“marijuana,” “pot,” “weed,” “grass”) is the most commonly used
illicit substance in the world.
■ The main psychoactive component which produces the “high” in cannabis is
THC (tetrahydrocannabinol).
■ Cannabinoid receptors in the brain inhibit adenylate cyclase.
■ Marijuana has shown some efficacy in treating nausea and vomiting in
chemotherapy patients, increasing appetite in AIDS patients, in chronic pain
(from cancer), and lowering intraocular pressure in glaucoma. A specific
class of compounds found in marijuana, cannabidiols (CBDs), is currently
being studied for management of pain, seizures, and anxiety/depression.
■ Marijuana causes euphoria, anxiety, impaired motor coordination,
perceptual disturbances (sensation of slowed time), mild tachycardia,
anxiety, conjunctival injection (red eyes), dry mouth, and increased appetite
(“the munchies”).
■ Cannabis-induced psychotic disorders with paranoia, hallucinations, and/or
delusions may occur. There is no overdose syndrome for marijuana use.
■ Cannabis use disorder occurs in approximately 10% of those who use (up to
50% of daily users).
■ Chronic use may cause respiratory problems such as asthma and chronic
bronchitis, immunosuppression, cancer, and possible effects on reproductive
hormones.
■ Treatment: Supportive, psychosocial interventions (e.g., contingency
management, groups).
■ Withdrawal symptoms may include irritability, anxiety, restlessness,
aggression, strange dreams, depression, headaches, sweating, chills,
insomnia, and low appetite.
■ Inhalants include a broad range of drugs that are inhaled and absorbed
through the lungs.
■ Inhalants generally act as CNS depressants.
■ Most commonly used by preadolescents or adolescents; rate of use is similar
between boys and girls (but rare in adult females).
■ Examples: Solvents, glue, paint thinners, fuels, isobutyl nitrates (“huffing,”
“laughing gas,” “rush,” “bolt”).
INTOXICATION
■ Effects: Perceptual disturbances, paranoia, lethargy, dizziness, nausea/vomiting,
headache, nystagmus, tremor, muscle weakness, hyporeflexia, ataxia, slurred
speech, euphoria, hypoxia, clouding of consciousness, stupor, or coma.
■ Acute intoxication: 15–30 minutes. May be sustained with repeated use.
■ Overdose: May be fatal secondary to respiratory depression or cardiac
arrhythmias.
■ Long-term use may cause permanent damage to CNS (e.g., neurocognitive
impairment, cerebellar dysfunction, Parkinsonism, seizures), peripheral
neuropathy, myopathy, aplastic anemia, malignancy, metabolic acidosis,
urinary calculi, glomerulonephritis, myocarditis, MI, and hepatotoxicity.
■ Treatment: Monitor airway, breathing, and circulation; may need oxygen
with hypoxic states.
■ Identify solvent because some (e.g., leaded gasoline) may require chelation.
WITHDRAWAL
A withdrawal syndrome does not usually occur, but symptoms may include
irritability, sleep disturbance, anxiety, depression, nausea, vomiting, and craving.
Caffeine
Caffeine is the most commonly used psychoactive substance in the United
States, usually in the form of coffee, tea, or energy drinks. It acts as an adenosine antagonist, causing increase in cyclic adenosine monophosphate (cAMP)
and stimulating the release of excitatory neurotransmitters.
OVERDOSE
■ More than 250 mg (2 cups of coffee): Anxiety, insomnia, muscle twitching,
rambling speech, flushed face, diuresis, gastrointestinal disturbance,
restlessness, excitement, and tachycardia.
■ More than 1 g: May cause tinnitus, severe agitation, visual light flashes, and
cardiac arrhythmias.
■ More than 10 g: Death may occur secondary to seizures and respiratory
failure.
■ Treatment: Supportive and symptomatic.
WITHDRAWAL
■ Caffeine withdrawal symptoms occur in 50–75% of caffeine users if
cessation is abrupt.
■ Withdrawal symptoms include headache, fatigue, irritability, nausea,
vomiting, drowsiness, muscle pain, and depression.
■ Usually resolves within 1½ weeks.
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
92
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
Nicotine
WARDS TIP
Cigarette smoking during pregnancy is associated with low birth
weight, SIDS, and a variety of
postnatal morbidities.
TREATMENT OF NICOTINE DEPENDENCE
FDA-approved pharmacotherapy:
■ Relapse after abstinence is common.
Gambling Disorder
DIAGNOSIS AND DSM-5 CRITERIA
■ Nicotine is derived from the tobacco plant, and stimulates nicotinic
receptors in autonomic ganglia of the sympathetic and parasympathetic
nervous systems. It is highly addictive through its effects on the
dopaminergic system.
■ Nicotine use causes both tolerance and physical dependence (i.e., prominent
craving and withdrawal).
■ Cigarette smoking is the leading cause of preventable morbidity and
mortality in the United States, posing many health risks including chronic
obstructive pulmonary disease (COPD), cardiovascular diseases, and
various cancers.
■ Current smoking prevalence is about 15% of U.S. adults.
■ Effects: Restlessness, insomnia, anxiety, and increase in gastrointestinal
motility.
■ Withdrawal symptoms: Intense craving, dysphoria, anxiety, poor
concentration, increase in appetite, weight gain, irritability, restlessness, and
insomnia.
■ Varenicline (Chantix): a4b2 nicotinic cholinergic receptor (nAChR) partial
agonist that mimics the action of nicotine, reducing the rewarding aspects
and preventing withdrawal symptoms.
■ Bupropion (Zyban): Antidepressant inhibits reuptake of dopamine and
norepinephrine; helps reduce craving and withdrawal symptoms.
■ Nicotine replacement therapy (NRT): Available as transdermal patch, gum,
lozenge, nasal spray, and inhaler.
■ Behavioral support/counseling should be part of every treatment.
Persistent and recurrent problematic gambling behavior, as evidenced by four
or more of the following in a 12-month period:
Preoccupation with gambling.
Need to gamble with increasing amount of money to achieve pleasure.
Repeated and unsuccessful attempts to cut down on or stop gambling.
Restlessness or irritability when attempting to stop gambling.
Gambling when feeling distressed (depressed, anxious, etc.).
Returning to reclaim losses after gambling (“get even”).
Lying to hide level of gambling.
Jeopardizing relationships or job because of gambling.
Relying on others to financially support gambling.
EPIDEMIOLOGY/ETIOLOGY
■ Prevalence: 0.4–1.0% of adults in the United States.
■ Men represent most of the cases.
■ More common in young adults and middle-aged, and lower rates in older
adults.
■ Similar to substance use disorders, the course is marked by periods of
abstinence and relapse.
■ Increased incidence of mood disorders, anxiety disorders, substance use
disorders, and personality disorders.
■ Etiology may involve genetic, temperamental, environmental, and
neurochemical factors.
■ One-third may achieve recovery without treatment.
TREATMENT
■ Participation in Gamblers Anonymous (a 12-step program) is the most
common treatment.
■ Cognitive-behavioral therapy has been shown to be effective, particularly
when combined with Gamblers Anonymous.
■ Important to treat comorbid mood disorders, anxiety disorders, and
substance use disorders where appropriate.
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
94
SUBSTANCE-RELATED AND ADDICTIVE DISORDERS
NOTES

11 - Chapter 8 Neurocognitive Disorders

01 - Chapter 8 Neurocognitive Disorders
Chapter 8 Neurocognitive Disorders
NEUROCOGNITIVE
CHAPTER 8
DISORDERS
Definition.................................................................................................................................96
Delirium....................................................................................................................................96
Epidemiology......................................................................................................................96
Risk Factors..........................................................................................................................96
Precipitating Factors............................................................................................................96
Etiology...............................................................................................................................97
Clinical Manifestations........................................................................................................97
Diagnosis.............................................................................................................................98
Treatment............................................................................................................................98
Mild and Major Neurocognitive Disorders...............................................................................100
Diagnosis...........................................................................................................................100
Alzheimer Disease (AD).....................................................................................................101
Vascular Disease (Vascular Cognitive Impairment)............................................................102
Lewy Body Disease (LBD)...................................................................................................103
Frontotemporal Degeneration (FTD)..................................................................................105
HIV Infection......................................................................................................................105
Huntington Disease (HD)...................................................................................................106
Parkinson Disease (PD)......................................................................................................106
Prion Disease (Transmissible Spongiform Encephalopathies)............................................107
Normal Pressure Hydrocephalus (NPH)..............................................................................108
96
NEUROCOGNITIVE DISORDERS
Definition
Delirium
WARDS TIP
■ Delirium is a medical emergency.
Terms commonly used for delirium
include toxic or metabolic encephalopathy, acute organic brain syndrome, acute confusional state, acute
toxic psychosis, and ICU psychosis.
■ Potentially reversible.
■ Can advance to coma, seizures, or death.
EPIDEMIOLOGY
WARDS TIP
Consider delirium as acute brain
failure—a medical emergency like
other acute organ failures.
RISK FACTORS
WARDS
QUESTIONS
■ Advanced age.
Q: What is the “ICU triad?”
A: Pain, Agitation, and Delirium.
■ Prior history of delirium.
■ Severe or terminal illness.
■ Multiple medical comorbidities.
■ Hearing or vision impairment.
PRECIPITATING FACTORS
WARDS TIP
Delirium is commonly experienced
by patients in the ICU and postoperative recovery.
■ Alcohol use or withdrawal.
■ Infection.
■ Pain.
■ Dehydration.
■ Malnutrition.
■ Impaired mobility.
■ Sleep deprivation.
■ Organ failure.
■ Mechanical ventilation.
The neurocognitive disorders (NCDs) comprise a group of conditions defined by
decline from a previous level of cognitive functioning. The six cognitive domains
that may be affected include complex attention, executive function, learning
and memory, language, perceptual-motor skills, and social cognition (interaction). By definition, cause(s) for the deficits may be ascertained from findings on
history, physical exam, and diagnostic testing. The DSM-5 divides the NCDs into
three main categories: delirium, mild NCDs, and major NCDs (dementias).
■ May be the only early manifestation of serious illness.
■ Associated with high mortality. Up to 40% of individuals die within 1 year
of diagnosis.
■ Up to one-half of hospitalized elderly patients develop delirium.
■ As many as 90% of patients with a preexisting NCD (dementia) will
experience a superimposed delirium when admitted to the hospital.
■ Delirium often goes unrecognized (65–88% of the time).
■ Delirium is associated with an increased risk for later development of
major NCD.
■ Preexisting cognitive impairment or depression.
■ Polypharmacy, including the use of psychotropic medications (especially
benzodiazepines and anticholinergic drugs).
TABLE 8-1. Clinical Scenarios of Delirium on Exam
Scenario
Likely Diagnosis
Diagnostic Testing
Delirium + fever + cough + rales
Pneumonia
Chest x-ray
Delirium + dysuria + suprapubic
tenderness
Urinary tract infection
Urinalysis and urine
culture
Delirium + constricted pupils (miosis) +
bradypnea
Opioid intoxication
Urine toxicology screen
Delirium + fever + nuchal rigidity +
photophobia
Meningitis
Lumbar puncture
Delirium + tachycardia + tremor +
thyromegaly
Thyrotoxicosis
TSH, free T4, T3
Delirium + insulin use
Hypoglycemia
Blood glucose
ETIOLOGY
■ Almost any medical condition can cause delirium (see examples in Table 8-1).
■ The DSM-5 recognizes five broad categories:
•• Substance intoxication delirium.
•• Substance withdrawal delirium.
•• Medication-induced delirium.
•• Delirium due to another medical condition.
•• Delirium due to multiple etiologies.
CLINICAL MANIFESTATIONS
■ Primarily a disorder of attention and awareness (i.e., orientation).
■ Cognitive deficits develop acutely over hours to days.
■ Symptoms fluctuate throughout the course of a day, typically worsening at
night.
■ Other features include deficits in recent memory, language abnormalities,
or perceptual disturbances (usually visual, such as illusions or
hallucinations).
■ Circadian rhythm disruption and emotional symptoms are common.
■ There are three types of delirium based on psychomotor activity.
•• Purely hypoactive (“quiet”) type
Decreased psychomotor activity, ranging from drowsiness to lethargy
to stupor.
More likely to go undetected.
More common in the elderly.
•• Purely hyperactive type (“ICU psychosis”)
Manifests with agitation, mood lability, and uncooperativeness.
More easily identified due to its disruptiveness.
More common in drug withdrawal or toxicity.
•• Mixed type
Psychomotor activity may remain stable at baseline or fluctuate rapidly
between hyperactivity and hypoactivity.
■ Hospitalized patients usually recover within 1 week, although some degree
of cognitive deficits can persist for months or even indefinitely.
NEUROCOGNITIVE DISORDERS
WARDS TIP
Common causes of
medication-induced delirium:
• Anticholinergics
• Benzodiazepines
• Nonbenzodiazepine hypnotics
(“Z-drugs”)
• Opioids (especially meperidine)
• Corticosteroids
• Tricyclic antidepressants
• H2 blockers
WARDS
QUESTION
Q: What are the two most common precipitants of delirium in
children?
A: Febrile illnesses and
­medications.
WARDS TIP
Suspect delirium if a patient presents with altered mental status,
disorientation, confusion, agitation, or sudden onset of psychotic
symptoms.
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NEUROCOGNITIVE DISORDERS
TABLE 8-2. DSM-5 Criteria for Delirium
WARDS TIP
■ Disturbance in attention and awareness.
■ Disturbance in an additional cognitive domain.
A quick, first-glance bedside exam
for suspected substance/medication intoxication is VALEUMS.
■ Not occurring during a coma.
• Vital signs
• Alertness Level
• Eyes (pupil size and position)
• Urine (bladder distention or
incontinence)
• Mucous membranes (moisture)
• Skin (temperature and
moisture)
DIAGNOSIS
KEY FACT
Delirium generally manifests as
diffuse background slowing on
electroencephalography (EEG).
An exception is delirium tremens,
which is associated with fast EEG
activity. EEG lacks sensitivity and
specificity for making the diagnosis but is useful for ruling out
nonconvulsive seizures.
WARDS TIP
Consider obtaining a head CT for
a patient with delirium under the
following circumstances:
• No underlying cause evident on
initial evaluation.
• In the context of head trauma.
• New focal neurologic deficits
detected on exam.
• Patient is unable or unwilling
to cooperate with a neurologic
examination.
• No improvement despite
treatment of already identified
causes.
TREATMENT
■ Treat the underlying cause(s).
■ Develops acutely over hours to days, represents a change from baseline, and tends to
fluctuate.
■ Not better accounted for by another neurocognitive disorder.
■ Evidence from history, physical, or labs that the disturbance is a direct consequence of
another medical condition, substance intoxication/withdrawal, exposure to toxin,
or due to multiple etiologies.
■ Table 8-2 summarizes the DSM-5 diagnostic criteria.
■ A useful clinical tool for evaluation of a patient with suspected delirium is
the Confusion Assessment Method (CAM).
•• This method takes 5 minutes to perform and has a high sensitivity and
specificity.
•• Delirium is diagnosed in a patient with inattention of acute onset and/
or fluctuating course along with either disorganized thinking or altered
consciousness.
Inattention manifests as distractibility or difficulty maintaining focus
during the evaluation.
Disorganized thinking is demonstrated via derailment or loose
­associations.
Level of consciousness ranges from vigilant (hyperalert) to alert (normal) to lethargic (drowsy, but easily aroused) to stuporous (difficult to
arouse) to comatose (unarousable to verbal stimulation).
■ Once delirium has been diagnosed, the cause(s) should be sought.
•• Finger-stick blood glucose, pulse-oximetry, arterial blood gases, and
electrocardiography can quickly provide useful data at bedside.
•• Labs typically obtained in a delirium workup include a basic metabolic
panel, serum magnesium, complete blood count with differential,
urinalysis, and urine culture.
•• Urine and blood drug screen, blood alcohol level, therapeutic drug levels
(e.g., antiepileptics, digoxin, lithium), hepatic panel, thyroid hormone
levels, inflammatory markers (e.g., C-reactive protein, erythrocyte
sedimentation rate), vitamin B12 level, or chest x-ray may also be
warranted depending on the clinical presentation.
•• Head imaging (head CT or brain MRI), EEG, and lumbar puncture
should be performed if focal neurological deficits are present or a cause of
delirium cannot be identified with the initial workup.
■ Address potential exacerbating factors: Mobility limitations, sensory
deficits, sleep cycle disruption, constipation, urinary retention, dehydration,
electrolyte abnormalities, uncontrolled pain, and medications.
■ Encourage a family member to stay at the bedside to help with supervision
and orientation.
■ Utilize a one-to-one sitter if needed.
■ Reorient the patient on a regular basis regarding time, place, and situation.
Open window shades during the day and place whiteboards, calendars, and
clocks in plain sight.
■ D2 antagonists (i.e., antipsychotics) are indicated for treatment of agitation
that endangers the patient or others.
•• Haloperidol is the preferred agent and can be administered orally,
intramuscularly, or intravenously.
•• D2 antagonists exacerbate extrapyramidal symptoms; use with caution in
patients with Parkinsonism.
■ Avoid benzodiazepines (except in alcohol or benzodiazepine withdrawal)
as they may worsen the delirium by causing paradoxical disinhibition or
over-sedation.
■ Avoid the use of restraints. They can worsen agitation and cause injury.
When restraints are necessary, reassess often and remove as soon as possible.
Use the least restrictive means appropriate for the situation.
An 83-year-old female is admitted to the hospital after presenting with a
fever and altered mental status. Her home nurse aide reports that the patient
was in her usual state of health until 24 hours prior to admission when she
became confused and seemed to be talking to herself. In a few hours, her
mental status improved then deteriorated again. After the patient dialed 911
to report that she was being held hostage by terrorists, her nurse aid called
an ambulance on her behalf.
On examination, the patient is somnolent and has difficulty responding to
questions appropriately. She is disoriented to place and time.
When the daughter calls to check in, she shares that her mother has had
progressive memory deficits over the past several years. The patient can no
longer drive and requires assistance with finances and meal preparation.
What is the most likely acute diagnosis?
The patient most likely has delirium. She presents with a sudden change
in cognition as manifested by confusion, disorientation, and hallucinations.
She has had an acute change from her baseline behavior. Her symptoms
wax and wane throughout the day, representing the typical fluctuation
found in delirium. She presents with a fever, likely secondary to an infection.
If confirmed, her diagnosis would be delirium due to the specific infectious
etiology.
Collateral information points to a prior diagnosis of major neurocognitive
disorder (dementia). She has a history of memory impairment that began
gradually and has progressively worsened. There is also history of impairment in executive functioning, and she can no longer care for herself. The
existence of a major neurocognitive disorder is a risk factor for the development of a superimposed delirium.
NEUROCOGNITIVE DISORDERS
WARDS
QUESTION
Q: In what scenarios is it appropriate to use benzodiazepines to
treat delirium?
A: Alcohol and benzodiazepine
withdrawal.
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NEUROCOGNITIVE DISORDERS
DIAGNOSIS
KEY FACT
Thyroid dysfunction can cause
reversible cognitive impairment.
Hypothyroidism is typically
accompanied by fatigue and cold
intolerance. Hyperthyroidism in
the elderly may manifest as an
“apathetic thyrotoxicosis,” characterized by depression and lethargy. Thyroid function tests are often
included in the initial workup of
any new onset psychiatric illness.
Objective findings on cognitive testing
(preferably standardized neuropsychological
testing)
Mild and Major Neurocognitive Disorders
■ The non-delirium NCDs are characterized by a chronic cognitive decline
that impacts functioning in daily activities (Table 8-3).
■ Individuals with mild NCDs (mild cognitive impairment [MCI] or
cognitive impairment, no dementia [CIND]) experience difficulty with some
of the more complex activities of daily living but are able to maintain their
independence.
■ Patients with major NCDs require assistance with independent activities
of daily living (IADLs), such as paying bills, managing medications,
or shopping for groceries. Over time, the basic activities of daily living
(e.g., feeding, toileting, bathing) are affected, eventually leading to total
dependence.
■ The mild and major NCDs are also subcategorized by etiology (Table 8-4).
•• The dementias comprise a large group of progressive and irreversible
major NCDs that primarily affect the elderly.
•• Several other major NCDs present similarly to the dementias, but
their progression may be arrested or even reversed with treatment
(e.g., vitamin B12 deficiency, thyroid dysfunction, normal pressure
hydrocephalus).
■ The Mini Mental State Exam (MMSE) is a screening test used due to its
speed and ease of administration.
•• Assesses orientation, attention/concentration, language, constructional
ability, and immediate and delayed recall.
•• Sensitive for major NCDs (e.g., dementias), particularly
moderate-to-severe forms.
Perfect score: 30.
Dysfunction: <25.
•• Not as sensitive for mild NCDs and early major NCDs.
•• Lacks specificity.
•• Norm tables are available to adjust for age and education.
TABLE 8-3. DSM-5 Criteria for Mild and Major NCDs
Criterion
Mild NCDs
Major NCDs
Functional decline in at least one cognitive domain relative to baseline as evidenced by
Concern (expressed by the patient or caretaker)
Mild decline
Significant decline
Modest
impairment
Substantial
impairment
Effect on functioning in daily life.
Ability to perform
IADLs preserved
Impaired
performance of
IADLs/ADLs
Deficits do not occur exclusively in the context of a delirium
Deficits are not better explained by another mental disorder.
ADLs, basic activities of daily living; IADLs, independent activities of daily living.
TABLE 8-4. Clinical Scenarios of Neurocognitive Disorders on Exam
Scenario
Likely Diagnosis
65-year-old patient with memory impairment + executive
dysfunction + poor insight progressing later to psychiatric/
behavioral disturbances + insomnia + apraxia.
65-year-old patient with executive dysfunction + cognitive
slowing + stepwise progression ± focal neurologic
abnormalities ± history of known stroke.
60-year-old patient with gait apraxia + urinary urgency →
incontinence + executive dysfunction + apathy.
Normal pressure
hydrocephalus
50-year-old patient with parkinsonism preceding cognitive
decline by several years.
Parkinson disease
50-year-old patient with concomitant development
of cognitive impairment (visuospatial dysfunction) +
parkinsonism, as well as REM sleep behaviors + fluctuating
alertness level + visual hallucinations.
Patient of any age with cognitive slowing + short-term memory
impairment + fatigue + cold intolerance.
Hypothyroidism
Patient of any age with cognitive slowing + depression + vegan
diet + paresthesias/numbness + ataxia.
Vitamin B12 deficiency
■ Another commonly used screening tool is the Mini-Cog.
•• Consists of three-item recall and clock-drawing tasks.
•• Positive screening for cognitive impairment:
No items recalled after 3 minutes.
Only one to two items recalled with abnormal clock drawing.
•• Negative screening:
All three items repeated correctly after 3 minutes.
One to two items recalled with normal clock drawing.
■ Other commonly used screening tools include:
•• Blessed Orientation-Memory-Concentration (BOMC).
•• Montreal Cognitive Assessment (MoCA).
•• Frontal Assessment Battery (FAB).
■ An abnormal screening test indicates the need for further testing, preferably
formal neuropsychological testing.
ALZHEIMER DISEASE (AD)
Alzheimer disease is the most common underlying etiology of major NCDs
(dementias).
Clinical Manifestations
■ Gradually progressive decline in cognitive functions.
■ The primary cognitive domains affected are memory, learning, and
language.
■ Personality changes, mood swings, and paranoia are very common.
■ Motor and sensory symptoms appear in advanced disease.
■ Death often occurs within 10 years of diagnosis.
NEUROCOGNITIVE DISORDERS
Alzheimer disease
Vascular NCD
NCD with Lewy bodies
WARDS
QUESTION
Q: What are the “four As” of Alzheimer disease?
A: Amnesia, agnosia, apraxia, and
aphasia.
KEY FACT
Postmortem pathological examination of the brain is the only way
to definitively diagnose Alzheimer
disease.
102
NEUROCOGNITIVE DISORDERS
Diagnosis
KEY FACT
Senile plaques and neurofibrillary
tangles are found in Alzheimer disease, as well as Down syndrome
and even in normal aging.
Etiology
KEY FACT
Adults with Down syndrome are
at increased risk of developing
Alzheimer disease in midlife.
Epidemiology
Treatment
WARDS TIP
Antipsychotics carry a black box
warning about increased risk of
death in patients with dementia.
■ A multidisciplinary approach is necessary.
■ A diagnosis of possible NCD due to AD is made based on the presence of
characteristic clinical findings:
•• Insidious onset.
•• Gradual progression.
•• Impairment in one (mild NCD) or more (major NCD) cognitive
domains.
■ NCD due to AD is probable if there is evidence of causation by one of
several single-gene variants.
■ Accumulation of extraneuronal beta-amyloid plaques and intraneuronal tau
protein tangles is associated with progressive brain atrophy.
■ Approximately 1% of AD results from an autosomal dominant single-gene
mutation (amyloid precursor protein, presenilin 1, or presenilin 2), which is
associated with an early onset of symptoms.
■ The epsilon-4 variant of the apolipoprotein gene is a risk factor for developing
early-onset AD.
■ AD pathology is estimated to play a role in 60–90% of major NCDs.
■ Approximately 50% of patients with AD pathology have an NCD due to
multiple etiologies.
■ Two-thirds of patients diagnosed with AD are female.
■ Diagnosis is made after the age of 65 in the vast majority of individuals.
■ No cure or truly effective treatment yet available.
■ Cholinesterase inhibitors (e.g., donepezil, rivastigmine, and galantamine)
may slow clinical deterioration by 6–12 months in up to 50% of patients
with mild-to-moderate AD.
■ The NMDA receptor antagonist, memantine, may provide a modest benefit
to patients with moderate-to-severe disease.
■ Antipsychotic medications are often used to treat agitation and aggression.
•• Because they are associated with increased mortality in patients with
dementia, low doses should be prescribed for short periods of time.
•• Ideally, informed consent should be obtained from patients and/or their
designated decision makers.
•• Monitor closely for side effects.
■ Supportive care via behavioral, social, and environmental interventions.
■ Any treatment plan must include caregiver support.
VASCULAR DISEASE (VASCULAR COGNITIVE IMPAIRMENT)
■ Second most common single cause of major NCD.
■ Evidence of vascular disease is found in half of all major NCDs, most
commonly comorbid with AD pathology (NCD due to multiple
etiologies).
■ Cognitive decline occurs as a result of at least one of the following
mechanisms:
•• Large vessel strokes, usually cortical.
•• Small vessel strokes (lacunar infarcts) to subcortical structures.
•• Microvascular disease affecting the periventricular white matter.
■ Effects vary based on the size, location, and number of infarcts.
Risk Factors
■ Hypertension.
■ Diabetes.
■ Smoking.
■ Obesity.
■ Hyperlipidemia.
■ Atrial fibrillation.
■ Coronary artery disease.
■ Advanced age.
Clinical Manifestations
■ Presentation and progression of cognitive impairment are variable.
•• Classically demonstrates a stepwise deterioration corresponding with the
occurrence of micro-infarcts (i.e., multi-infarct dementia).
•• May present with acute onset followed by partial improvement.
•• May have an insidious onset with gradual decline similar to AD.
■ Complex attention and executive function are the cognitive domains
typically affected in small vessel disease.
■ Confirmation of the diagnosis requires neuroimaging with clinical
correlation.
Treatment
■ No cure or truly effective treatment yet available.
■ Manage and mitigate risk factors with the goal of preventing future strokes.
■ Symptomatic treatment is similar to AD.
A 68-year-old female is brought to the clinic by her husband. He reports that
his wife has recently seemed confused and overly emotional. The patient
is able to complete her daily activities, but reports increased difficulty with
planning and decision-making. Her medical history is significant for hypertension and transient ischemic attacks (TIAs). A physical exam reveals a
carotid bruit.
What is the likely diagnosis?
Mild vascular NCD.
LEWY BODY DISEASE (LBD)
As reflected in its name, the major pathologic features of LBD are Lewy bodies
(pathologic aggregations of alpha-synuclein) and Lewy neurites in the brain,
primarily in the basal ganglia.
NEUROCOGNITIVE DISORDERS
KEY FACT
A lesion to the frontal lobe can
manifest with a spectrum of
symptoms including personality
changes, disinhibition, inappropriate behavior, aggression, apathy,
amotivation, and paranoia.
104
NEUROCOGNITIVE DISORDERS
Clinical Manifestations
■ Progressive cognitive decline.
■ Core features:
■ Suggestive features:
■ Indicative biomarkers:
Diagnosis
Treatment
■ Levodopa-carbidopa for Parkinsonism.
■ Commonly coexists with AD and/or cerebrovascular disease as NCD due to
multiple etiologies.
•• Waxing and waning of cognition, especially in the areas of attention and
alertness.
•• Visual hallucinations—U­sually vivid, colorful, well-formed images of
(commonly small) people, animals, or objects.
•• Rapid eye movement (REM) sleep behavior disorder (not included
in the DSM-5 core features but often associated)—Violent movements
during sleep in response to dreams (often fighting).
•• Development of extrapyramidal signs (Parkinsonism) at least 1 year after
cognitive decline becomes evident.
•• Pronounced antipsychotic sensitivity (i.e., extrapyramidal symptoms).
•• Postural instability and recurrent falls.
•• Loss of consciousness or transient unresponsiveness.
•• Autonomic dysfunction.
•• Olfactory agnosia or diminished sense of smell.
•• Nonvisual hallucinations and delusions.
•• Excessive sleepiness.
•• Depression, apathy, and anxiety.
•• REM sleep without atonia (RWSA) demonstrated via polysomnography.
•• Decreased 123iodine-MIBG uptake on myocardial scintigraphy.
•• Evidence of reduced dopamine receptor uptake in the basal ganglia via
SPECT or PET.
■ Definitive diagnosis can only be made with autopsy.
■ Possible NCD with Lewy bodies: Only one core feature without evidence
from indicative biomarkers OR one or more indicative biomarker(s), but no
core clinical features.
■ Probable NCD with Lewy bodies: Two or more core features OR one core
feature and one or more indicative biomarker(s).
■ Cholinesterase inhibitors for cognitive and behavioral symptoms.
■ Quetiapine or clozapine for psychotic symptoms.
•• Use the lowest effective dose for the shortest period of time possible.
•• Monitor closely for adverse effects, such as extrapyramidal signs,
sedation, increased confusion, autonomic dysfunction, and signs of
neuroleptic malignant syndrome (NMS).
•• Not as effective as in idiopathic Parkinson disease.
•• May exacerbate psychosis or REM sleep behavior disorder.
■ Melatonin and/or clonazepam for REM sleep behavior disorder.
FRONTOTEMPORAL DEGENERATION (FTD)
■ FTD includes a diverse group of clinical and pathological disorders that
typically present between the ages of 45 and 65.
■ Approximately 40% are familial, and 10% are autosomal dominant.
Clinical Manifestations
■ Cognitive deficits in attention, abstraction, planning, and problem
solving.
■ Behavioral variant:
•• Disinhibited verbal, physical, or sexual behavior.
•• Overeating or oral exploration of inanimate objects.
•• Lack of emotional warmth, empathy, or sympathy.
•• Apathy or inertia.
•• Perseveration, repetitive speech, rituals, or obsessions.
•• Decline in social cognition and/or executive abilities.
■ Language variant (primary progressive aphasia):
•• Difficulties with speech and comprehension.
■ Relative sparing of learning/memory and perceptual-motor function.
■ Many individuals have features of both the behavioral and language variants.
■ Increased sensitivity to adverse effects of antipsychotics.
Pathology
Marked atrophy of the frontal and temporal lobes.
Diagnosis
■ Definitive diagnosis cannot be made until autopsy.
■ FTD is probable if frontotemporal atrophy is evident on structural
imaging or hypoactivity is visualized on functional imaging with clinical
correlates.
Treatment
■ Symptom-focused.
■ Serotonergic medications (e.g., SSRIs, trazodone) may help reduce
disinhibition, anxiety, impulsivity, repetitive behaviors, and eating
disorders.
HIV INFECTION
■ HIV is the most common infectious agent known to cause cognitive
impairment.
■ In patients with HIV, 33% have asymptomatic neurocognitive impairment
that appears on exam, 12% have mild NCD, and 2% have major NCD.
■ Severe forms of NCD due to HIV infection have become much less common
with the widespread use of antiretroviral drugs.
Risk Factors
■ History of severe immunosuppression.
■ High viral loads in the CSF.
■ Advanced HIV infection.
NEUROCOGNITIVE DISORDERS
106
NEUROCOGNITIVE DISORDERS
Clinical Manifestations
Treatment
HUNTINGTON DISEASE (HD)
■ Autosomal dominant mode of inheritance.
Clinical Manifestations
■ Average age at diagnosis is 40 years.
■ Increased rate of suicide (7%).
Diagnosis
PARKINSON DISEASE (PD)
■ Variable presentation depending on the part(s) of the brain affected.
■ Decline may be observed in executive functioning, attention, working
memory, and psychomotor activity.
■ Psychiatric and neuromotor symptoms may also be present.
Diagnosis
Mild or major NCD attributable to confirmed HIV infection.
■ Antiretroviral therapy (ART) improves cognition in some patients.
■ Psychostimulants target fatigue, apathy, and psychomotor retardation.
■ A genetic disorder resulting from trinucleotide (CAG) repeats in the gene
encoding the huntingtin (HTT) protein on chromosome 4.
■ Characterized by a triad of motor, cognitive, and psychiatric symptoms.
■ Cognitive decline and behavioral changes can precede onset of motor signs
by up to 15 years.
■ Executive function is the primary cognitive domain affected.
■ Psychiatric manifestations include depression, apathy, irritability, obsessions,
impulsivity, paranoia, delusions, and hallucinations.
■ Patients are often aware of deteriorating mentation.
■ Movement disorders include chorea (jerky, dance-like movements) and
bradykinesia.
■ Extrapyramidal movement disorder in an individual with either a family
history of HD or genetic testing that confirms an increased number of CAG
trinucleotide repeats in the HTT gene.
■ Mild or major NCD may be diagnosed prior to onset of motor signs if an
individual is determined to be at risk based on family history or genetic
testing.
Treatment
Symptom-directed therapy with tetrabenazine or atypical
(second-generation) antipsychotics.
■ An idiopathic, progressive neurodegenerative disease characterized by
depletion of dopamine in the substantia nigra pars compacta (located in the
basal ganglia).
■ Up to 75% of patients with PD meet the criteria for major NCD, typically in
advanced disease.
Clinical Manifestations
■ Motor signs include muscular (lead-pipe or cogwheel) rigidity, resting
tremor, bradykinesia, and postural instability.
■ Cognitive manifestations consist of executive dysfunction and visuospatial
impairments.
■ Depression, anxiety, personality changes, and apathy are common.
■ Psychotic symptoms, including visual hallucinations and paranoid delusions,
may result from the disease itself or from adverse effects of the medications
used to treat the motor symptoms.
■ Prodromal symptoms and signs (e.g., micrographia, hyposmia, hypogeusia,
constipation, personality changes, mood disorders, and REM-sleep behavior
disorder) may occur up to two decades before motor abnormalities appear.
Diagnosis
■ Diagnosis of PD requires the presence of bradykinesia and either tremor or
rigidity.
■ Associated with asymmetry of motor symptoms.
■ Mild or major NCD is attributed to PD if cognitive decline appears
after the onset of motor symptoms and no other underlying etiology is
identified.
■ Typically responds favorably to dopaminergic therapy.
Treatment
■ Motor symptoms are most commonly treated with carbidopa-levodopa
and/or dopamine agonists.
■ High-frequency deep brain stimulation may lessen severe motor symptoms,
but is associated with increased risk of depression.
■ Cholinesterase inhibitors are used to target cognitive symptoms and may
also ameliorate some of the neuropsychiatric symptoms (hallucinations).
■ Psychotic symptoms may respond to a reduction in the dose of dopamine
agonists.
■ Low-dose quetiapine and clozapine are the preferred medications for
treatment of psychosis. Avoid other antipsychotics since they can worsen the
motor symptoms of PD.
■ Pimavanserin is a serotonergic medication approved by the FDA to treat PD
psychosis.
PRION DISEASE (TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES)
■ A form of subacute spongiform encephalopathy caused by proteinaceous
infectious particles (prions).
■ The most common type is sporadic Creutzfeldt–Jakob disease (sCJD).
■ Variant CJD (vCJD, aka bovine spongiform encephalopathy or mad cow
disease) is a rare food-borne prion disease.
■ Up to 15% are familial (autosomal dominant), involving prion protein
(PRNP) gene mutations.
■ Less than 1% of cases are iatrogenic.
Clinical Manifestations
■ Insidious onset with rapidly progressive cognitive decline (over months to
years).
NEUROCOGNITIVE DISORDERS
KEY FACT
Symptoms of Parkinson disease
can be exacerbated by antipsychotic medications.
KEY FACT
Rapidly progressive cognitive decline with myoclonus is suggestive of Creutzfeldt–Jakob disease.
108
NEUROCOGNITIVE DISORDERS
■ Presentation and progression vary by type.
■ Typical clinical features of CJD.
Evaluation
■ EEG: Periodic sharp wave complexes.
Diagnosis
Treatment
■ No effective treatment yet available.
WARDS
QUESTION
Q: What are the “three Ws” of NPH?
A: Wobbly (abnormal gait), Wet
(urinary urgency → incontinence),
Wacky (cognitive impairment).
Clinical Manifestations
■ Classically presents with a clinical triad:
•• Gait disturbance (“Wobbly”).
May begin as urinary urgency.
•• Myoclonus (often triggered by startle response) is found in most
individuals.
•• Visual (e.g., hallucinations, cortical blindness) or cerebellar disturbance
(e.g., nystagmus, ataxia).
•• Pyramidal (e.g. positive Babinski sign, spasticity, hyperactive reflexes) or
extrapyramidal dysfunction (e.g., bradykinesia, rigidity, dystonia).
•• Akinetic mutism in end-stage disease.
■ Brain MRI: Hyperintensities in the caudate head, putamen, or at least two
cortical regions on DWI or FLAIR.
■ CSF analysis: Positive RT QuIC assay and/or presence of 14-3-3 protein.
■ A diagnosis of probable sCJD requires either of the following scenarios:
•• A neuropsychiatric disorder with a positive CSF RT-QuIC assay.
•• Rapid progression of cognitive decline with two or more of the typical
clinical features listed above AND typical findings on MRI, EEG, or CSF
analysis.
■ Definitive diagnosis requires analysis of brain tissue obtained via biopsy or
autopsy.
■ Death usually occurs within 1 year of diagnosis.
NORMAL PRESSURE HYDROCEPHALUS (NPH)
■ NPH is a potentially reversible cause of cognitive dysfunction.
■ The etiology is either idiopathic or secondary to obstruction of CSF
reabsorption sites due to infection (meningitis) or hemorrhage
(subarachnoid or intraventricular).
Most likely to be the first manifestation.
Slow with short steps.
Broad-based with outwardly rotated feet.
Feet appear to be stuck to the floor (magnetic gait).
Postural instability leads to recurrent falls.
•• Urinary incontinence (“Wet”).
Gait disturbance may interfere with reaching the toilet before urinary
incontinence.
In later stages, apathy may contribute.
•• Cognitive impairment (“Wacky”).
Insidious onset.
Executive dysfunction.
Psychomotor retardation.
Decreased attention.
Apathy.
•• Enlargement of ventricles out of proportion to cortical atrophy on
imaging.
Localized elevation of cerebrospinal fluid (CSF) pressure but normal
opening pressures on lumbar puncture.
•• Clinical improvement following CSF removal via lumbar puncture.
Treatment
■ Placement of a shunt (usually ventriculoperitoneal) may improve symptoms.
■ Cognitive impairment is least likely to improve.
NEUROCOGNITIVE DISORDERS
110
NEUROCOGNITIVE DISORDERS
NOTES

