16 - 11 Trauma and Stressor Related Disorders

01 - 11.1 Posttraumatic Stress Disorder and Acute
11.1 Posttraumatic Stress Disorder and Acute Stress Disorder
Trauma- and Stressor-Related Disorders
11.1 Posttraumatic Stress Disorder and Acute Stress
Disorder
Both posttraumatic stress disorder (PTSD) and acute stress disorder are marked by
increased stress and anxiety following exposure to a traumatic or stressful event.
Traumatic or stressful events may include being a witness to or being involved in a
violent accident or crime, military combat, or assault, being kidnapped, being involved
in a natural disaster, being diagnosed with a life-threatening illness, or experiencing
systematic physical or sexual abuse. The person reacts to the experience with fear and
helplessness, persistently relives the event, and tries to avoid being reminded of it. The
event may be relived in dreams and waking thoughts (flashbacks).
The stressors causing both acute stress disorder and PTSD are sufficiently
overwhelming to affect almost everyone. They can arise from experiences in war,
torture (discussed in detail below), natural catastrophes, assault, rape, and serious
accidents, for example, in cars and in burning buildings. Persons reexperience the
traumatic event in their dreams and their daily thoughts; they are determined to avoid
anything that brings the event to mind and they undergo a numbing of responsiveness
along with a state of hyperarousal. Other symptoms are depression, anxiety, and
cognitive difficulties such as poor concentration.
A link between acute mental syndromes and traumatic events has been recognized for more than 200 years. Observations
of trauma-related syndromes were documented following the Civil War, and early psychoanalytic writers, including
Sigmund Freud, noted a relation between neurosis and trauma. Considerable interest in posttraumatic mental disorders was
stimulated by observations of “battle fatigue,” “shell shock,” and “soldier’s heart” in both World Wars I and II. Moreover,
increasing documentation of mental reactions to the Holocaust, to a series of natural disasters, and to assault contributed to
the growing recognition of a close relation between trauma and psychopathology.
EPIDEMIOLOGY
The lifetime incidence of PTSD is estimated to be 9 to 15 percent and the lifetime
prevalence of PTSD is estimated to be about 8 percent of the general population,
although an additional 5 to 15 percent may experience subclinical forms of the disorder.
The lifetime prevalence rate is 10 percent in women and 4 percent in men. According to
the National Vietnam Veterans Readjustment Study (NVVRS), 30 percent of men develop
full-blown PTSD after having served in the war and an additional 22.5 percent develop
partial PTSD, falling just short of qualifying for the disorder. Among veterans of the Iraq
and Afghanistan wars, 13 percent received the diagnosis of PTSD.
Although PTSD can appear at any age, it is most prevalent in young adults, because
they tend to be more exposed to precipitating situations. Children can also have the
disorder (see Section 31.11b). Men and women differ in the types of traumas to which
they are exposed. Historically, men’s trauma was usually combat experience, and
women’s trauma was most commonly assault or rape. The disorder is most likely to
occur in those who are single, divorced, widowed, socially withdrawn, or of low
socioeconomic level, but anyone can be effected, no one is immune. The most important
risk factors, however, for this disorder are the severity, duration, and proximity of a
person’s exposure to the actual trauma. A familial pattern seems to exist for this
disorder, and first-degree biological relatives of persons with a history of depression
have an increased risk for developing PTSD following a traumatic event.
COMORBIDITY
Comorbidity rates are high among patients with PTSD, with about two thirds having at
least two other disorders. Common comorbid conditions include depressive disorders,
substance-related disorders, anxiety disorders, and bipolar disorders. Comorbid disorders
make persons more vulnerable to develop PTSD.
ETIOLOGY
Stressor
By definition, a stressor is the prime causative factor in the development of PTSD. Not
everyone experiences the disorder after a traumatic event, however. The stressor alone
does not suffice to cause the disorder. Clinicians must also consider individual’s
preexisting biological and psychosocial factors and events that happened before and
after the trauma. For example, a member of a group who lived through a disaster can
sometimes better deal with trauma because others have also shared the experience. The
stressor’s subjective meaning to a person is also important. For example, survivors of a
catastrophe may experience guilt feelings (survivor guilt) that can predispose to, or
exacerbate, PTSD.
Three weeks after a train derailment, a 42-year-old budget analyst presented to the
mental health clinic. He noted that he was embarrassed to seek care, as he was
previously a firefighter, but he felt he needed “some reassurance that what I’m
experiencing is normal.” He reported that, since the wreck, he had been feeling
nervous and on edge. He experienced some difficulty focusing his attention at work,
and he had occasional intrusive recollections of “the way the ground just shook; the
tremendous ‘bang’ and then the screaming when the train rolled over.” He noted that
he had spoken with five business colleagues who were also on the train, and three
acknowledged similar symptoms. However, they said that they were improving. He
was more concerned about the frequency of tearful episodes, sometimes brought on by
hearing the name of a severely injured friend, but, at other times, occurring “for no
particular reason.” In addition, he noted that, when he evacuated the train, rescue
workers gave him explicit directions about where to report, and, although he
complied, he now felt extremely guilty about not returning to the train to assist in the
rescue of others. He reported a modest decrease in appetite and denied weight loss but
noted that he had stopped jogging during his lunch break. He had difficulty initiating
sleep, so he had begun consuming a “glass or two” of wine before bed to help with
this. He did not feel rested on awakening. He denied suicidal ideation or any
psychotic symptoms. His sister had taken an antidepressant several years ago, but he
did not desire medication. He feared that side effects could further diminish his ability
to function at the workplace and could cause him to gain weight. (Courtesy of D. M.
Benedek, M.D., R. J. Ursano, M.D., and H. C. Holloway, M.D.)
Risk Factors
Even when faced with overwhelming trauma, most persons do not experience PTSD
symptoms. The National Comorbidity Study found that 60 percent of males and 50
percent of females had experienced some significant trauma, whereas the reported
lifetime prevalence of PTSD, as mentioned earlier, was only about 8 percent. Similarly,
events that may appear mundane or less than catastrophic to most persons can produce
PTSD in some. Evidence indicates of a dose–response relationship between the degree of
trauma and the likelihood of symptoms. Table 11.1-1 summarizes vulnerability factors
that appear to play etiological roles in the disorder.
Table 11.1-1
Predisposing Vulnerability Factors in Posttraumatic Stress Disorder
Psychodynamic Factors
The psychoanalytic model of the PTSD hypothesizes that the trauma has reactivated a
previously quiescent, yet unresolved psychological conflict. The revival of the childhood
trauma results in regression and the use of the defense mechanisms of repression,
denial, reaction formation, and undoing. According to Freud, a splitting of
consciousness occurs in patients who reported a history of childhood sexual trauma. A
preexisting conflict might be symbolically reawakened by the new traumatic event. The
ego relives and thereby tries to master and reduce the anxiety. Psychodynamic themes in
PTSD are summarized in Table 11.1-2. Persons who suffer from alexithymia, the
inability to identify or verbalize feeling states, are incapable of soothing themselves
when under stress.
Table 11.1-2
Psychodynamic Themes in Posttraumatic Stress Disorder
Cognitive-Behavioral Factors
The cognitive model of PTSD posits that affected persons cannot process or rationalize
the trauma that precipitated the disorder. They continue to experience the stress and
attempt to avoid experiencing it by avoidance techniques. Consistent with their partial
ability to cope cognitively with the event, persons experience alternating periods of
acknowledging and blocking the event. The attempt of the brain to process the massive
amount of information provoked by the trauma is thought to produce these alternating
periods. The behavioral model of PTSD emphasizes two phases in its development. First,
the trauma (the unconditioned stimulus) that produces a fear response is paired, through
classic conditioning, with a conditioned stimulus (physical or mental reminders of the
trauma, such as sights, smells, or sounds). Second, through instrumental learning, the
conditioned stimuli elicit the fear response independent of the original unconditioned
stimulus, and persons develop a pattern of avoiding both the conditioned stimulus and
the unconditioned stimulus. Some persons also receive secondary gains from the
external world, commonly monetary compensation, increased attention or sympathy,
and the satisfaction of dependency needs. These gains reinforce the disorder and its
persistence.
Biological Factors
The biological theories of PTSD have developed both from preclinical studies of animal
models of stress and from measures of biological variables in clinical populations with
the disorder. Many neurotransmitter systems have been implicated by both sets of data.
Preclinical models of learned helplessness, kindling, and sensitization in animals have
led
to
theories
about
norepinephrine,
dopamine,
endogenous
opioids,
and
benzodiazepine receptors and the hypothalamic-pituitary-adrenal (HPA) axis. In clinical
populations, data have supported hypotheses that the noradrenergic and endogenous
opiate systems, as well as the HPA axis, are hyperactive in at least some patients with
PTSD. Other major biological findings are increased activity and responsiveness of the
autonomic nervous system, as evidenced by elevated heart rates and blood pressure
readings and by abnormal sleep architecture (e.g., sleep fragmentation and increased
sleep latency). Some researchers have suggested a similarity between PTSD and two
other psychiatric disorders: major depressive disorder and panic disorder.
Noradrenergic System.
Soldiers with PTSD-like symptoms exhibit nervousness,
increased blood pressure and heart rate, palpitations, sweating, flushing, and tremors—
symptoms associated with adrenergic drugs. Studies found increased 24-hour urine
epinephrine concentrations in veterans with PTSD and increased urine catecholamine
concentrations in sexually abused girls. Further, platelet α2- and lymphocyte βadrenergic receptors are downregulated in PTSD, possibly in response to chronically
elevated catecholamine concentrations. About 30 to 40 percent of patients with PTSD
report flashbacks after yohimbine (Yocon) administration. Such findings are strong
evidence for altered function in the noradrenergic system in PTSD.