12 - Chapter 9 Geriatric Psychiatry

01 - Chapter 9 Geriatric Psychiatry
Chapter 9 Geriatric Psychiatry
GERIATRIC
CHAPTER 9
PSYCHIATRY
Normal Aging.........................................................................................................................112
Major Depression....................................................................................................................112
Pseudodementia.....................................................................................................................112
Treatment..........................................................................................................................113
Bereavement..........................................................................................................................114
Substance Use.........................................................................................................................115
Psychiatric Manifestations of Major Neurocognitive Disorders (Dementia).............................116
Treatment..........................................................................................................................116
Sleep Disturbance...................................................................................................................117
Other Issues............................................................................................................................117
Restraints..........................................................................................................................117
Medications.......................................................................................................................118
Elder Abuse........................................................................................................................118
Nursing Homes..................................................................................................................118
112
GERIATRIC PSYCHIATRY
WARDS TIP
Work up an elderly patient for major depression when they present
with memory loss or nonspecific
physical complaints.
Normal Aging
Factors associated with normal aging include:
■ Decreased muscle mass/increased fat.
■ Impaired vision and hearing.
WARDS TIP
Patients with a major neurocognitive disorder are more likely to
confabulate when they do not
know an answer, whereas depressed patients may just say that
they don’t know. When pressed for
an answer, depressed patients will
often show the ability to answer
correctly.
Major Depression
Pseudodementia
WARDS
QUESTION
Q: What is the most common psychiatric disorder in the elderly?
A: Major depressive disorder.
The geriatric population of the United States is projected to more than double
by the year 2050, boosted in a large part by the aging Baby Boomer generation.
Nearly 20% of people over the age of 60 have a psychiatric disorder. The suicide
rate of elderly (aged 85 and older) white men is five times the national average.
Common diagnoses in elderly patients include mood disorders, anxiety disorders, and neurocognitive disorders, though many psychiatric disorders in this
population remain underreported and untreated.
■ Decreased brain weight/enlarged ventricles and sulci.
■ Minor forgetfulness (sometimes called age-associated memory impairment
or benign senescent forgetfulness).
Major depression is a common disorder in the geriatric population, with
depressive symptoms present in 5–15% of the elderly. Depression is associated
with poor physical health:
■ Post-myocardial infarction (MI) patients who develop depression have a
four times increased rate of death.
■ Stroke patients who develop depression have a greater than three times
increased rate of death during the 10 years following their stroke.
■ Patients with depression newly admitted to nursing homes have an increase
in 1-year mortality rate.
Symptoms of major depression in the elderly often include problems with
memory and cognitive functioning. Because this clinical picture may be
mistaken for a major neurocognitive disorder (dementia), it is termed
­pseudodementia.
Pseudodementia is the presence of apparent cognitive deficits in patients with
major depression. Patients may appear to be suffering from a neurocognitive
disorder (dementia); however, their symptoms are secondary to their underlying
depression, although it can be difficult to differentiate the two (see Table 9-1).
TABLE 9-1. Dementia versus Pseudodementia (Depression)
Dementia
Pseudodementia (Depression)
Onset is insidious.
Onset is more acute.
Sundowning is common
(↑ confusion at night).
Sundowning is uncommon.
Will guess at answers (confabulate).
Often answers “I don’t know.”
Patient is unaware of problems.
Patient is aware of problems.
Cognitive deficits do not improve with
antidepressant treatment.
Cognitive deficits improve with
antidepressants.
TREATMENT
■ Supportive psychotherapy.
■ Community resources: Senior centers, senior services, support groups, etc.
■ Antidepressant medications (selective serotonin reuptake inhibitors [SSRIs]
and other newer antidepressants have fewer side effects and are preferable to
tricyclic antidepressants [TCAs] or monoamine oxidase [MAO] inhibitors).
■ Elderly patients are sensitive to side effects of medications so it’s important
to start at a very low dose and titrate slowly up to the full dose of the
antidepressant: “Start low and go slow!”
■ If using TCAs in elderly patients, nortriptyline is favored because it has the
fewest anticholinergic side effects.
■ At lower doses, mirtazapine can increase appetite and be sedating; it
is dosed at bedtime for depressed patients who particularly suffer from
decreased appetite and sleep disturbances.
■ Methylphenidate can be used at low doses as an adjunct to antidepressants
for patients with severe depression and/or psychomotor retardation;
however, it may cause insomnia if given in the afternoon or evening. Also,
be aware of the risk of arrhythmia in patients with cardiac disease.
■ Electroconvulsive therapy (ECT) may be used in place of antidepressants
(ECT is safe and effective in the elderly).
Mrs. Brennan is a 72-year-old female who considers herself to be in good
health. She goes out to lunch with friends three times a week and looks
forward to her Saturday bridge games at the local senior center. Unfortunately, her husband has suffered from years of ill health, including five
myocardial infarctions and a serious stroke last year that left him barely able
to walk. You are a geriatric psychiatrist who has been treating Mrs. Brennan’s
husband for depression that began after his last stroke. Mrs. Brennan always
comes along to appointments so that she can stay informed about her
husband’s medical care.
You become concerned when your patient uncharacteristically misses
an appointment and does not return your phone message. Finally, a month
later, you are surprised to see Mrs. Brennan walk into your office alone. She
enters the room slowly, and you notice that she has lost some weight since
you last saw her.
She sits down but does not make eye contact. Finally, she begins to talk
in a soft, monotone voice, explaining that her husband had another stroke
last month and was moved to a hospice facility, where he passed away 2
weeks ago. She begins to cry, and you hand her some tissues. The two of
you talk some more about her husband’s death and how she is coping with
it. She reports that her daughter visits her frequently and has invited her to
spend the weekends with her.
Although Mrs. Brennan reports that she feels “down,” she reports that
she is making an effort to go on with her life because that is what her
husband would have wanted. She says that she went out to lunch with
her friends this week and adds that they are very supportive. Mrs. Brennan also reports that it is difficult for her to realize that her husband is no
longer there and says that she has heard his voice calling her a couple of
times this week. As she leaves your office, you tell her she is welcome to
come back whenever she wants.
Is Mrs. Brennan having a normal grief reaction?
Yes, Mrs. Brennan is going through a normal grieving process, also known
as bereavement. Although she displays some symptoms ­suggestive of
GERIATRIC PSYCHIATRY
WARDS
QUESTION
Q: What demographic has the
highest rate of completed
­suicides?
A: White elderly males.
114
GERIATRIC PSYCHIATRY
 WARDS TIP
The elderly are very sensitive to side
effects of medications, particularly
anticholinergic effects of antidepressants.
Bereavement
­major depression (psychomotor retardation, depressed mood), and reports
the presence of auditory hallucinations (her husband’s voice), these symptoms are commonly encountered in bereavement and are considered a
normal reaction to her sudden loss.
Three months later, you receive a phone call from Mrs. Brennan’s daughter,
who expresses concern about her mother. She tells you that her mother has
to be urged to shower, wear clean clothes, and eat regularly. Mrs. Brennan
has stopped participating in her bridge group and has not been out with
her friends in many weeks. The daughter also worries about Mrs. Brennan’s
increasing forgetfulness and memory problems. She asks if she can bring her
in for an appointment with you. You agree and schedule Mrs. Brennan the
next day.
Mrs. Brennan enters your office with her daughter by her side. She is
dressed in a wrinkled pantsuit and is wearing scuffed shoes. Her hair is clean
but lies limply against her head. She appears much thinner than the last time
you saw her. Her eyes are downcast, and she appears sad. You try to engage
her in conversation, but her answers to your questions are soft and short.
When you do an assessment of her memory, you note that she answers basic
questions with “I don’t know” and scores poorly on the mini-mental state
exam questions.
What is Mrs. Brennan’s most likely diagnosis now?
Mrs. Brennan is most likely suffering from a major depressive episode. Her
symptoms now fulfill criteria for major depressive disorder and have been
present for over 2 weeks. Since her memory problems began after she began
experiencing depressive symptoms, these are likely secondary to depression.
When this occurs, it is often referred to as “pseudodementia.” If this is the case,
as her depression is treated her memory deficits will improve.
What are possible treatment options for Mrs. Brennan?
Supportive psychotherapy and a medication trial of an SSRI would be excellent first-line treatments. In addition, you suggest to Mrs. Brennan and her
daughter to consider visiting her local senior center to learn what kinds of
services from which she might benefit.
In 1969, Elisabeth Kübler-Ross, MD, published a book called On Death and
Dying, in which she proposed a model of bereavement, the Five Stages of Grief.
■ Denial: “This isn’t happening to me. I don’t feel sick.”
■ Anger: “It’s my ex-husband’s fault for smoking around me all those years!”
■ Bargaining: “Maybe if I exercise and improve my diet, I’ll get better.”
■ Depression: “There’s no hope for a cure. I will die of this cancer.”
■ Acceptance: “I may have cancer, but I’ve always been a fighter—why stop
now?”
There is some controversy surrounding this model (e.g., people may not experience all of the stages or they may go through them in a different order) as
grief is a very individualized experience; there is no “correct” way to mourn a
loss. However, it is important to be able to distinguish normal grief reactions
from unhealthy, pathological ones.
■ Normal grief may involve many intense feelings, including guilt and
sadness, sleep disturbances, appetite changes, and illusions/hallucinations
(not always pathological in some cultures). These feelings generally
abate within 6 months of the loss, and the patient’s ability to function
appropriately in their life is preserved.
■ Bereavement-associated depression is a major depression that begins with
a concrete death or loss in the patient’s life. It is often difficult to distinguish
between depression and grief, since many symptoms are similar.
•• Look for generalized feelings of hopelessness, helplessness, severe guilt
and worthlessness, neurovegetative symptoms (e.g., insomnia, appetite/
weight changes, low energy), and suicidal ideation, in addition to grief
symptoms.
•• Treatment for depression is recommended in patients who have at least
2 weeks of persistent depressive symptoms.
Substance Use
■ Forty percent of the 65 plus-year-old population drink alcohol, and up to
16% are heavy drinkers who may experience adverse health events from
the amount of alcohol they use or from its interaction with medications
and impact on chronic disease processes. It is important to screen elderly
patients for substance use.
■ Age-related effects of alcohol:
•• Elderly people have a lower amount of alcohol dehydrogenase in their
livers which can lead to higher blood alcohol levels (BALs) with fewer
drinks as compared to younger adults.
•• The amount of water in the body lessens with age, resulting in a higher
percentage of alcohol in the blood of elderly compared to younger
individuals after drinking the same amount of alcohol.
•• The central nervous system becomes more sensitive to alcohol with age.
■ Chronic medical conditions worsened by alcohol:
•• Liver diseases (cirrhosis, hepatitis).
•• Gastrointestinal (GI) diseases (GI bleeding, gastric reflux, ulcer).
•• Cardiovascular diseases (hypertension, heart failure).
•• Metabolic/endocrine diseases (gout, diabetes).
•• Mental disorders (depression, anxiety).
■ Alcohol and medication interactions (see Table 9-2).
TABLE 9-2. Alcohol and Medication Interactions
Medication
Result of Concurrent Alcohol Use
H2 blockers
Higher BALs
Benzodiazepines, tricyclics, narcotics,
barbiturates, antihistamines
↑ sedation
Aspirin, NSAIDs
Prolonged bleeding time; irritation of
gastric lining
Metronidazole, sulfonamides, long-acting
hypoglycemics
Nausea and vomiting
Reserpine, nitroglycerin, hydralazine
↑ risk of hypotension
Acetaminophen, isoniazid, phenylbutazone
↑hepatotoxicity
Antihypertensives, antidiabetics, ulcer drugs,
gout medications
Worsen underlying disease
GERIATRIC PSYCHIATRY
116
GERIATRIC PSYCHIATRY
■ Mood disorders:
■ Psychosis:
 WARDS TIP
Visual hallucinations early in
dementia suggest a diagnosis of
neurocognitive disorder due to
Lewy body disease. Antipsychotics
should be avoided as these patients
are sensitive to extrapyramidal
symptoms (EPS).
TREATMENT
■ Nonpharmacological treatments:
          WARDS
QUESTION
Q: What is common condition in the
geriatric population that can mimic
depression?
A: Delirium.
■ Pharmacological treatments:
•• Antipsychotics:
Psychiatric Manifestations of Major Neurocognitive
Disorders (Dementia)
Behavioral symptoms are quite common in patients with major neurocognitive
disorders, and are often the source of many psychosocial problems surrounding their care. Agitation and aggression can be distressing and dangerous
for caregivers, as well as unsafe for patients. Behavioral disinhibition is fairly
common in major neurocognitive disorders and causes patients to act in ways
that are quite unlike their typical behaviors (e.g., stripping off clothes in public,
sexualized behavior, cursing).
•• Difficult to diagnose in a patient with confirmed major neurocognitive
disorder.
•• Patients with major neurocognitive disorders may display many
symptoms of depression (such as apathy) that are merely natural
manifestations of their disease.
■ Aggression may be provoked by the following:
•• Patient’s confusion in the setting of cognitive, memory, and language
deficits.
•• Patient’s inability to communicate discomfort or basic needs such as
constipation, hunger, thirst, need to urinate, or pain.
•• Patient’s hallucinations or delusions.
•• Patient with additional delirium
•• Delusions are reported in up to 50% of Alzheimer patients.
•• Hallucinations (mostly auditory and/or visual) can be seen in at least 25%
of patients with a major neurocognitive disorder.
•• If hallucinations do not bother the patient or interfere with caring for the
patient, pharmacotherapy is unnecessary.
Behavioral and environmental treatments for behavioral symptoms are much
preferred in the elderly. Pharmacological methods are appropriate in the setting of potentially harmful behaviors, but care must be taken in dosing, duration of treatment, and interactions with other medications.
•• Music, art, exercise, and pet therapy.
•• Strict daily schedules to minimize changes in routine.
•• Continual reorientation of patient.
•• Reducing stimuli (quiet living environments that are light during the day
and dark at night).
•• Surrounding with familiar objects (family photos, a favorite quilt, etc.).
•• Ensuring patient has hearing aids, eyeglasses, and other basic needs.
Limited efficacy in treating agitation, and carry increased risk of mortality that must be discussed in a risk-benefit assessment with patient
and caregivers.
Try olanzapine (Zyprexa) or quetiapine (Seroquel) in patients with
severe symptoms.
Can also use short-term haloperidol (Haldol) or risperidone (Risperdal).
Can be useful in psychiatric emergencies.
•• Anxiolytics:
Anxiety symptoms may be due to unrecognized depression and respond well to an SSRI.
Reserve benzodiazepines for very short-term, acute episodes and remember to watch for disinhibition (paradoxical agitation) and worsening confusion.
Mood stabilizers: Few studies on their efficacy in the elderly.
Sleep Disturbance
The incidence of sleep disorders increases with aging. Elderly people often
report difficulty sleeping, daytime drowsiness, and daytime napping.
■ Outside of normal changes associated with aging (see Table 9-3), causes of
sleep disturbances may include other medical conditions, drug/alcohol use,
social stressors, and medications.
■ Patients with movement disorders (Parkinson disease, progressive
supranuclear palsy) have shallow sleep and may be more restless at night
because of trouble turning in bed.
■ Restless leg movements during sleep, likely due to a dopamine imbalance,
are called periodic leg movements (PLMs).
■ Nonpharmacological treatment approaches should be tried first (alcohol
cessation, increased daily structure, elimination of daytime naps,
encouraging daylight exposure, treatment of underlying medical conditions
that may be exacerbating sleep problems).
■ Sedative-hypnotic drugs are more likely to cause side effects when used
by the elderly (memory impairment, ataxia, paradoxical excitement, and
rebound insomnia) and increase risk of falls.
■ If sedative-hypnotics must be prescribed, medications such as trazodone are
safer than the more sedating benzodiazepines, but be careful of orthostasis.
Other Issues
RESTRAINTS
■ In nonemergency situations, restraints should be used as a last resort and
the patient should be reassessed at regular intervals.
TABLE 9-3. Normal Sleep Changes in Geriatric Patients
Rapid eye movement (REM) sleep
↓ REM latency and ↓ total REM
Non-REM sleep
↑ amounts of stage 1 and 2 sleep, ↓ amounts of
stage 3 and 4 sleep (deep sleep)
Sleep efficiency
↓ (frequent nocturnal awakenings)
Amount of total sleep
↓
Sleep cycle
Sleep cycle advances (earlier to bed, earlier to rise)
GERIATRIC PSYCHIATRY
118
GERIATRIC PSYCHIATRY
MEDICATIONS
ELDER ABUSE
NURSING HOMES
■ Patient safety, health, and well-being should be the most important concern
in the matter of restraint use.
■ Evaluate ABCs in a restrained patient: airway, breathing, and circulation.
■ Many older people are on multiple medications (“polypharmacy”).
■ They suffer from more side effects because of decreased lean body mass and
impaired liver and kidney function.
■ When confronted with a new symptom in an elderly patient on multiple
medications, always try to remove a medication before adding one.
■ Types: Physical abuse, psychological abuse (threats, insults, etc.), neglect
(withholding of care), exploitation (misuse of finances), and rarely sexual
abuse.
■ Approximately 10% of all people more than 65 years old; underreported by
victims.
■ Perpetrator is usually a caregiver (spouse or adult child) who lives with the
victim.
■ Physicians are mandated to report suspected elder abuse.
■ Provide care and rehabilitation for chronically ill and impaired patients as
well as for those who are in need of short-term care before returning to their
prior living arrangements.
■ The majority of patients stay permanently, and fewer than half are
discharged after only a short period of time.
■ Careful medication review is imperative for nursing home patients who
experience frequent hospitalizations and subsequent medication changes.
■ Caregiver burnout is very common in families of these patients, and can
negatively affect patient care.

13 - Chapter 10 Psychiatric Disorders in Children

01 - Chapter 10 Psychiatric Disorders in Children
Chapter 10 Psychiatric Disorders in Children
Psychiatric Examination of a Child..........................................................................................121
Sources of Information......................................................................................................121
Methods of Gathering Information....................................................................................121
Safety Assessment.............................................................................................................121
Intellectual Disability..............................................................................................................121
Diagnosis and DSM-5 Criteria.............................................................................................121
Epidemiology....................................................................................................................122
Etiology.............................................................................................................................122
Global Developmental Delay...................................................................................................122
Specific Learning Disorder (LD)...............................................................................................122
Diagnosis and DSM-5 Criteria.............................................................................................123
Epidemiology....................................................................................................................123
Etiology.............................................................................................................................123
Comorbidity.......................................................................................................................123
Treatment..........................................................................................................................123
Communication Disorders.......................................................................................................123
Treatment..........................................................................................................................124
Attention Deficit/Hyperactivity Disorder (ADHD)....................................................................124
Diagnosis and DSM-5 Criteria.............................................................................................124
Epidemiology....................................................................................................................125
Etiology.............................................................................................................................125
Course/Prognosis...............................................................................................................125
Treatment..........................................................................................................................125
Autism Spectrum Disorder (ASD)............................................................................................126
Diagnosis and DSM-5 Criteria.............................................................................................126
Epidemiology....................................................................................................................126
Etiology.............................................................................................................................126
Prognosis and Treatment...................................................................................................127
Tic Disorders...........................................................................................................................127
Tourette’s Disorder.............................................................................................................127
Disruptive and Conduct Disorders...........................................................................................128
Oppositional Defiant Disorder (ODD).................................................................................128
DISORDERS IN CHILDREN
CHAPTER 10
PSYCHIATRIC
120
PSYCHIATRIC DISORDERS IN CHILDREN
Conduct Disorder (CD)........................................................................................................129
Elimination Disorders..............................................................................................................130
DSM-5 Diagnosis................................................................................................................130
Epidemiology....................................................................................................................130
Etiology.............................................................................................................................130
Treatment..........................................................................................................................131
PANS/PANDAS.........................................................................................................................131
Child Abuse.............................................................................................................................132
Physical Abuse...................................................................................................................132
Sexual Abuse.....................................................................................................................132
Psychological Abuse..........................................................................................................132
Neglect..............................................................................................................................132
Treatment..........................................................................................................................133
Sequelae............................................................................................................................133
Psychiatric Examination of a Child
SOURCES OF INFORMATION
Gather and integrate collateral information from multiple sources to obtain as
accurate a clinical picture as possible: primary caregivers, teachers, pediatricians, and the child welfare system (if relevant).
METHODS OF GATHERING INFORMATION
Determine the child’s developmental stage and tailor the interview
appropriately.
■ Play therapy: Utilizes the child’s symbolic play, storytelling, or drawing as a
forum for expression of emotions and experiences.
■ Classroom observation: A window into the child’s functioning in school.
■ Formal neuropsychological testing: Quantitatively assesses a child’s
strengths and weaknesses by examination of their cognitive profile:
intelligence quotient (IQ); language and visual-motor skills; memory,
attention, and organizational abilities.
■ Kaufman Assessment Battery for Children (K-ABC): Intelligence test
comparing intellectual capacity with acquired knowledge of patients
between 2 and 12 years old.
■ Wechsler Intelligence Scale for Children-Revised (WISC-R): Assesses
verbal, performance, and full-scale IQ of patients between 6 and 16 years
old.
SAFETY ASSESSMENT
■ Always screen for safety issues including self-injurious behavior, suicidal
ideation, homicidal ideation, and command auditory hallucinations in a
developmentally appropriate manner.
■ In the United States, suicide rates have increased significantly and are
currently the second leading cause of death in individuals 10–34 years old.
In the United States, 2½ times as many suicides occurred as homicides.
Collectively, deaths due to suicide and homicide have remained a major
cause of premature death for victims between 10 and 24 years old.
Intellectual Disability
Intellectual disability (ID), or intellectual developmental disorder, is characterized by impaired cognitive and adaptive/social functioning. Severity level
is currently based on adaptive functioning, indicating the degree of support
required. A single IQ score does not adequately capture this and is no longer
used solely to determine ID severity.
DIAGNOSIS AND DSM-5 CRITERIA
■ Deficits in intellectual functioning include learning, reasoning, judgment,
planning, abstract thinking, and problem solving.
■ Deficits in adaptive functioning include communication, social
participation, and independent living.
PSYCHIATRIC DISORDERS IN CHILDREN
WARDS
QUESTION
Q: Should you screen a new patient
for suicidal ideation?
A: Yes. Asking a patient directly
about suicidal thoughts may help
save their life and does not cause
suicidal tendencies.
122
PSYCHIATRIC DISORDERS IN CHILDREN
WARDS TIP
Characteristic physical features of
genetic syndromes:
• Down syndrome: Epicanthic
folds, flat nasal bridge, and palmar crease.
• Fragile X syndrome: long, narrow
face, joint hyperlaxity, and macroorchidism in postpubertal males.
• Prader–Willi syndrome:
Obese, small stature, and almond-shaped eyes.
EPIDEMIOLOGY
■ Overall: 1% of population.
■ Severe ID: 6/1000.
ETIOLOGY
KEY FACT
Fragile X Syndrome Facts and Stats
• Most common inherited form
of ID.
• Second most common cause
of ID.
• Due to FMR-1 gene mutation.
• Males > females.
KEY FACT
TABLE 10-1. Causes of Intellectual Disability
Cause
Examples
Down Syndrome Facts and Stats
• 1/700 live births.
• Most common chromosomal
disorder.
• Trisomy 21 = 3 copies of chromosome 21.
Prenatal
Infection and toxins (TORCH):
■ Deficits affect multiple domains including conceptual, practical, and social.
■ Onset occurs during the developmental period.
■ Intellectual deficits are confirmed by clinical assessment and standardized
intelligence testing (scores at least two standard deviations below the
population mean).
■ Adaptive functioning deficits require ongoing support for activities of daily
life.
■ Severity levels: Mild, moderate, severe, and profound.
■ Causes include genetic, prenatal, perinatal, and postnatal conditions (see
Table 10-1).
■ Fifty percent of ID cases have no identifiable cause.
Global Developmental Delay
■ Failure to meet expected developmental milestones in several areas of
intellectual functioning.
■ Diagnosis reserved for patients less than 5 years old when severity level
cannot be reliably assessed via standardized testing. Patients will need to be
reevaluated when older to clarify the diagnosis.
Specific Learning Disorder (LD)
Characterized by delayed cognitive development in a particular academic
domain.
Genetic
■ Down syndrome: Trisomy 21 (1/700 live births)
■ Fragile X syndrome: Involves mutation of X chromosome, 2nd most
common cause of intellectual disability, males >females
■ Other causes: Phenylketonuria, familial mental retardation, Prader–
Willi syndrome, Williams syndrome, Angelman syndrome, tuberous
sclerosis
■ Toxoplasmosis
■ Other (syphilis, AIDS, alcohol/illicit drugs)
■ Rubella (German measles)
■ Cytomegalovirus (CMV)
■ Herpes simplex
Perinatal
Anoxia, prematurity, birth trauma, meningitis, hyperbilirubinemia
Postnatal
Hypothyroidism, malnutrition, toxin exposure, trauma
DIAGNOSIS AND DSM-5 CRITERIA
■ Significantly impaired academic skills which are below expectation for
chronological age and interfere with academics, occupation, or activities of
daily living (ADLs).
■ Begins during school but may become more impairing as demands increase.
■ Affected areas: Reading (e.g., dyslexia), writing (e.g., dysgraphia), or
arithmetic (e.g., dyscalculia).
■ Not better accounted for by intellectual disabilities, visual/auditory deficits,
language barriers, or subpar education.
EPIDEMIOLOGY
■ Prevalence in school age children: 5–15%.
■ Males > females affected.
ETIOLOGY
■ Environmental factors: Increased risk with prematurity, very low birth
weight, and prenatal nicotine exposure.
■ Genetic factors: Increased risk in first-degree relatives of affected
individuals.
COMORBIDITY
■ Commonly co-occurs with other neurodevelopmental disorders, such as
attention deficit/hyperactivity disorder (ADHD), communication disorders,
developmental coordination disorder, and autism spectrum disorder (ASD).
■ Comorbid with other mental disorders, including anxiety, depressive, and
bipolar disorders.
TREATMENT
■ Systematic, individualized education tailored to child’s specific needs.
■ Behavioral techniques may be used to improve learning skills.
Communication Disorders
Communication disorder includes impaired speech, language or social communication that are below expectation for chronological age. Symptoms begin
in the early developmental period and lead to academic or adaptive issues.
■ Language disorder—Difficulty acquiring and using language due to
expressive and/or receptive impairment (e.g., reduced vocabulary, limited
sentence structure, impairments in discourse). Increased risk in families of
affected individuals.
■ Speech sound disorder (phonological disorder)—Difficulty producing
articulate, intelligible speech.
■ Childhood-onset fluency disorder (stuttering)—Dysfluency and speech
motor production issues. Increased risk of stuttering in first-degree relatives
of affected individuals.
PSYCHIATRIC DISORDERS IN CHILDREN
KEY FACT
Fetal Alcohol Exposure Facts
Fetal alcohol syndrome (FAS) =
Leading preventable cause of birth
defects and ID.
Three features of FAS:
Growth retardation
CNS involvement (structural,
neurologic, functional)
Facial dysmorphology
(smooth philtrum, short palpebral fissures, thin vermillion
border)
Fetal alcohol spectrum disorders:
Fetal alcohol exposure of any
amount may cause a range of
developmental disabilities, which
are often underrecognized.
WARDS TIP
Always rule out sensory deficits before diagnosing a specific learning
disorder.
124
PSYCHIATRIC DISORDERS IN CHILDREN
TREATMENT
What treatment is indicated?
DIAGNOSIS AND DSM-5 CRITERIA
■ At least six inattentive symptoms:
■ Social (pragmatic) communication disorder—Challenges with the social use
of verbal and nonverbal communication. If restricted/repetitive behaviors,
activities, or interests are also present, consider diagnosis of ASD. Increased
risk with family history of communication disorders, ASD, or specific LD.
■ Speech and language therapy, family counseling.
■ Tailor educational supports to meet the individual’s needs.
A 10-year-old girl is referred for psychiatric evaluation because of academic and behavioral issues over the last year. The student has an above
average IQ and seems to comprehend class material. Her teachers share
concerns that she makes careless mistakes on homework and rushes
through tests, leading to lower than predicted grades. She also blurts
out answers without waiting for her turn. During the interview, she has
difficulty staying focused and asks the examiner to repeat the question
several times. Her mother complains that she does not clean her room or
complete assigned chores.
What is the most likely diagnosis?
The patient has classic symptoms of attention deficit/hyperactivity disorder (ADHD) occurring in two different settings (home and school).
If the child does not have any contraindications, stimulant medications are
usually the first-line treatment for ADHD.
Attention Deficit/Hyperactivity Disorder (ADHD)
ADHD is characterized by persistent inattention, hyperactivity, and impulsivity inconsistent with the patient’s developmental stage. There are three subcategories of ADHD: predominantly inattentive type, predominantly hyperactive/impulsive type, and combined type.
■ Two symptom domains: Inattentiveness and hyperactivity/impulsivity.
•• Does not pay attention to details or makes careless mistakes.
•• Has difficulty sustaining attention.
• Difficulty listening.
• Struggles to follow instructions.
• Is unorganized.
• Avoids tasks requiring high cognitive demands.
• Misplaces/loses objects frequently.
• Is easily distracted.
• Is forgetful.
And/or
■ At least six hyperactivity/impulsivity symptoms:
•• Fidgets with hands/feet or squirms in seat.
• Has difficulty remaining still.
• Runs/climbs excessively in childhood (extreme restlessness in adults).
• Has difficulty engaging in activities quietly.
• Acts as if driven by a motor (an internal sensation in adults).
• Talks excessively.
• Blurts out answers before questions have been completed.
• Has difficulty waiting or taking turns.
• Interrupts or intrudes upon others.
■ Symptoms more than 6 months and present in two or more settings (e.g.,
home, school, work).
■ Symptoms interfere with or reduce quality of social, academic, and/or
occupational functioning.
■ Onset prior to age 12, but can be diagnosed retrospectively in adulthood.
■ Not due to the physiological effects of a substance, another medical or
neurological condition (e.g., traumatic brain injury), or another mental
disorder.
EPIDEMIOLOGY
■ Prevalence: 10% of children and 4.5% of adults.
■ Males > females with 2:1 ratio.
■ Females present more often with inattentive symptoms.
ETIOLOGY
The etiology of ADHD is multifactorial and may include:
■ Genetic factors: Increased rate in first-degree relatives of affected
individuals.
■ Environmental factors: Potentially in utero exposure to neurotoxin, low
birth weight, or childhood abuse or neglect.
COURSE/PROGNOSIS
■ Stable through adolescence.
■ Many continue to have symptoms as adults (inattentive > hyperactive).
■ High incidence of comorbid oppositional defiant disorder, conduct disorder,
and specific LD.
TREATMENT
Multimodal treatment plan: Medications are the most effective treatment for
decreasing core symptoms, but should be used in conjunction with educational
and behavioral interventions.
■ Pharmacological treatments:
•• First-line: Stimulants (e.g., methylphenidate compounds,
dextroamphetamine, mixed amphetamine salts).
• Second-line: Alpha-2 agonists (e.g., clonidine, guanfacine) can be used
instead or as adjunctive therapy to stimulants. May be used in children
who respond poorly to other medications, experience side effects, or have
coexisting conditions such as tics.
PSYCHIATRIC DISORDERS IN CHILDREN
WARDS
QUESTION
Q: What are first-line treatments in
ADHD?
A: Stimulants.
126
PSYCHIATRIC DISORDERS IN CHILDREN
■ Nonpharmacological treatments:
WARDS TIP
DIAGNOSIS AND DSM-5 CRITERIA
Consider ASD as the diagnosis if
there is a rapid deterioration of social and/or language skills during
the first 2 years of life.
  Complete an appropriate workup, such as auditory testing, prior
to diagnosing ASD.
  An extensive medical workup
needs to be initiated if skills are
lost after age 2, or more expansive
losses occur (e.g., self-care, motor
skills).
WARDS TIP
Assess for a potential cause of
pain/discomfort if a nonverbal
child with ASD presents with new
onset aggression or self-injurious
behavior.
EPIDEMIOLOGY
■ Ratio in males to females is 4:1.
ETIOLOGY
Etiology of ASD is multifactorial:
• Second-line: Atomoxetine, a norepinephrine reuptake inhibitor. May be
more appropriate when a history or family history of illicit substance use
is present.
•• Parental psychoeducation, parent management training.
• Executive function coaching, behavior modification techniques and social
skills training.
• Educational accommodations such as classroom modifications.
Autism Spectrum Disorder (ASD)
ASD is characterized by impairments in social communication/interaction
and restrictive, repetitive behaviors/interests. This disorder encompasses the
spectrum of symptomatology formerly diagnosed as autism, Asperger’s disorder, childhood disintegrative disorder, and pervasive developmental disorder.
■ Problems with social interaction and communication:
•• Impaired social/emotional reciprocity (e.g., inability to hold
conversations).
• Deficits in nonverbal communication skills (e.g., decreased eye contact).
• Interpersonal/relational challenges (e.g., lack of interest in peers).
■ Restricted, repetitive patterns of behavior, interests, and activities:
•• Intense, peculiar interests (e.g., preoccupation with unusual objects).
• Inflexible adherence to rituals (e.g., rigid thought patterns).
• Stereotyped, repetitive motor mannerisms (e.g., hand flapping).
• Hyper/hyporeactivity to sensory input (e.g., hypersensitive to particular
textures).
■ Abnormalities in functioning begin in the early developmental period.
■ Not better accounted for by ID or global developmental delay. When ID
and ASD co-occur, social communication is below expectation based on
developmental level.
■ Causes significant social or occupational impairment.
■ Recent increase in prevalence to 1% of population. May be related to
expansion of diagnostic classification and/or increased awareness/
recognition.
■ Symptoms typically recognized between 12 and 24 months old but varies
based on severity.
■ Prenatal neurological insults (e.g., infections, drugs), advanced paternal age,
and low birth weight.
■ Fifteen percent of ASD cases are associated with a known genetic mutation.
■ Fragile X syndrome = most common known single gene cause of ASD.
■ Other genetic causes of ASD: Down syndrome, Rett syndrome, and tuberous
sclerosis.
■ High comorbidity with ID.
■ Association with epilepsy.
PROGNOSIS AND TREATMENT
ASD is a chronic condition. The prognosis is variable, but the two most important predictors of adult outcome are level of intellectual functioning and
language impairment. Only a minority of patients can live and work independently in adulthood. Treatment targets associated symptoms in order to
improve basic social, communicative, and cognitive skills:
■ Alpha-2 agonists (e.g., clonidine, guanfacine) and low-dose atypical
antipsychotic medications (e.g., risperidone, aripiprazole) may help reduce
disruptive behavior, aggression, and irritability.
■ Early intervention.
■ Remedial education.
■ Behavioral therapy.
■ Psychoeducation.
Tic Disorders
TOURETTE’S DISORDER
Tics are defined as sudden, rapid, repetitive, stereotyped movements or vocalizations. Although experienced as involuntary, patients can learn to temporarily suppress tics. Prior to the tic, patients may feel a premonitory urge (somatic
sensation), with subsequent tension release after the tic. Anxiety, excitement,
and fatigue can be aggravating factors for tics. Tics may present as simple or
complex, depending on length of time, purpose, and orchestration.
Tourette’s disorder is the most severe of the tic disorders. It is characterized by
multiple motor tics and at least one vocal tic lasting for at least 1 year. Vocal
tics may appear many years after the motor tics, and they may wax and wane in
frequency. The most common motor tics involve the face and head, such as eye
blinking and throat clearing.
Examples of vocal tics:
■ Coprolalia—Utterance of obscene, taboo words as a bark or grunt.
■ Echolalia—Repeating others’ words.
Diagnosis and DSM-5 Criteria
■ Multiple motor and at least one vocal tic present (not required to occur
concurrently) for more than 1 year since onset of first tic.
■ Onset prior to age 18 years.
■ Not caused by a substance (e.g., cocaine) or another medical condition (e.g.,
Huntington disease).
PSYCHIATRIC DISORDERS IN CHILDREN
WARDS TIP
Tic disorders are one of the few
psychiatric disorders in which
diagnostic criteria do not require
symptoms to cause significant
distress.
128
PSYCHIATRIC DISORDERS IN CHILDREN
Epidemiology
■ Prevalence: Boys > girls.
Etiology
Course/Prognosis
■ Tics wax and wane and change in type.
Treatment
■ Psychoeducation.
WARDS TIP
A child may have oppositional
defiant disorder if they no difficulty getting along with peers but
will not comply with rules from
parents or teachers.
Other tic disorders include:
OPPOSITIONAL DEFIANT DISORDER (ODD)
KEY FACT
Unlike conduct disorder, ODD
does not involve physical aggression or violating the basic rights
of others.
■ Transient tic behaviors: Common in children.
■ Tourette’s disorder: 3 per 1000 school-age children.
■ Genetic factors: > 55% concordance rate in monozygotic twins.
■ Prenatal/perinatal factors: Older paternal age, obstetrical complications,
maternal smoking, and low birth weight.
■ Psychological factors: Symptom exacerbations with stressful life events.
■ Onset typically occurs between 4 and 6 years, with the peak severity between
ages 10 and 12.
■ Symptoms tend to decrease in adolescence and significantly diminish in
adulthood.
■ High comorbidity with ADHD, OCD, and LD.
■ Behavioral interventions—Habit reversal therapy.
■ Medications—Utilize only if tics become severely impairing or also treating
comorbidities. Due to the fluctuating course of the disorder, it can be
difficult to determine medication efficacy.
•• Alpha-2 agonists: guanfacine (usually first choice), clonidine.
• In severe cases, can consider treatment with atypical (e.g., risperidone) or
typical antipsychotics (e.g., pimozide).
■ Persistent (chronic) motor or vocal tic disorder: Single or multiple motor
or vocal tics (but not both) that have never met criteria for Tourette’s.
■ Provisional tic disorder: Single or multiple motor and/or vocal tics less
than 1 year that have never met criteria for Tourette’s.
Disruptive and Conduct Disorders
These disorders involve problematic interactions with or inflicting harm on
others. While disruptive behaviors may appear within the scope of normal
development, they become pathologic when the frequency, pervasiveness, and
severity impair functioning of the individual or others.
A maladaptive pattern of irritability/anger, defiance, or vindictiveness, which
causes dysfunction or distress in the patient or those affected. These interpersonal difficulties involve at least one non-sibling (usually an authority figure).
Diagnosis and DSM-5 Criteria
Characterized by at least four symptoms present for more than or equal to 6
months (with at least one individual who is not a sibling):
■ Anger/Irritable mood—Loses temper frequently; often angry and resentful.
■ Argumentative/Defiant behavior—Breaks rules, blames others, argues with
authority figures, and deliberately aggravates others.
■ Vindictiveness—Is spiteful/vindictive at least two times in the past 6
months.
■ Behaviors are associated with distress in the individual or others, or
negatively impact functioning.
■ Behaviors cannot be explained exclusively by the diagnosis of another
mental disorder.
Epidemiology
■ Prevalence: Approximately 3%.
■ Onset usually during preschool years: Seen more often in boys before
adolescence.
■ Increased incidence of comorbid substance use and ADHD.
■ Although ODD often precedes CD, most do not develop CD.
Treatment
■ Behavior modification, conflict management training, and problem-solving
skills.
■ Parent management training (PMT) can help with setting limits and
enforcing consistent rules.
■ Medications are used to treat comorbid conditions, such as ADHD.
CONDUCT DISORDER (CD)
CD includes the most serious disruptive behaviors, which violate the rights
of other humans and animals. These individuals inflict cruelty and harm
through physical and sexual violence. They may lack remorse for committing
crimes or lack empathy for their victims.
Diagnosis and DSM-5 Criteria
A pattern of recurrently violating the basic rights of others or societal
norms. The individual has displayed at least three of the following behaviors
exhibited over the last year and at least one occurring within the past 6 months:
■ Aggression to people and animals: Bullies/threatens/intimidates others;
initiation of physical aggression, including use of a weapon; robbery; rape;
cruelty to animals.
■ Destruction of property (e.g., fire setting).
■ Deceitfulness or theft: Burglary; lying to obtain goods/favors.
■ Serious violations of rules: Runs away from home, stays out late at night, and
often truant from school before age 13 years old.
Epidemiology
■ Lifetime prevalence: 9%.
■ More common in males.
■ High incidence of comorbid ADHD and ODD.
■ Associated with antisocial personality disorder.
PSYCHIATRIC DISORDERS IN CHILDREN
KEY FACT
Cruelty to animals may be indicative of Conduct disorder.
KEY FACT
Males: Higher risk of fighting,
stealing, fire setting, and vandalism.
Females: Higher risk of lying,
running away, sex-work, and substance use.
130
PSYCHIATRIC DISORDERS IN CHILDREN
Treatment
Elimination Disorders
WARDS
QUESTION
Q: What is the most common drug
of abuse by adolescents?
A: Alcohol, followed by cannabis
and vaping products.
DSM-5 DIAGNOSIS
Enuresis:
■ At least 5 years old developmentally.
■ At least 4 years old developmentally.
EPIDEMIOLOGY
■ Prevalence of enuresis decreases with age:
WARDS TIP
The majority of enuresis cases
spontaneously remit (5–10% per
year) by adolescence.
ETIOLOGY
■ A multimodal treatment approach with behavior modification, family, and
community involvement.
■ PMT can help parents with limit setting and enforcing consistent rules.
■ Medications can be used to target comorbid symptoms and aggression (e.g.,
SSRIs, guanfacine, propranolol, mood stabilizers, antipsychotics).
Characterized by developmentally inappropriate elimination of urine or feces.
Though typically involuntary, this may be intentional. The course may be
primary (never established continence) or secondary (continence achieved for
a period and then lost). Incontinence can cause significant distress or impair
social or other areas of functioning.
■ Recurrent voiding of urine onto clothes or bed.
■ Occurs two times per week for at least 3 consecutive months or results in
clinical distress or marked impairment.
■ Can occur during sleep (nocturnal), waking hours (diurnal), or both.
■ Not due to a substance (e.g., diuretic) or another medical condition (e.g.,
urinary tract infection, neurogenic bladder, diabetes).
Encopresis:
■ Recurrent defecation into inappropriate places (e.g., clothes, floor), which
may be voluntary or involuntary.
■ Occurs at least one time per month for at least 3 months.
■ Not due to the physiological effects of a substance (e.g., laxatives) or another
medical condition (e.g., hypothyroidism, anal fissure, spina bifida), except
via a constipation-related mechanism.
•• 5—10% of 5 year olds; 3—5% of 10 year olds; 1% of >15 year olds.
• Nocturnal enuresis more common in boys; diurnal enuresis more
common in girls.
■ Prevalence of encopresis: 1% of 5-year-old children; boys >girls.
■ Genetic predisposition for nocturnal enuresis:
•• Approximately 4 times increased risk if history of maternal urinary
incontinence.
• Approximately 10 times increased risk if history of paternal urinary
incontinence.
■ Psychosocial stressors may contribute to secondary incontinence.
■ Encopresis: Often related to constipation/impaction with overflow
incontinence.
TREATMENT
■ Psychoeducation is key for children and their primary caregivers; provide
information about high spontaneous remission rates.
■ Treat if symptoms are distressing and impairing. Engage the patient as
an active participant in the treatment plan. Encourage investment in a
waterproof mattress.
■ PMT for managing intentional elimination.
■ Enuresis treatment:
•• Limit fluid intake and caffeine at night.
• Behavioral program with monitoring and reward system, “bladder
training” exercises, or urine alarm (upgrade from the “bell and pad”
method).
• Pharmacology can be used if the above methods are ineffective or for
diurnal enuresis.
First line: Desmopressin (DDAVP), an antidiuretic hormone analogue.
Second line: Imipramine, a tricyclic antidepressant, can be used at low
doses for refractory cases but has less tolerable side effects.
■ Encopresis without constipation: Comprehensive behavioral program
(“bowel retraining”) for appropriate elimination.
■ Encopresis due to constipation: Initial bowel cleaning followed by stool
softeners, high-fiber diet, and toileting routine in conjunction with a
behavioral program.
PANS/PANDAS
Pediatric acute-onset neuropsychiatric syndrome (PANS aka childhood acute
neuropsychiatric symptoms or CANS) refers to a group of disorders characterized by the presence of obsessive compulsive disorder or severely restricted
food intake. As suggested by the name, the onset is typically rapid, often described by parents as “appearing overnight.” The presence of severe symptoms
from two or more of the following categories are necessary to meet the diagnostic criteria:
■ Anxiety.
■ Emotional lability and/or depression.
■ Irritability, aggression, and/or oppositional behaviors.
■ Behavioral/developmental regression.
■ Sudden deterioration in school performance.
■ Motor or sensory abnormalities.
■ Somatic symptoms and signs, including sleep disturbances, enuresis, or
urinary frequency.
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal
infections (PANDAS) is a subtype of PANS. Diagnosis requires OCD and/or
a tic disorder. The initial onset and/or periodic exacerbations are temporally
associated with group A streptococcal infections. Motoric hyperactivity and/or
adventitious movements are commonly present. While both PANS and
PSYCHIATRIC DISORDERS IN CHILDREN
132
PSYCHIATRIC DISORDERS IN CHILDREN
Child Abuse
WARDS TIP
• Red flags for physical abuse: Delayed medical care for injury, inconsistent explanation of injury,
multiple injuries in various stages
of healing, head injuries, cigarette burns, spiral bone fractures,
bruising patterns consistent with
hand or belt.
• Red flags for sexual abuse:
Sexually transmitted diseases,
recurrent urinary tract infections,
prepubertal vaginal bleeding,
pregnancy, or trauma/bruising/
inflammation of genitals/anus.
PHYSICAL ABUSE
SEXUAL ABUSE
WARDS TIP
If a child reports sexual abuse, it
should be taken seriously as it is
rarely unfounded.
PSYCHOLOGICAL ABUSE
NEGLECT
PANDAS have been topics of debate in regards to their etiologies, evaluation,
and treatment, PANDAS is listed in the DSM-5, as an Obsessive Compulsive
and Related Disorder due to Another Medical Condition.
Child abuse encompasses physical abuse, sexual abuse, emotional abuse, and
neglect. Toxic stress may result when children endure prolonged, severe trauma
and adversity without the buffer of supportive caregivers. This can disrupt a
child’s development and lead to a spectrum of pathologic sequelae.
■ About 1 million cases of child maltreatment in the United States.
■ Up to 2500 deaths per year caused by abuse in the United States.
These numbers may be an underestimation as many cases go undetected and
unreported.
■ Any act that results in non-accidental injury and may be the result of severe
corporal punishment committed by an individual responsible for the child.
■ Physical exam and x-rays may demonstrate multiple injuries not consistent
with child’s developmental age.
■ Most common perpetrator is a first-degree male caregiver (e.g., parent,
guardian, mother’s partner).
■ Any sexual act involving a child intended to provide sexual gratification to
an individual responsible for the child.
■ Sexual abuse is the most invasive form of abuse and results in detrimental
lifetime effects on the victim.
■ Data indicates approximately 25% of girls and 9% of boys are exposed to
sexual abuse. Abuse is generally underreported, and males are less likely
than females to report it.
■ Children are most at risk of sexual abuse during preadolescence.
Non-accidental verbal or symbolic acts that result in psychological damage.
■ Failure to provide a child with adequate food, shelter, supervision, medical
care, education, and/or affection.
■ Victims of neglect may exhibit poor hygiene, malnutrition, stunted growth,
developmental delays, and failure to thrive.
■ Severe deprivation can result in death, particularly in infants.
■ Neglect accounts for the majority of cases reported to child protection
services.
TREATMENT
Early intervention can potentially mitigate the negative sequelae and facilitate
recovery.
SEQUELAE
■ Increased risk of developing posttraumatic stress disorder, anxiety disorders,
depressive disorders, dissociative disorders, self-destructive behaviors, and
substance use disorders.
■ Increased risk of continuing intergenerational abuse cycle with partners and
children.
PSYCHIATRIC DISORDERS IN CHILDREN
WARDS TIP
Doctors are mandated reporters,
thus legally required to report all
cases of suspected child abuse
to the appropriate social service
agencies.
134
PSYCHIATRIC DISORDERS IN CHILDREN
NOTES

14 - Chapter 11 Dissociative Disorders

01 - Chapter 11 Dissociative Disorders
Chapter 11 Dissociative Disorders
CHAPTER 11
DISSOCIATIVE
DISORDERS
Dissociative Amnesia..............................................................................................................136
Diagnosis and DSM-5 Criteria.............................................................................................136
Epidemiology/Etiology......................................................................................................136
Treatment..........................................................................................................................136
Depersonalization/Derealization Disorder..............................................................................137
Diagnosis and DSM-5 Criteria.............................................................................................137
Epidemiology/Etiology......................................................................................................137
Course and Prognosis.........................................................................................................137
Treatment..........................................................................................................................137
Dissociative Identity Disorder (Multiple Personality Disorder).................................................138
Diagnosis and DSM-5 Criteria.............................................................................................138
Epidemiology/Etiology......................................................................................................138
Course and Prognosis.........................................................................................................138
Treatment..........................................................................................................................138
Other Specified Dissociative Disorder......................................................................................139
DSM-5 Examples................................................................................................................139
136
DISSOCIATIVE DISORDERS
WARDS
QUESTION
Q: When do dissociative responses
typically occur?
A: During stressful and traumatic
events.
Dissociative Amnesia
KEY FACT
Dissociative amnesia refers to
disruption in the continuity of an
individual’s memory. Patients with
dissociative amnesia report gaps
in the recollection of particular
events, usually traumatic ones.
WARDS TIP
DIAGNOSIS AND DSM-5 CRITERIA
Patients suffering from dissociative
amnesia can experience periods of
flashbacks, nightmares, or behavioral reenactments of their trauma.
KEY FACT
Although dissociative fugue is
now considered a subtype of
dissociative amnesia disorder, it
more commonly occurs in patients
with dissociative identity disorder.
EPIDEMIOLOGY/ETIOLOGY
■ Lifetime prevalence is 6–7%.
■ Higher incidence in female patients.
■ Amnesia often develops after trauma.
KEY FACT
TREATMENT
■ Important to establish the patient’s safety.
Abreaction: The strong emotional
reaction patients may experience while retrieving traumatic
memories.
Dissociation can be understood as a disruption in the integrated sense of self.
This may involve lapses in autobiographical memory (amnesia) and feelings
of detachment from one’s self (depersonalization) or from one’s surroundings
(derealization). These symptoms often develop in the context or aftermath of
significant trauma, particularly during childhood. Dissociation may initially help buffer the impact of a trauma, but can also become pathological and
maladaptive. While the dissociative disorders are closely related to the stressorand trauma-related disorders, they are classified separately in the DSM-5.
Individuals with dissociative amnesia are unable to remember important personal information or history, often traumatic in nature. Procedural memory
(e.g., how to ride a bike) is preserved, distinguishing dissociative amnesia from
other conditions resulting in memory loss (e.g., major neurocognitive disorders/dementias). The unrecalled autobiographical information has been stored
in memory and is thus potentially retrievable. Dissociative amnesia rarely generalizes to encompass complete memory loss. More commonly, a single period
of time (localized amnesia) or certain events (selective amnesia) are forgotten.
Affected individuals often do not have insight regarding their deficits. There is
a significant incidence of comorbid major depressive disorder or persistent
depressive disorder (dysthymia) and an increased risk for suicide—particularly
as amnesia resolves and the overwhelming memories return.
■ An inability to recall important autobiographical information, usually
involving a traumatic or stressful event, that is inconsistent with ordinary
forgetfulness.
■ May present with dissociative fugue: Sudden, unexpected travel away from
home, accompanied by amnesia for identity or other autobiographical
information.
■ Not due to the physiological effects of a substance, another medical or
neurological condition (e.g., traumatic brain injury), or another mental
disorder.
■ Symptoms cause significant distress or impairment in daily functioning.
■ Psychotherapy (e.g., supportive, CBT, hypnosis) is the mainstay of treatment.
■ Medications have not demonstrated efficacy in dissociative amnesia.
A 19-year-old male is found wandering several miles from home several days
after a missing persons report was filed by his family. He cannot recall his full
name or address, even when shown his ID card. His family reports that he
recently returned from combat deployment.
Likely diagnosis?
Dissociative amnesia with dissociative fugue
Depersonalization/Derealization Disorder
Characterized by repeated experiences of detachment from one’s self or surroundings. Patients may feel as though they are observing themselves from a
distance or have an “out-of-body” experience (depersonalization). They may
experience the world around them as if in a dream or movie (derealization).
DIAGNOSIS AND DSM-5 CRITERIA
■ Persistent or recurrent experiences of one or both:
•• Depersonalization—Experiences of unreality or detachment from one’s
body, thoughts, feelings, or actions
• Derealization—Experiences of unreality or detachment from one’s
surroundings.
■ Reality testing remains intact during an episode, as opposed to during
psychosis, when one cannot distinguish between what is real and what is
not.
■ The symptoms cause significant distress or social/occupational impairment.
■ Not accounted for by a substance (e.g., drug of abuse, medication), another
medical condition, or another mental disorder.
EPIDEMIOLOGY/ETIOLOGY
■ Lifetime prevalence is 2%.
■ Gender ratio 1:1.
■ Mean age of onset is about 16 years.
■ Increased incidence of comorbid anxiety disorders and major depression.
■ Predisposing factors include severe stress and trauma.
COURSE AND PROGNOSIS
Often persistent but may wax and wane.
TREATMENT
■ Psychodynamic, cognitive-behavioral, hypnotherapy, and supportive
therapies may be helpful.
■ There is a lack of evidence for use of medications to treat depersonalization/
derealization disorder.
DISSOCIATIVE DISORDERS
WARDS TIP
Fugue: Think of a forgetful fugitive
who runs away and forms a new
identity.
WARDS
QUESTION
True or False? Transient experiences of depersonalization or derealization commonly occur in many
otherwise healthy individuals.
True. Depersonalization and derealization can occur under stress,
intoxication with substances, and
even in benign circumstances (e.g.,
staring into a mirror for a prolonged period).
138
DISSOCIATIVE DISORDERS
DIAGNOSIS AND DSM-5 CRITERIA
EPIDEMIOLOGY/ETIOLOGY
■ Increased prevalence in women.
WARDS TIP
Symptoms of DID overlap with
symptoms in borderline personality disorder or, to an extent,
psychotic disorders.
COURSE AND PROGNOSIS
■ Course is fluctuating but chronic.
TREATMENT
Dissociative Identity Disorder (Multiple Personality
Disorder)
Dissociative identity disorder (DID) is characterized by the presence of more
than one distinct personality state resulting from a fragmented sense of self.
DID encompasses features of the other dissociative disorders, such as amnesia,
depersonalization, and derealization. DID predominantly develops in victims
of significant and chronic childhood trauma. Patients diagnosed with DID
often cope with posttraumatic stress disorder (PTSD), depression, and suicidality.
■ Disruption of identity manifested as two or more distinct personality
states dominating at different times. These symptoms may be observed by
others or self-reported.
■ Extensive memory lapses in autobiographical information, daily
occurrences, and/or traumatic events.
■ Not due to effects of a substance (drug or medication) or another medical
condition.
■ The condition causes significant distress or impairment in social/
occupational functioning.
■ Rare. No epidemiologic studies of the national prevalence, although a few
community-based studies claim 1% prevalence.
■ 90% of patients with DID have suffered from childhood physical abuse,
sexual abuse, or neglect.
■ Symptoms usually begin to manifest to some extent in childhood but may
occur at any age.
■ High incidence of comorbid PTSD, major depressive disorder, eating
disorders, borderline personality disorder, and substance use disorders.
■ More than 70% of patients attempt suicide, often with frequent attempts and
self-mutilation.
■ Worst prognosis of all dissociative disorders.
■ Psychotherapy is the standard treatment. Goals include maintenance of
safety, stabilization, identity integration, and symptom reduction by working
directly with traumatic memories.
■ Pharmacotherapy: SSRIs to target comorbid depressive and/or PTSD
symptoms (especially hyperarousal). Prazosin may ameliorate nightmares,
and naltrexone may reduce self-injurious behaviors.
A 21-year-old female is brought to the clinic by her boyfriend for evaluation
of “memory issues.” The patient recently visited her family for the holidays.
The boyfriend states that “she had to deal with her abusive, alcoholic father.
She seems like someone else ever since.” The patient speaks in a childlike
singsong voice and asks to be called by a name different than what is listed
on her driver’s license. She denies any concerns.
Most likely diagnosis?
Dissociative identity disorder (DID).
Other Specified Dissociative Disorder
Characterized by symptoms of dissociation that cause significant distress or
impairment of functioning, but do not meet the full criteria for a specific
dissociative disorder.
DSM-5 EXAMPLES
■ Identity disturbance due to prolonged and intense coercive persuasion (e.g.,
brainwashing, cult rituals).
■ Chronic and recurrent syndromes of mixed dissociative symptoms (without
dissociative amnesia).
■ Dissociative trance: An acute narrowing or loss of awareness of
surroundings manifesting as unresponsiveness, potentially with minor
stereotyped behaviors (not part of a cultural or religious practice).
■ Acute dissociative reactions to stressful events (lasting hours/days →
1 month).
DISSOCIATIVE DISORDERS
140
DISSOCIATIVE DISORDERS
NOTES

15 - Chapter 12 Somatic Symptom and Factitious Disorder

01 - Chapter 12 Somatic Symptom and Factitious Dis
Chapter 12 Somatic Symptom and Factitious Disorders
Somatic Symptom Disorder....................................................................................................142
Diagnosis and DSM-5 Criteria.............................................................................................143
Epidemiology....................................................................................................................143
Treatment and Prognosis...................................................................................................143
Conversion Disorder (Functional Neurological Symptom Disorder).........................................143
Diagnosis and DSM-5 Criteria.............................................................................................143
Epidemiology....................................................................................................................144
Treatment and Prognosis...................................................................................................144
Illness Anxiety Disorder..........................................................................................................144
Diagnosis and DSM-5 Criteria.............................................................................................144
Epidemiology....................................................................................................................144
Treatment..........................................................................................................................144
Prognosis...........................................................................................................................144
Psychological Factors Affecting Other Medical Conditions......................................................145
Diagnosis and DSM-5 Criteria.............................................................................................145
Epidemiology....................................................................................................................145
Treatment and Prognosis...................................................................................................145
Factitious Disorder..................................................................................................................145
Diagnosis and DSM-5 Criteria.............................................................................................145
Epidemiology....................................................................................................................146
Treatment and Prognosis...................................................................................................146
Malingering............................................................................................................................146
Presentation......................................................................................................................146
Epidemiology....................................................................................................................147
Management.....................................................................................................................147
Review of Distinguishing Features..........................................................................................147
S OMAT I C SYM P TO M A ND
CHAPTER 12
FACTITIOUS DISORDERS
142
SOMATIC SYMPTOM AND FACTITIOUS DISORDERS
Patients with somatic symptom disorders present with prominent physical
symptoms; these are associated with significant distress or impairment in
social, occupational, or other areas of functioning. While these patients may or
may not have an associated medical condition, their focus is on their distressing somatic symptoms as well as their thoughts, feelings, and behaviors in
response to these symptoms.
■ Types of somatic symptom and related disorders include:
• Somatic symptom disorder.
• Conversion disorder (functional neurological symptom disorder).
• Illness anxiety disorder.
• Psychological factors affecting other medical conditions.
• Factitious disorder.
• Other specified somatic symptom and related disorder.
• Unspecified somatic symptom and related disorder.
Up to 30% of primary care patients present with medically unexplained
­symptoms. In many cases, unspoken psychological needs manifest as physical symptoms. The symptoms may not make physiological “sense” but rather
follow the patient’s conception of how their body works.
Ms. Thomas is a 31-year-old woman who was referred to a psychiatrist by her
gynecologist after undergoing multiple exploratory surgeries for abdominal pain and gynecologic concerns with no definitive findings. The patient
reports that she has had extensive medical problems dating back to adolescence. She reports periods of extreme abdominal pain, vomiting, diarrhea, and possible food intolerances. The obstetrician is her fourth provider
because “my other doctors were not able to help me.” Ms. Thomas reports
fear that her current physician will also fail to relieve her distress. She was
reluctant to see a psychiatrist and did so only after her obstetrician agreed to
follow her after her psychiatric appointment.
Ms. Thomas states that her problems worsened in college, which was
the first time she underwent surgery. She reports that due to her health
problems and severe lack of energy, it took her 5½ years to graduate from
college. She did better for a year or two after college but then had a return of
symptoms. She reports recently feeling very lonely and isolated because she
has not been able to find a boyfriend who can tolerate her frequent illnesses.
She also reports that physical intimacy is difficult for her because she finds
sex painful. Additionally, she is concerned that she might lose her job due to
the number of days she has missed from work due to her abdominal pain,
fatigue, and weakness.
What is the diagnosis?
Somatic symptom disorder. Ms. Thomas has a history of multiple somatic complaints lasting at least 6 months, along with a high level of anxiety about her
symptoms and excessive time and energy devoted to her health concerns.
She has had multiple medical procedures and significant impairment in her
social and occupational functioning.
Somatic Symptom Disorder
Patients with somatic symptom disorder present with at least one (and ­often
multiple) physical symptom. They frequently seek treatment from many
doctors, often resulting in extensive lab work, diagnostic procedures, hospitalizations, and/or surgeries. Note that somatic symptom disorder and a related
medical illness are not mutually exclusive.
DIAGNOSIS AND DSM-5 CRITERIA
■ One or more somatic symptoms (may be predominantly pain) that are
distressing or result in significant disruption.
■ At least one of the following:
• Disproportionate and persistent thoughts about the seriousness of one’s
symptoms.
• Persistently high level of anxiety about health or symptoms.
• Excessive time and energy devoted to these symptoms.
■ Persistent state of being symptomatic (typically >6 months; though the
specific somatic symptoms may shift over time).
EPIDEMIOLOGY
■ Incidence in females likely greater than males.
■ Prevalence in general adult population: 5–7%.
■ Risk factors include older age, fewer years of education, lower
socioeconomic status, unemployment, and history of traumatic experiences
in childhood.
TREATMENT AND PROGNOSIS
■ The course tends to be chronic and debilitating. Symptoms may periodically
improve and then worsen under stress.
■ The patient should have regularly scheduled visits with a single primary
care physician, who should minimize unnecessary medical workups and
treatments.
■ All treating physicians should recognize that the patient’s suffering is
genuine, whether or not there is an identifiable medical cause.
■ Address psychological issues slowly. Patients will likely resist referral to a
mental health professional.
Conversion Disorder (Functional Neurological
Symptom Disorder)
Patients with conversion disorder have at least one neurological symptom
(sensory or motor) which cannot be fully explained by a neurological condition. Examples include blindness, paralysis, and paresthesia. Patients may be
surprisingly calm and unconcerned (la belle indifference) when describing their
symptoms.
DIAGNOSIS AND DSM-5 CRITERIA
■ At least one symptom of altered voluntary motor or sensory function.
■ Evidence of incompatibility between the symptom and recognized
neurological or medical conditions.
■ Not better explained by another medical or mental disorder.
SOMATIC SYMPTOM AND FACTITIOUS DISORDERS
KEY FACT
Somatic symptom disorder
patients typically express lots of
concern over their condition and
chronically perseverate over it.
Conversion disorder patients often
have an abrupt onset of their neurological symptoms (blindness,
etc.) but appear unconcerned.
WARDS TIP
When treating a patient with a
somatic symptom disorder, it is
important for the psychiatrist to
work closely with the patient’s
primary care physician.
WARDS
QUESTION
Q: Are patients with conversion
disorder consciously faking their
symptoms?
A: No. Patients with conversion
disorder unconsciously produce
symptoms, and cannot control
when they occur. Symptoms may
persist even after they become
aware of their conversion disorder.
144
SOMATIC SYMPTOM AND FACTITIOUS DISORDERS
KEY FACT
Conversion-like presentations in
elderly patients have a higher
likelihood of representing an
underlying neurological deficit.
EPIDEMIOLOGY
TREATMENT AND PROGNOSIS
Illness Anxiety Disorder
DIAGNOSIS AND DSM-5 CRITERIA
■ High level of anxiety about health.
WARDS
QUESTION
Q: In what setting are you most
likely to diagnose a somatic
symptom-related disorder?
A: Patients most commonly seek
out care in medical settings—for
example, primary care offices, medical specialty clinics, or
­emergency rooms. Patients are
­relatively unlikely to present
to psychiatric settings, unless
­referred by a medical provider.
EPIDEMIOLOGY
■ Men are affected as often as women.
■ Average age of onset 20–30 years.
TREATMENT
■ Psychotherapy (primarily CBT).
PROGNOSIS
■ Can result in significant disability.
■ Causes significant distress or impairment in social or occupational
functioning or warrants medical evaluation.
■ Common symptoms: Paralysis, weakness, blindness, mutism, sensory
complaints (paresthesias), psychogenic nonepileptic seizures (PNES), globus
sensation (globus hystericus or sensation of lump in throat).
■ Two to three times more common in women than men.
■ Onset at any age, but more often in adolescence or early adulthood.
■ High incidence of comorbid neurological, depressive, or anxiety disorders.
■ The primary treatment is education about the illness. Cognitive-behavioral
therapy (CBT), with or without physical therapy, can be used if education
alone is not effective.
■ While patients often spontaneously recover, the prognosis is poor:
Symptoms may persist, recur, or worsen in 40–66% of patients.
■ Preoccupation with having or acquiring a serious illness.
■ Somatic symptoms are not present, or if present, are mild in intensity.
■ Performs excessive health-related behaviors or exhibits maladaptive behaviors.
■ Persists for at least 6 months (the specific illness that is feared may change
over time).
■ Not better explained by another mental disorder (such as somatic symptom
disorder).
■ Approximately 67% have a coexisting major mental disorder.
■ Regularly scheduled visits with one primary care physician.
■ Comorbid anxiety and depressive disorders should be treated with selective
serotonin reuptake inhibitors (SSRIs) or other appropriate psychotropic
medications.
■ Chronic but episodic—Symptoms may wax and wane periodically.
■ Up to 60% of patients improve significantly.
■ Factors predicting better prognosis include fewer somatic symptoms, shorter
duration of illness, and absence of childhood physical punishment.
Psychological Factors Affecting
Other Medical Conditions
A patient with one or more psychological or behavioral factors (e.g., distress,
coping styles, maladaptive health behaviors) adversely affecting a medical
symptom or condition. Examples include anxiety worsening asthma, denial
that acute chest pain needs treatment, and manipulating insulin doses in order
to lose weight.
DIAGNOSIS AND DSM-5 CRITERIA
■ A medical symptom or condition (other than mental disorder) is present.
■ Psychological or behavioral factors adversely affect the medical condition
in at least one way, such as influencing the course or treatment, constituting
an additional health risk factor, influencing the underlying pathophysiology,
precipitating, or exacerbating symptoms or necessitating medical attention.
■ Psychological or behavioral factors are not better explained by another
mental disorder.
EPIDEMIOLOGY
■ Prevalence and gender differences are unclear.
■ Can occur across the lifespan.
TREATMENT AND PROGNOSIS
■ Treatment includes education and frequent contact with a primary care
physician.
■ SSRIs and/or psychotherapy (especially CBT) should be used to treat
underlying anxiety or depression.
Factitious Disorder
Patients with factitious disorder intentionally falsify medical or psychological
signs or symptoms in order to assume the role of a sick patient. They often do
this in a way that can cause legitimate danger (central line infections, insulin
injections, etc.). The absence of external rewards is a prominent feature of this
disorder.
DIAGNOSIS AND DSM-5 CRITERIA
■ Falsification of physical or psychological signs or symptoms, or induction of
injury or disease, associated with identified deception.
■ The deceptive behavior is evident even in the absence of obvious external
rewards.
■ Behavior is not better explained by another mental disorder, such as
delusional disorder or another psychotic disorder.
SOMATIC SYMPTOM AND FACTITIOUS DISORDERS
146
SOMATIC SYMPTOM AND FACTITIOUS DISORDERS
KEY FACT
■ Commonly feigned symptoms:
Münchhausen syndrome is
­another, older name for factitious disorder with predominantly ­physical complaints.
­Münchhausen syndrome by
proxy is intentionally producing
symptoms in someone else who
is under one’s care (usually one’s
child).
EPIDEMIOLOGY
■ May be at least 1% of hospitalized patients.
■ More common in women.
■ Associated with personality disorders.
TREATMENT AND PROGNOSIS
Malingering
PRESENTATION
■ Individual can present themself, or another individual (as in factitious
disorder imposed on another).
• Psychiatric—Hallucinations, depression.
• Medical—Fever (by heating the thermometer), infection, hypoglycemia,
abdominal pain, seizures, and hematuria.
■ Higher incidence in hospital and health care workers (who have learned
how to feign symptoms).
■ Many patients have a history of illness and hospitalization, as well as
childhood physical or sexual abuse.
■ Collect collateral information from medical providers and family.
Collaborate with primary care physician and treatment team to avoid
unnecessary procedures.
■ Patients may require confrontation in a nonthreatening manner; however,
patients who are confronted may leave against medical advice and seek
hospitalization elsewhere.
■ Repeated and long-term hospitalizations are common.
A 37-year-old patient claims that he has frequent episodes of “seizures,” starts
on medications, and joins an epilepsy support group. It becomes known that
he is doing this in order to collect social security disability money. Diagnosis?
Malingering. In contrast, in factitious disorder, patients look for some kind
of unconscious emotional gain by playing the “sick role,” such as sympathy
from the physician. The fundamental difference between malingering and
factitious disorder is in the intention of the patient; in malingering, the motivation is external, whereas in factitious disorder, the motivation is internal.
Malingering involves the intentional reporting of physical or psychological
symptoms in order to achieve secondary (external) gain. Common external
motivations include avoiding incarceration, receiving room and board, obtaining narcotics, and receiving monetary compensation. Note that malingering is
not considered a psychiatric condition.
■ Patients usually present with multiple vague complaints that do not conform
to a known medical condition.
■ They often have a long medical history with many hospital stays.
■ They are generally uncooperative and refuse to accept a good prognosis even
after extensive medical evaluation.
■ Symptoms quickly improve or resolve once the desired objective is obtained.
EPIDEMIOLOGY
■ Not uncommon in hospitalized patients.
■ Significantly more common in men than women.
MANAGEMENT
■ Neuropsychological testing can help to identify feigned or exaggerated
cognitive symptoms. Assessments routinely include embedded validity
measures and tests more specifically designed to catch malingering or low
effort, such as the TOMM (Test of Memory Malingering).
■ Work with the patient to manage their underlying distress, if possible.
■ Gentle confrontation may be necessary; however, patients who are
confronted may leave the hospital Against Medical Advice (AMA) and
seek treatment elsewhere.
Review of Distinguishing Features
■ Somatic symptom disorders: Patients believe they are ill and do not
intentionally produce or feign symptoms.
■ Factitious disorder: Patients intentionally produce symptoms of a
psychological or physical illness because of a desire to assume the sick role,
not for external rewards.
■ Malingering: Patients intentionally produce or feign symptoms for external
rewards.
SOMATIC SYMPTOM AND FACTITIOUS DISORDERS
KEY FACT
Malingering is the conscious
feigning of symptoms for some
secondary gain (e.g., monetary compensation or avoiding
­incarceration).
148
SOMATIC SYMPTOM AND FACTITIOUS DISORDERS
NOTES