Opioid System.
Abnormality in the opioid system is suggested by low plasma βendorphin concentrations in PTSD. Combat veterans with PTSD demonstrate a naloxone
(Narcan)-reversible analgesic response to combat-related stimuli, raising the possibility
of opioid system hyperregulation similar to that in the HPA axis. One study showed that
nalmefene (Revex), an opioid receptor antagonist, was of use in reducing symptoms of
PTSD in combat veterans.
Corticotropin-Releasing Factor and the HPA Axis.
Several factors point to
dysfunction of the HPA axis. Studies have demonstrated low plasma and urinary free
cortisol concentrations in PTSD. More glucocorticoid receptors are found on
lymphocytes, and challenge with exogenous corticotropin-releasing factor (CRF) yields a
blunted corticotropin (ACTH) response. Further, suppression of cortisol by challenge
with low-dose dexamethasone (Decadron) is enhanced in PTSD. This indicates
hyperregulation of the HPA axis in PTSD. Also, some studies have revealed cortisol
hypersuppression in trauma-exposed patients who develop PTSD, compared with
patients exposed to trauma who do not develop PTSD, indicating that it might be
specifically associated with PTSD and not just trauma. Overall, this hyperregulation of
the HPA axis differs from the neuroendocrine activity usually seen during stress and in
other disorders such as depression. Recently, the role of the hippocampus in PTSD has
received increased attention, although the issue remains controversial. Animal studies
have shown that stress is associated with structural changes in the hippocampus, and
studies of combat veterans with PTSD have revealed a lower average volume in the
hippocampal region of the brain. Structural changes in the amygdala, an area of the
brain associated with fear, have also been demonstrated.
DIAGNOSIS
The 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) criteria
for PTSD (Table 11.1-3) specify that the symptoms of intrusion, avoidance, alternations
of mood and cognition, and hyperarousal must have lasted more than 1 month. The
DSM-5 diagnosis of PTSD allows the physician to specify if the symptoms occur in
preschool-aged
children
or
with
dissociative
(depersonalization/derealization)
symptoms. For patients whose symptoms have been present less than 1 month, the
appropriate diagnosis may be acute stress disorder (Table 11.1-4).
Table 11.1-3
DSM-5 Diagnostic Criteria for Posttraumatic Stress Disorder
Table 11.1-4
DSM-5 Diagnostic Criteria for Acute Stress Disorder
Mrs. M sought treatment for symptoms that she developed in the wake of an assault
that had occurred about 6 weeks prior to her psychiatric evaluation. While leaving
work late one evening, Mrs. M was attacked in a parking lot next to the hospital in
which she worked. She was raped and badly beaten but was able to escape and call
for help. On referral, Mrs. M reported frequent intrusive thoughts about the assault,
including nightmares about the event and recurrent intrusive visions of her assailant.
She reported that she now took the bus to work to avoid the scene of the attack and
that she had to change her work hours so that she did not have to leave the building
after dark. In addition, she reported that she had difficulty interacting with men,
particularly those who resembled her attacker, and that she consequently avoided
such interactions whenever possible. Mrs. M described increased irritability, difficulty
staying asleep at night, poor concentration, and an increased focus on her
environment, particularly after dark. (Courtesy of Erin B. McClure-Tone, Ph.D., and
Daniel S. Pine, M.D.)
CLINICAL FEATURES
Individuals with PTSD show symptoms in three domains: intrusion symptoms following
the trauma, avoiding stimuli associated with the trauma, and experiencing symptoms of
increased automatic arousal, such as an enhanced startle. Flashbacks, in which the
individual may act and feel as if the trauma were reoccurring, represent a classic
intrusion symptom. Other intrusion symptoms include distressing recollections or
dreams and either physiological or psychological stress reactions to exposure to stimuli
that are linked to the trauma. An individual must exhibit at least one intrusion symptom
to meet the criteria for PTSD. Symptoms of avoidance associated with PTSD include
efforts to avoid thoughts or activities related to the trauma, anhedonia, reduced capacity
to remember events related to the trauma, blunted affect, feelings of detachment or
derealization, and a sense of a foreshortened future. Symptoms of increased arousal
include insomnia, irritability, hypervigilance, and exaggerated startle.