16 - Chapter 13 Impulse Control Disorders

01 - Chapter 13 Impulse Control Disorders
Chapter 13 Impulse Control Disorders
IM P U LSE CON T R O L
CHAPTER 13
DISORDERS
Intermittent Explosive Disorder..............................................................................................151
Diagnosis and DSM-5 Criteria.............................................................................................151
Epidemiology/Etiology......................................................................................................151
Treatment..........................................................................................................................151
Kleptomania...........................................................................................................................151
Diagnosis and DSM-5 Criteria.............................................................................................151
Epidemiology/Etiology......................................................................................................152
Treatment..........................................................................................................................152
Pyromania..............................................................................................................................152
Diagnosis and DSM-5 Criteria.............................................................................................152
Epidemiology/Etiology......................................................................................................152
Treatment..........................................................................................................................152
150
IMPULSE CONTROL DISORDERS
■ Little control over the negative behavior.
Impulse control disorders are characterized by problems in the self-regulation
of emotions and behaviors. The behaviors violate the rights of others and/
or conflict with societal norms. Impulse control disorders are not caused by
another mental disorder, medical condition, or substance use.
Core qualities of the impulse control disorders are as follows:
■ Repetitive or compulsive engagement in behavior despite adverse
consequences.
■ Anxiety or craving experienced prior to engagement in impulsive behavior.
■ Relief or satisfaction during or after completion of the behavior.
Mr. Baker is a 27-year-old married accountant who arrives at the outpatient
psychiatry clinic complaining of difficulty in managing his anger. He has no
prior psychiatric history, but reports that he has had difficulty controlling his
temper since adolescence. He reports that he is easily angered by small occurrences, such as his wife’s failing to make coffee or a coworker’s forgetting
a pen at work. He reacts quickly and in a volatile way, describing it as “going
from 0 to 60 before I know it.” Mr. Baker feels that he is unable to control his
anger; on several occasions he has thrown objects and destroyed property
in fits of rage, and has made threatening statements to his wife and coworkers in the past year. Because of these incidents, one coworker has recently
threatened to pursue legal action.
Mr. Baker describes these episodes as brief, lasting only 10–15 minutes,
and feels embarrassed shortly after the episode has transpired. He is concerned he may lose his job because of his behavior, and he worries about the
fate of his relationships. He rarely drinks alcohol, and denies any history of
illicit drug use.
What is his most likely diagnosis?
Based on Mr. Baker’s history, his most likely diagnosis is intermittent explosive disorder. However, it is important to recognize that impulsivity is a common characteristic of other psychiatric diagnoses, and these must be ruled
out prior to diagnosing a patient with this disorder.
What would be your recommended treatment?
Treatment for this disorder usually involves medications to treat impulsive
aggression. These include selective serotonin reuptake inhibitors (SSRIs)—
fluoxetine being the most studied—and mood stabilizers such as anticonvulsants and lithium. Individual psychotherapy is difficult and has limited efficacy given the nature of the disease and lack of individual control. However,
cognitive-behavioral therapy (CBT) has been used in the treatment of anger
management. Group therapy and/or family therapy may be useful to create
behavior plans to help manage episodes.
What are associated laboratory findings?
In some impulsive individuals, cerebrospinal fluid testing shows low mean
5-hydroxyindoleacetic acid (5-HIAA) concentration. There may also be
nonspecific electroencephalographic findings or abnormalities on
­neuropsychological testing.
Intermittent Explosive Disorder
DIAGNOSIS AND DSM-5 CRITERIA
■ Recurrent behavioral outbursts resulting in verbal and/or physical
aggression against people or property.
Either:
■ Frequent verbal/physical outbursts (that do not result in physical damage to
people, animals, or property) twice weekly for 3 months.
Or:
■ Rare (more than three times per year) outbursts resulting in physical
damage to others, animals, or property.
■ Outbursts and aggression are grossly out of proportion to the triggering
event or stressor.
■ Outbursts are not premeditated and not committed to obtain a desired
reward.
■ Aggressive outbursts cause either marked distress or impairment in
occupational/interpersonal functioning, or are associated with financial/
legal consequences.
■ Aggression is not better explained by another mental disorder, medical
condition, or due to the effects of a substance (drug or medication).
EPIDEMIOLOGY/ETIOLOGY
■ More common in men than women.
■ Onset usually in late childhood or adolescence.
■ May be episodic, but course is generally chronic and persistent.
■ Genetic, perinatal, environmental, and neurobiological factors may play
a role in etiology. Patients may have a history of childhood physical or
emotional abuse or head trauma.
TREATMENT
■ Treatment involves use of SSRIs, anticonvulsants, or lithium.
■ CBT has been shown to be effective and is often used in combination with
medications.
■ Group therapy and/or family therapy may be useful to create behavior plans
to help manage episodes.
Kleptomania
DIAGNOSIS AND DSM-5 CRITERIA
■ Failure to resist uncontrollable urges to steal objects that are not needed for
personal use or monetary value.
■ Increasing internal tension immediately prior to the theft.
■ Pleasure or relief is experienced while stealing; however, those with the
disorder often report intense guilt and depression.
IMPULSE CONTROL DISORDERS
KEY FACT
Low levels of serotonin in the CSF
have been shown to be associated with impulsiveness and
aggression.
WARDS
QUESTION
Q: What conditions should be
considered in the differential diagnosis for an adult with possible
intermittent explosive disorder?
A: Substance intoxication or
withdrawal, antisocial or borderline personality disorders, neurologic disorders (e.g., TBI, seizures),
ADHD, bipolar disorder, and
psychotic disorders.
152
IMPULSE CONTROL DISORDERS
EPIDEMIOLOGY/ETIOLOGY
WARDS
QUESTION
Q: What eating disorder is most
commonly comorbid with kleptomania?
A: Bulimia nervosa. An estimated
65% of patients with kleptomania
also suffer from bulimia nervosa.
■ Occurs in 4–24% of shoplifters.
TREATMENT
Pyromania
DIAGNOSIS AND DSM-5 CRITERIA
KEY FACT
Pyromania is the impulse to start
fires, typically with feelings of
gratification or relief afterward.
EPIDEMIOLOGY/ETIOLOGY
TREATMENT
■Stealing is not committed to express anger/vengeance and does not occur in
response to a delusion or hallucination.
■ Objects stolen are typically given or thrown away, returned, or hoarded.
■ Three times more common in women than men, though rare in the general
population.
■ Higher incidence of comorbid mood disorders, eating disorders (especially
bulimia nervosa), anxiety disorders, substance use disorders, and personality
disorders.
■ Higher risk of OCD and substance use disorders in family members.
■ Illness usually begins in adolescence and course is episodic.
Treatment may include CBT (including systematic desensitization and aversive
conditioning) and SSRIs. There is also some anecdotal evidence for the use of
naltrexone, which blocks reward pathways mediated by endogenous opioids.
■ At least two episodes of deliberate fire setting.
■ Tension or arousal experienced before the act; pleasure, gratification, or
relief experienced when setting fires or witnessing/participating in their
aftermath.
■ Fascination with, interest in, curiosity about, or attraction to fire and
contexts.
■ Purpose of fire setting is not for monetary gain, for expression of anger or
vengeance, to conceal criminal activity, or as an expression of sociopolitical
ideology. It is not in response to a hallucination, delusion, or impaired
judgment (intoxication, neurocognitive disorder).
■ Fire setting is not better explained by conduct disorder, a manic episode, or
antisocial personality disorder.
■ Rare disorder but much more common in men.
■ Most begin to set fires in adolescence or early adulthood.
■ High comorbidity with mood disorders, substance use disorders, gambling
disorder, and conduct disorder.
■ Episodes are episodic and wax and wane in frequency.
Most don’t go into treatment and symptoms will remain chronic. While there is
no standard treatment, CBT, SSRIs, mood stabilizers, and antipsychotics have
all been used.

17 - Chapter 14 Eating Disorders

01 - Chapter 14 Eating Disorders
Chapter 14 Eating Disorders
EATI N G
CHAPTER 14
DISORDERS
Definition...............................................................................................................................154
Anorexia Nervosa....................................................................................................................155
Diagnosis and DSM-5 Criteria.............................................................................................155
Physical Findings and Medical Complications....................................................................155
Epidemiology....................................................................................................................155
Etiology.............................................................................................................................156
Differential Diagnosis........................................................................................................156
Course and Prognosis.........................................................................................................156
Treatment..........................................................................................................................156
Bulimia Nervosa.....................................................................................................................157
Diagnosis and DSM-5 Criteria.............................................................................................157
Physical Findings and Medical Complications....................................................................157
Epidemiology....................................................................................................................157
Etiology.............................................................................................................................157
Course and Prognosis.........................................................................................................157
Treatment..........................................................................................................................158
Binge-Eating Disorder.............................................................................................................158
Diagnosis and DSM-5 Criteria.............................................................................................158
Physical Findings and Medical Complications....................................................................159
Epidemiology....................................................................................................................159
Etiology.............................................................................................................................159
Course and Prognosis.........................................................................................................159
Treatment..........................................................................................................................159
154
EATING DISORDERS
Definition
WARDS TIP
Suspect an eating disorder? Ask the
patient what is their highest/lowest
weight, their ideal body weight, if
they count calories/fat/carbs/protein, how much they exercise, if they
binge and purge, and if they have
food rituals (e.g., drinking water
between bites).
Eating disorders include anorexia nervosa, bulimia nervosa, and binge-eating
disorder. Patients with anorexia or bulimia have a disturbed body image and
use extreme measures to avoid gaining weight (vomiting, laxatives, diuretics,
enemas, fasting, and excessive exercise). Patients with binge-eating disorder
typically binge in response to negative emotions.
Ms. Williams is a 17-year-old female without prior psychiatric history who
is brought to the emergency room by ambulance after her parents called
911 when they found her having a seizure in their living room. She was
admitted to the medical intensive care unit in status epilepticus and was
quickly stabilized with intramuscular lorazepam and fosphenytoin loading. Her height is 5 feet 6 inches, she is of medium build, and her weight is
101 pounds (BMI 16.3 kg/m2). She has no significant medical history, and
this is her first seizure. Laboratory workup shows an electrolyte imbalance
as the most likely cause for her seizures. Although initially reluctant, she
admits to self-induced vomiting several times this week. She reports that
although she normally restricts her daily caloric intake to 500 calories, she
regularly induces vomiting if her weight is above 100 pounds. Her last
menstrual cycle was 1 year ago. Psychiatric consultation is requested in
order to confirm her diagnosis.
As the psychiatrist on call, you evaluate Ms. Williams and find that she
appears underweight and younger than her stated age. She is in mild distress, has a nasogastric tube in place, and exhibits poor eye contact. She
reports feeling “sad” and admits to experiencing constant preoccupation
about her physical appearance, stating “I’m fat. I hate my body.” She also
reports insomnia, low energy levels, and a history of self-harm behavior by
cutting her forearms. She reports that she is careful in hiding her symptoms from her parents, whom she describes as strict disciplinarians. She
also expresses concerns that she will disappoint them.
Ms. Williams’s parents describe her as a perfectionist. They say that she
is involved in multiple school activities, takes advanced placement classes,
and has been recently concerned about being accepted to her college of
choice. They report that she has maintained a 4.0 grade point average in
high school, and they expect her to become a doctor. Her parents have
noticed that she is underweight and rarely see her eat, but have attributed this to stress from her many academic pursuits. Ms. Williams’s mother
receives treatment for obsessive-compulsive disorder.
What is Ms. Williams’s most likely diagnosis?
The most likely diagnosis is anorexia nervosa—binge-eating/purging
type. As described above, she refuses to weigh more than 100 pounds,
which is significantly below the minimal normal weight for her height.
Despite being underweight, she expresses intense fear of gaining weight
and has a disturbed self-image. In addition, she has engaged in bingeeating/purging behavior regularly. You should also explore for comorbid
depression, anxiety, and a personality disorder. Remember that malnutrition in itself can lead to some of the symptoms experienced in depression, and that many patients show an improvement in their mood when
nutrition is replenished.
What are some of the medical complications associated with
this condition?
Patients with anorexia nervosa can present with bradycardia, orthostatic hypotension, arrhythmias, QTc prolongation, and ST-T wave changes
on electrocardiogram, as well as anemia and leukopenia. They may also
experience cognitive impairment, evidence of enlarged ventricles and/or
decrease in gray and white matter on brain imaging, and peripheral neuropathy. Lanugo and muscle wasting sometimes become evident. Amenorrhea and loss of libido are commonly reported. In patients who regularly
engage in self-induced vomiting, parotid enlargement, increased amylase
levels, and electrolyte imbalances (e.g., hypokalemia) not uncommonly
occur as a result, and may lead to seizures if severe.
Anorexia Nervosa
Patients with anorexia nervosa are preoccupied with their weight, their body
image, and being thin. It is often associated with obsessive-compulsive personality traits. There are two main subtypes:
■ Restricting type: Has not regularly engaged in binge-eating or purging
behavior; weight loss is achieved through diet, fasting, and/or excessive
exercise.
■ Binge-eating/purging type: Eating binges followed by purges including selfinduced vomiting, using laxatives, enemas, or diuretics. Some individuals
purge after eating small amounts of food without binging.
DIAGNOSIS AND DSM-5 CRITERIA
■ Restriction of energy intake relative to requirements, leading to significant
low body weight—defined as less than minimally normal or expected.
■ Intense fear of gaining weight or becoming fat, or persistent behaviors that
prevent weight gain.
■ Disturbed body image, undue influence of weight or shape on selfevaluation, or denial of the seriousness of the current low body weight.
PHYSICAL FINDINGS AND MEDICAL COMPLICATIONS
■ The medical complications of eating disorders are related to weight loss and
purging (e.g., vomiting and laxative abuse).
■ Physical manifestations: Amenorrhea, cold intolerance/hypothermia,
hypotension (especially orthostasis), bradycardia, arrhythmia, acute
coronary syndrome, cardiomyopathy, mitral valve prolapse, constipation,
lanugo (fine, soft body hair typically found in newborns), alopecia, edema,
dehydration, peripheral neuropathy, seizures, hypothyroidism, osteopenia,
osteoporosis.
■ Laboratory/Imaging abnormalities: Hyponatremia, hypochloremic
hypokalemic alkalosis (if vomiting), arrhythmia (especially QTc
prolongation), hypercholesterolemia, transaminitis, leukopenia, anemia
(normocytic, normochromic), elevated blood urea nitrogen (BUN),
increased growth hormone (GH), increased cortisol, reduced gonadotropins
(luteinizing hormone [LH], follicle-stimulating hormone [FSH]),
reduced sex steroid hormones (estrogen, testosterone), hypothyroidism,
hypoglycemia, osteopenia.
EPIDEMIOLOGY
■ Ten to one female to male ratio. Twelve-month prevalence among young
females is 0.4%.
EATING DISORDERS
WARDS
QUESTION
Q: What are the core differences
between anorexia and bulimia?
A: Anorexia is marked by low body
weight and restriction of caloric
intake, while bulimia is marked by
normal (or over) body weight.
KEY FACT
Classic example of anorexia nervosa:
An extremely thin teenage girl
with amenorrhea, whose mother
says she eats very little, does
aerobic exercise for 2 hours a day,
and ritualistically performs 400
sit-ups every day (500 if she has
“overeaten”).
156
EATING DISORDERS
KEY FACT
Anorexia nervosa versus major
depressive disorder: Appetite
Anorexia nervosa: Patients have
a good appetite but starve themselves due to distorted body
image. They are often quite preoccupied with food (e.g., preparing
it for others) but do not eat it
themselves.
Major depressive disorder: Patients
usually have poor appetite, which
leads to weight loss. These
patients have no or decreased
interest in food.
ETIOLOGY
■ Multifactorial.
DIFFERENTIAL DIAGNOSIS
KEY FACT
COURSE AND PROGNOSIS
Refeeding syndrome refers to
dangerous electrolyte and fluid
shifts that occur when severely
malnourished patients are refed
too quickly. Look for fluid retention and decreased levels of
phosphorus, magnesium, and
calcium. Complications include
arrhythmias, respiratory failure,
delirium, and seizures. Manage by
replacing electrolytes and slowing
the feedings.
TREATMENT
■ Food is the best medicine.
WARDS TIP
When a patient with anorexia
learns that weight gain is a common side effect, they may refuse
medication.
■ Bimodal age of onset (age 13–14: hormonal influences; age 17–18:
environmental influences). More common in industrialized countries where
food is abundant and a thin body ideal is held.
■ Common in sports that involve thinness, revealing attire, subjective judging,
and weight classes (e.g., running, ballet, wrestling, diving, cheerleading,
figure skating).
■ Genetics: Higher concordance in monozygotic than dizygotic twin studies.
■ Social theories: Exaggeration of social values (achievement, control, and
perfectionism), idealization of thin body and prepubescent appearance in
Western cultures, increased prevalence of dieting at earlier ages.
■ Medical conditions: Endocrine disorders (e.g., hypothalamic disease,
diabetes mellitus, hyperthyroidism), gastrointestinal illnesses (e.g.,
malabsorption, inflammatory bowel disease), genetic disorders (e.g., Turner
syndrome, Gaucher disease), cancer, AIDS.
■ Psychiatric disorders: Major depression, bulimia, or other disorders (such as
somatic symptom disorder or schizophrenia).
■ Chronic and relapsing illness. Variable course—may completely recover,
have fluctuating symptoms with relapses, or progressively deteriorate. Most
remit within 5 years.
■ Mortality rate is cumulative and approximately 5% per decade due to
starvation, suicide, or cardiac failure. Rates of suicide are approximately 12
per 100,000 per year.
■ Patients may be treated as outpatients unless they are dangerously below
ideal body weight (>20–25% below) or if there are serious medical or
psychiatric complications, in which case they should be hospitalized for
supervised refeeding.
■ Treatment involves cognitive-behavioral therapy, family therapy (e.g.,
Maudsley approach—the gold standard for treatment of anorexia nervosa in
teenagers), and supervised weight-gain programs.
■ Selective serotonin reuptake inhibitors (SSRIs) have not been effective in
the treatment of anorexia nervosa but may be used for comorbid anxiety or
depression.
■ Little evidence that second-generation antipsychotics can treat
preoccupation with weight and food, or independently promote weight
gain. Olanzapine has the most evidence in this regard.
■ There is some consensus that a premeal anxiolytic (such as alprazolam) can
help encourage eating by decreasing anticipatory anxiety.
Bulimia Nervosa
Bulimia nervosa involves binge eating combined with behaviors intended to
counteract weight gain, such as vomiting; use of laxatives, enemas, or diuretics;
fasting; or excessive exercise. Patients are embarrassed by their binge eating
and are overly concerned with body weight. However, unlike patients with
anorexia, they usually maintain a normal weight (and may be overweight).
DIAGNOSIS AND DSM-5 CRITERIA
■ Recurrent episodes of binge eating.
■ Recurrent, inappropriate attempts to compensate for overeating and prevent
weight gain (such as laxative abuse, vomiting, diuretics, fasting, or excessive
exercise).
■ The binge eating and compensatory behaviors occur at least once a week for
3 months.
■ Perception of self-worth is excessively influenced by body weight and shape.
■ Does not occur exclusively during an episode of anorexia nervosa.
PHYSICAL FINDINGS AND MEDICAL COMPLICATIONS
■ Patients with anorexia and bulimia may have similar medical complications
related to weight loss and vomiting.
■ Physical manifestations: Salivary gland enlargement (sialadenosis), dental
erosion/caries, esophageal tear or ruptures, callouses/abrasions on dorsum
of hand (“Russell’s sign” from self-induced vomiting), petechiae, peripheral
edema, aspiration.
■ Laboratory/Imaging abnormalities: Hypochloremic hypokalemic alkalosis,
metabolic acidosis (laxative abuse), elevated bicarbonate (compensation),
hypernatremia, increased BUN, increased amylase, altered thyroid hormone,
esophagitis.
EPIDEMIOLOGY
■ Twelve-month prevalence in young females is 1–1.5%.
■ Significantly more common in women than men (10:1 ratio).
■ Onset is in late adolescence or early adulthood.
■ More common in developed countries.
■ High incidence of comorbid mood disorders, anxiety disorders, impulse
control disorders, substance use, prior physical/sexual abuse, as well as
increased prevalence of borderline personality disorder.
ETIOLOGY
■ Multifactorial, with similar factors as for anorexia (e.g., genetic and social
theories).
■ Childhood obesity and early pubertal maturation increase risk for bulimia
nervosa.
COURSE AND PROGNOSIS
■ Chronic and relapsing illness.
■ Better prognosis than anorexia nervosa.
EATING DISORDERS
WARDS TIP
Unlike patients with anorexia
nervosa, bulimic patients usually
maintain a normal weight (or are
overweight) and their symptoms
are more ego-dystonic (distressing); they are therefore more likely
to seek help.
WARDS
QUESTION
Q: What is binge eating?
A: Excessive food intake within a
2-hour period accompanied by a
sense of lack of control.
WARDS
QUESTION
Q: What is a potentially lethal complication of both anorexia nervosa
and bulimia nervosa?
A: Cardiac arrhythmias due to
electrolyte disturbances such as
hypokalemia.
KEY FACT
Compared to patients with
bulimia nervosa, cortisol is often
increased in patients with anorexia nervosa.
158
EATING DISORDERS
KEY FACT
Classic example of bulimia
nervosa: A 20-year-old college
student is referred by her dentist
because of multiple dental caries.
She is normal weight for her
height but feels that “she needs
to lose 15 pounds.” She reluctantly admits to eating large quantities of food in a short period of
time and then inducing vomiting.
■ Crude mortality rate is 2% per decade.
TREATMENT
■ SSRIs are first-line medication.
■ Nutritional counseling and education.
WARDS
QUESTION
Q: What is the only FDA-approved
medication for the treatment of
bulimia?
A: Fluoxetine.
KEY FACT
In patients with bulimia, make
sure to check that they aren’t on
medications that could further
lower their seizure threshold, such
as the antidepressant Wellbutrin
(bupropion).
Binge-Eating Disorder
DIAGNOSIS AND DSM-5 CRITERIA
■ Severe distress over binge eating.
■ Symptoms are usually exacerbated by stressful conditions.
■ One-half recover fully with treatment; the other half have a chronic course
with fluctuating symptoms.
■ Elevated suicide risk compared to the general population.
■ Antidepressants plus therapy are more efficacious for treating bulimia
nervosa than either treatment alone.
■ Fluoxetine is the only Food and Drug Administration (FDA)-approved
medication for bulimia (60–80 mg/day).
■ Therapy includes cognitive-behavioral therapy, interpersonal psychotherapy,
group therapy, and family therapy. Cognitive behavioral therapy has
demonstrated more efficacy than the other therapies.
■ Avoid bupropion due to its potential side effect to lower seizure threshold.
Key Differences: Anorexia vs. Bulimia
Anorexia Nervosa
Bulimia Nervosa
Concern about body weight
Main concern
Concern about body weight
with intense fear of gaining
weight
Eating behavior
Avoids eating (restricting),
± purging
Binge eating with compensatory
behavior (purging, exercise)
Weight
Underweight
Normal weight/Overweight
Medical complications
Nutritional deficiencies
Hypotension
Nutritional deficiencies
Russel’s sign
Dental/esophageal problems
Patients with binge-eating disorder suffer emotional distress over their binge
eating, but they do not try to control their weight by purging or restricting
calories, as do individuals with anorexia or bulimia. Unlike in anorexia and
bulimia, patients with binge-eating disorder are not as fixated on their body
shape and weight.
■ Recurrent episodes of binge eating (eating an excessive amount of food in
a 2-hour period associated with a lack of control), with at least three of the
following: eating very rapidly, eating until uncomfortably full, eating large
amounts when not hungry, eating alone due to embarrassment, and feeling
disgusted/depressed/guilty after eating.
■ Binge eating occurs at least once a week for 3 months.
■ Binge eating is not associated with compensatory behaviors (such as
vomiting and laxative use), and doesn’t occur exclusively during the course
of anorexia or bulimia.
PHYSICAL FINDINGS AND MEDICAL COMPLICATIONS
Patients are typically obese and suffer from medical problems related to obesity
including metabolic syndrome, type 2 diabetes, and cardiovascular disease.
EPIDEMIOLOGY
■ Twelve-month prevalence is 1.6% for females and 0.8% for males.
■ Equal prevalence in females across ethnicities.
■ Increased prevalence among individuals seeking weight-loss treatment
compared to the general population.
ETIOLOGY
Runs in families, reflecting likely genetic influences.
COURSE AND PROGNOSIS
■ Typically begins in adolescence or young adulthood.
■ Appears to be relatively persistent, though remission rates are higher than
for other eating disorders.
■ Most obese individuals do not binge eat; those who do have more functional
impairment, lower quality of life, and more subjective distress than weightmatched controls.
■ Higher rates of psychiatric comorbidities than in obese individuals without
binge-eating disorder.
TREATMENT
■ Treatment involves individual (cognitive-behavioral or interpersonal)
psychotherapy with a strict diet and exercise program coordinated by a
registered dietician. Comorbid mood disorders or anxiety disorders should
be treated as necessary.
■ SSRIs are first-line treatment due to their efficacy and tolerability.
■ Although not frequently used due to significant side effects and limited
long-term efficacy, pharmacotherapy may be used adjunctively to directly
promote weight loss:
• Lisdexamfetamine (Vyvanse)—Stimulant that suppresses appetite and is
FDA-approved for the treatment of binge-eating disorder.
• Topiramate and zonisimide—Antiepileptics associated with weight loss.
• Orlistat (Xenical)—Inhibits pancreatic lipase, thus decreasing amount of
fat absorbed from the gastrointestinal tract.
• Comorbid medical problems such as diabetes and metabolic syndrome
should be monitored and treated appropriately.
EATING DISORDERS
160
EATING DISORDERS
NOTES

18 - Chapter 15 Sleep Wake Disorders

01 - Chapter 15 Sleep Wake Disorders
Chapter 15 Sleep-Wake Disorders
S L EEP -WAKE
CHAPTER 15
DISORDERS
Normal Sleep-Wake Cycle.......................................................................................................162
Sleep Disorders.......................................................................................................................162
Dyssomnias............................................................................................................................163
Insomnia Disorder.............................................................................................................163
Hypersomnolence Disorder................................................................................................164
Obstructive Sleep Apnea Hypopnea...................................................................................165
Central Sleep Apnea..........................................................................................................166
Sleep-Related Hypoventilation..........................................................................................166
Narcolepsy.........................................................................................................................167
Circadian Rhythm Sleep-Wake Disorders...........................................................................168
Parasomnias...........................................................................................................................169
Non-REM Sleep Arousal Disorders......................................................................................169
Sleepwalking.....................................................................................................................169
Sleep Terrors......................................................................................................................171
Nightmare Disorder...........................................................................................................171
REM Sleep Behavior Disorder.............................................................................................172
Restless Legs Syndrome.....................................................................................................172
Substance/Medication-Induced Sleep Disorder.................................................................173
162
SLEEP-WAKE DISORDERS
Normal Sleep-Wake Cycle
KEY FACT
As one ages there are the following changes that occur in the
sleep pattern:
• Increase in time it takes to fall
asleep, known as sleep latency
• Decline in total amount of REM
sleep achieved
• Increase in sleep fragmentation
with more frequent nighttime
awakening
Sleep Disorders
■ Classified as either:
■ When taking a sleep history, ask about:
Awake
Movement
REM
Stage 1
Stage 2
Stage 3
Stage 4
Sleep disorders affect as many as 40% of the U.S. adult population. Current data
demonstrate a high rate of comorbidity between sleep disorders and various
psychiatric illnesses. Disturbances in sleep can potentiate and/or exacerbate
psychological distress and other mental illnesses.
■ Normal sleep-wake cycle is defined in terms of characteristic changes
in several physiological parameters, including brain wave activity, eye
movements, and motor activity.
■ The two stages of normal sleep are rapid eye movement (REM) sleep and
non-rapid eye movement (NREM) sleep.
■ About every 90 minutes, NREM sleep alternates with REM sleep.
■ NREM induces transition from the waking state to deep sleep.
■ Progression through NREM sleep results in slower brain wave patterns and
higher arousal thresholds.
■ In REM sleep, brain wave patterns resemble the electroencephalogram
(EEG) of an aroused person.
■ Awakening from REM sleep is associated with vivid dream recall.
See Figure 15-1.
• Dyssomnias: Insufficient, excessive, or altered timing of sleep.
• Parasomnias: Unusual sleep-related behaviors.
• Activities prior to bedtime that may interfere with restful sleep.
• Bed partner history.
• Consequence on waking function; quality of life.
• Drug regimen, medications.
• Exacerbating or relieving factors.
• Frequency and duration.
• Genetic factors or family history.
• Habits (alcohol consumption, use of caffeine, nicotine, illicit substances,
and hypnotics).
FIGURE 15-1. The sleep cycle. © 2008 LLS. Adapted, with permission of the publisher, Les
Laboratoires Servier, from Figure 1 in Nutt D, Wilson S, Paterson L. Sleep disorders as core
symptoms of depression. Dialogues Clin Neurosci. 2008;10(3):329–336.
Dyssomnias
Dyssomnias are disorders that make it difficult to fall or remain asleep (insomnias), or cause excessive daytime sleeping (hypersomnias).
INSOMNIA DISORDER
■ Refers to a number of symptoms that interfere with duration and/or quality
of sleep despite adequate opportunity for sleep. Symptoms may include:
• Difficulty initiating sleep (initial or sleep-onset insomnia).
• Difficulty maintaining sleep (middle or sleep-maintenance insomnia).
• Early morning awakenings (late or sleep-offset insomnia).
• Waking up feeling fatigued and unrefreshed (nonrestorative sleep).
■ Acute insomnia (less than 3 months) is generally associated with stress or
changes in sleep schedule and usually resolves spontaneously.
■ Chronic insomnia lasts greater than or equal to 3 months to years and
is associated with reduced quality of life and increased risk of psychiatric
illness.
■ Diagnosis is often assisted by use of subjective sleep tracking measures
such as the Consensus Sleep Diary.
DSM-5 Criteria
■ Difficulty initiating/maintaining sleep or early-morning awakening with
inability to return to sleep.
■ Occurs at least 3 days a week for at least 3 months.
■ Causes clinically significant distress or impairment in functioning.
■ Occurs despite adequate opportunity to sleep.
■ Does not occur exclusively during the course of another sleep-wake disorder.
■ Not due to the physiologic effects of a substance or medication.
■ Coexisting mental and medical disorders do not adequately explain the
insomnia.
Epidemiology
Prevalence: 6–10% (the most prevalent of all sleep-wake disorders).
Etiology
■ Subclinical mood and/or anxiety disorders.
■ Preoccupation with a perceived inability to sleep.
■ Bedtime behavior not conducive to adequate sleep (poor sleep hygiene).
■ Idiopathic.
Treatment
■ Sleep hygiene measures.
■ Cognitive-behavioral therapy (CBT) is the first-line treatment.
■ Chronotherapy (bright light therapy) has evidence supporting its use in
treating insomnia by entraining the circadian rhythm.
■ Pharmacotherapy:
• Benzodiazepines:
Reduce sleep latency and nocturnal awakening.
As effective as CBT during short periods of treatment (4–8 weeks);
insufficient evidence to support long-term efficacy.
SLEEP-WAKE DISORDERS
WARDS TIP
REM sleep is characterized by
increase in blood pressure, heart
rate, and respiratory rate.
WARDS
QUESTION
Q: What is the first-line therapy for
chronic insomnia?
A: Cognitive-behavioral therapy;
hypnotic medications are reserved
for those who do not improve with
CBT.
KEY FACT
Insomnia is the most common reason patients are put on long-term
benzodiazepines.
164
SLEEP-WAKE DISORDERS
WARDS
QUESTION
Q: What is the most common antidepressant prescribed for chronic
insomnia?
A: Trazodone.
HYPERSOMNOLENCE DISORDER
KEY FACT
DSM-5 Criteria
Breathing-related disorders are the
most common of the hypersomnias and include obstructive sleep
apnea and central sleep apnea.
Epidemiology
■ Equal frequency in men and women.
Etiology
■ Head trauma.
Side effects include development of tolerance, addiction, daytime
sleepiness, and rebound insomnia.
In the elderly, falls, confusion, and dizziness are of particular concern.
• Non-benzodiazepines:
Include melatonin, zolpidem (Ambien), eszopiclone (Lunesta), zaleplon (Sonata), and suvorexant (Belsomra).
Effective for short-term treatment.
Associated with low incidence of daytime sleepiness and orthostatic
hypotension.
In the elderly, zolpidem causes increased risk of falls and may induce
cognitive impairment.
Doses of zolpidem more than 10 mg can cause increase in cognitive
impairment in women.
• Antidepressants:
Trazodone, amitriptyline, and doxepin (off-label use).
Mirtazapine (in low doses) is often used to promote sleep in patients
with coexisting depressive disorders.
Side effects include sedation, dizziness, and psychomotor impairment.
■ Refers to symptoms of excessive quantity of sleep, reduced quality of
wakefulness, and sleep inertia/sleep drunkenness (i.e., impaired performance
and reduced alertness after awakening).
■ Complain of nonrestorative sleep, automatic behaviors (routine behavior
performed with little to no recall), and difficulty awakening in the morning.
■ Excessive sleepiness despite at least 7 hours of sleep, with at least one of
the following: recurrent periods of sleep within the same day; prolonged,
nonrestorative sleep more than 9 hours; difficulty being fully awake after
awakening.
■ Occurs at least three times per week for at least 3 months.
■ Causes clinically significant distress or impairment in functioning.
■ Does not occur exclusively during the course of another sleep-wake
disorder.
■ Not due to the physiologic effects of a substance or medication.
■ Coexisting mental and medical disorders do not adequately explain the
hypersomnolence.
■ Prevalence: 5–10% of individuals presenting to sleep disorders clinics.
■ Viral infections (e.g., HIV pneumonia, infectious mononucleosis, Guillain–
Barré).
■ Genetic—May have autosomal dominant mode of inheritance in some
individuals.
Course
■ Progressive onset, beginning between ages 15 and 25.
■ Persistent course unless treated.
Treatment
■ Life-long therapy with modafinil (first-line) or stimulants such as
methylphenidate; amphetamine-like antidepressants such as atomoxetine
are second-line therapy.
■ Pitolisant (Wakix) and sodium oxybate (Xyrem) have shown benefit as well.
■ Scheduled napping.
OBSTRUCTIVE SLEEP APNEA HYPOPNEA
Chronic breathing-related disorder characterized by repetitive collapse of the
upper airway during sleep and evidence by polysomnography of multiple episodes of apnea or hypopnea per hour of sleep.
A 40-year-old businessman states that over the past 2 years he has had trouble staying awake for more than 2 hours before eventually falling asleep. He
then has a hard time sleeping through the night. As a result, his performance
at work is suffering. Diagnosis? Many possible diagnoses, but you must
always consider obstructive sleep apnea in addition to insomnia disorder,
narcolepsy, etc.
Features
■ Excessive daytime sleepiness.
■ Apneic episodes characterized by cessation of breathing or hypopneic
episodes of reduced airflow (more than 15 per hour).
■ Sleep fragmentation.
■ Snoring.
■ Frequent awakenings due to gasping or choking.
■ Nonrefreshing sleep or fatigue.
■ Morning headaches.
■ Hypertension.
Risk Factors
Obesity, increased neck circumference, airway narrowing.
Prevalence
■ Most common in middle-aged men and women.
■ Male to female ratio ranges from 2:1 to 4:1.
■ Children: 1–2%; middle-aged adults: 2–15%; older adults: >20%.
Treatment
■ Positive airway pressure: Continuous (CPAP) and in some cases bilevel
(BiPAP).
■ Behavioral strategies such as weight loss and exercise.
■ Surgery, including tonsillectomy and selective upper airway stimulation
implants.
SLEEP-WAKE DISORDERS
166
SLEEP-WAKE DISORDERS
CENTRAL SLEEP APNEA
Prevalence
■ Idiopathic subtype rare.
■ Higher frequency in men than women.
Course
■ May be chronic in opioid users.
Treatment
■ Treat the underlying condition.
■ CPAP/BiPAP.
■ Supplemental O2.
SLEEP-RELATED HYPOVENTILATION
Prevalence
Very uncommon.
Course
Slowly progressive.
Treatment
■ Treat the underlying condition.
■ CPAP/BiPAP.
Evidenced by five or more central apneas per hour of sleep. It can be idiopathic, with Cheyne–Stokes breathing (pattern of periodic crescendo–
decrescendo variation in tidal volume due to heart failure, stroke, or renal
failure), or due to opioid use. It is associated with insomnia and daytime
sleepiness.
■ Cheyne–Stokes subtype increased in patients with decreased ejection
fraction and acute stroke.
■ Thirty percent of chronic opioid users have central sleep apnea.
■ Tied to comorbid medical conditions, although may be transient.
■ Medications (e.g., acetazolamide [Diamox], theophylline, sedativehypnotics).
Polysomnography demonstrates decreased respiration and elevated CO2 levels. Individuals report frequent arousals, morning headaches, insomnia, and
excessive daytime sleepiness. Frequently comorbid with medical or neurologic
disorders, medication use, or substance use disorder. Over time it can result in
pulmonary hypertension, cor pulmonale, cardiac arrhythmias, polycythemia,
neurocognitive dysfunction, and eventually respiratory failure due to severe
blood gas abnormalities.
■ Medications to stimulate/promote breathing (e.g., bronchodilators,
theophylline).
Mr. Richards is a 22-year-old college student with a history of persistent
depressive disorder (dysthymic disorder) who arrives at the outpatient psychiatry clinic complaining of daytime sleepiness. He reports that during the
past 2 years, he has fallen asleep while in social situations and during his college classes. He often takes naps during class, in movie theaters, and sometimes in the middle of conversations with his girlfriend. His naps typically last
for 5–10 minutes and he awakens feeling better. However, within the next
2–3 hours he feels sleepy again. His colleagues joke about his tendency to
sleep everywhere, and he feels embarrassed by this.
Mr. Richards also complains of “weird” experiences while sleeping. He
reports that he sometimes sees bright colors and hears loud sounds that feel
real to him. He says that when this occurs it is difficult to distinguish if he is
dreaming or is awake. He feels frightened by these experiences because he is
unable to move when they happen. However, after a few minutes he reports
that these feelings resolve, and he is able to move and is fully awake.
In performing a thorough history, you learn that he has had episodes
during which he has experienced weakness and has dropped objects from
his hands while laughing or becoming angry. Last week, his legs buckled and
he fell to the ground after his friends startled him at a surprise birthday party.
He denies ever losing consciousness during these episodes, and there have
been no reports of witnessed convulsions.
What is this patient’s diagnosis?
This patient’s symptoms are consistent with a diagnosis of narcolepsy.
The classic narcolepsy tetrad (all four present in less than 25% of patients)
consists of excessive daytime sleepiness or “sleep attacks,” REM-related sleep
phenomena including inability to move during the transition from sleep to
wakefulness, hypnagogic or hypnopompic hallucinations, and a sudden loss
of muscle tone evoked by strong emotion without loss of consciousness
(cataplexy). Cataplexy may be mild, affecting only the voice, face, or arms,
or generalized, causing patients to fall to the ground, and it occurs in 70% of
those diagnosed with narcolepsy.
What are Mr. Richards’s treatment options?
In the treatment of narcolepsy, it is important for patients to schedule daytime
naps and to maintain a regular sleep schedule at night. They should get at
least 8 hours of sleep and keep consistent times for sleeping and awakening.
Pharmacological treatments may include the use of stimulants (methylphenidate) and antidepressants. The stimulant modafinil and sodium oxybate (nonstimulant) are also effective in the treatment of narcolepsy. Sodium oxybate
(Xyrem) is particularly effective in the treatment of cataplexy.
NARCOLEPSY
Narcolepsy is characterized by excessive daytime sleepiness and falling asleep at
inappropriate times.
DSM-5 Criteria
■ Recurrent episodes of need to sleep, lapsing into sleep, or napping during
the day, occurring at least three times per week for at least 3 months
associated with at least one of the following:
• Cataplexy (brief episodes of sudden bilateral loss of muscle tone, most
often associated with intense emotion).
• Hypocretin deficiency in the CSF.
• Reduced REM sleep latency on polysomnography.
■ Hallucinations and/or sleep paralysis at the beginning or end of sleep
episodes are common (but not necessary for diagnosis in the DSM-5).
SLEEP-WAKE DISORDERS
KEY FACT
Hypnagogic hallucination: When
going to sleep.
Hyponopompic hallucination:
When transitioning from sleep.
168
SLEEP-WAKE DISORDERS
Epidemiology/Prevalence
WARDS
QUESTION
Q: What study is useful in
diagnosing narcolepsy?
A: Polysomnography.
Pathophysiology
■ May have autoimmune component.
KEY FACT
Treatment
Don’t confuse narcoleptic cataplexy with catatonic catalepsy
(unprovoked muscular rigidity).
■ Sleep hygiene.
■ Scheduled daytime naps.
■ Avoidance of shift work.
■ For excessive daytime sleepiness:
■ For cataplexy:
KEY FACT
The suprachiasmatic nucleus (SCN)
in the hypothalamus coordinates
24-hour or circadian rhythmicity.
Symptoms
■ Excessive daytime sleepiness.
■ Insomnia.
■ Sleep inertia.
■ Headaches.
■ Difficulty concentrating.
■ Irritability.
■ Waking up at inappropriate times.
■ Narcolepsy with cataplexy occurs in 0.02–0.04% worldwide.
■ Slightly more common in males than females.
■ Linked to a loss of hypothalamic neurons that produce hypocretin which
has excitatory effects promoting wakefulness.
■ Secondary causes include lesions to the posterior hypothalamus and
midbrain.
• Modafinil is first-line pharmacologic treatment.
• Amphetamines (d-amphetamine, methamphetamine).
• Other non-amphetamines such as methylphenidate, sodium oxybate, and
pitolisant (a novel histamine H3 receptor inverse agonist that is effective
for both daytime sleepiness and cataplexy).
• Sodium oxybate (drug of choice).
• Tricyclic antidepressants (TCAs): Imipramine, desipramine, and
clomipramine.
• REM suppression drugs such as selective serotonin reuptake inhibitor
(SSRI)/serotonin-norepinephrine reuptake inhibitor (SNRI): Fluoxetine,
duloxetine, atomoxetine, venlafaxine.
■ Sedative hypnotics are given in some cases to correct disturbed nighttime
sleep.
CIRCADIAN RHYTHM SLEEP-WAKE DISORDERS
Circadian rhythm sleep-wake disorders are recurrent patterns of sleep disruption due to an alteration of the circadian system or misalignment between the
endogenous circadian rhythm and sleep-wake schedule required by an individual’s environment or schedule. Subtypes include delayed sleep phase, advanced
sleep phase, irregular sleep-wake, non-24-hour sleep-wake, and shift work (see
Table 15-1).
■ Increased reaction times and frequent performance errors.
SLEEP-WAKE DISORDERS
Parasomnias
■ Abnormal behaviors, experiences, or physiological events that occur during
sleep or sleep-wake transitions.
■ Symptoms may include abnormal movements, emotions, dreams, and
autonomic activity.
■ Isolated episodes common in childhood and adolescence.
■ Include non-REM sleep arousal disorders, nightmare disorder, REM sleep
behavior disorder, restless leg syndrome.
See Table 15-2.
NON-REM SLEEP AROUSAL DISORDERS
Repeated episodes of incomplete arousals that are brief and usually occur
during the first one-third of the sleep episode. Include sleepwalking and sleep
terrors.
SLEEPWALKING
Features
■ Repeated episodes of simple to complex behaviors that occur during slowwave (NREM) sleep.
■ Behaviors may include sitting up in bed, walking around, eating, and in
some cases “escaping” outdoors.
■ Eyes are usually open with a blank stare and “glassy look.”
■ Difficulty arousing the sleepwalker during an episode.
■ Dreams are not remembered and there is amnesia for the episode.
■ Episodes usually end with patients returning to bed or awakening (briefly)
confused and disoriented.
■ Rare cases associated with violent behavior.
TABLE 15-1. Circadian Rhythm Sleep-Wake Disorders
Disorders
Definitions
Risk Factors
Treatments
Delayed sleep
phase disorder
(DSPD)
Chronic or recurrent delay in sleep
onset and awakening times with
preserved quality and duration of
sleep
■ Puberty (secondary to temporal
changes in melatonin secretion)
■ Caffeine and nicotine use
■ Irregular sleep schedules
■ Timed bright light phototherapy
during early morning
■ Administration of melatonin in
the evening
■ Chronotherapy (delaying bedtime by a few hours each night)
Advanced sleep
phase disorder
Normal duration and quality
of sleep with sleep onset and
awakening times earlier than
desired
Older age
■Timed bright light phototherapy
prior to bedtime
■ Early morning melatonin not
recommended (may cause
daytime sedation)
Shift-work
disorder (SWD)
Sleep deprivation and
misalignment of the circadian
rhythm secondary to
nontraditional work hours
■ Night shift work
■ Rotating shifts
■ Shifts >16 hours
■ Medical and psychiatry residents
■ Avoid risk factors
■ Bright light phototherapy to
facilitate rapid adaptation to
night shift
■ Modafinil may be helpful for
patients with severe SWD
Jet lag disorder
Sleep disturbances (insomnia,
hypersomnia) associated with
travel across multiple time zones
Recent sleep deprivation
■Disorder is usually self-limiting
■ Sleep disturbances generally
resolve 2–3 days after travel
170
SLEEP-WAKE DISORDERS
Examples
■Sleepwalking
Timing
■Slow wave sleep
Behaviors
■ Simple to complex (e.g.,
sitting, walking, eating)
Recall and
orientation upon
awakening
Risk factors
■ Sleep deprivation
Epidemiology
Risk Factors
■ Sleep deprivation.
■ Irregular sleep schedules.
■ Stress.
■ Fatigue.
■ Obstructive sleep apnea.
■ Nocturnal seizures.
■ Fever.
■ Family history.
Etiology
■ Unknown.
■ Family history in 80% of cases.
Treatment
TABLE 15-2. Comparison of REM and NREM Sleep Disorders
NREM Disorders
REM Disorders
■ REM sleep behavior disorder
■ Sleep terrors
■ Nightmares
■ REM sleep
■ First one-third of sleep
■ Last third of sleep
■ Complex behaviors with
gross motor movements,
vocalizations (e.g., yelling, limb
jerking, punching, kicking)
■ Disoriented
■ Oriented
■ Confused
■ Vivid recall
■ Amnesia for the episode
■ REM sleep behavior disorder
(RSBD):
■ Stress
■ OSA
■
■Older age
■ Medications
■
■Medications
■ Seizures
■
■Narcolepsy
■ Fever
■
■Neurogenerative disorder
■ Nightmares:
■
■Adolescence and early
adulthood
■
■PTSD
■ 1–7% of adults have sleepwalking episodes (not disorder).
■ 10–30% of children have at least one episode and 2–3% sleepwalk often.
■ Medications, including sedatives/hypnotics, lithium, and anticholinergics.
■ Usually not associated with any significant underlying psychiatric or
psychological problems.
■ Most cases do not need to be treated as they are self-limiting.
■ Patients may benefit from education, reassurance, addressing precipitating
factors, ensuring a safe environment, and proper sleep hygiene.
■ Refractory cases may respond to low-dose benzodiazepine (e.g.,
clonazepam).
SLEEP TERRORS
Features
■ Recurrent episodes of sudden terror arousals, usually beginning with
screaming or crying, that occur during slow-wave sleep.
■ Signs of autonomic arousal, including tachycardia, tachypnea, diaphoresis,
and mydriasis.
■ Difficulty arousing during an episode.
■ After episode, patients usually return to sleep without awakening.
■ Dreams are not remembered and there is amnesia for the episode.
■ In rare cases, awakening elicits aggressive behavior.
Epidemiology
■ Approximately 2% of adults and 20% of young children have sleep terrors
(not disorder).
■ Tenfold increase in first-degree biological relatives of affected patients.
■ High comorbidity with sleepwalking.
Risk Factors
■ Same as for sleepwalking.
■ Other sleep disorder such as sleep apnea.
Treatment
■ Reassurance that the condition is benign and self-limited.
■ Same as for sleepwalking.
NIGHTMARE DISORDER
Features
■ Recurrent frightening dreams that occur during the second half of the sleep
episode (i.e., during REM sleep).
■ Terminate in awakening with vivid recall.
■ No confusion or disorientation upon awakening.
■ Causes clinically significant distress or impairment in functioning.
Epidemiology
■ Frequent nightmares in 1–2% of adults, higher prevalence in women.
■ Peak prevalence in late adolescence or early adulthood.
■ Nightmares are seen in at least 50–70% of posttraumatic stress disorder
(PTSD) cases.
Treatment
■ Not always needed. Reassurance may help in many cases.
■ Desensitization/Imagery rehearsal therapy (IRT) involves the use of
mental imagery to modify the outcome of a recurrent nightmare, writing
down the improved outcome, and then mentally rehearsing it in a relaxed
state.
■ Medications are rarely indicated. Prazosin and antidepressants are often
used to treat nightmares related to PTSD.
SLEEP-WAKE DISORDERS
KEY FACT
Imagery rehearsal therapy (IRT)
has been successful in treating
recurrent nightmares in patients
with PTSD.
172
SLEEP-WAKE DISORDERS
REM SLEEP BEHAVIOR DISORDER
Features
■ Dream-enacting behaviors include:
Epidemiology
■ Occurs mostly in males.
Risk Factors
■ Older age, generally more than 50 years.
■ Narcolepsy.
WARDS
QUESTION
Treatment
■ Clonazepam is efficacious in most patients.
Q: Which neurocognitive disorder
is commonly associated with REM
sleep behavior disorder?
A: Neurocognitive disorder with
Lewy bodies.
■ Melatonin may also be helpful.
RESTLESS LEGS SYNDROME
Epidemiology
■ Repeated arousals during sleep associated with vocalization or complex
motor behavior (dream-enacting behaviors) occurring during REM, more
often in the second half of the sleep episode.
■ Characterized by lack of normal muscle atonia during REM sleep.
■ No confusion or disorientation upon awakening.
• Sleep talking.
• Yelling.
• Limb jerking.
• Walking and/or running.
• Punching and/or other violent behaviors.
■ Presenting complaint is often violent behaviors during sleep resulting in
injury to the patient and/or to the bed partner.
■ Prevalence in general population is approximately 0.5%, likely higher in
people with psychiatric disorders.
■ Psychiatric medications such as TCAs, SSRIs, SNRIs, and b-blockers.
■ Highly associated with underlying neurodegenerative disorders, especially
Parkinson, multiple system atrophy, and neurocognitive disorder with Lewy
bodies.
■ Discontinuation of likely causative medications if possible.
■ Ensure environmental safety such as removing potentially dangerous objects
from the bedroom and sleeping on the ground until behaviors can be
managed effectively.
Features
The urge to move legs accompanied by unpleasant sensation in the legs, characterized by relief with movement, aggravation with inactivity, and only occurring or worsening in the evening.
■ Prevalence is 2–7% in the general population.
■ Females 1.5–2 times more likely than males.
Risk Factors
■ Increases with age.
■ Strong familial component.
■ Iron deficiency.
■ Antidepressants, antipsychotics, dopamine-blocking antiemetics, and
antihistamines can contribute to or worsen symptoms.
■ Multiple medical comorbidities, including cardiovascular disease, diabetes
mellitus, chronic kidney disease, and Parkinson disease.
Treatment
■ Behavioral strategies including regular exercise, reduced caffeine intake, and
avoiding aggravating factors have been shown to be beneficial.
■ Responds well to pharmacologic treatments.
■ Remove offending agents if possible.
■ Iron replacement if low ferritin.
■ Dopamine agonists, such as pramipexole and ropinirole, and
benzodiazepines are first-line treatments.
■ Gabapentin, gabapentin enacarbil (prodrug to gabapentin), and pregablin
are also used.
■ Low-potency opioids can be used for treatment-refractory patients.
SUBSTANCE/MEDICATION-INDUCED SLEEP DISORDER
■ Severe sleep disorder due to substance intoxication/withdrawal or
medication.
■ Sleep disturbance not better explained by another sleep disorder (e.g.,
symptoms do not last longer than 1 month after intoxication or withdrawal).
■ Can be insomnia, daytime sleepiness, parasomnia, or mixed type.
■ Treatment is to remove the offending substance, or reduce, discontinue, or
switch medications (if clinically appropriate).
SLEEP-WAKE DISORDERS
WARDS
QUESTION
Q: What laboratory test should
be ordered in a person diagnosed
with Restless legs syndrome (RLS)?
A: Serum ferritin.
174
SLEEP-WAKE DISORDERS
NOTES

19 - Chapter 16 Sexual Dysfunctions and Paraphilic Diso

01 - Chapter 16 Sexual Dysfunctions and Paraphilic
Chapter 16 Sexual Dysfunctions and Paraphilic Disorders
Sexual Response Cycle............................................................................................................176
Sexual Changes with Aging....................................................................................................176
Differential Diagnosis of Sexual Dysfunctions.........................................................................176
Sexual Dysfunctions................................................................................................................177
Treatment of Sexual Disorders................................................................................................178
Sex Therapy.......................................................................................................................178
Cognitive-Behavioral Therapy............................................................................................179
Group Therapy...................................................................................................................179
Analytically Oriented (Psychodynamic) Psychotherapy......................................................179
Pharmacologic Treatment..................................................................................................179
Mechanical Therapies........................................................................................................179
Gender Dysphoria...................................................................................................................180
Diagnosis and DSM-5 Criteria.............................................................................................180
Treatment..........................................................................................................................180
Paraphilias..............................................................................................................................181
Examples of Paraphilic Disorders.......................................................................................181
Course and Prognosis.........................................................................................................181
Treatment..........................................................................................................................181
PARAPHILIC DISORDERS
S EX UAL DYSFU NC T I O NS A ND
CHAPTER 16
176
SEXUAL DYSFUNCTIONS AND PARAPHILIC DISORDERS
Sexual Response Cycle
WARDS
QUESTION
Q: Which class of antidepressants
is most likely to cause sexual dysfunction?
A: Selective serotonin reuptake
inhibitors (SSRIs).
■ Depression.
■ Substance use.
Sexual dysfunctions include clinically significant disturbances in individuals’
ability to respond sexually or to experience sexual pleasure.
There are several stages of normal sexual response in men and women:
Desire: The motivation or interest in sexual activity, often reflected by sexual
fantasies.
Excitement/Arousal: Begins with either fantasy or physical contact. It is
characterized by erections and testicular enlargement in men and by vaginal
lubrication, clitoral erection, labial swelling, and elevation of the uterus in
the pelvis (tenting) in women. Both men and women experience flushing,
nipple erection, and increased respiration, pulse, and blood pressure.
Orgasm: In men just prior there is tightening of the scrotal sac and secretion of a few drops of seminal fluid. Women experience contraction of the
outer one-third of the vagina and enlargement of the upper one-third of the
vagina.
Men ejaculate and women have contractions of the uterus and lower onethird of the vagina. There is facial grimacing, release of tension, slight clouding of consciousness, involuntary anal sphincter contractions, and acute
increase in blood pressure and pulse in both men and women.
Resolution: Muscles relax and cardiovascular state returns to baseline. Detumescence of genitalia in both sexes. Men have a refractory period lasting
minutes to hours during which they cannot reexperience orgasm; women
have little or no refractory period.
Sexual Changes with Aging
The desire for sexual activity does not usually change as people age. However, men usually require more direct stimulation of genitals and more time to
achieve orgasm, with less reliable/strong erections. The intensity of ejaculation
usually decreases, and the length of refractory period increases.
After menopause, women experience vaginal dryness and thinning due to decreased levels of estrogen and lubrication. They may also have decreased libido
and reduced nipple/clitoral/vulvar sensitivity. These conditions can be treated
with hormone replacement therapy or vaginal creams.
Differential Diagnosis of Sexual Dysfunctions
Problems with sexual functioning may be due to any of the following:
■ Medical conditions: Examples include atherosclerosis (causing erectile
dysfunction from vascular occlusion), diabetes (causing erectile dysfunction
from vascular changes and peripheral neuropathy), and pelvic adhesions
(causing dyspareunia in women).
■ Medication side effects: Antihypertensives, anticholinergics, antidepressants
(especially selective serotonin reuptake inhibitors [SSRIs]), and
antipsychotics.
■ Abnormal levels of gonadal hormones:
• Estrogen: Decreased levels after menopause cause vaginal dryness and
thinning in women (without affecting desire).
• Testosterone: Promotes libido (desire) in both men and women.
• Progesterone: May inhibit libido in both men and women by blocking
androgen receptors; found in oral contraceptives, hormone replacement
therapy, and, occasionally, treatments for prostate cancer.
■ Presence of a sexual dysfunction (see below).
Sexual Dysfunctions
Sexual dysfunctions are problems involving any stage of the sexual response
cycle. They all share the following Diagnostic and Statistical Manual of Mental
Disorders, 5th ed. (DSM-5) criteria:
■ The disorder causes clinically significant distress.
■ The dysfunction is not better explained by a nonsexual mental disorder,
as a consequence of severe relationship distress or other stressors, and not
attributable to the effects of a substance/medication or another medical
condition.
Mr. Jones is a 58-year-old married man with a history of major depressive
disorder who arrives at your outpatient clinic for a yearly follow-up visit. He
complains of recent marital problems with his wife of 30 years. He is being
treated with an SSRI, and his depressive symptoms have been stable for over
3 years on his current dose. Upon further questioning, he reveals that he
has been having sex with his wife less often than usual, only once or twice
a month. He states that this is a marked decrease since his last visit with
you. He feels that lately they have been arguing more and feels that their
decrease in sexual activity has adversely affected their relationship. He also
reports a mild decrease in his energy.
Mr. Jones denies having urges to masturbate in the times between sexual
intercourse with his wife. He also denies having any affairs, laughing nervously while saying, “I can barely satisfy my own wife.” He appears sad and
states that he is beginning to feel “down” about this. When he does have sex,
he reports that it is initiated by his wife, and he is initially reluctant to engage
in sexual activity. However, once he does, he denies any problems with having or sustaining an erection and denies any difficulties in reaching orgasm.
Mr. Jones reports that he drinks two or three drinks per day on the weekends,
and he does not use any recreational drugs.
What is his most likely diagnosis? What other considerations should be
made?
The patient’s most likely diagnosis is male hypoactive sexual desire disorder.
Although decreased sexual interest is more prevalent in women, it should
not be overlooked in men. As this clinical case shows, the patient does not
seem to fantasize or desire sexual activity despite prior history of doing so.
He appears distressed by this and reports that it is causing interpersonal
dysfunction. Although his depression has remained stable during the past 3
years and the patient does not report symptoms that would suggest a current depressive episode, his sexual complaints and fatigue symptoms might
suggest a relapse of depressive symptoms and should be monitored closely.
It is also very important to consider if his treatment with an SSRI is affecting
his sexual functioning.
SEXUAL DYSFUNCTIONS AND PARAPHILIC DISORDERS
KEY FACT
Dopamine enhances libido. Serotonin inhibits sexual function.
WARDS TIP
Causes of sexual dysfunctions may
be physiological, psychological,
or both. Psychological causes
of sexual dysfunctions are often
comorbid with other psychiatric
disorders, such as depression or
anxiety.
WARDS TIP
Problems with sexual desire may
be due to stress, relationship difficulties or conflict, poor selfesteem, or unconscious fears
about sex.
178
SEXUAL DYSFUNCTIONS AND PARAPHILIC DISORDERS
WARDS
QUESTION
Q: What are the most common
sexual dysfunctions in men?
A: Erectile disorder and premature
ejaculation.
KEY FACT
Other DSM-5 categories of sexual
dysfunction include substance/
medication-induced sexual
dysfunction and other specified/
unspecified sexual dysfunction.
SEX THERAPY
What should you consider in the initial management of this patient’s
complaints?
His initial management should consist of a thorough history, a physical
examination, and laboratory tests (complete metabolic profile, testosterone
levels, thyroid-stimulating hormone levels) that might rule out medical (e.g.,
endocrine) abnormalities. If another medical disorder, mental disorder, or
substance is not believed to be responsible, treatment considerations should
include outpatient psychotherapy, sex therapy, cognitive-behavioral therapy,
or group therapy.
■ Male hypoactive sexual desire disorder: Absence or deficiency of sexual
thoughts, desire, or fantasies for more than 6 months (self-reported in
approximately 5% of men).
■ Female sexual interest/Arousal disorder: Absence or reduced sexual
interest, thoughts/fantasies, initiation of sex, sexual excitement/pleasure,
sexual arousal, and/or genital/nongenital sensations during sex for more
than 6 months (unclear prevalence of DSM-5 disorder, but self-reported in
26–43% of women).
■ Erectile disorder: Marked difficulty obtaining or maintaining an erection,
or marked decreased in erectile rigidity for more than 6 months. Commonly
referred to as erectile dysfunction (ED) or impotence. May be lifelong (always
had difficulty) or acquired (after previous ability to maintain erections). ED
is the most common sexual disorder diagnosed in men; the prevalence is age
dependent, from 5% at age 40 to 15% at age 70.
■ Premature (early) ejaculation: Recurrent pattern of ejaculation during sex
within 1 minute and before the individual wishes it for more than 6 months.
Likely the most common sexual disorder in men, but underreported.
Worldwide prevalence up to 30%.
■ Female orgasmic disorder: Marked delay in infrequency/absence/reduced
intensity of orgasm for more than 6 months. The international prevalence
ranges from 20% to 40%.
■ Delayed ejaculation: Marked delay in infrequency/absence of ejaculation
for more than 6 months. Worse as men age and likely underreported,
approximately 6% of men over 50 years report ejaculatory difficulty.
■ Genito-pelvic pain/Penetration disorder: Persistent or recurrent
difficulties in one of the following: vaginal penetration during intercourse,
marked vulvovaginal or pelvic pain during intercourse or penetration,
marked anticipatory fear or anxiety about vulvovaginal or pelvic pain, or
marked tensing or tightening of pelvic floor muscles during attempted
vaginal penetration for more than 6 months. Prevalence unknown but
10–20% of American women complain of pain during intercourse. Prior
sexual/physical abuse is considered to be a risk factor.
Treatment of Sexual Disorders
Sex therapy utilizes the concept of the couple, rather than the individual, as the
target of therapy. Couples meet with a therapist together in sessions to identify
and discuss their sexual problems. The therapist recommends sexual exercises
for the couple to attempt at home; activities initially focus on heightening
sensory awareness (sensate focus exercises) and progressively incorporate
increased levels of sexual contact. Treatment is short term. This therapy is most
useful when no other psychopathology is involved.
COGNITIVE-BEHAVIORAL THERAPY
Cognitive-behavioral therapy (CBT) approaches sexual dysfunction as a
learned maladaptive behavior. It utilizes traditional therapies such as cognitive
restructuring, partner communication training, systematic desensitization,
and exposure, where patients are progressively exposed to increasing levels
of stimuli that provoke their anxiety. Eventually, patients are able to respond
appropriately to the stimuli. Other forms of therapy may include muscle relaxation techniques, assertiveness training, and prescribed sexual exercises to try
at home. It is also a short-term therapy.
GROUP THERAPY
May be used as a primary or adjunctive therapy.
ANALYTICALLY ORIENTED (PSYCHODYNAMIC) PSYCHOTHERAPY
Individual, long-term therapy that focuses on feelings, past relationships
(including familial), fears, fantasies, dreams, and interpersonal problems that
may be contributing to the sexual disorder.
PHARMACOLOGIC TREATMENT
■ Erectile disorder: Phosphodiesterase-5 inhibitors (e.g., sildenafil) are given
orally, which enhance blood flow to the penis; they require psychological
or physical stimulation to achieve an erection. A second-line treatment
is alprostadil, either injected into the corpora cavernosa or transurethral,
which acts locally; it produces an erection within 2–3 minutes and works in
the absence of sexual stimulation.
■ Premature ejaculation: SSRIs and the serotonergic tricyclic antidepressant
(TCA) clomipramine prolong the time from stimulation to orgasm. Topical
aesthetics are also occasionally used.
■ Male hypoactive sexual desire disorder/female sexual interest/arousal
disorder: Testosterone is used as replacement therapy for men with
low levels. Low doses may also improve libido in women, especially
in postmenopausal women. Medications that increase dopamine and
norepinephrine, such as Flibanserin and bupropion, may also be used.
Low-dose vaginal estrogen replacement may improve vaginal dryness and
atrophy in postmenopausal women.
MECHANICAL THERAPIES
■ Erectile disorder: Vacuum-assisted erection devices, penile prostheses, or
surgical insertion of semirigid or inflatable tubes into the corpora cavernosa
(used only for end-stage impotence).
■ Female orgasmic disorder: Directed masturbation (education and selfawareness exercises to reach orgasm through self-stimulation).
SEXUAL DYSFUNCTIONS AND PARAPHILIC DISORDERS
180
■ Premature ejaculation:
SEXUAL DYSFUNCTIONS AND PARAPHILIC DISORDERS
Gender Dysphoria
DIAGNOSIS AND DSM-5 CRITERIA
■ At least two of the following:
KEY FACT
Gender-expansive patients may
use a wide range of terms to
self-identify, such as transgender, nonbinary, or genderqueer.
Transitioning is different for every
individual, and may involve psychosocial changes, medications, or
gender-affirming surgeries.
TREATMENT
• The squeeze technique is used to increase the threshold of excitability.
When the man is excited to near ejaculation, he or his sexual partner
is instructed to squeeze the glans of his penis in order to prevent
ejaculation. Gradually, he gains awareness about his sexual sensations and
learns to achieve greater ejaculatory control.
• The stop-start technique involves cessation of all penile stimulation when
the man is near ejaculation. This technique functions in the same manner
as the squeeze technique.
■ Genito-pelvic pain/Penetration disorder: Gradual desensitization to
achieve intercourse, starting with muscle relaxation techniques, progressing
to erotic massage, and finally achieving sexual intercourse.
Previous versions of the DSM included the diagnosis of gender identity disorder.
This was revised to gender dysphoria in DSM-5 to emphasize that the pathology
is not gender diversity itself, but rather the distress caused by incongruence
between the gender a person was assigned at birth and their identified gender.
Gender-expansive people experience disproportionately high rates of harassment, violence, and discrimination. One-third of transgender adults have had
negative experiences related to their gender in healthcare settings, and nearly
one-third are not “out” to any of their medical providers; therefore, clinicians
should ask, not assume, a patient’s gender, and use the patient’s identified pronouns in all communication and documentation.
Common psychiatric comorbidities include suicidal ideation, mood/anxiety
disorders, PTSD, substance use, and eating disorders.
• A marked incongruence between one’s experienced gender and primary/
secondary sex characteristics.
• A strong desire to be rid of one’s primary/secondary sex characteristics
because of the above.
• A strong desire for the primary/secondary sex characteristics of the other
gender.
• A strong desire to be of the other gender.
• A strong desire to be treated as the other gender.
• A strong conviction that one has the typical feelings/reactions of the other
gender.
■ Clinically significant distress or impairment in functioning.
Gender-affirming psychotherapy, and engagement of family support especially
for children or adolescents. Transitioning may be social (e.g., changes to name,
clothing, or hairstyle), medical (hormone therapy), or surgical. Surgical sex
reassignment surgery can be performed after living 1 year in the desired gender
role and 1 year of continuous hormone therapy. It’s essential to screen carefully
for comorbid psychiatric conditions and treat these as usual.
Paraphilias
Paraphilic disorders are characterized by engagement in unusual sexual activities and/or preoccupation with unusual sexual urges or fantasies for at least 6
months that either are acted on with a nonconsenting person or cause significant distress or impairment in functioning. Paraphilic fantasies alone are not
considered disorders unless they are intense, recurrent, and interfere with daily
life; occasional fantasies are considered normal components of sexuality (even
if unusual).
Only a small percentage of people suffer from paraphilic disorders. Most paraphilic disorders occur almost exclusively in men, but sadism, masochism, and
pedophilia may also occur in women. Voyeuristic and pedophilic disorders are
the most common paraphilic disorders.
EXAMPLES OF PARAPHILIC DISORDERS
■ Pedophilic disorder: Sexual fantasies/urges/behaviors involving sexual acts
with prepubescent children (age 13 years or younger). DSM-5 specifies that
the person is at least age 16 and at least 5 years older than the child.
■ Frotteuristic disorder: Sexual arousal from touching or rubbing against a
nonconsenting person.
■ Voyeuristic disorder: Sexual arousal from observing an unsuspecting nude,
or disrobing individual (often with binoculars).
■ Exhibitionistic disorder: Sexual arousal from exposure of one’s genitals to
an unsuspecting person.
■ Sexual masochism disorder: Sexual arousal from the act of being
humiliated, beaten, bound, or made to suffer.
■ Sexual sadism disorder: Sexual arousal from the physical or psychological
suffering of another person.
■ Fetishistic disorder: Sexual arousal from either the use of nonliving objects
(e.g., shoes or pantyhose) or nongenital body parts.
■ Transvestic disorder: Sexual arousal from cross-dressing (e.g., man wearing
women’s clothing such as underwear).
COURSE AND PROGNOSIS
■ Poor prognostic factors are having multiple paraphilias, early age of onset,
comorbid substance use, high frequency of behavior, and referral by law
enforcement agencies (i.e., after an arrest).
■ Good prognostic factors are having only one paraphilia, self-referral
for treatment, sense of guilt associated with the behavior, and
history of otherwise normal sexual activity in addition to the
paraphilia.
TREATMENT
■ Difficult to treat; studied mostly in pedophilia.
■ Psychotropic medication if associated with a comorbid psychiatric
illness.
SEXUAL DYSFUNCTIONS AND PARAPHILIC DISORDERS
WARDS
QUESTION
Q: What are the three most common types of paraphilia?
A: Pedophilia, voyeurism, and
exhibitionism.
KEY FACT
Patients often have more than one
paraphilia.
KEY FACT
An example of fetishistic disorder
is a man being primarily sexually aroused by women’s shoes
resulting in significant distress and
marital problems.
KEY FACT
An example of transvestic disorder
is a person significantly distressed
by being sexually aroused when
dressing up as a member of the
opposite gender. This is not the
same as homosexuality or gender
dysphoria.
182
SEXUAL DYSFUNCTIONS AND PARAPHILIC DISORDERS
KEY FACT
Rape is a violent crime and not a
paraphilia.
■ Social skills training.
■ Twelve-step programs.
■ Group therapy.
■ Although controversial, antiandrogens, long-acting gonadotropin-releasing
hormones, SSRIs, and naltrexone have been used to decrease sex drive and
fantasies.
■ Cognitive-behavioral therapy can be used to disrupt learned patterns and
modify behavior.