A 40-year-old man watched the September 11, 2001, terrorist attack on the World
Trade Center on television. Immediately thereafter he developed feelings of panic
associated with thoughts that he was going to die. The panic disappeared within a few
hours; however, for the next few nights he had nightmares with obsessive thoughts
about dying. He sought consultation and reported to the psychiatrist that his wife had
been killed in a plane crash 20 years earlier. He described having adapted to the loss
“normally” and was aware that his current symptoms were probably related to that
traumatic event. On further exploration in brief psychotherapy, he realized that his
reactions to his wife’s death were muted and that his relationship with her was
ambivalent. At the time of her death, he was contemplating divorce and frequently
had wished her dead. He had never fully worked through the mourning process for his
wife, and his catastrophic reaction to the terrorist attack was related, in part, to those
suppressed feelings. He was able to recognize his feelings of guilt related to his wife
and his need for punishment manifested by thinking he was going to die.
Gulf War Syndrome
In the Persian Gulf War against Iraq, which began in 1990 and ended in 1991,
approximately 700,000 American soldiers served in the coalition forces. Upon their
return, more than 100,000 US veterans reported a vast array of health problems,
including irritability, chronic fatigue, shortness of breath, muscle and joint pain,
migraine headaches, digestive disturbances, rash, hair loss, forgetfulness, and difficulty
concentrating. Collectively, these symptoms were called the Gulf War syndrome. The US
Department of Defense acknowledges that up to 20,000 troops serving in the combat
area may have been exposed to chemical weapons, and the best evidence indicates that
the condition is a disorder that in some cases may have been precipitated by exposure to
an unidentified toxin (Table 11.1-5). One study of loss of memory found structural
change in the right parietal lobe and damage to the basal ganglia with associated
neurotransmitter dysfunction. A significant number of veterans have developed
amyotrophic lateral sclerosis (ALS), thought to be the result of genetic mutations.
Table 11.1-5
Syndromes Associated with Toxic Exposurea
In a 1997 editorial in the Journal of the American Medical Association, the relationship
of the Persian Gulf War syndrome and stress was stated as follows:
Physicians need to acknowledge that many Gulf War veterans are experiencing stress-related disorders and the physical
consequences of stress. These conditions should not be hidden or denied, but rather are well-recognized entities that have
been studied extensively in survivors of past wars, most notably the Vietnam conflict. As physicians, we should not accept
a diagnosis of stress-related disorder in veterans prior to excluding treatable physical factors, but at the same time, we need
to recognize the pervasive presence of stress-related illness such as hypertension, fibromyalgia, and chronic fatigue among
Persian Gulf War veterans and manage these illnesses appropriately. As a nation, we need to get beyond the fallacious idea
that diseases of the mind either are not real or are shameful and to better recognize that the mind and the body are
inextricably linked.
In addition, thousands of Gulf War veterans developed PTSD and the differentiation
between the two disorders has proved difficult. PTSD is caused by psychological stress,
and Gulf War syndrome is presumed to be caused by environmental biological stressors.
Signs and symptoms often overlap and both conditions may exist at the same time.
9/11/01
On September 11, 2001, terrorist activity destroyed the World Trade Center in New York
City and damaged the Pentagon in Washington (Fig. 11.1-1). It resulted in more than
3,500 deaths and injuries and left many citizens in need of therapeutic intervention.
One survey found a prevalence rate of 11.4 percent for PTSD and 9.7 percent for
depression in US citizens 1 month after 9/11. It is estimated that more than 25,000
people suffer symptoms of PTSD related to the 9/11 attacks beyond the 1-year mark.
FIGURE 11.1-1
The World Trade Center, New York City, prior to 9/11/01. (Courtesy of Kimsamoon,
Inc.)
Iraq and Afghanistan
In October 2001, the United States, along with Australia, Canada, and the United
Kingdom, began the invasion of Afghanistan in the wake of the September 11, 2001,
attacks. US forces are scheduled to withdraw by the end of 2014. On March 20, 2003, US
forces, along with their allies, invaded Iraq, marking the beginning of the Iraq War,
which officially ended on December 15, 2011.
Both wars caused an estimated 17 percent of returning soldiers to develop PTSD. The
rate of PTSD is higher in women soldiers. Women account for 11 percent of those who
served in Iraq and Afghanistan and for 14 percent of patients at Veterans
Administration (VA) hospitals and clinics. Women soldiers are more likely to seek help
than men soldiers. The rate of suicide for active duty personnel in both of these wars
have assumed epidemic proportions, with the likelihood of suicide being double that of
the general population.
Traumatic brain injury (TBI), the result of direct or indirect trauma to the brain,
causes changes in either the gross or microscopic structure of the brain with associated
signs and symptoms depending on the location of the lesion. In most cases of TBI there
will be signs and symptoms of PTSD as well, complicating the picture. According to the
Department of Veterans Affairs, 19 percent of veterans may have TBI.
Natural Disasters
Tsunami.
On December 26, 2004, a massive tsunami struck the shores of Indonesia,
Sri Lanka, South India, and Thailand and caused serious damage and deaths as far west
as the coast of Africa and South Africa. The tsunami caused nearly 300,000 deaths and
left more than 1 million people without homes. Many survivors continue to live in fear
and show signs of PTSD; fishermen fear venturing out to sea, children fear playing at
beaches they once enjoyed, and many families have trouble sleeping for fear of another
tsunami.