20 - Chapter 17 Psychotherapies

01 - Chapter 17 Psychotherapies
Chapter 17 Psychotherapies
Psychoanalysis and Related Therapies....................................................................................184
Freud’s Theories of the Mind...................................................................................................184
Topographic Theory...........................................................................................................184
Structural Theory...............................................................................................................184
Defense Mechanisms..............................................................................................................184
Mature Defenses................................................................................................................185
Neurotic Defenses..............................................................................................................185
Immature Defenses...........................................................................................................186
Other Defense Mechanisms...............................................................................................186
Psychoanalysis........................................................................................................................186
Important Concepts and Techniques Used in Psychoanalysis.............................................187
Psychoanalysis-Related Therapies.....................................................................................187
Behavioral Therapy.................................................................................................................187
Learning Theory.................................................................................................................187
Conditioning......................................................................................................................188
Behavioral Therapy Techniques (Deconditioning)..............................................................188
Cognitive Therapy...................................................................................................................188
Clinical Example of the Cognitive Theory of Depression.....................................................189
Cognitive-Behavioral Therapy (CBT)........................................................................................189
Dialectical Behavioral Therapy (DBT)......................................................................................190
Group Therapy........................................................................................................................190
Family Therapy........................................................................................................................190
Couples Therapy......................................................................................................................191
PSYCHOTHERAPIES
CHAPTER 17
184
PSYCHOTHERAPIES 
KEY FACT
Normal development: Id is present
at birth, ego develops after birth,
and superego development is
traditionally considered to be
completed by age 6.
■ Psychoanalysis.
■ Psychoanalytically oriented psychotherapy.
■ Brief dynamic therapy.
KEY FACT
■ Interpersonal therapy.
According to Freud, the superego
is the aspect of one’s psyche that
represents “morality, society, and
parental teaching.”
TOPOGRAPHIC THEORY
KEY FACT
The Freudian superego represents
internalization of cultural rules.
STRUCTURAL THEORY
Defense Mechanisms
It is common to combine psychotherapy with medications. Split treatment
describes the arrangement where a physician prescribes medication and someone else provides therapy. In these cases, the physician and therapist should
­regularly communicate regarding the patient’s treatment.
Psychoanalysis and Related Therapies
Psychoanalysis and its related therapies are derived from Sigmund Freud’s psychoanalytic theories of the mind. Freud proposed that behaviors, or symptoms,
result from unconscious mental processes, including defense mechanisms and
conflicts between one’s ego, id, superego, and external reality. Since the time
of Freud, many other psychoanalytic theories have been developed. Influential
theorists have included Melanie Klein, Heinz Kohut, Michael Balint, Margaret
Mahler, and others.
Examples of psychoanalytic therapies include the following:
Freud’s Theories of the Mind
Unconscious: Includes repressed thoughts that are out of one’s awareness;
involves primary process thinking (primitive, pleasure-seeking urges with no
regard to logic or time, prominent in children and psychosis). Thoughts and
ideas may be repressed into the unconscious because they are embarrassing,
shameful, or otherwise too painful.
Preconscious: Contains memories that are easy to bring into awareness, but
not unless consciously retrieved.
Conscious: Involves current thoughts and secondary process thinking (logical, organized, mature, and can delay gratification).
Id: Unconscious; involves instinctual sexual/aggressive urges and primary
process thinking.
Superego: Moral conscience and ego ideal (inner image of oneself that one
wants to become).
Ego: Serves as a mediator between the id, superego, and external environment, and seeks to develop satisfying interpersonal relationships; uses
defense mechanisms (see below) to control instinctual urges and distinguishes fantasy from reality using reality testing. Problems with reality testing
occur in psychotic individuals.
Defense mechanisms are used by the ego to protect oneself and relieve anxiety
by keeping conflicts out of awareness. They are (mostly) unconscious processes
that are normal and healthy if they are mature and used in moderation (i.e.,
adaptive). They may be unhealthy if immature (i.e., maladaptive). Immature
defense mechanisms can be used excessively as seen in some psychiatric
disorders.
Defense mechanisms are often classified hierarchically. Mature defense mechanisms are healthy and adaptive, and they are seen in high-functioning and
healthy adults. Neurotic defenses are encountered in obsessive-compulsive
patients, patients with other anxiety disorders, and adults under stress. Immature defenses are seen in children, adolescents, psychotic patients, and some
nonpsychotic patients, such as those with severe personality disorders. They are
the most primitive defense mechanisms.
MATURE DEFENSES
Mature ego defenses are commonly found in healthy, high-functioning adults.
These defenses often help people integrate conflicting emotions and thoughts.
Altruism: Performing acts that benefit others so as to vicariously experience pleasure. (Clinical example: A patient’s child recently died from ovarian
cancer. As part of the grieving process, the patient donates money to help
raise community awareness about the symptoms of ovarian cancer so other
patients could potentially benefit from early intervention.)
Humor: Expressing (usually) unpleasant or uncomfortable feelings without
causing discomfort to self or others. (Clinical Example: When talking about
lifestyle modifications, a diabetic patient jokingly reports that they are exercising their arm muscles when they eat.)
Sublimation: Satisfying socially objectionable impulses in an acceptable manner (thus channeling them rather than preventing them). (Clinical ­example: Person with unconscious urges to physically control others
­becomes a prison guard.)
Suppression: Purposely ignoring an unacceptable impulse or emotion so as
to diminish discomfort and accomplish a task. (Clinical example: Nurse who
feels nauseated by an infected wound puts aside feelings of disgust to clean
wound and provides necessary patient care.)
NEUROTIC DEFENSES
Displacement: Shifting emotions from an undesirable situation to one
that is personally tolerable. (Clinical example: Student who is angry with
their mother talks back to their teacher the next day and refuses to obey
­instructions.)
Intellectualization: Avoiding negative feelings by excessive use of intellectual functions and by focusing on irrelevant details. (Clinical example: Physician dying from colon cancer describes the pathophysiology of the disease in
detail to their 12-year-old child.)
Isolation of affect: Unconsciously limiting the experience of feelings or
emotions associated with a stressful life event so as to avoid anxiety. (Clinical
example: Patient describes the recent death of their beloved spouse without
emotion.)
Rationalization: Explanations of an event to justify outcomes or behaviors and
to make them acceptable. (Clinical example: “My boss fired me today because
they aren’t meeting their quotas, not because I haven’t done a good job.”)
Reaction formation: Doing the opposite of an unacceptable impulse. (Clinical
example: Patient who is attracted to their married coworker insults them.)
PSYCHOTHERAPIES 
KEY FACT
Suppression, as a defense mechanism, is a conscious process that
involves avoiding paying attention
to a particular emotion.
WARDS
QUESTION
Q: A former gang member becomes a police officer working
in the intercity to prevent gang
violence. What is the defense
mechanism?
A: Sublimation—The channeling
of destructive impulses to create
something constructive.
186
PSYCHOTHERAPIES 
KEY FACT
Intellectualization is a defense
mechanism where reasoning is
used to block confrontation with
an unconscious conflict or undesirable thought or feeling.
IMMATURE DEFENSES
WARDS
QUESTION
Q: An individual buys an unreasonably expensive new watch and
tells their friends that they needed
it because their old one was not
reliable enough and they have
to make sure to get to appointments on time. What is the defense
mechanism?
A: Rationalization—Attempting
to justify behavior to make it
­acceptable.
OTHER DEFENSE MECHANISMS
WARDS
QUESTION
Psychoanalysis
Q: A person accuses their partner
of cheating when they themselves
are involved in numerous affairs.
What is the defense mechanism?
A: Projection—Ascribing one’s
objectional qualities onto others.
KEY FACT
Remember for individuals with
borderline personality disorder,
splitting is their major defense
mechanism.
■ Clusters B and C personality disorders.
■ Anxiety disorders.
■ Problems coping with life events.
■ Sexual disorders.
■ Persistent depressive disorder.
6. Repression: Preventing a thought or feeling from entering consciousness. (Repression is unconscious, whereas suppression is a conscious act.)
(­Clinical Example: A sexual assault victim tries hard but cannot recall details
of the crime when questioned by police.)
Acting out: Giving in to an impulse, even if socially inappropriate, so as to
avoid the anxiety of suppressing that impulse. (Clinical example: Patient who
has been told their therapist is going on vacation “forgets” their last appointment and skips it.)
Denial: Not accepting reality that is too painful. (Clinical example: Woman
who has been scheduled for a breast mass biopsy cancels her appointment
because she believes she is healthy.)
Regression: Performing behaviors from an earlier stage of development so
as to avoid tension associated with current phase of development. (Clinical
example: Patient brings their childhood teddy bear to the hospital when they
have to spend the night.)
Projection: Attributing objectionable thoughts, qualities, or emotions to
others. (Clinical example: An individual who is attracted to others believes
their partner is having an affair.)
Splitting: Labeling people as all good or all bad; often seen in borderline
personality disorder. (Clinical example: Patient who tells their doctor, “You
and the nurses are the only people who understand me; all the other doctors
are mean and impatient.”)
Undoing: Attempting to reverse a situation by adopting a new behavior.
(Clinical example: An individual who has had a brief fantasy of killing their
spouse by sabotaging their car, takes the car in for a complete checkup.)
The goal of psychoanalysis is to resolve unconscious conflicts by bringing repressed experiences and feelings into awareness and integrating them into the
patient’s conscious experience. Psychoanalysis is therefore considered insight
oriented. Patients best suited for psychoanalysis have the following characteristics: not psychotic, intelligent, and stable in relationships and daily living.
Treatment is usually 3–5 days per week for many years. During therapy sessions, the patient usually lies on a couch with the therapist seated out of view.
To become an analyst, professionals (MDs, PhDs, PsyDs, and MSWs) must
complete training at a psychoanalytic institute. In addition to attending seminars and treating patients under supervision, the training requires that they
receive their own analysis.
Psychoanalysis can be useful in the treatment of the following:
IMPORTANT CONCEPTS AND TECHNIQUES USED IN PSYCHOANALYSIS
■ Free association: The patient is asked to say whatever comes into their mind
during therapy sessions. The purpose is to bring forth thoughts and feelings
from the unconscious so that the therapist may interpret them.
■ Dream interpretation: Dreams are seen to represent conflict between urges
and fears. Interpretation of dreams by the psychoanalyst is used to help
achieve therapeutic goals.
■ Therapeutic alliance: This is the bond between the therapist and the patient,
who work together toward a therapeutic goal.
■ Transference: Projection of unconscious feelings regarding important
figures in the patient’s life onto the therapist. Interpretation of transference is
used to help the patient gain insight and resolve unconscious conflict.
■ Countertransference: Projection of unconscious feelings about important
figures in the therapist’s life onto the patient. The therapist must remain
aware of countertransference issues, as they may interfere with their
objectivity.
PSYCHOANALYSIS-RELATED THERAPIES
Examples of psychoanalysis-related therapies include:
Psychoanalytically oriented psychotherapy and brief dynamic psychotherapy: These employ similar techniques and theories as psychoanalysis,
but they are less frequent, less intense, usually briefer (weekly sessions for
6 months to several years), and involve face-to-face sessions between the
therapist and patient (no couch).
Interpersonal therapy: Attachment-focused psychotherapy that centers on
the development of skills to treat certain psychiatric disorders. Treatment is
brief (once-weekly sessions for 3–4 months). The idea is to improve interpersonal relations. Sessions focus on reassurance, clarification of emotions,
improving interpersonal communication, and testing perceptions. It has
demonstrated efficacy in the treatment of depression and has been modified
for use in adolescents.
Supportive psychotherapy: Purpose is to help patient feel safe during a
difficult time and help to build up the patient’s healthy defenses. Treatment
is not insight oriented but instead focuses on empathy, understanding, and
education. Supportive therapy is commonly used as adjunctive treatment in
even the most severe mental disorders.
Behavioral Therapy
Behavioral therapy, pioneered by B. F. Skinner, seeks to treat psychiatric disorders by helping patients change behaviors that contribute to their symptoms.
It can be used to extinguish maladaptive behaviors (such as phobic avoidance, compulsions, etc.) by replacing them with healthy alternatives. The time
course is usually brief, and it is almost always combined with cognitive therapy
as CBT.
LEARNING THEORY
Behavioral therapy is based on learning theory, which states that behaviors are
learned by conditioning and can similarly be unlearned by deconditioning.
PSYCHOTHERAPIES 
WARDS TIP
Psychoanalysis is not indicated for
people who have problems with
reality testing, such as actively
psychotic or manic patients.
KEY FACT
An example of transference would
be when a patient who has repressed feelings of abandonment
by their parent becomes angry
when their therapist is late for the
appointment.
188
PSYCHOTHERAPIES 
CONDITIONING
KEY FACT
Positive reinforcement: Giving a
reward for a desired behavior.
KEY FACT
Negative reinforcement: Encouraging a behavior by removing
an aversive stimulus. (Example:
Putting on the seatbelt in the car
to stop the beeping.) Punishment,
in contrast, is an aversive response
to a behavior. Punishment is not
negative reinforcement.
KEY FACT
Biofeedback is used to treat a
wide scope of clinical conditions
including agoraphobia, fecal
incontinence, tension headache,
and hypertension.
Cognitive Therapy
■ Classical conditioning: A neutral stimulus can evoke a conditioned
response. (Example: Pavlov’s dog would salivate when hearing a bell because
the dog had learned that bells were always followed by food.)
■ Operant conditioning: Behaviors can be learned when followed by positive
or negative reinforcement. (Example: Skinner box—a rat presses a lever by
accident and receives food; eventually, it learns to press the lever for food
[trial-and-error learning].)
BEHAVIORAL THERAPY TECHNIQUES (DECONDITIONING)
■ Systematic desensitization: The patient performs relaxation techniques
while being exposed to increasing doses of an anxiety-provoking stimulus.
Gradually, they learn to use relaxation skills to tolerate and cope with the
anxiety-provoking stimulus. Commonly used to treat phobic disorders.
(Example: A patient who has a fear of spiders is first shown a photograph of
a spider, followed by exposure to a stuffed toy spider, then a videotape of a
spider, and finally a live spider. At each step, the patient learns to relax while
exposed to an increasing dose of the phobia.)
■ Flooding and implosion: Through habituation, the patient is confronted
with a real (flooding) or imagined (implosion) anxiety-provoking stimulus
and not allowed to withdraw from it until they feel calm and in control.
Relaxation exercises are used to help the patient tolerate the stimulus. Less
commonly used than systematic desensitization to treat phobic disorders.
(Example: A patient who has a fear of flying is made to fly in an airplane
[flooding] or imagine flying [implosion].)
■ Aversion therapy: A negative stimulus (such as an electric shock) is
repeatedly paired with a specific behavior to create an unpleasant response.
Used to treat addictions or paraphilic disorders. (Example: An alcoholic
patient is prescribed Antabuse (disulfiram), which makes them ill every time
they drink alcohol.)
■ Token economy: Rewards are given after specific behaviors to positively
reinforce them. Commonly used to encourage showering, shaving, and
other positive behaviors in disorganized patients. Also frequently used in
treatment of substance use disorders on rehabilitation units as part of a
contingency management program where abstinence is reinforced with
material rewards or privileges.
■ Biofeedback: Physiological data (such as heart rate and blood pressure
measurements) are given to patients as they try to mentally control
physiological states. Can be used to treat anxiety disorders, migraines,
hypertension, chronic pain, asthma, and incontinence. (Example: A patient
is given their heart rate and blood pressure measurements during a migraine
while being instructed to mentally control visceral changes that affect the pain.)
Cognitive therapy, pioneered by Aaron T. Beck, seeks to correct faulty assumptions and negative feelings that exacerbate psychiatric symptoms. The patient
is taught to identify maladaptive thoughts and replace them with positive ones.
It is most commonly used to treat depressive and anxiety disorders, and is
usually combined with behavioral therapy in CBT. It may also be used for paranoid personality disorder, obsessive-compulsive disorder, somatic symptom
­disorders, and eating disorders. Cognitive therapy can be as effective as medication for some disorders.
CLINICAL EXAMPLE OF THE COGNITIVE THEORY OF DEPRESSION
■ Cognitive distortions, also known as faulty assumptions or automatic
thoughts. (Example: If I were smart, I would do well on tests. I must not be
smart since I received average grades this semester.)
■ Negative thoughts. (Example: I am stupid. I will never amount to anything
worthwhile. Nobody likes a worthless person.)
Cognitive-Behavioral Therapy (CBT)
CBT combines theories and approaches from cognitive therapy and behavior
therapy. Treatment follows a protocol or manual with homework assignments
between therapy sessions. During therapy sessions, the patient and therapist
set an agenda, review homework, and challenge cognitive distortions. The
patients learn how their feelings and behavior are influenced by their thoughts.
Treatment is usually brief and may last from 6 weeks to 6 months. Research has
shown that CBT is effective for many psychiatric illnesses, including depression, anxiety disorders, schizophrenia, and substance use disorders.
Mrs. R is a 22-year-old college student who is hospitalized after she tried to
kill herself by taking an overdose of fluoxetine. This is her fifth overdose, and
all have been in response to perceived rejections. She often feels “empty
inside” and reports that she has had many intense relationships that have
ended abruptly. She reports that she has been married for 1 year but fights
constantly with her husband because of suspicions that he is unfaithful. Her
husband denies these allegations and reports that he is tired of her outbursts, explaining that she yells at him and has become physically abusive.
He has threatened to divorce her if these behaviors continue. During your
evaluation, you notice multiple healed scars over her forearms, and she
admits to self-harm behavior by cutting and burning herself because, “When
I get angry, it helps me feel better.”
During her hospitalization, you notice that her mood has improved and
that she has become close to other patients. She says, “They are like family.”
Although you have seen her only twice, she thinks you are “a great doctor,”
unlike the psychiatrists who have treated her in the past, who have all been
“idiots.” You call her outpatient therapist, who confirms that she has been
diagnosed with borderline personality disorder.
What are the recommended psychotherapeutic modalities
for this patient?
Dialectical behavioral therapy (DBT) and psychoanalytic/psychodynamic
therapy have shown to be effective treatments in randomized controlled
­trials for borderline personality disorder. DBT is a form of cognitivebehavioral therapy that is effective in reducing the urges to ­engage in
self-harm behavior and leads to fewer hospital days. Although the efficacy
of couples therapy in borderline patients has been debated, it might be
­considered in this case.
What special considerations should be taken into account when engaging
in psychotherapy?
The psychotherapist should always be aware of positive or negative
­countertransference developed toward the patient. Frequent discussion and
PSYCHOTHERAPIES 
WARDS TIP
CBT focuses on a patient’s current
symptoms and problems by examining the connection between
thoughts, feelings, and behaviors.
190
PSYCHOTHERAPIES 
Group Therapy
WARDS
QUESTION
Q: What is the primary treatment for borderline personality
disorder?
A: Dialectical behavioral therapy
(DBT).
Family Therapy
counseling with colleagues is useful. Patients with borderline personality
disorder are challenging to treat due to their intense emotions, impulsivity,
and anger.
What particular defense mechanism is exhibited by Mrs. R?
She exhibits splitting as evidenced by her extreme dichotomous thinking in
expressing that you are a “great” psychiatrist, whereas other psychiatrists who
have treated her in the past are “idiots.”
Dialectical Behavioral Therapy (DBT)
DBT was developed by Marsha Linehan, and its effectiveness has been demonstrated in research trials. Once-weekly individual and group treatment can
effectively diminish the self-destructive behaviors and hospitalizations of
patients with borderline personality disorder. It incorporates cognitive and
supportive techniques, along with “mindfulness” derived from traditional
­Buddhist practice. DBT has demonstrated effectiveness in patients with borderline ­personality disorders and eating disorders.
■ Three or more patients with a similar problem or pathology meet together
with a therapist for group sessions. Many of the psychotherapeutic
techniques already reviewed are used, including behavioral, cognitive, and
supportive.
■ Certain groups are peer led (including 12-step groups like Alcoholics
Anonymous) and do not have a therapist present to facilitate the group.
These groups meet to discuss problems, share feelings, and provide support
to each other.
■ Group therapy is especially useful in the treatment of substance use
disorders, adjustment disorders, and personality disorders. Advantages of
group therapy over individual therapy include:
• Patients get immediate feedback and support from their peers.
• Patients gain insight into their own condition by listening to others with
similar problems.
• If a therapist is present, there is an opportunity to observe interactions
between others who may be eliciting a variety of transferences.
Family therapy is useful as an adjunctive treatment in many psychiatric
­conditions because:
An individual’s problems usually affect the entire family. They may be
viewed differently and treated differently after the development of psychopathology, and new tensions and conflicts within the family may arise.
Psychopathology may arise or worsen due to dysfunction within the family
unit. These conditions are most effectively treated with the entire family
present. Evidence demonstrates that high expressed emotion (critical and
emotionally over-involved attitudes toward a family member) negatively
impacts mental health in psychiatric patients.
The goals of family therapy are to reduce conflict, help members understand
each other’s needs (mutual accommodation), and help the family unit cope with
internally destructive forces. Boundaries between family members may be too
rigid or too permeable, and “triangles” may result when two family members
form an alliance against a third member. The therapist may assist in correcting
these problems. (Example of boundaries that may be too permeable: A parent
and child smoke marijuana together and share intimate details about their sexual activities.) Family therapy is especially useful in treating schizophrenia and
anorexia in adolescents.
Couples Therapy
Couples therapy is useful in the treatment of conflicts, sexual problems, and
communication problems within the context of an intimate relationship. The
therapist sees the couple together (conjoint therapy), but they may also be
seen separately (concurrent therapy). In addition, each person may have a separate therapist and be seen individually (collaborative therapy). In the treatment of sexual problems, two therapists may see the couple together (four-way
therapy). Relative contraindications include lack of motivation by one or both
spouses and severe illness in one of the spouses (e.g., schizophrenia).
PSYCHOTHERAPIES 
192
PSYCHOTHERAPIES 
NOTES

21 - Chapter 18 Psychopharmacology

01 - Chapter 18 Psychopharmacology
Chapter 18 Psychopharmacology
Side Effects in a Nutshell.........................................................................................................195
Antidepressants......................................................................................................................196
Selective Serotonin Reuptake Inhibitors............................................................................197
Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs).....................................................198
Miscellaneous Antidepressants..........................................................................................199
Heterocyclic Antidepressants.............................................................................................200
Tricyclic Antidepressants....................................................................................................200
Tetracyclic Antidepressants................................................................................................201
Monoamine Oxidase Inhibitors..........................................................................................201
Antidepressant Use in Other Disorders....................................................................................202
Antipsychotics........................................................................................................................203
Typical (First-Generation) Antipsychotics...........................................................................203
Atypical (Second-Generation) Antipsychotics....................................................................206
Mood Stabilizers.....................................................................................................................208
Lithium..............................................................................................................................208
Anticonvulsants......................................................................................................................209
Carbamazepine (Tegretol).................................................................................................209
Valproic Acid (Depakote and Depakene)............................................................................210
Anxiolytics/Hypnotics.............................................................................................................211
Benzodiazepines................................................................................................................211
Non-BDZ Hypnotics...........................................................................................................212
Non-BDZ Anxiolytics..........................................................................................................212
Psychostimulants....................................................................................................................213
Cognitive Enhancers................................................................................................................213
Acetylcholinesterase Inhibitors..........................................................................................213
NMDA (Glutamate) Receptor Antagonist...........................................................................214
Reference List of Medications That May Cause Psychiatric Symptoms.....................................214
Psychosis...........................................................................................................................214
Agitation/Confusion/Delirium...........................................................................................214
Depression.........................................................................................................................214
Anxiety..............................................................................................................................214
PSYCHOPHARMACOLOGY
CHAPTER 18
194
PSYCHOPHARMACOLOGY 
Sedation/Poor Concentration.............................................................................................214
Selected Medications.........................................................................................................214
Other Treatments....................................................................................................................215
Electroconvulsive Therapy (ECT)........................................................................................215
Deep Brain Stimulation (DBS)............................................................................................215
Repetitive Transcranial Magnetic Stimulation (rTMS)........................................................215
Light Therapy.....................................................................................................................215
Ketamine Infusion.............................................................................................................216
Side Effects in a Nutshell
HAM side effects (antiHistamine—sedation, weight gain; antiAdrenergic—
hypotension; antiMuscarinic (anticholinergic)—dry mouth, blurred vision,
urinary retention, constipation, exacerbation of neurocognitive disorders
(i.e., dementias).
■ Found in tricyclic antidepressants (TCAs) and low-potency antipsychotics.
■ Associated with increased risk of falls and delirium in elderly patients.
Serotonin syndrome: Confusion, flushing, diaphoresis, tremor, myoclonic
jerks, hyperthermia, hypertonicity, rhabdomyolysis, renal failure, and death.
■ This uncommon psychiatric emergency occurs when there is too much
serotonin, classically when selective serotonin reuptake inhibitors (SSRIs) and
monoamine oxidase inhibitors (MAOIs) are combined. As this combination
is rarely seen in practice anymore, serotonin syndrome is more commonly
seen when a patient is prescribed multiple medications with serotonergic
activity (e.g., SSRIs/SNRIs, lithium, trazodone, linezolid, Tramadol, triptans,
dextromethorphan, St. John’s wort, ondansetron), or other illicit drugs with
serotonergic activity (e.g., cocaine, MDMA, amphetamine).
■ Treatment: Stop medications, supportive care, possibly use
cyproheptadine or even ECT.
Hypertensive crisis: Caused by a buildup of stored catecholamines (norepinephrine); triggered by the combination of MAOIs with tyramine-rich foods
(e.g., red wine, cheese, chicken liver, cured meats) or with sympathomimetics. Treated with IV phentolamine or sublingual nifedipine.
Extrapyramidal side effects (EPS): Parkinsonism—mask-like face, cogwheel rigidity, bradykinesia, pill-rolling tremor; akathisia—restlessness,
need to move, and agitation; dystonia—sustained, painful contraction of
muscles of neck, tongue, eyes, diaphragm.
■ Occur more frequently with high-potency, typical (first generation)
antipsychotics, but can also be seen with atypical (second generation)
antipsychotics.
■ Reversible.
■ All EPS can be treated with benztropine (Cogentin), although for
akathisia, beta-blockers such as propranolol are first-line.
■ Occur within hours to days of starting medications or increasing doses.
■ In rare cases, can be life threatening (e.g., dystonia of the diaphragm
causing asphyxiation).
■ Drug-induced parkinsonism should be differentiated from primary
neurodegenerative Parkinson disease.
Hyperprolactinemia: Occurs with high-potency, typical (first generation)
antipsychotics and risperidone.
Tardive dyskinesia (TD): Choreoathetoid (involuntary, irregular, and
repetitive) muscle movements, usually of the mouth and tongue (can affect
extremities, as well).
■ Occurs after years of antipsychotic use (more likely with high-potency,
first-generation antipsychotics).
■ Usually irreversible.
Neuroleptic malignant syndrome: Mental status changes, fever, tachycardia, hypertension, tremor, hyporeflexia, elevated creatine phosphokinase
(CPK), “lead pipe” rigidity.
■ Can be caused by any antipsychotic after a short or long time (increased
with high-potency, typical antipsychotics).
PSYCHOPHARMACOLOGY 
196
PSYCHOPHARMACOLOGY 
WARDS TIP
Drugs that increase serotonin may
be found in over-the-counter medicines (e.g., dextromethorphan,
St. John’s wort). They can cause
serotonin syndrome when taken in
high doses or in combination with
other serotonergic agents.
KEY FACT
Keeping the “kinesias” (impairment of body function) straight:
• Tardive dyskinesia is characterized by potentially permanent
choreoathetoid movements
and tongue protrusion.
• Acute dystonia is characterized by (painful and reversible) twisting and abnormal
postures.
• Akathisia is characterized by
the inability to sit still; feels like
“ants in the pants.”
• Bradykinesia is characterized
by decreased or slow body
movement.
Antidepressants
■ The major categories of antidepressants are:
WARDS
QUESTION
Q: What are the key differences
between serotonin syndrome and
neuroleptic malignant syndrome
(NMS)?
A: Serotonin syndrome includes
myoclonic jerks, hyperreflexia,
hyperactive bowels, while NMS
is marked by “lead pipe” rigidity,
hyporeflexia, and ↑ CPK.
■ A medical emergency with up to a 20% mortality rate.
■ Treatment includes dantroline, bromocriptine, and ECT in emergencies.
8. Drug interactions: Cytochrome P450 is a group of enzymes in the liver that
metabolizes many common drugs, including psychiatric medications.
■ Some medications induce the system, in other words the system
metabolizes medications faster—drug levels decrease.
■ Some medications inhibit the system, in other words the system
metabolizes medications more slowly—drug levels increase.
■ Common cytochrome P450 enzymes important in metabolizing
psychiatric medications include CYP3A4, CYP2D6, CYP1A2, CYP2C9,
and CYP2C19.
■ For example: A patient with schizophrenia who smokes a pack of
cigarettes a day is prescribed olanzapine. The tobacco induces CYP450
enzyme to metabolize the olanzapine quickly, the drug level of olanzapine
decreases, and the patient therefore requires a higher dose.
CYP450 InDucers
CYP450 Inhibitors
Tobacco (1A2)
Fluoxetine (2C19, 2C9, 2D6)
Carbamazepine (1A2, 2C9, 3A4)
Fluvoxamine (1A2, 2C19, 3A4)
Barbiturates (2C9)
Paroxetine (2D6)
St. John’s wort (2C19, 3A4)
Sertraline (2D6)
Duloxetine (2D6)
9. Metabolic syndrome: Antipsychotic medications (especially
second-generation antipsychotics such as clozapine, olanzapine, quetiapine)
can cause a metabolic syndrome which includes weight gain, hyperlipidemia,
hyperglycemia, and hypertension that are associated with increased cardiovascular morbidity and mortality. Routine monitoring of patients on these
medications should include weight checks or BMI, fasting lipid profile, A1C or
fasting glucose, and vital signs; treatment with metformin may be considered.
• SSRIs.
• SNRIs.
• Heterocyclic antidepressants, including TCAs and tetracyclic antidepressants.
• MAOIs.
• Miscellaneous antidepressants.
■ All antidepressants have similar response rates in treating major depression
but differ in safety and side-effect profiles.
■ Approximately 60–70% of patients with major depression will respond to an
antidepressant medication.
■ It usually takes 4–6 weeks on a given dose of an antidepressant for a patient
to fully benefit from a trial of the medication, although many patients start
responding sooner.
■ For patients who are prone to side effects, it’s important to start at a low dose
and titrate up slowly.
■ Some antidepressants have a withdrawal phenomenon, characterized by
dizziness, headaches, nausea, insomnia, anxiety, electric-like shocks (“zaps”),
and malaise; depending on the dose and half-life, they may need to be
tapered slowly before discontinuing.
■ Because of their safety and tolerability, SSRIs and related antidepressants
have become the most common agents used to treat major depression.
However, the choice of a particular medication used for a given patient
should be made based on:
• Patient’s particular symptoms
• Previous treatment responses by the patient or a family member to a
particular medication
• Side-effect profile
• Comorbid (medical and psychiatric) conditions
• Risk of suicide via overdose on the medication
• Cost (newer medications may be prohibitively expensive)
SELECTIVE SEROTONIN REUPTAKE INHIBITORS
■ SSRIs inhibit presynaptic serotonin reuptake pumps, leading to increased
availability of serotonin in synaptic clefts. Additionally, SSRIs cause
downstream effects increasing brain plasticity—this mechanism has been
hypothesized to explain the delay to onset of antidepressant effect.
■ Although structural differences are minimal, patients often respond
differently (in regards to efficacy and side effects) to different SSRIs.
■ Based on their half-lives, most SSRIs can be dosed daily. Fluoxetine has a
weekly dosing form available, as well.
■ There is no correlation between plasma levels and efficacy or side effects.
■ SSRIs are the most commonly prescribed antidepressants due to several
distinct advantages:
• Low incidence of side effects, most of which resolve with time.
• No food restrictions.
• Much safer in overdose.
■ Examples of SSRIs include:
• Fluoxetine (Prozac):
Longest half-life, with active metabolites; therefore, no need to taper.
Safe in pregnancy, approved for use in children and adolescents.
Common side effects: Insomnia, anxiety, sexual dysfunction.
Can elevate levels of antipsychotics, leading to increased side effects.
• Sertraline (Zoloft):
Higher risk for gastrointestinal (GI) disturbances.
Very few drug interactions.
Other common side effects: Insomnia, anxiety, sexual dysfunction.
• Paroxetine (Paxil):
A potent inhibitor of CYP26, which can lead to several drug–drug
interactions.
Common side effects: Anticholinergic effects (e.g., sedation, constipation, weight gain) and sexual dysfunction.
Short half-life leading to uncomfortable withdrawal phenomena if not
taken consistently.
PSYCHOPHARMACOLOGY 
KEY FACT
First-generation antipsychotics
(typicals) are more associated
with EPS and second-generation
antipsychotics (atypicals) are more
associated with metabolic side
effects.
KEY FACT
The Food and Drug Administration
(FDA) has a black box warning for
all SSRIs potentially increasing
“suicidal thinking and behavior.”
This warning applies to children
and young adults to age 25, but
may be accurate for older adults
as well. The absolute risk remains
low and must be weighed against
the risks of an untreated mood
disorder.
WARDS
QUESTION
Q: How are sexual side effects of
SSRI treated?
A: Either reducing the dose (if
clinically appropriate), changing
to a non-SSRI antidepressant,
augmenting with bupropion, or, in
men, by adding medications like
sildenafil.
WARDS TIP
Patients should receive an adequate trial of antidepressant medication, usually at least 4–6 weeks
at a full dose, before the medication is deemed non-efficacious.
198
PSYCHOPHARMACOLOGY 
• Fluvoxamine (Luvox):
WARDS
QUESTION
Q: What are the SSRIs associated
with most and least weight gain?
A: Paroxetine is the most associated with weight gain. Fluoxetine and sertraline are the most
weight-neutral.
Fewest drug–drug interactions.
Dose-dependent QTc prolongation.
• Escitalopram (Lexapro):
WARDS TIP
Side Effects
SSRIs can increase levels of warfarin, requiring increased monitoring when starting and stopping
these medications.
KEY FACT
Serotonin syndrome is common
when serotonergic drugs are used
with MAOIs. SSRIs should not be
used for at least 2 weeks before or
after use of an MAOI, and at least
5–6 weeks with fluoxetine given
its long half-life.
■ Other side effects include:
■ Venlafaxine (Effexor):
Currently approved only for use in obsessive-compulsive disorder
(OCD).
Common side effects: Nausea and vomiting.
Multiple drug interactions due to CYP inhibition.
• Citalopram (Celexa):
Levo-enantiomer of citalopram; similar efficacy, possibly fewer side
effects.
Dose-dependent QTc prolongation.
■ SSRIs have significantly fewer side effects than TCAs and MAOIs due to
serotonin selectivity (not as much activity on histamine, adrenergic, or
muscarinic receptors).
■ They are much safer in overdose. Most side effects occur because of the
extensive number of serotonin receptors throughout the body, including the
GI tract.
■ Many of the side effects of SSRIs resolve within a few days to weeks and
include:
• GI disturbance: Mostly nausea and diarrhea; giving with food can help.
• Insomnia; also vivid dreams, often resolves over time.
• Headache.
• Weight changes (up or down).
• Sexual dysfunction (30–40%): Decreased libido, anorgasmia, delayed
ejaculation. These may occur weeks to months after taking an SSRI and
typically do not resolve.
• Restlessness: An akathisia-like state.
• Serotonin syndrome: Caused by an excess of serotonin in the body. It
can result from taking a single serotonergic agent, or by taking multiple
serotonergic agents in combination. One example is triptans (for migraine
headaches) used with SSRIs. Serotonin syndrome is characterized by fever,
diaphoresis, tachycardia, hypertension, delirium, and neuromuscular
excitability (especially hyperreflexia and “electric jolt” limb movements),
potentially death. Treatment includes stopping all serotonergic agents,
administering cyproheptadine, and ECT in emergencies.
• Hyponatremia: Rare.
• Decreased platelet aggregation leading to increased risk of bleeding and
bruising.
• Seizures: Rate of approximately 0.2%, slightly lower than TCAs.
SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIS)
• Often used for depressive disorders, anxiety disorders like generalized
anxiety disorder (GAD), and neuropathic pain.
• Low drug interaction potential.
• Extended release (XR form) allows for once-daily dosing.
• Due to its short half-life, discontinuation of this drug should be tapered
to avoid an uncomfortable discontinuation syndrome.
• Side-effect profile similar to SSRIs, with the exception of increased blood
pressure (BP) in higher doses; do not use in patients with untreated or
labile BP.
• New form, desvenlafaxine (Pristiq), is the active metabolite of
venlafaxine; it is expensive and without known benefit over venlafaxine.
■ Duloxetine (Cymbalta):
• Often used for people with depression, neuropathic pain, and in
fibromyalgia.
• Side effects are similar to SSRIs (no hypertensive risk), but more
constipation relating to its norepinephrine effects.
• Hepatotoxicity may be more likely in patients with liver disease or heavy
alcohol use, so liver function tests should be monitored when indicated.
MISCELLANEOUS ANTIDEPRESSANTS
■ Bupropion (Wellbutrin):
• Norepinephrine-dopamine reuptake inhibitor.
• Relative lack of sexual side effects as compared to the SSRIs. Can be
added to other antidepressants to treat sexual dysfunction.
• Some efficacy in treatment of adult attention deficit hyperactivity disorder
(ADHD).
• Effective for smoking cessation.
• Weight neutral.
• Side effects include increased anxiety, as well as increased risk of seizures
and psychosis at high doses.
• Contraindicated in patients with epilepsy or active eating disorders, and
in those currently on an MAOI. Use with caution with agents that also
lower the seizure threshold (like stimulants).
Serotonin Receptor Antagonists and Agonists
■ Trazodone (Desyrel) and Nefazodone (Serzone):
• Useful in the treatment of major depression, major depression with
anxiety, and insomnia (secondary to its sedative effects).
• They do not have the sexual side effects of SSRIs and do not affect rapid
eye movement (REM) sleep.
• Side effects include nausea, dizziness, orthostatic hypotension, cardiac
arrhythmias, sedation, and priapism (especially with trazodone).
• Because of orthostatic hypotension and sedation in higher doses,
trazodone is not frequently used solely as an antidepressant. It is
commonly used to treat insomnia often when initiating an SSRI (until
insomnia improves as the depression resolves).
• Nefazodone carries a black box warning for rare but serious liver failure
(1 per 250,000–300,000 people) and is now off the market.
PSYCHOPHARMACOLOGY 
WARDS
QUESTION
Q: Which antidepressant is least
likely to cause sexual side effects?
A: Wellbutrin (bupropion).
KEY FACT
Trazodone causes priapism: Remember the phrase “Trazo-bone.”
200
PSYCHOPHARMACOLOGY 
α2-Adrenergic Receptor Antagonists
■ Mirtazapine (Remeron):
KEY FACT
HETEROCYCLIC ANTIDEPRESSANTS
Mirtazapine (Remeron) is good for
treating major depression in the
elderly—It helps with both sleep
and appetite.
TRICYCLIC ANTIDEPRESSANTS
Useful in treating chronic pain.
Used as a sleep aid in low doses.
More activating/least sedating.
Least anticholinergic.
• Mechanism of action is antagonism of the central presynaptic alpha-2adrenergic receptors, which causes an increased release of serotonin and
norepinephrine.
• Useful in the treatment of major depression, especially in patients who
have significant weight loss and/or insomnia.
• At lower doses, mirtazapine acts preferentially on histamine receptors
causing sedation and increased appetite, but at higher doses acts
preferentially on the norepinephrine receptors and can be more
activating.
• Side effects include sedation, weight gain, dizziness, tremor, dry mouth,
constipation, and (rarely) agranulocytosis.
• Fewer sexual side effects compared to SSRIs and few drug interactions.
■ TCAs inhibit the reuptake of norepinephrine and serotonin, increasing
availability of monoamines in the synapse.
■ Because of the long half-lives, most are dosed once daily.
■ They are rarely used as first-line agents due to a higher incidence of side
effects, titration of dosing, and lethality in overdose.
■ Tertiary amines (highly anticholinergic/antihistaminergic [more sedating]/
antiadrenergic [more orthostasis] with a greater lethality in overdose):
• Amitriptyline (Elavil): Useful in chronic pain, migraines, and insomnia.
• Imipramine (Tofranil):
Has intramuscular form.
Useful in enuresis and panic disorder.
• Clomipramine (Anafranil): Most serotonin-specific, therefore has
efficacy in the treatment of OCD.
• Doxepin (Sinequan):
■ Secondary amines—Metabolites of tertiary amines (less anticholinergic/
antihistaminic/antiadrenergic):
• Nortriptyline (Pamelor, Aventyl):
Least likely to cause orthostatic hypotension.
Useful therapeutic blood levels.
Useful in treating chronic pain.
Can be safely used in geriatric population.
• Desipramine (Norpramin):
TETRACYCLIC ANTIDEPRESSANTS
■ Amoxapine (Asendin):
• Metabolite of antipsychotic loxapine.
• May cause EPS and has a similar side-effect profile to typical
antipsychotics.
Side Effects
■ TCAs are highly protein bound and lipid soluble, and therefore can interact
with other medications that have high protein binding.
■ The side effects of TCAs are mostly due to their lack of specificity and
interaction with other receptors.
■ Antihistaminic properties: Sedation and weight gain.
■ Antiadrenergic properties (cardiovascular side effects): Orthostatic
hypotension, dizziness, reflex tachycardia, arrhythmias (block cardiac
sodium channel), and electrocardiographic (ECG) changes (widening
QRS, QT, and PR intervals). Avoid in patients with preexisting conduction
abnormalities or recent MI, or with increased fall risk.
■ Antimuscarinic effects (also called anticholinergic): Dry mouth,
constipation, urinary retention, blurred vision, tachycardia, and
exacerbation of narrow angle glaucoma. Can lead to delirium in the elderly
population.
■ Lethal in overdose—Must carefully assess the suicide risk when prescribing.
Symptoms of overdose include agitation, tremors, ataxia, arrhythmias,
delirium, hypoventilation from central nervous system (CNS) depression,
myoclonus, hyperreflexia, seizures, and coma.
■ Seizures: Risk of seizure is directly related to the dose and serum level (i.e.,
higher risk of seizures at high doses and overdoses).
■ Serotonergic effects: Erectile/ejaculatory dysfunction in males, anorgasmia
in females.
MONOAMINE OXIDASE INHIBITORS
■ MAOIs prevent the inactivation of biogenic amines such as norepinephrine,
serotonin, dopamine, and tyramine (an intermediate in the conversion of
tyrosine to norepinephrine).
■ By irreversibly inhibiting the enzymes MAO-A and B, MAOIs increase the
number of neurotransmitters available in synapses.
■ MAO-A preferentially deactivates serotonin and norepinephrine, and
MAO-B preferentially deactivates phenethylamine; both types also act on
dopamine and tyramine.
■ MAOIs are not used as first-line agents because of the increased safety and
tolerability of newer agents, notably SSRIs/SNRIs. However, MAOIs are
rarely used for certain types of refractory depression and in refractory
anxiety disorders:
• Phenelzine (Nardil).
• Tranylcypromine (Parnate).
• Isocarboxazid (Marplan).
PSYCHOPHARMACOLOGY 
WARDS TIP
A 1-week supply of TCAs (as
little as 1–2 g) can be lethal in
overdose.
WARDS
QUESTION
Q: What is the treatment for TCA
overdose?
A: IV sodium bicarbonate.
WARDS TIP
Major complications of TCAs—3Cs:
Cardiotoxicity
Convulsions
Coma
WARDS
QUESTION
Q: What are the most common
side effects of TCAs?
A: Anticholinergic effects: Dry
mouth, urinary retention, constipation, and blurry vision.
WARDS TIP
MAOIs are considered more effective than TCAs in depression with
atypical features, characterized by
hypersomnia, increased appetite,
heavy feeling in extremities, and
increased sensitivity to interpersonal rejection.
202
PSYCHOPHARMACOLOGY 
Side Effects
WARDS TIP
■ Orthostatic hypotension (most common).
■ Drowsiness.
Selegiline (Emsam transdermal
patch) is a MAOI used to treat
depression that does not require
following the dietary restrictions when used in low dosages.
However, decongestants, opiates
(such as meperidine, fentanyl, and
tramadol), and serotonergic drugs
must still be avoided.
■ Weight gain.
■ Sexual dysfunction.
■ Dry mouth.
■ Sleep dysfunction.
■ Liver toxicity, seizures, and edema (rare).
■ GAD: SSRIs, SNRIs (venlafaxine), TCAs.
■ Posttraumatic stress disorder: SSRIs.
■ Irritable bowel syndrome: SSRIs, TCAs.
■ Enuresis: TCAs (imipramine).
■ Chronic pain: SNRIs, TCAs.
■ Fibromyalgia: SNRIs.
■ Migraine headaches: TCAs (amitriptyline).
■ Serotonin syndrome occurs when SSRIs and MAOIs are taken together or
if other drugs cause increase in serotonin levels.
• Initially characterized by lethargy, restlessness, confusion, flushing,
hyperactive bowels, diaphoresis, tremor, and myoclonic jerks.
• May progress to hyperthermia, hypertonicity, rhabdomyolysis, renal
failure, convulsions, coma, and death.
• Treatment includes immediately discontinuing serotonergic medications,
ICU monitoring, and administration of cyproheptadine. ECT can be
effective.
• Wait at least 2 weeks before switching from SSRI to MAOI, and at least
5–6 weeks with fluoxetine.
■ Hypertensive crisis: Risk when MAOIs are taken with tyramine-rich foods
or sympathomimetics.
• Foods with tyramine (red wine, cheese, chicken liver, fava beans, cured
meats) cause a buildup of stored catecholamines.
• In addition to a markedly elevated BP, it is also characterized by
headache, sweating, nausea, and vomiting, photophobia, autonomic
instability, chest pain, arrhythmias, and death.
■ Patients with pyridoxine deficiency can have numbness or paresthesias, so
they should supplement with B6.
■ “Start low and go slow” (low doses that are increased slowly).
Antidepressant Use in Other Disorders
■ OCD: SSRIs (in high doses), TCAs (clomipramine).
■ Panic disorder: SSRIs, SNRIs, TCAs, MAOIs.
■ Eating disorders: SSRIs (in high doses), TCAs.
■ Persistent depressive disorder (dysthymia): SSRIs, SNRIs (e.g., venlafaxine,
duloxetine).
■ Social anxiety disorder (social phobia): SSRIs, SNRIs, MAOIs.
■ Neuropathic pain: TCAs (amitriptyline and nortriptyline), SNRIs.
■ Smoking cessation: Bupropion.
■ Premenstrual dysphoric disorder: SSRIs.
■ Insomnia: Mirtazapine, trazodone, TCAs (doxepin).
Antipsychotics
■ Antipsychotics are used to treat psychotic disorders and bipolar disorders,
as well as psychotic symptoms associated with other psychiatric and medical
illnesses.
• Typical or first-generation antipsychotics, sometimes referred to as
neuroleptics, are classified according to potency and treat psychosis by
primarily by blocking dopamine (D2) receptors.
• Atypical or second-generation antipsychotics block both dopamine (D2)
and serotonin (5HT-2A) receptors.
■ Most antipsychotics have a number of actions and receptor interactions in
the brain that contribute to their varied efficacy and side-effect profiles.
■ Both typical and atypical antipsychotics have similar efficacies in treating
the presence of positive psychotic symptoms, such as hallucinations and
delusions.
■ Atypical antipsychotics were thought to be more effective at treating negative
symptoms (such as flattened affect and social withdrawal), although this has
not been consistently shown in the literature.
■ Atypical antipsychotics have largely replaced typical antipsychotics in use
due to their side-effect profile. However, the risk of metabolic syndrome/
weight gain and other side effects, as well as the significant cost of the
atypical antipsychotics means that currently both classes are used as
first-line treatments.
■ The choice of which specific medication to prescribe should be made based
on the patient’s individual clinical presentation, past response (favorable and
unfavorable), side-effect profile, and preference.
TYPICAL (FIRST-GENERATION) ANTIPSYCHOTICS
All typical antipsychotics have similar efficacy, but vary in potency.
Low-Potency, Typical Antipsychotics
■ Lower affinity for dopamine receptors and therefore a higher dose is
required. Remember, potency refers to the action on dopamine receptors, not
the level of efficacy.
■ Higher incidence of antiadrenergic, anticholinergic, and antihistaminic side
effects compared to high-potency typical antipsychotics.
■ Lower incidence of EPS and (possibly) neuroleptic malignant syndrome.
■ More lethality in overdose due to QTc prolongation, and the potential for
heart block and ventricular tachycardia.
■ Rare risk of agranulocytosis, and slightly higher seizure risk than
high-potency antipsychotics.
• Chlorpromazine (Thorazine):
Commonly causes orthostatic hypotension.
Can cause blue-gray skin discoloration as well as corneal and lens
deposits.
PSYCHOPHARMACOLOGY 
WARDS
QUESTION
Q: How is serotonin syndrome
treated?
A: First, discontinue the medication(s), next, provide supportive
care and benzodiazepines. The
serotonin antagonist cyproheptadine and ECT can also be used.
WARDS TIP
Warning about atypical antipsychotics: Although they are used to
treat the behavioral symptoms of
neurocognitive disorders (dementias) and delirium, studies show an
increased risk of all-cause mortality and stroke when using these
agents in the elderly, which, as a
result, is listed as a FDA black box
warning for these medications.
204
PSYCHOPHARMACOLOGY 
Midpotency, Typical Antipsychotics
■ Have midrange properties.
• Loxapine (Loxitane):
High-Potency, Typical Antipsychotics
Can lead to photosensitivity.
Also used to treat nausea and vomiting, as well as intractable hiccups.
Comes in PO and IM formulations (effective in treating agitation in
emergencies).
• Thioridazine (Mellaril): Associated with retinitis pigmentosa.
Higher risk of seizures.
Metabolite is an antidepressant.
• Thiothixene (Navane): Can cause ocular pigment changes.
• Molindone (Moban).
• Perphenazine (Trilafon).
■ Greater affinity for dopamine receptors; therefore, a relatively low dose is
needed to achieve effect.
■ Less sedation, orthostatic hypotension, and anticholinergic effects.
■ Greater risk for extrapyramidal symptoms and (likely) TD.
• Haloperidol (Haldol): Can be given PO/IM/IV. Decanoate (long acting)
form available.
• Fluphenazine (Prolixin): Can be given PO/IM. Decanoate form available.
• Trifluoperazine (Stelazine): Approved for nonpsychotic anxiety.
• Pimozide (Orap): Associated with QTc prolongation and ventricular
tachycardia.
Ms. B is a 28-year-old, overweight female who presents to your outpatient
clinic following discharge from an inpatient psychiatry unit. Police found
her in a local shopping mall, talking to herself and telling a passerby that
the devil had “stolen her soul.” She appeared disheveled and scared. During
the hospitalization, she was diagnosed with schizophrenia, and olanzapine
was prescribed and titrated to 30 mg at bedtime for delusional thinking and
disorganized behavior. She has since been living with her parents, and her
hygiene and self-care have improved. Although Ms. B reports occasional auditory hallucinations telling her that her parents do not like her, she recognizes that the voices are not real and is not distressed by them. She has become
involved in a vocational skills program and hopes to work at a local supermarket. However, during her last appointment with her primary care doctor,
she was told she had an elevated fasting glucose of 115 and triglycerides of
180, and that she had gained 12 pounds in the past 3 months with a waist
circumference of 36 inches. Her blood pressure was normal, but she reported
a family history of diabetes and high blood pressure.
What is the next step?
Given her diagnosis of schizophrenia, and that Ms. B has had an adequate
partial response to pharmacological treatment, she should continue to be
treated with an antipsychotic. However, her recent laboratory results are
suggestive of metabolic syndrome, and thus she is at an increased risk for
cardiovascular disease. While this patient has responded well to olanzapine,
this medication along with other atypical antipsychotics have been associated with increased weight gain and impaired glucose metabolism. It is unclear if her laboratory test results were abnormal prior to starting olanzapine,
are elevated secondary to treatment, or a combination of both. In treating
Ms. B, first steps include recommending lifestyle modifications and close
monitoring of her weight, blood sugar levels, lipids, and waist circumference,
while collaborating closely with her primary care physician. If a change in her
antipsychotic medication is warranted after weighing the risks and benefits
of altering her treatment, other atypical antipsychotics such as ziprasidone or
aripiprazole (both less associated with weight gain), or typical antipsychotics
might be considered; these medications would then be cross-tapered. When
choosing medications, consideration must be given to a history of response,
tolerability, side-effect profile, patient preference, and cost.
Side Effects
■ The positive symptoms of schizophrenia are treated by action of the medications
in the mesolimbic dopamine pathway. The mesolimbic pathway includes the
nucleus accumbens, the fornix, the amygdala, and the hippocampus.
■ The negative symptoms of schizophrenia are thought to occur due to
(decreased) dopaminergic action in the mesocortical pathway.
■ Extrapyramidal symptoms occur through blockade of the dopamine
pathways in the nigrostriatum.
■ Increased prolactin is caused by dopamine blockade in the
tuberoinfundibular area.
■ Antidopaminergic effects:
• EPS:
Parkinsonism—Bradykinesia, mask-like face, cogwheel rigidity,
pill-rolling tremor. Treat with benztropine (Cogentin) or lower dose if
appropriate.
Akathisia—Subjective anxiety and restlessness, objective fidgetiness.
Patients may report a sensation of inability to sit still. Best treated with
dose reduction (if appropriate), b-blockers, or benzodiazepines.
Dystonia—Sustained painful contraction of muscles of neck (torticollis), tongue, eyes (oculogyric crisis). It can be life threatening if it
involves the airway or diaphragm. Treat with benztropine (Cogentin)
or diphenhydramine (Benadryl), or lower the dose if appropriate.
• Hyperprolactinemia—Leads to decreased libido, galactorrhea,
gynecomastia, impotence, amenorrhea.
■ Anti-HAM effects: Caused by actions on Histaminic, Adrenergic, and
Muscarinic receptors:
• Antihistaminic—Results in sedation, weight gain.
• Anti-a1 adrenergic—Results in orthostatic hypotension, cardiac
abnormalities, and sexual dysfunction.
• Antimuscarinic—Anticholinergic effects, resulting in dry mouth,
tachycardia, urinary retention, blurry vision, constipation, and
precipitation of narrow-angle glaucoma.
■ Tardive dyskinesia:
• Choreoathetoid (writhing, irregular) movements of mouth and tongue
(or other body parts) that may occur in patients who have used
antipsychotics for more than 6 months.
PSYCHOPHARMACOLOGY 
KEY FACT
Haloperidol (Haldol) is often given
as an intramuscular injection to
treat acute agitation or psychosis.
The commonly used phrase: “5
and 2,” in psychiatric emergencies
refers to 5 mg of IM haloperidol
and 2 mg of IM lorazepam in order
to quickly sedate an agitated
patient.
WARDS TIP
Haloperidol and fluphenazine
are also available in long-acting,
intramuscular forms (decanoate)
that are useful if patients are
poorly compliant with their oral
medication. Risperidone (Consta),
aripiprazole (Maintena), and paliperidone (Invega Sustenna) also
have long-acting injectibles, but
they are more expensive.
KEY FACT
There is a roughly 5% chance of
developing tardive dyskinesia for
each year treated with a typical
antipsychotic.
WARDS
QUESTION
Q: How are dystonia and akathisia
treated?
A: The first-line treatment for dystonia is benztropine (Cogentin).
Diphenhydramine (Benadryl) can
also be used. The first-line treatment for akathisia is decreasing
the dose of the causative agent (if
appropriate), or adding propranolol or a benzodiazepine.
206
PSYCHOPHARMACOLOGY 
KEY FACT
Clozapine, the first atypical antipsychotic, is less likely to cause
tardive dyskinesia.
■ Elevated liver enzymes, jaundice.
• Older age is a risk factor.
• Women and patients with affective disorders may be at an increased risk.
• Although up to 50% of cases will remit (without further antipsychotic
use), most cases are permanent.
• Treatment involves discontinuation of current antipsychotic if clinically
possible and changing to a medication with less potential to cause TD.
■ Less common side effects include neuroleptic malignant syndrome (NMS):
• Though uncommon, occurs more often in young males early in treatment
with high-potency typical antipsychotics.
• It is a medical emergency and has up to a 20% mortality rate if left
untreated.
• It is characterized by FALTERED:
Fever (most common presenting symptom).
Autonomic instability (tachycardia, labile hypertension, diaphoresis).
Leukocytosis.
Tremor.
Elevated CPK.
Rigidity (lead pipe rigidity is considered almost universal).
Excessive sweating (diaphoresis).
Delirium (mental status changes).
• Treatment involves discontinuation of current medications and
administration of supportive medical care (hydration, cooling, etc.).
• Sodium dantrolene, bromocriptine, and amantadine may be used but
have their own side effects and unclear efficacy. ECT can also be effective.
• This is not an allergic reaction.
• Patient is not prevented from restarting the same antipsychotic at a later
time, but will have an increased risk for another episode of neuroleptic
malignant syndrome.
■ Ophthalmologic problems (irreversible retinal pigmentation with high
doses of thioridazine, deposits in lens and cornea with chlorpromazine).
■ Dermatologic problems, including rashes and photosensitivity (blue-gray
skin discoloration with chlorpromazine).
■ Seizures: All antipsychotics lower the seizure threshold, although
low-potency antipsychotics are more likely.
ATYPICAL (SECOND-GENERATION) ANTIPSYCHOTICS
■ Atypical antipsychotics block both dopamine and serotonin receptors and
are associated with different side effects than typical antipsychotics.
■ In particular, they are less likely to cause EPS, TD, or neuroleptic malignant
syndrome.
■ They may be more effective than typical antipsychotics in treating negative
symptoms of schizophrenia.
■ Atypical antipsychotics are also used to treat acute mania, bipolar disorder,
and as adjunctive medications in unipolar depression.
■ They are also used in treating borderline personality disorder, PTSD, and
certain psychiatric disorders in childhood (e.g., tic disorders).
• Clozapine (Clozaril):
Less likely to cause TD.
Only antipsychotic shown to be more efficacious than the others; used
in treatment refractory schizophrenia.
Only antipsychotic shown to decrease the risk of suicide.
More anticholinergic side effects than other atypical or high-potency
typical antipsychotics. Associated with tachycardia, constipation, and
hypersalivation.
Risk of severe side effects
• 1% incidence of agranulocytosis; clozapine must be stopped if the
absolute neutrophil count (ANC) drops below 1500 per microliter.
All patients must undergo regular ANC monitoring weekly for the
first 6 months of treatment, followed by biweekly for 6 months, and
then monthly monitoring.
• 4% incidence of seizures.
• Small risk of myocarditis.
• Risperidone (Risperdal):
Can cause increased prolactin.
Associated with orthostatic hypotension and reflex tachycardia.
Long-acting injectable (LAI) form named Consta.
• Quetiapine (Seroquel): Much less likely to cause EPS; common side
effects include sedation, orthostatic hypotension, and weight gain.
• Olanzapine (Zyprexa): Common side effects include significant weight
gain, sedation, and dyslipidemia. Comes in PO/IM/LAI formulations.
• Ziprasidone (Geodon): Less likely to cause significant weight gain,
associated with QTc prolongation, and must be taken with food (50%
reduction in absorption without a 300-calorie meal). Comes in PO and
IM formulations.
• Aripiprazole (Abilify):
Unique mechanism of partial D2 agonism.
Can be more activating (akathisia) and less sedating.
Less potential for weight gain.
Comes in PO, IM, and LAI formulations.
■ Newer (more expensive) antipsychotics:
• Paliperidone (Invega):
Metabolite of risperidone.
Long-acting injectable forms: Sustenna—monthly; Trinza—every
3 months.
• Asenapine (Saphris) orally dissolving (sublingual) tablet.
• Iloperidone (Fanapt).
• Lurasidone (Latuda): Must be taken with food; used in bipolar
depression.
Side Effects
■ Metabolic syndrome.
• This must be monitored with baseline weight, waist circumference
(measured at iliac crest), BP, HbA1c, and fasting lipids.
PSYCHOPHARMACOLOGY 
WARDS TIP
Onset of antipsychotic side effects
NMS: Any time (but usually early in
treatment)
Acute dystonia: Hours to days
Parkinsonism/Akathisia: Days
to weeks
Tardive dyskinesia: Months
to years
The Abnormal Involuntary
Movement Scale (AIMS) can be
used to quantify and monitor for
tardive dyskinesia.
WARDS TIP
Thirty percent of patients with
treatment-resistant psychosis will
respond to clozapine.
208
PSYCHOPHARMACOLOGY 
WARDS TIP
Patients on clozapine must have
weekly blood draws for the first 6
months to check WBC and absolute neutrophil counts because
of the risk of agranulocytosis.
With time, the frequency of blood
draws decreases.
■ QTc prolongation.
Mood Stabilizers
WARDS TIP
Quetiapine, olanzapine, aripiprazole, risperidone, asenapine, and
ziprasidone have FDA approval for
treatment of mania.
WARDS TIP
Antipsychotics may be used as
adjuncts to mood stabilizers early
in the course of a manic episode.
Atypical antipsychotics are often
prescribed as monotherapy in the
acute or maintenance treatment of
bipolar disorder.
LITHIUM
■ Onset of action takes 5–7 days.
WARDS
QUESTION
Q: What is the only mood stabilizer
shown to decrease suicidality?
A: Lithium.
Side Effects
• Weight gain: Metformin can be used to reduce or prevent.
• Hyperlipidemia.
• Hyperglycemia—Rarely, diabetic ketoacidosis has been reported.
■ Some anti-HAM effects (antihistaminic, antiadrenergic, and
antimuscarinic).
■ Elevated liver function tests (LFTs)—Monitor yearly for elevation in LFTs
and ammonia.
■ Mood stabilizers are used to treat acute mania and to help prevent relapses
of manic episodes (maintenance treatment) in bipolar disorder and
schizoaffective disorder. Less commonly, they may be used for:
• Augmentation of antidepressants in patients with major depression
refractory to monotherapy.
• Potentiation of antipsychotics in patients with schizophrenia or
schizoaffective disorder.
• Treatment of aggression and impulsivity (e.g., neurocognitive disorders,
intellectual disability, personality disorders, other medical conditions).
• Enhancement of abstinence in treatment of alcoholism.
■ Mood stabilizers include lithium and anticonvulsants, most commonly
valproic acid, lamotrigine, and carbamazepine.
■ Lithium is the drug of choice in acute mania and as prophylaxis for both
manic and depressive episodes in bipolar and schizoaffective disorders.
■ It is also used in cyclothymic disorder and unipolar depression.
■ Lithium is metabolized by the kidney, so dosing adjustments may be
necessary in patients with renal dysfunction.
■ Prior to initiating, patients should have an ECG, basic chemistries, thyroid
function tests, a complete blood count (CBC), and a pregnancy test.
■ Blood levels correlate with clinical efficacy and should be checked 4–5 days
after initiation of treatment and after every dose change.
■ The major drawback of lithium is its high incidence of side effects and very
narrow therapeutic index:
• Therapeutic range: 0.6–1.2. (Individual patients can have significant side
effects even within this range.)
• Toxic: >1.5.
• Potentially lethal: >2.0.
■ Toxic levels of lithium cause altered mental status, coarse tremors,
convulsions, delirium, coma, and death.
■ Clinicians need to regularly monitor blood levels of lithium, thyroid
function (thyroid-stimulating hormone), and kidney function.
■ Fine tremor.
■ Cognitive slowing or dulling.
■ Nephrogenic diabetes insipidus (polydipsia, polyuria).
■ GI disturbance.
■ Weight gain.
■ Sedation.
■ Thyroid enlargement, hypothyroidism.
■ ECG changes.
■ Benign leukocytosis.
■ Lithium is associated with an increased risk of Ebstein’s anomaly, a cardiac
defect in babies born to mothers taking lithium, although the absolute risk
is very low. Weighed against the risk of untreated bipolar disorder, many
women take lithium during pregnancy.
Anticonvulsants
CARBAMAZEPINE (TEGRETOL)
■ Especially useful in treating mania with mixed features and rapid-cycling
bipolar disorder; less effective for the depressed phase.
■ Acts by blocking sodium channels and inhibiting action potentials.
■ Onset of action is 5–7 days.
■ Must check pregnancy test prior to initiating therapy as it increases the risk
of neural tube defects.
■ Carries risk of rash, SIADH, hyponatremia, benign leukopenia, and aplastic
anemia (rare).
■ CBC, LFTs must be obtained before initiating treatment and regularly
monitored during treatment.
■ Carbamazepine induces its own metabolism. Patients may therefore need a
dose increase in the first few weeks to months.
• Serum carbamazepine levels should be measured initially and after every
few weeks for the first several months. Therapeutic level is 8–12 mcg/mL.
Side Effects
■ The most common side effects are GI and CNS (e.g., drowsiness, ataxia,
sedation, confusion).
■ Potential dangerous skin rash (Stevens–Johnson syndrome).
■ Leukopenia, hyponatremia, aplastic anemia, thrombocytopenia, and
agranulocytosis.
■ Elevation of liver enzymes, causing hepatitis.
■ Teratogenic effects when used during pregnancy (neural tube defects).
■ Significant drug interactions with many medications metabolized by the
cytochrome P450 pathway, including inducing its own metabolism through
autoinduction (requiring increasing dosages).
■ Toxicity: Confusion, stupor, motor restlessness, ataxia, tremor, nystagmus,
twitching, and vomiting.
PSYCHOPHARMACOLOGY 
KEY FACT
When prescribing lithium, it is important to monitor lithium levels,
creatinine, and thyroid function
tests. To remember labs for lithium:
P THY BEER
Pregnancy
Thyroid
Benign leukocytosis
Electrolytes
EKG
Renal
WARDS TIP
Blood levels are useful for lithium,
valproic acid, carbamazepine, and
clozapine. Remember the 8–12
rule for therapeutic windows of
lithium (0.8–1.2), carbamazepine
(8–12), and valproic acid (80–120).
WARDS TIP
The following factors increase Li+
levels:
• NSAIDs (e.g., ibuprofen)
• Aspirin (+/–)
• Thiazide diuretics
• Dehydration
• Salt deprivation
• Sweating (salt loss)
• Impaired renal function
210
PSYCHOPHARMACOLOGY 
VALPROIC ACID (DEPAKOTE AND DEPAKENE)
KEY FACT
Carbamazepine is like “PacMan”:
It causes the CYP450 enzyme to
chew up medications, resulting in
low medication levels and requiring higher dosages than usual.
■ Monitoring of LFTs and CBC is necessary.
WARDS TIP
Lithium’s side effect of leukocytosis can be advantageous when
combined with other medications that decrease WBC count
(e.g., clozapine).
Lamotrigine (Lamictal)
WARDS
QUESTION
Q: What is a potential consequence of using benzodiazepines
(BDZ) with alcohol?
A: BDZs can be lethal when mixed
with alcohol. Respiratory depression may cause death.
Oxcarbazepine (Trileptal)
■ Less risk of rash and hepatic toxicity.
■ Monitor sodium levels for hyponatremia.
Gabapentin (Neurontin)
WARDS TIP
■ Little efficacy in bipolar disorder.
Pregabalin (Lyrica)
In chronic alcoholics or those with
liver disease, use benzodiazepines
that are not metabolized by the
liver. There are a LOT of them:
Lorazepam
Oxazepam
Temazepam
■ Little efficacy in bipolar disorder.
■ Beneficial side effect is weight loss.
■ Useful in treating acute mania, mania with mixed features, and rapid
cycling.
■ Multiple mechanisms of action: Blocks sodium channels and increases
GABA concentrations in the brain.
■ Comes in PO (Depakote), liquid (Depakene), and IV formulations.
■ Drug levels should be checked after 4–5 days. Therapeutic range is
80–120 µg/mL.
■ Contraindicated in pregnancy, so care should be given in women of
childbearing age (neural tube defects).
■ Side effects include GI distress, sedation, cognitive slowing, weight gain, LFT
elevations, hyperammonemia, thrombocytopenia, pancreatitis.
■ Efficacy for bipolar depression, though little efficacy for acute mania or
prevention of mania.
■ Believed to work on sodium channels that modulate glutamate and
aspartate.
■ Most common side effects are dizziness, sedation, headaches, and ataxia.
■ Most serious side effect is Stevens–Johnson syndrome (life-threatening rash
involving skin and mucous membranes) in 0.1%. This is most likely in the
first 2–8 weeks, but is minimized by starting with low doses and increasing
slowly.
■ Valproate will increase lamotrigine levels, and lamotrigine will decrease
valproate levels.
■ As effective in mood disorders as carbamazepine, but better tolerated.
■ Often used adjunctively to help with anxiety, sleep, neuropathic pain.
■ Used in GAD (second-line) and fibromyalgia.
Tiagabine (Gabitril): Questionable benefit in treating anxiety
Topiramate (Topamax)
■ May be helpful with impulse control disorders.
■ Can cause hypochloremic, metabolic acidosis as well as kidney stones.
■ The most limiting side effect is cognitive slowing and sleepiness resulting in
its nickname, “Dope-a-max.”
Anxiolytics/Hypnotics
■ Include benzodiazepines (BDZs), barbiturates, and buspirone.
■ Common indications for anxiolytics/hypnotics include:
• Anxiety disorders.
• Muscle spasm.
• Seizures.
• Sleep disorders.
• Alcohol withdrawal.
• Anesthesia induction.
BENZODIAZEPINES
■ BDZs are the most widely prescribed psychotropic medications.
■ BDZs work by potentiating the effects of gamma-aminobutyric acid
(GABA).
■ They reduce anxiety and can be used to treat akathisia.
■ Many patients become physically dependent on these medications and
require increasing amounts for the same clinical effect (i.e., tolerance).
■ Potential for abuse.
■ Choice of BDZ is based on time to onset of action, duration of action, and
method of metabolism.
■ Relatively safer in overdose than barbiturates.
■ Long acting (half-life: >20 hours)
• Diazepam (Valium):
Rapid onset.
Used during detoxification from alcohol or
sedative-hypnotic-anxiolytics, and for seizures.
Effective for muscle spasm.
Less commonly prescribed to treat anxiety because of euphoria.
• Clonazepam (Klonopin):
Treatment of anxiety, including panic attacks.
Avoid with renal dysfunction; longer half-life allows for once or twice
daily dosing.
■ Intermediate acting (half-life: 6–20 hours)
• Alprazolam (Xanax):
Treatment of anxiety, including panic attacks.
Short onset of action leads to euphoria, high abuse potential.
• Lorazepam (Ativan):
Treatment of panic attacks, alcohol and sedative-hypnotic-anxiolytic
detoxification, agitation.
Not metabolized by liver.
Used with haloperidol in IM formulations to quickly sedate agitated
patients.
• Oxazepam (Serax):
Alcohol and sedative-hypnotic-anxiolytic detoxification.
Not metabolized by liver.
PSYCHOPHARMACOLOGY 
212
PSYCHOPHARMACOLOGY 
• Temazepam (Restoril):
WARDS
QUESTION
Q: How is benzodiazepine (BDZ)
overdose treated?
A: Flumazenil; however, be
careful not to induce withdrawal too quickly—this can be life
threatening.
■ Short acting (half-life: <6 hours)
• Midazolam (Versed):
Side Effects
■ Drowsiness.
■ Impairment of intellectual function.
■ Anterograde amnesia.
NON-BDZ HYPNOTICS
■ Diphenhydramine (Benadryl):
■ Ramelteon (Rozerem):
NON-BDZ ANXIOLYTICS
■ Buspirone (BuSpar):
Because of dependence, rarely used for treatment of insomnia.
Not metabolized by liver.
Very short half-life.
Primarily used in medical and surgical settings.
■ Reduced motor coordination (careful in elderly).
■ Withdrawal can be life threatening and cause seizures.
■ Toxicity: Respiratory depression in overdose, especially when combined
with alcohol.
■ Zolpidem (Ambien)/Zaleplon (Sonata)/Eszopiclone (Lunesta):
• Work by selective receptor binding to the omega-1 receptor on the
GABA-A receptor, which is responsible for sedation.
• Should be used for short-term treatment of insomnia.
• Compared to BDZs, less tolerance/dependence occurs with prolonged use
(but still can occur).
• Zaleplon has a shorter half-life than zolpidem, which has a shorter
half-life than eszopiclone.
• Reports of anterograde amnesia, hallucinations, parasomnias
(e.g., sleepwalking, sleepeating), increased fall risk, and GI side effects
may limit their tolerability.
• An antihistamine with moderate anticholinergic effects.
• Side effects include sedation, dry mouth, constipation, urinary retention,
and blurry vision.
• Selective melatonin MT1 and MT2 agonist.
• No tolerance or dependence, making it an effective and safe sleep aid.
• Partial agonist at 5HT-1A receptor, thereby decreasing serotonergic activity.
• Slower onset of action than BDZs (takes several weeks for effect).
• Not considered as effective as other options, and so it is often used in
combination with another agent (e.g., an SSRI) for the treatment of
generalized anxiety disorder.
• Does not potentiate the CNS depression of alcohol (useful in alcoholics),
and has a low potential for abuse/addiction.
• Dosed three times per day.
■ Hydroxyzine (Atarax):
• An antihistamine.
• Side effects include sedation, dry mouth, constipation, urinary retention,
and blurry vision.
• Useful for patients who want quick-acting, short-term medication, but
who cannot take BDZs for various reasons.
■ Barbiturates (e.g., butalbitol, phenobarbital, amobarbitol, pentobarbital):
Rarely used because of the lethality of overdose, significant withdrawal,
potential for abuse, and side-effect profile.
■ Propranolol:
• Beta-blocker.
• Useful in treating the autonomic effects of panic attacks or social phobia
(i.e., performance anxiety), such as palpitations, sweating, and tachycardia.
• Also used to treat akathisia (side effect of antipsychotics).
Psychostimulants
Used in ADHD and in treatment refractory depression.
■ Dextroamphetamine and amphetamines (Dexedrine, Adderall):
• Dextroamphetamine is the d-isomer of amphetamine.
• Schedule II due to high potential for abuse/diversion.
• Monitor BP, and watch for weight loss, insomnia, exacerbation of tics,
decreased seizure threshold.
■ Methylphenidate (Ritalin, Concerta):
• CNS stimulant, similar to amphetamine.
• Schedule II.
• Watch for leukopenia or anemia.
• Monitor BP and CBC with differential, and watch for weight loss,
insomnia, exacerbation of tics, decreased seizure threshold.
■ Atomoxetine (Strattera):
• Inhibits presynaptic norepinephrine reuptake, resulting in increased
synaptic norepinephrine and dopamine.
• Less appetite suppression and insomnia.
• Not classified as a controlled substance.
• Less abuse potential than dextroamphetamine/methylphenidate but less
effective.
• Rare liver toxicity, and possible increase in suicidal ideation in children/
adolescents.
■ Modafinil (Provigil): Used in narcolepsy, not ADHD.
Cognitive Enhancers
Used in major neurocognitive disorders (dementias).
ACETYLCHOLINESTERASE INHIBITORS
■ Donepezil (Aricept):
• Once-daily dosing.
• Some GI side effects.
• Used in mild-to-moderate neurocognitive disorders (dementias).
PSYCHOPHARMACOLOGY 
214
PSYCHOPHARMACOLOGY 
■ Galantamine (Razadyne):
KEY FACT
Alzheimer medications, such as
donepezil and rivastigmine, work
by reversible inhibition of acetylcholine esterase.
■ Rivastigmine (Exelon):
■ Memantine (Namenda):
PSYCHOSIS
AGITATION/CONFUSION/DELIRIUM
DEPRESSION
ANXIETY
SEDATION/POOR CONCENTRATION
SELECTED MEDICATIONS
■ Albuterol: Anxiety, confusion.
■ Isoniazid: Psychosis.
• Twice-daily dosing.
• GI side effects.
• Used in mild-to-moderate neurocognitive disorders (dementias).
• Twice-daily dosing.
• Has daily patch form, with fewer side effects.
• Used in mild-to-moderate neurocognitive disorders (dementias).
NMDA (GLUTAMATE) RECEPTOR ANTAGONIST
• Used in moderate-to-severe neurocognitive disorders (dementia).
• Fewer side effects than cholinesterase inhibitors.
• Should be used in conjunction with acetylcholinesterase inhibitor.
Reference List of Medications That May
Cause Psychiatric Symptoms
Sympathomimetics, analgesics, antibiotics (e.g., isoniazid, antimalarials), anticholinergics, anticonvulsants, antihistamines, corticosteroids, antiparkinsonian
agents.
Antipsychotics, anticholinergics, antihistamines, antidepressants, antiarrhythmics, antineoplastics, corticosteroids, NSAIDs, antiasthmatics, antibiotics, antihypertensives, antiparkinsonian agents, thyroid hormones.
Antihypertensives, antiparkinsonian agents, corticosteroids, calcium channel
blockers, NSAIDs, antibiotics, peptic ulcer drugs.
Sympathomimetics, antiasthmatics, antiparkinsonian agents, hypoglycemic
agents, NSAIDs, thyroid hormones.
Antianxiety agents/hypnotics, anticholinergics, mood stabilizers, antibiotics,
antihistamines, antipsychotics (e.g., clozapine, quetiapine, olanzapine).
■ Procainamide, quinidine: Confusion, delirium.
■ Tetracycline: Depression.
■ Nifedipine, verapamil: Depression.
■ Cimetidine: Depression, confusion, psychosis.
■ Steroids: Aggressiveness/agitation, mania, depression, anxiety, psychosis.
Other Treatments
ELECTROCONVULSIVE THERAPY (ECT)
Patients are often premedicated with atropine, and then given general anesthesia
and muscle relaxants (e.g., succinylcholine). A generalized tonic-clonic seizure is
then induced using unilateral or bilateral electrodes placed on the head. While the
mechanism of action of ECT is not fully known, there are likely anticonvulsant
effects, as well as brain perfusion and connectivity changes involved. ECT is the
most effective treatment for major depressive disorder, especially with psychotic
features, as well as for acute mania and catatonia. It is often used in patients who
cannot tolerate medications or who have failed other treatments. ECT is discontinued after symptomatic improvement, typically a course of 8–12 sessions given
three times weekly. Monthly maintenance ECT is often used to prevent relapse of
symptoms, and the addition of nortriptyline or venlafaxine may prolong remission even further. The most common side effects are muscle soreness, headaches,
amnesia, and confusion. Bilateral electrode placement is more efficacious, but
increases memory impairment and confusion. Evidence shows that the memory
loss is almost always temporary and returns to baseline at 6 months.
DEEP BRAIN STIMULATION (DBS)
DBS is a surgical treatment involving the implantation of a medical device
that sends electrical impulses to specific parts of the brain. DBS in select brain
regions has provided benefits for Parkinson disease and disabling dystonia, as
well as for chronic pain and tremors. Its underlying principles and mechanisms
are still not clear. DBS directly changes brain activity in a controlled manner
and its effects are reversible (unlike those of lesioning techniques). DBS has
been used to treat various affective disorders, including major depression.
While DBS has proven helpful for some patients, there is potential for serious
complications and side effects.
REPETITIVE TRANSCRANIAL MAGNETIC STIMULATION (rTMS)
rTMS is a noninvasive method to excite neurons in the brain. Weak electric
currents are induced in the tissue by rapidly changing magnetic fields, a process called electromagnetic induction. In this way, brain activity can be triggered with minimal discomfort. rTMS can produce longer-lasting changes than
nonrepetitive stimulation. Numerous small-scale studies have demonstrated
efficacy in the treatment of major depression; however, studies show less efficacy than for ECT, and the price of treatment is high. Side effects include seizures
(rare), as well as headache and scalp pain.
LIGHT THERAPY
Light therapy, or phototherapy, consists of exposure to daylight or to specific
wavelengths of light using lasers, light-emitting diodes, fluorescent lamps, dichroic
lamps or very bright, full-spectrum light, for a prescribed amount of time and, in
PSYCHOPHARMACOLOGY 
216
PSYCHOPHARMACOLOGY 
KETAMINE INFUSION
Typical Antipsychotics (D2 antagonism)
Watch for NMS (fever, lead pipe rigidity).
some cases, at a specific time of day. The recommendation is for using a 10,000
lux bright white light for 30 minutes per day in the early morning. Light therapy is used to treat major depression with a seasonal pattern (seasonal affective
­disorder), with some support for its use with nonseasonal psychiatric disorders.
Ketamine is an NMDA receptor antagonist that is most commonly used as an
anesthetic agent. Ketamine can be given as an IV infusion for the treatment
of unipolar major depression. It’s effect is rapid (with response within 40–120
­minutes), but the effect dissipates by day 10–14. Ketamine carries a risk of dissociation/psychosis, bladder toxicity, and neurotoxicity. Currently, use of IV ketamine for depression is still mostly limited to research settings, but increasingly
through specialized ketamine clinics. Esketamine, the intranasal formulation of
ketamine, was recently FDA approved for treatment-resistant depression.
Most Common Psychiatric Medications for Wards
Drug name (Brand)
Dosing
Side Effects
Monitoring
Other
chlorpromazine
(Thorazine)
200–800 mg
Hypotension,
sedation,
orthostasis
EKG, BMI, QTc
Least potent
PO, IM
fluphenazine (Prolixin)
6–20 mg
EPS, sedation
PO, IM, LAI
haloperidol (Haldol)
2–20 mg
EPS, sedation
PO, IM, LAI
perphenazine (Triaflon)
8–32 mg
EPS, sedation
PO, IM
EPS tx: Akathisia (propranolol 10 mg TID), Parkinsonism/Dystonia
­(benztropine 1–2 mg daily)
Atypical Antipsychotics (D2 and 5HT2a antagonism)
Drug name
(Brand)
Dosing
Side Effects
Monitoring
Other
clozapine
(Clozaril)
300–900 mg
Anticholinergic,
orthostatis,
agranulocytosis, drooling
Weekly ANC
Most efficacious
Lower
suicide risk
aripiprazole
(Abilify)
5–30 mg
Akathisia
For all: A1C,
fasting
glucose,
lipid profile,
BMI, LFTs,
renal
function
PO and LAI
lurasidone
(Latuda)
40–120 mg
Akathisia
Give with food
olanzapine
(Zyprexa)
10–30 mg
Metabolic syndrome,
orthostasis, sedating
PO, IM, LAI
paliperidone
(Invega)
3–12 mg
Hyperprolactinemia,
EPS, sedation, metabolic
syndrome
PO and LAI
quetiapine
(Seroquel)
50–800 mg
Metabolic syndrome,
orthostasis, sedating
PO, check QTc
risperidone
(Risperdal)
2–6 mg
Hyperprolactinemia,
EPS, sedation, metabolic
syndrome
PO and LAI
Mood Stabilizers
Drug name
Brand)
Dosing
Side Effects
Monitoring
Other
Lithium
900–1800 mg
GI upset, tremor,
nephrogenic DI,
renal failure
Thyroid, renal,
serum drug
level (0.8–1.2)
lamotrigine
(Lamictal)
100–200 mg
GI upset,
SJS rash
Monitor for rash
Dose slowly
valproic acid
(Depakote)
500–2000 mg
GI upset, weight
gain, liver
toxicity
Liver, ammonia,
serum drug
level (80–120)
carbamazepine
(Tegretol)
800–1600 mg
Hyponatremia,
agranulocytosis
Liver, renal,
serum drug
level (8–10)
Antidepressants
Drug name (Brand)
Dosing
Side Effects/Monitor
Other
fluoxetine (Prozac)
20–80 mg
SSRI’s: GI upset,
sexual dysfunction,
bleeding,
discontinuation
syndrome
sertraline (Zoloft)
50–200 mg
Safe in pregnancy
escitalopram
(Lexapro)
10–20 mg
Few med
interactions
venlafaxine
(Effexor)
75–225 mg
Tremor, HTN,
akathisia
Short half-life
duloxetine
(Cymbalta)
40–120 mg
Monitor LFTs
Treats pain,
fibromyalgia
mirtazapine
(Remeron)
15–45 mg
Sedation,
weight gain
Activating at
higher doses
buproprion
(Wellbutrin)
150–450 mg
Activating, insomnia
Increased seizure risk
Watch for 5HT syndrome (Fever, hyperreflexia, myoclonus, GI disturbance)
PSYCHOPHARMACOLOGY 
Ebstein’s
anomaly
Lower
suicide risk
Contraindicated
in pregnancy:
neural tube
defect
Contraindicated
in pregnancy:
neural tube
defect
PacMan inducer
Long half-life
218
PSYCHOPHARMACOLOGY 
NOTES