Hurricane.
In August 2005, a category 5 hurricane, Hurricane Katrina, ravaged the
Gulf of Mexico, the Bahamas, South Florida, Louisiana, Mississippi, and Alabama. Its
high winds and torrential rainfall breached the levee system that protected New
Orleans, Louisiana, causing major flooding. More than 1,300 people were killed and
tens of thousands were left stranded. In October 2012, Hurricane Sandy landed on the
eastern coast of the United States and in the New York–New Jersey metropolitan area
caused almost 150 deaths with an estimated 650,000 homes damaged or destroyed. Over
50,000 persons were believed to have developed full blown PTSD as a result.
Earthquake.
On January 12, 2010, a 7.0 magnitude earthquake hit Port-au-Prince,
the capital of the Republic of Haiti, which had a population of approximately 3 million
people. Approximately 316,000 people died, 300,000 were injured, and 1 million were
made homeless. The government of Haiti also estimated that 250,000 residences and
30,000 commercial buildings had collapsed or were severely damaged, leaving
10 million cubic meters of rubble.
On March 11, 2011, a 9.0 magnitude earthquake hit northeastern Japan, causing a
10-meter tsunami that reached as far as the western coast of the United States, making
it the fifth largest earthquake since 1900. Approximately 15,700 people were killed,
4,700 were missing, and 5,700 were injured. It also brought Japan into its second
recession in 3 years and triggered the world’s biggest nuclear disaster since Chernobyl in
1986.
PTSD developed among those who experienced these disasters, the full extent of which
remains to be determined. Some estimates range from 50 to 75 percent of survivors
experienced some or all of the signs and symptoms of PTSD.
Torture
The intentional physical and psychological torture of one human by another can have
emotionally damaging effects comparable to, and possibly worse than, those seen with
combat and other types of trauma. As defined by the United Nations, torture is any
deliberate infliction of severe mental pain or suffering, usually through cruel, inhuman,
or degrading treatment or punishment. This broad definition includes various forms of
interpersonal violence, from chronic domestic abuse to broad-scale genocide. According
to Amnesty International, torture is common and widespread in most of the 150
countries worldwide where human rights violations have been documented. Recent
figures estimate that between 5 and 35 percent of the world’s 14 million refugees have
had at least one torture experience, and these numbers do not even account for the
consequences of the current political, regional, and religious disputes in various parts of
the world where torture is still practiced.
DIFFERENTIAL DIAGNOSIS
Because patients often exhibit complex reactions to trauma, the clinician must be careful
to exclude other syndromes as well when evaluating patients presenting in the wake of
trauma. It is particularly important to recognize potentially treatable medical
contributors to posttraumatic symptomatology, especially head injury during the
trauma. Medical contributors can usually be detected through a careful history and
physical examination. Other organic considerations that can both cause and exacerbate
the symptoms are epilepsy, alcohol-use disorders, and other substance-related disorders.
Acute intoxication or withdrawal from some substances may also present a clinical
picture that is difficult to distinguish from the disorder until the effects of the substance
have worn off.
Symptoms of PTSD can be difficult to distinguish from both panic disorder and
generalized anxiety disorder, because all three syndromes are associated with prominent
anxiety and autonomic arousal. Keys to correctly diagnosing PTSD involve a careful
review of the time course relating the symptoms to a traumatic event. PTSD is also
associated with re-experiencing and avoidance of a trauma, features typically not
present in panic or generalized anxiety disorder. Major depression is also a frequent
concomitant of PTSD. Although the two syndromes are not usually difficult to distinguish
phenomenologically, it is important to note the presence of comorbid depression,
because this can influence treatment of PTSD. PTSD must be differentiated from a series
of related disorders that can exhibit phenomenological similarities, including borderline
personality disorder, dissociative disorders, and factitious disorders. Borderline
personality disorder can be difficult to distinguish from PTSD. The two disorders can
coexist or even be causally related. Patients with dissociative disorders do not usually
have the degree of avoidance behavior, the autonomic hyperarousal, or the history of
trauma that patients with PTSD report.
COURSE AND PROGNOSIS
PTSD usually develops some time after the trauma. The delay can be as short as 1 week
or as long as 30 years. Symptoms can fluctuate over time and may be most intense
during periods of stress. Untreated, about 30 percent of patients recover completely, 40
percent continue to have mild symptoms, 20 percent continue to have moderate
symptoms, and 10 percent remain unchanged or become worse. After 1 year, about 50
percent of patients will recover. A good prognosis is predicted by rapid onset of the
symptoms, short duration of the symptoms (less than 6 months), good premorbid
functioning, strong social supports, and the absence of other psychiatric, medical, or
substance-related disorders or other risk factors.