22 - Chapter 19 Forensic Psychiatry

01 - Chapter 19 Forensic Psychiatry
Chapter 19 Forensic Psychiatry
Standard of Care and Malpractice ..........................................................................................220
Confidentiality .......................................................................................................................220
Decision Making ....................................................................................................................221
Emancipated Minors .........................................................................................................221
Decisional Capacity ...........................................................................................................222
Guardians and Conservators .............................................................................................222
Admission to a Psychiatric Hospital ........................................................................................223
Disability ..........................................................................................................................223
Competence to Stand Trial ......................................................................................................223
Not Guilty by Reason of Insanity (NGRI)..................................................................................224
Risk Assessment ...............................................................................................................224
Malingering............................................................................................................................225
Child and Family Law..............................................................................................................225
Correctional Psychiatry ..........................................................................................................225
FORENSIC PSYCHIATRY
CHAPTER 19
220
FORENSIC PSYCHIATRY
WARDS TIP
A wrong prediction or a bad outcome is not necessarily proof of
malpractice.
■ Risk assessment.
■ Criminal responsibility.
KEY FACT
■ Competence/Decisional capacity.
■ Child custody and visitation.
Four Ds of malpractice: Dereliction
of Duty that was the Direct cause
of Damage.
■ Trauma.
■ Mental disability.
■ Malpractice.
■ Involuntary treatment.
WARDS
QUESTION
Q: What legal case set the precedent that physicians have a duty to
report patients who are potentially
dangerous to others?
A: Tarasoff v. Regents of the University of California which called for
the duty to warn.
Confidentiality
KEY FACT
Doctors are required to report
child abuse, but lawyers are not.
Forensic psychiatry is a medical subspecialty that includes areas in which psychiatry is applied to legal matters. Forensic psychiatrists often conduct evaluations requested by the court or attorneys.
While some forensic psychiatrists specialize exclusively in legal issues, almost
all psychiatrists have to work within one of the many spheres where the mental
health and legal system overlap. These areas include the following:
■ Correctional psychiatry.
Legal issues are considered criminal in nature if someone is being charged with
a crime. Civil cases involve other kinds of rights and may result in monetary
awards. It is important to note that the specific laws pertaining to the various
topics discussed in this chapter may vary by state.
Standard of Care and Malpractice
■ The standard of care in psychiatry is generally defined as the skill level and
knowledge base of the average, prudent psychiatrist in a given community.
■ Negligence is practicing below the standard of care.
■ Malpractice is the act of being negligent as a doctor.
■ The following four conditions typically must be proven by a preponderance
of the evidence in order to sustain a claim of malpractice:
The physician had a duty of care (psychiatrist–patient relationship).
The physician breached their duty by practice that did not meet the standard of care (negligence).
The patient was harmed.
The harm was directly caused by the physician’s negligence.
■ If a malpractice case is successful, the patient can receive compensatory
damages (reimbursement for medical expenses, lost salary, or physical
suffering) and punitive damages (money awarded to “punish” the doctor).
All information regarding a doctor–patient relationship should be held confidential, except when otherwise exempted by statute, such as:
■ When sharing relevant information with other staff members who are also
treating the patient.
■ If subpoenaed—Physician must supply all requested information.
■ If child abuse is suspected—Obligated to report to the proper authorities.
■ If a patient is suicidal—Physician may need to admit the patient, with or
without the patient’s consent, and share information with the hospital staff.
■ If a patient threatens direct harm to another person—Physician may have a
duty to warn the intended victim.
Decision Making
■ Process by which patients knowingly and voluntarily agree to a treatment or
procedure.
■ In order to make informed decisions, patients must know the purpose of
the treatment, alternative treatments, and the potential risks and benefits of
undergoing and of refusing the treatment.
■ The patient should have the opportunity to ask questions.
■ Situations that do not require informed consent:
• Lifesaving medical emergency.
• Prevention of suicidal or homicidal behavior.
• Unemancipated minors (typically require informed consent from the
parent or legal guardian).
EMANCIPATED MINORS
■ Considered competent to give consent for all medical care without parental
input or consent.
■ Minors are considered emancipated if they are:
• Self-supporting.
• In the military.
• Married.
• Have children or pregnant.
A 74-year-old male with insulin-dependent diabetes mellitus and severe major depressive disorder was admitted to the intensive care unit for treatment
of diabetic ketoacidosis. The internal medicine team calls your psychiatry
consult-liaison service to evaluate the patient for depression and provide
treatment recommendations.
When you meet the patient, he is disoriented, confused, and has a waxing
and waning level of consciousness. His mini-mental state exam (MMSE) score
is 18/30. You identify that the patient is likely delirious, and you are unable
to obtain any useful historical information. After interviewing the patient’s
daughter by phone, you learn that the patient’s wife passed away 2 years
ago, and in the past he had told family members that he can no longer live
without her. One year ago, his daughter found him in the garage taping a
hose to his car’s exhaust pipe. She said that he broke down crying and admitted that he was going to kill himself by carbon monoxide poisoning. His
daughter has been very concerned because he refuses to check his glucose
or take his insulin as recommended. She stated, “I think he was trying to kill
himself by not taking care of his diabetes.”
He is followed daily by your consult-liaison team, and his MMSE score
improves to 28/30. On hospital day 5, the internal medicine team informs
you that he has developed wet gangrene in his right lower extremity and will
need to have a below-knee amputation as soon as possible. The team asks
you to assess the patient’s capacity to make medical decisions because he is
adamantly refusing to consent to this procedure.
You meet with the patient to discuss his medical situation. He is alert, lucid, and fully oriented. His affect is euthymic and appropriate. He states, “My
doctor told me that I had an ulcer on my foot from poorly controlled diabetes that has become severely infected. I was told that I need to have my right
FORENSIC PSYCHIATRY
WARDS
QUESTION
Q: In what situations is informed
consent not required?
A: In a lifesaving medical emergency, to prevent suicide or
homicide, or when treating an
unemancipated minor.
KEY FACT
Elements of informed consent
(4 Rs):
• Reason for treatment
• Risks and benefits
• Reasonable alternatives
• Refused treatment
­consequences
WARDS
QUESTION
Q: What is the key difference between capacity and competency?
A: Capacity is a clinical term
assessed by physicians, while competency is a legal term decided by
a judge.
222
FORENSIC PSYCHIATRY
WARDS TIP
When evaluating for decisionmaking capacity think CURA:
Communicate a clear choice
Understand the situation, proposed treatment, and treatment
alternatives
Reason logically through information and decision
Appreciate consequences, including risk/benefits of treatment or
refusal of treatment
WARDS
QUESTION
Q: What is the standard hierarchy
for choosing a surrogate decision
maker?
A: 1. Durable POA or
court-appointed guardian
2. Spouse
3. Adult offspring
4. Parent
5. Sibling
6. Other relative in close contact
with patient
7. Close friend
DECISIONAL CAPACITY
KEY FACT
Emancipated minors do not need
parental consent to make medical
decisions.
GUARDIANS AND CONSERVATORS
leg amputated very soon or else I could die from the infection.” He maintains
that he is not interested in the surgical procedure that has been recommended. He adds, “My daughter is begging me to have the surgery, but I’m already
old and I don’t want to have to use a prosthetic leg or a wheelchair. I do not
think life would be worth living if I had this amputation.” He denies suicidal
thoughts, plan, or intent.
Does this patient with history of severe major depressive disorder demonstrate the capacity to refuse a potentially lifesaving procedure?
Yes, he demonstrates the capacity to refuse the recommended amputation.
Legal standards for decision-making capacity to consent or refuse medical
treatment involve the following: the ability to communicate a choice, to
understand the relevant information, to appreciate the medical consequences of the situation, and to reason about treatment choices. In this case, the
patient demonstrated the ability to discuss all of these topics. Although he
was cognitively impaired on admission, his delirium eventually cleared.
However, the case is complicated by the fact that the patient may be
currently suffering from major depression. This should be further assessed.
While a history of current major depression does not preclude having decisional capacity, the patient should be evaluated carefully to ensure that his
refusal of treatment does not stem from intent to commit suicide. If it does,
then his suicidal intent would be interfering with his ability to reason. Optimally, the consult-liaison team may recommend treating the depression and
readdressing the surgical procedure when his depression is in remission, but
this may take many weeks and failure to amputate the limb in a timely manner could result in death. Since the patient demonstrates decision-making
capacity and does not appear to be suicidal at this time, the medical team
must respect the patient’s wishes and treat the condition without surgery
Competence and capacity are terms that refer to a patient’s ability to make informed treatment decisions.
■ Capacity is a clinical term and may be assessed by physicians.
■ Competence is a legal term and can be decided only by a judge.
■ Decisional capacity is task specific and can fluctuate over time.
■ In order for a patient to have decisional capacity, they must be able to:
• Understand the relevant information regarding treatment (purpose, risks,
benefits).
• Appreciate the appropriate weight and impact of the decision.
• Logically manipulate the information to make a decision.
• Communicate a choice or preference.
• Criteria for determining capacity may be more stringent if the
consequences of a patient’s decision are very serious.
■ If a patient is determined not to have decisional capacity, the decision is
typically made by a surrogate decision maker, usually a power of attorney,
spouse, or close family member.
■ May be appointed by a judge to make treatment decisions for incompetent
patients.
■ Make decisions by “substituted judgment.” This means making decisions
based on what the patient would most likely have wanted, were the patient
competent.
■ Patients can express their wishes for treatment in advance of losing
competence or capacity using a mental health advance directive form called
“Declaration for Mental Health Treatment.”
Admission to a Psychiatric Hospital
The two main categories of admission to a psychiatric hospital are voluntary
and involuntary.
■ Voluntary:
• Patient requests or agrees to be admitted to the psychiatric ward.
• Voluntary patients often have to meet the same symptom severity criteria
as involuntary patients as listed below.
• Voluntary patients may not have the right to be discharged immediately
upon request.
• Patient must have capacity and be competent to be admitted as a
voluntary patient to an inpatient facility.
■ Involuntary:
• Patient must be found to be imminently at risk of harm to one’s self or
others or unable to provide for their basic needs.
• Involuntary patients have legal rights to a trial to challenge their
hospitalization.
• Involuntary patients do not automatically lose the right to refuse
treatment, including the involuntary administration of nonemergent
medication.
• Involuntary commitment is supported by legal principles of police power
(protecting citizens from each other) and parens patriae (protecting
citizens who can’t care for themselves).
Disability
■ Mental impairment: Any mental or psychological disorder.
■ Mental disability: Alteration of an individual’s capacity to meet personal,
social, or occupational demands due to a mental impairment.
■ To assess whether an impairment is also a disability, consider four
categories:
• Activities of daily living.
• Social functioning.
• Concentration, persistence, and pace.
• Deterioration or decompensation in work settings.
Competence to Stand Trial
■ Competence is a legal term for the capacity to understand, rationally
manipulate, and apply information to make a reasoned decision on a specific
issue. This definition varies by state.
FORENSIC PSYCHIATRY
WARDS
QUESTION
Q: When can a patient be involuntarily hospitalized on a psychiatric unit?
A: When they pose a risk of harm
to self, others, or cannot provide
for their basic needs.
WARDS TIP
If a child presents to the emergency department with various
bruises, suspicious injuries in
various stages of healing, and
numerous prior emergency room
visits, your next step would most
likely be to contact the appropriate authorities.
KEY FACT
Sixth Amendment: Right to counsel, a speedy trial, and to confront
witnesses.
KEY FACT
Fourteenth Amendment: Right to
due process of law.
224
FORENSIC PSYCHIATRY
KEY FACT
The fact that someone is mentally ill doesn’t mean they aren’t
­competent to stand trial.
■ To stand trial, a defendant must:
WARDS TIP
After John Hinckley received NGRI
for an assassination attempt on
President Reagan, there was public
outcry against lenient NGRI standards, contributing to the Insanity
Defense Reform Act of 1984.
Risk Assessment
WARDS
QUESTION
Q: What is the most important
factor in assessing a patient’s risk
of violence?
A: The individual’s history of
violence.
TABLE 19-1. Insanity Defense Standards
Standard
Definition
American Law
Institute (ALI) Model
Penal Code
■ The Sixth and Fourteenth Amendments to the Constitution are the basis for
the law that someone cannot be tried if they are not mentally competent to
stand trial.
■ This was established by the legal case Dusky v. United States in 1960.
■ If a defendant has significant mental health problems or behaves irrationally
in court, their competency to stand trial should be considered.
■ Competence to stand trial may change over time.
• Understand the charges against them.
• Be familiar with the courtroom personnel and procedure.
• Have the ability to work with an attorney and participate in their trial.
• Understand possible consequences.
Not Guilty by Reason of Insanity (NGRI)
■ Conviction of a crime requires both an “evil deed” (actus reus) and “evil
intent” (mens rea).
■ Insanity is a legal term, and its definition varies by state (see Table 19-1).
■ If someone is declared legally insane, they are not criminally responsible for
their act.
■ Some states have a ruling of Guilty but Mentally Ill (GBMI) instead of
NGRI, or no criminal insanity defense at all.
■ NGRI is used in less than 1% of criminal cases.
■ It is successful in 26% of cases that continue to use it throughout the trial.
■ Those found NGRI often spend the same amount of time (or more) as
involuntary psychiatric patients than they would have spent in prison if they
were found guilty.
■ Mental disorders are neither necessary nor sufficient causes of violence.
■ The major risk factors of violence are a history of violence, being young,
male, and of lower socioeconomic status.
■ Substance use is a major determinant of violence, whether it occurs in the
context of a mental illness or not.
M’Naghten
■ Person did not understand what they were doing or its
wrongfulness.
■ Most stringent test.
Person could neither appreciate the criminality of their conduct
nor conform their conduct to the requirements of the law.
Irresistible Impulse
Person could not appreciate right from wrong or could not control
actions.
Durham
■ The person’s criminal act has resulted from mental illness.
■ Most lenient test and is rarely used.
■ Predicting dangerousness:
• Short term easier than long term.
• High false positives because of low base rates (most people are not
violent).
Malingering
■ Feigning or exaggerating symptoms for “secondary gain,” including:
• Financial gain (injury law suit).
• Avoiding school, work, or other responsibilities.
• Obtaining medications of abuse (opioids, benzodiazepines).
• Avoiding legal consequences.
■ Signs for detecting malingering:
• Atypical presentation.
• “Textbook” description of the illness.
• History of working in the medical field.
• Symptoms that are present only when the patient knows they are being
observed.
• History of substance use or antisocial personality disorder.
• Reluctant to engage in invasive/in-depth testing or treatment.
Child and Family Law
Evaluations for which a child forensic psychiatrist may be needed include:
■ Child custody.
■ Termination of parental rights.
■ Child abuse or neglect.
Correctional Psychiatry
■ With the closing of state psychiatric hospitals (i.e., deinstitutionalization),
many persons with mental illness have moved to correctional institutions.
■ Psychiatrists who practice in jails and prisons must balance treating the
inmates as their patients and maintaining safety in the institution.
■ Issues of confidentiality and violence are key.
FORENSIC PSYCHIATRY
WARDS
QUESTION
Q: What is the key difference between malingering and factitious
disorder?
A: The motivation for malingering
is for secondary gain (external motivations, such as avoiding work or
jail), whereas factitious disorder is
primary gain (internal motivations,
such as to assume the sick-role).
WARDS TIP
The contribution of people with
mental illness to overall rates
of violence is small. Those with
mental illness are more likely to
be the victims of violence than the
perpetrators.
226
FORENSIC PSYCHIATRY
NOTES

23 - Chapter 20 Approach to the Psychiatric Patient in

01 - Chapter 20 Approach to the Psychiatric Patien
Chapter 20 Approach to the Psychiatric Patient in the Emergency Department
EMERGENCY
DEPARTMENT
A P P R OACH TO T H E P S YC H IAT RI C PAT I E N T IN T HE
CHAPTER 20
Safety Assessment .................................................................................................................228
Medical Clearance Orders .......................................................................................................228
De-escalation Techniques.......................................................................................................228
Communication with ED.........................................................................................................230
Acutely Agitated Patients........................................................................................................230
Assessment of a Sleeping or Unresponsive Patient.................................................................230
Medication Interactions .........................................................................................................230
Causes of Mental Status Changes ...........................................................................................231
228
APPROACH TO THE PSYCHIATRIC PATIENT IN THE EMERGENCY DEPARTMENT
Safety Assessment
■ Position yourself close to the exit
Medical Clearance Orders
■ De-escalating the situation:
De-escalation Techniques
During the course of your psychiatry clerkship, you may be asked to see a
patient who is in the Emergency Department (ED). Unlike on the psychiatry
floor/ward or even a psychiatric emergency holding unit, the ED sees patients
with all sorts of complaints, and is not particularly well-suited for psychiatric patients. Reasons contributing to the ED environment being challenging
include staff frequently entering and exiting the patient’s room, which may
interrupt your interview; a high level of activity and noise; and a large number of distractions. Psychiatric patients in the ED are from some of the most
marginalized segments of society. They may be homeless, may have untreated,
undertreated or mistreated psychiatric illness, and their presentation may be
confounded by acute intoxication with alcohol, drugs, or co-existing medical
illness.
Many patients are brought in by law enforcement/police, which may unfortunately exacerbate a patient’s aggression or paranoia. When patients are hostile
or scared, it is difficult to develop a rapport with them.
When interviewing such patients, it is preferable to enter the room without
law enforcement as long as there does not seem to be an immediate threat of
physical harm to you or your team (see Figure 20-1).
How to assess whether the room/patient is safe (see Table 20-1):
■ Position yourself on the patient’s nondominant side
• This is usually the patient’s left in 95% of cases.
• Patients usually wear their watch on their nondominant hand.
• Their belt buckle usually faces to the nondominant side.
■ Do a quick visual to make sure no objects that can be used as weapons are
around. ED rooms designated as psychiatric rooms are usually devoid of
such objects, but if the patient is in a regular medical room, then there may
be many items that could be dangerous (e.g., suction canisters, trashcans,
needles, intravenous [IV] poles).
■ Be prepared to de-escalate the situation. Recognize that the patient may not
be there by choice; that they may be been treated poorly by law enforcement;
that they fear losing their independence; that this new environment
aggravates their paranoia; and that the ED may be a place that they mistrust.
• Speak softly (if they have to strain to hear you, they will have to be quiet
themselves).
• Offer them food or drink (they rarely have to go to surgery, so keeping them
NPO is not usually a concern, and most ED psychiatric patients are hungry).
• Bring them a blanket (it is usually cold in the ED).
When you
enter the
room, do a
quick visual to
make sure
there are no
immediate
hazards in
sight.
Ensure exit
is clear in case
you need to
get out of
there fast.
Ensure your
own safety and
that of your
team
Stand on the
patient’s non
dominant side
FIGURE 20-1.  Suggested steps for approaching a psychiatric patient in the ED.
TABLE 20-1. Typical Medical “Clearance” Orders
Undress patient, place in hospital gown
Continuous pulse oximetry
Cardiac monitor
Electrocardiogram (ECG)
Peripheral IV
Complete blood count (CBC)
Complete metabolic panel (electrolytes and liver function tests)
b-hCG (if female)
Magnesium
Alcohol
Salicylate
Acetaminophen
Urinalysis
Urine drug screen
Suicide precautions (sitter)
Seizure precautions (padded bedrails)
• Speak to them like an individual. Pick your favorite benign topic of
conversation, such as the weather. One choice is: “Where were you born
and raised?” It’s unusual to be asked something like that, so it tends to
catch the patient off guard and put them more into a conversation mode.
• Ask their permission to examine them. Respecting anyone’s personal space
is important, but especially so with the psychiatric patient.
• If they are going to be admitted to the psychiatric unit, explain what is going
to happen to them. Hopefully they have been seen by an ED physician and
the process has been discussed, but this is not always the case. If you are
the first student they are talking to, explain that the ED will do a medical
clearance evaluation (see Table 20-1), and then they will be brought to the
behavioral health unit/psychiatry floor. While respecting their dignity and
APPROACH TO THE PSYCHIATRIC PATIENT IN THE EMERGENCY DEPARTMENT
Review patient’s ED
workup to see if there are
urgent medical conditions
that need to be addressed
Determine if
patient meets
criteria for
involuntary
commitment
(suicidal,
homicidal).
Ensure
patient is in a
hospital gown
and has been
searched for
weapons
Check labs for electrolyte
abnormalities, replete if indicated
Review any imaging (especially
head CT if ordered)
Review EKG
230
APPROACH TO THE PSYCHIATRIC PATIENT IN THE EMERGENCY DEPARTMENT
Communication with ED
WARDS
QUESTION
Q: What medication is used to
reverse opiate/opioid overdose?
A: Naloxone.
Acutely Agitated Patients
WARDS TIP
Case: You are called to the ED
to see a patient. You encounter
a 22-year-old male who is very
agitated, trying to break free of
the numerous paramedics and
security officers trying to hold him
down. He is loudly yelling to be let
go as well as clearly responding to
internal stimuli. How should you
manage the situation?
Answer: Try verbally de-escalating
the situation while you order
chemical restraints. Order a benzodiazepine and an antipsychotic
together, as that will result in less
total benzodiazepine dose being
needed.
■ Assess the patient’s ABCs
KEY FACT
Medication Interactions
Flumazenil is used for benzodiazepine overdose reversal BUT its use
can cause seizures, especially in
those patients with a low seizure
threshold. Use with caution, and
have an airway cart ready in case
airway control becomes necessary.
Remember that benzodiazepine
withdrawal can be life threatening.
privacy, ED psychiatric patients should be placed in a gown and searched for
items such as weapons, drugs, drug paraphernalia, and medication patches.
Communicate with the ED team any plans you have made with your psychiatry
attending.
■ Let them know if there are any medications the patient should or should not
receive.
■ Expedite the patient’s movement out of the ED if possible, as it is the least
restful place for them.
In the event that an acutely agitated patient cannot be de-escalated, medication(s) may be required. The most common choice is an antipsychotic with
or without a benzodiazepine. Either class can achieve control on its own, but
benzodiazepines tend to be more sedating. Table 20-2 lists the most common
medications used to control acute agitation in the ED. The ability to administer
oral or intramuscular medications is very helpful as an acutely agitated patient
may not cooperate for the team to safely place an IV.
[
Assessment of a Sleeping or Unresponsive Patient
If you walk in the room and the patient appears to be sleeping or unresponsive,
you should do the following:
• Airway: Can the patient speak? (if yes, airway is patent)
• Breathing: Is the patient breathing? (look for chest rise, auscultate lungs)
• Circulation: Does the patient have a pulse? (auscultate heart, check blood
pressure)
■ If the patient’s ABCs are compromised, immediately get an ED physician.
Pull the panic cord if you need to.
■ If the patient’s ABCs are stable but they appear somnolent, explore with
the ED team whether the patient has received any medications from the
ED or paramedics/emergency medical services (EMS) which could be
contributing.
Psychiatric medications can adversely interact with many other medications.
Using a drug interaction calculator to verify interactions will be a huge service
to your patient as well as your team. Do not assume that just because patient is
prescribed a set of medications, that they are all safe to be taken together. Often, patients get prescriptions for various medications from several prescribers,
and concurrent prescriptions are not cross-checked.
APPROACH TO THE PSYCHIATRIC PATIENT IN THE EMERGENCY DEPARTMENT
Causes of Mental Status Changes
Lab and vital sign abnormalities that can cause altered mental status or
­delirium:
■ Hypoglycemia/Hyperglycemia.
■ Hyponatremia/Hypernatremia.
■ Hypocalcemia/Hypercalcemia.
■ Hypothermia/Hyperthermia.
■ Hypothyroidism.
■ Hypovolemia.
■ Hypercarbia.
■ Hypoxemia.
Geriatric patients (>65 years) are
often sensitive to medications so
it is recommended to start with
smaller doses. Also some geriatric
patients can have paradoxical agitation with benzodiazepines. Remember that it is unusual for a patient
over age 40 to have a first episode
of psychosis. Be sure to search for
other medical causes of psychosis.
KEY FACT
TABLE 20-2. Common Medications Used in Adults for Control of Acute Agitation in the ED
Medication
(Brand Name)
Drug Class
Initial Dose
Onset of
Action
(minutes)
Half-Life
(hours)
Adverse Effects/Notes
Lorazepam
(Ativan®)
Benzodiazepine
PO, IM, PR,
IV: 2 mg
IM: 15
PO: 30–60
More sedating than antipsychotics alone
Midazolam
(Versed®)
Benzodiazepine
PO, IM, IN,
IV 2 mg
PO, IN: 12–15
IV: 2–5
1–3
Shortest onset of action
Short duration of action may be both an
advantage and disadvantage; intranasal
route unique
Haloperidol
Typical (1st generation)
antipsychotic
PO, IM,
IV: 5 mg
20
Extrapyramidal symptoms; anticholinergic
symptoms; QT prolongation; neuroleptic
malignant syndrome
Olanzapine
(Zyprexa®)
Atypical (2nd generation)
antipsychotic
ODT: 5, 10,
15, 20 mg
IM: 10 mg
15–60
20–50
Safety and efficacy not established for
children less than 13 years.
Life-threatening sedation and
hypotension when co-administered with a
benzodiazepine.
Ziprasidone
(Geodon®)
Atypical (2nd generation)
antipsychotic
IM; 20 mg
2–5
Causes QTc prolongation; important
to assess known history of QTc
prolongation, recent myocardial infarction,
uncompensated heart failure, or if taking
other medications known to prolong the
QTc interval.
Risperidone
(Risperdal®)
Atypical (2nd generation)
antipsychotic
ODT and
solution
IM: 30–60
PO: 60–120
Quetiapine
(Seroquel®)
Atypical (2nd generation)
antipsychotic
Oral tablet
form only
6
Long time of onset limits use in acute
agitation
232
APPROACH TO THE PSYCHIATRIC PATIENT IN THE EMERGENCY DEPARTMENT
WARDS TIP
KEY FACT
Normal QTc—Men: <440 ms and
women: <460 ms.
An increase in 10 ms is associated
with a 5–7% increase in Torsades
de pointes.
KEY FACT
Visual hallucinations should
always prompt search for an
underlying medical pathology.
Although visual hallucinations can
occur with psychiatric disorders,
auditory hallucinations are more
common.
Case: You are called to the ED to see an elderly patient who you are told
is psychotic. The patient has a history of Parkinson for which he takes
carbidopa-levodopa. He had vomited earlier so he was given one oral dissolving
tablet of ondansetron. The ED team wants to give him some Olanzapine to help
control his symptoms. As the team that will take over the care of this patient, what
would you advise?
Answer: Most anti-parkinsonian medications including carbidopa-levodopa can
induce psychosis in Parkinson patients, usually manifested as visual hallucinations.
It is the most common nonmotor disabling symptom in PD. A quick drug interaction search will reveal that carbidopa-levodopa has a serious interaction with
olanzapine, in that it reduces the activity of carbidopa-levodopa. In addition, the
combination of ondansetron and olanzapine can result in dangerously prolonged
QTc, so be sure to check an ECG.