In general, the very young and the very old have more difficulty with traumatic
events than do those in midlife. For example, about 80 percent of young children who
sustain a burn injury show symptoms of PTSD 1 or 2 years after the initial injury; only
30 percent of adults who suffer such an injury have symptoms of PTSD after 1 year.
Presumably, young children do not yet have adequate coping mechanisms to deal with
the physical and emotional insults of the trauma. Likewise, older persons are likely to
have more rigid coping mechanisms than younger adults and to be less able to muster a
flexible approach to dealing with the effects of trauma. Furthermore, the traumatic
effects can be exacerbated by physical disabilities characteristic of late life, particularly
disabilities of the nervous system and the cardiovascular system, such as reduced
cerebral blood flow, failing vision, palpitations, and arrhythmias. Preexisting
psychiatric disability, whether a personality disorder or a more serious condition, also
increases the effects of particular stressors. PTSD that is comorbid with other disorders is
often more severe and perhaps more chronic and may be difficult to treat. The
availability of social supports may also influence the development, severity, and
duration of PTSD. In general, patients who have a good network of social support are
less likely to have the disorder and to experience it in its severe forms and are more
likely to recover faster.
TREATMENT
When a clinician is faced with a patient who has experienced a significant trauma, the
major approaches are support, encouragement to discuss the event, and education about
a variety of coping mechanisms (e.g., relaxation). In encouraging persons to talk about
the event it is imperative that the clinician allow the person to proceed at his or her
own pace. Some patients will not be willing to talk until well after the event has passed,
and those wishes should be respected. To press a person who is reluctant to talk about a
trauma into doing so is likely to increase rather than decrease the risk of developing
PTSD. The use of sedatives and hypnotics can also be helpful in some cases. When a
patient has experienced a traumatic event in the past and has now developed PTSD, the
emphasis should be on education about the disorder and its treatment, both
pharmacological and psychotherapeutic. The clinician should also work to destigmatize
the notion of mental illness and PTSD. Additional support for the patient and the family
can be obtained through local and national support groups for patients with PTSD.
Pharmacotherapy
Selective serotonin reuptake inhibitors (SSRIs), such as sertraline (Zoloft) and
paroxetine (Paxil), are considered first-line treatments for PTSD, owing to their efficacy,
tolerability, and safety ratings. SSRIs reduce symptoms from all PTSD symptom clusters
and are effective in improving symptoms unique to PTSD, not just symptoms similar to
those of depression or other anxiety disorders. Buspirone (BuSpar) is serotonergic and
may also be of use.
The efficacy of imipramine (Tofranil) and amitriptyline (Elavil), two tricyclic drugs,
in the treatment of PTSD is supported by a number of well-controlled clinical trials.
Although some trials of the two drugs have had negative findings, most of these trials
had serious design flaws, including too short a duration. Dosages of imipramine and
amitriptyline should be the same as those used to treat depressive disorders, and an
adequate trial should last at least 8 weeks. Patients who respond well should probably
continue the pharmacotherapy for at least 1 year before an attempt is made to
withdraw the drug. Some studies indicate that pharmacotherapy is more effective in
treating the depression, anxiety, and hyperarousal than in treating the avoidance,
denial, and emotional numbing.
Other drugs that may be useful in the treatment of PTSD include the monoamine
oxidase inhibitors (MAOIs) (e.g., phenelzine [Nardil]), trazodone (Desyrel), and the
anticonvulsants (e.g., carbamazepine [Tegretol], valproate [Depakene]). Some studies
have also revealed improvement in PTSD in patients treated with reversible monoamine
oxidase inhibitors (RIMAs). Use of clonidine (Catapres) and propranolol (Inderal),
which are antiadrenergic agents, is suggested by the theories about noradrenergic
hyperactivity in the disorder. There are almost no positive data concerning the use of
antipsychotic drugs in the disorder, so the use of drugs such as haloperidol (Haldol)
should be reserved for the short-term control of severe aggression and agitation.
Research is ongoing about the use of opioid receptor agonists during traumatic events as
a preventative against developing PTSD.
Psychotherapy
Psychodynamic psychotherapy may be useful in the treatment of many patients with
PTSD. In some cases, reconstruction of the traumatic events with associated abreaction
and catharsis may be therapeutic, but psychotherapy must be individualized because
reexperiencing the trauma overwhelms some patients.
Psychotherapeutic interventions for PTSD include behavior therapy, cognitive
therapy, and hypnosis. Many clinicians advocate time-limited psychotherapy for the
victims of trauma. Such therapy usually takes a cognitive approach and also provides
support and security. The short-term nature of psychotherapy minimizes the risk of
dependence and chronicity, but issues of suspicion, paranoia, and trust often adversely
affect compliance. Therapists should overcome patients’ denial of the traumatic event,
encourage them to relax, and remove them from the source of the stress. Patients should
be encouraged to sleep, using medication if necessary. Support from persons in their
environment (e.g., friends and relatives) should be provided. Patients should be
encouraged to review and abreact emotional feelings associated with the traumatic
event and to plan for future recovery. Abreaction—experiencing the emotions associated
with the event—may be helpful for some patients. The amobarbital (Amytal) interview
has been used to facilitate this process.
Psychotherapy after a traumatic event should follow a model of crisis intervention
with support, education, and the development of coping mechanisms and acceptance of
the event. When PTSD has developed, two major psychotherapeutic approaches can be
taken. The first is exposure therapy, in which the patient re-experiences the traumatic
event through imaging techniques or in vivo exposure. The exposures can be intense, as
in implosive therapy, or graded, as in systematic desensitization. The second approach
is to teach the patient methods of stress management, including relaxation techniques
and cognitive approaches, to coping with stress. Some preliminary data indicate that,
although stress management techniques are effective more rapidly than exposure
techniques, the results of exposure techniques last longer.
Another psychotherapeutic technique that is relatively novel and somewhat
controversial is eye movement desensitization and reprocessing (EMDR), in which the
patient focuses on the lateral movement of the clinician’s finger while maintaining a
mental image of the trauma experience. The general belief is that symptoms can be
relieved as patients work through the traumatic event while in a state of deep
relaxation. Proponents of this treatment state it is as effective, and possibly more
effective, than other treatments for PTSD and that it is preferred by both clinicians and
patients who have tried it.
In addition to individual therapy techniques, group therapy and family therapy have
been reported to be effective in cases of PTSD. The advantages of group therapy include
sharing of traumatic experiences and support from other group members. Group therapy
has been particularly successful with Vietnam veterans and survivors of catastrophic
disasters such as earthquakes. Family therapy often helps sustain a marriage through
periods of exacerbated symptoms. Hospitalization may be necessary when symptoms are
particularly severe or when a risk of suicide or other violence exists.
UNSPECIFIED TRAUMA- OR STRESSOR-RELATED DISORDER
In DSM-5, the category of “unspecified trauma- or stressor-related disorder” is used for
patients who develop emotional or behavioral symptoms in response to an identifiable
stressor but do not meet the full criteria of any other specified trauma- or stressorrelated disorder (e.g., acute stress disorder, PTSD, or adjustment disorder). The
symptoms cannot meet the criteria for another mental, medical disorder and is not an
exacerbation of a preexisting mental disorder. The symptoms also cannot be attributed
to the direct physiological effects of a substance. See Section 11.2 for a discussion of
adjustment disorders.
REFERENCES
Alexander S, Kuntz S. PTSD-related sleep disturbances: Is there evidence-based treatment? JAAPA. 2012;25:44.
Barnes JB, Dickstein BD, Maguen S, Neria Y, Litz BT. The distinctiveness of prolonged grief and posttraumatic stress
disorder in adults bereaved by the attacks of September 11th. J Affect Disord. 2012;136:366.
Benedek DM, Ursano RJ, Holloway HC. Disaster psychology: Disaster, terrorism, and war. In: Sadock BJ, Sadock VA, Ruiz
P, eds. Kaplan & Sadock’s Comprehensive Textbook of Psychiatry. 9th ed. Philadelphia: Lippincott Williams & Wilkins;
2009:2187.
Biggs QM, Fullerton CS, Reeves JJ, Grieger TA, Reissman D, Ursano RJ. Acute stress disorder, depression, and tobacco use
in disaster workers following 9/11. Am J Orthopsychiatry. 2010;80:586.
Bryant RA. Acute stress disorder as a predictor of posttraumatic stress disorder: A systematic review. J Clin Psychiatry.
2011;72:233.
Cloitre M, Garvert DW, Brewin CR, Bryant RA, Maercker A. Evidence for proposed ICD-11 PTSD and complex PTSD: A
latent profile analysis. Eur J Psychotraumatol. 2013;4.
Elklit A, Christiansen DM. Acute stress disorder and posttraumatic stress disorder in rape victims. J Interper Viol.
2010;25(8):1470–1488.
Fareed A, Eilender P, Haber M, Bremner J, Whitfield N, Drexler K. Comorbid posttraumatic stress disorder and opiate
addiction: A literature review. J Addict Dis. 2013;32(2):168–179.
Forneris CA, Gartlehner G, Brownley KA, Gaynes BN, Sonis J, Coker-Schwimmer E, Jonas DE, Greenblatt A, Wilkins TM,
Woodell CL, Lohr KN. Interventions to prevent post-traumatic stress disorder: A systematic review. Am J Prev Med.
2013;44(6):635–650.
Jamieson JP, Mendes WB, Nock MK. Improving acute stress responses: The power of reappraisal. Curr Dir Psychol Sci.
2013;22(1):51–56.
Jovanovic T, Sakoman AJ, Kozari´c-Kovacˇi´c D, Meštrovi´c AH, Duncan EJ, Davis M, Norrholm SD. Acute stress disorder
versus chronic posttraumatic stress disorder: Inhibition of fear as a function of time since trauma. Depress Anxiety.
2013;30(3):217–224.
Le QA, Doctor JN, Zoellner LA, Feeny NC. Cost-Effectiveness of prolonged exposure therapy versus pharmacotherapy and
treatment choice in posttraumatic stress disorder (the optimizing PTSD treatment trial): a doubly randomized
preference trial. J Clin Psychiatry. 2014;75(3):222–230.
McNally RJ. Posttraumatic stress disorder. In: Sadock BJ, Sadock VA, Ruiz P, eds. Kaplan & Sadock’s Comprehensive
Textbook of Psychiatry. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2009:2650.

02 - 11.2 Adjustment Disorders
11.2 Adjustment Disorders
Panagioti M, Gooding PA, Tarrier N. Hopelessness, defeat, and entrapment in posttraumatic stress disorder: Their
association with suicidal behavior and severity of depression. J Nerv Ment Dis. 2012;200:676.
Ponniah K, Hollon SD. Empirically supported psychological treatments for adult acute stress disorder and posttraumatic
stress disorder: A review. Depress Anxiety. 2009;26:1086.
Sones HM, Thorp SR, Raskind M. Prevention of posttraumatic stress disorder. Psychiatr Clin North Am. 2011;34:79.
Zantvoord JB, Diehle J, Lindauer RJ. Using neurobiological measures to predict and assess treatment outcome of
psychotherapy in posttraumatic stress disorder: Systematic review. Psychother Psychosom. 2013;82(3):142–151.
11.2 Adjustment Disorders
The diagnostic category of adjustment disorders is widely used among clinicians in
practice. Adjustment disorders are characterized by an emotional response to a stressful
event. It is one of the few diagnostic entities in which an external stressful event is
linked to the development of symptoms. Typically, the stressor involves financial issues,
a medical illness, or relationship problem. The symptom complex that develops may
involve anxious or depressive affect or may present with a disturbance of conduct. By
definition, the symptoms must begin within 3 months of the stressor. A variety of
subtypes of adjustment disorder are identified in the fifth edition of the Diagnostic and
Statistical Manual of Mental Disorders (DSM-5). These include adjustment disorder with
depressed mood, mixed anxiety and depressed mood, disturbance of conduct, mixed
disturbance of emotions and conduct, features of acute stress disorder or posttraumatic
stress disorder (PTSD), bereavement, and unspecified type.
EPIDEMIOLOGY
The prevalence of the disorder is estimated to be from 2 to 8 percent of the general
population. Women are diagnosed with the disorder twice as often as men, and single
women are generally overly represented as most at risk. In children and adolescents,
boys and girls are equally diagnosed with adjustment disorders. The disorders can occur
at any age but are most frequently diagnosed in adolescents. Among adolescents of
either sex, common precipitating stresses are school problems, parental rejection and
divorce, and substance abuse. Among adults, common precipitating stresses are marital
problems, divorce, moving to a new environment, and financial problems.
Adjustment disorders are one of the most common psychiatric diagnoses for disorders
of patients hospitalized for medical and surgical problems. In one study, 5 percent of
persons admitted to a hospital over a 3-year period were classified as having an
adjustment disorder. Up to 50 percent of persons with specific medical problems or
stressors have been diagnosed with adjustment disorders. Furthermore, 10 to 30 percent
of mental health outpatients and up to 50 percent of general hospital inpatients referred
for mental health consultations have been diagnosed with adjustment disorders.
ETIOLOGY
By definition, an adjustment disorder is precipitated by one or more stressors. The
severity of the stressor or stressors does not always predict the severity of the disorder;
the stressor severity is a complex function of degree, quantity, duration, reversibility,
environment, and personal context. For example, the loss of a parent is different for a
child 10 years of age than for a person 40 years of age. Personality organization and
cultural or group norms and values also contribute to the disproportionate responses to
stressors.
Stressors may be single, such as a divorce or the loss of a job, or multiple, such as the
death of a person important to a patient, which coincides with the patient’s own
physical illness and loss of a job. Stressors may be recurrent, such as seasonal business
difficulties, or continuous, such as chronic illness or poverty. A discordant intrafamilial
relationship can produce an adjustment disorder that affects the entire family system, or
the disorder may be limited to a patient who was perhaps the victim of a crime or who
has a physical illness. Sometimes, adjustment disorders occur in a group or community
setting, and the stressors affect several persons, as in a natural disaster or in racial,
social, or religious persecution. Specific developmental stages, such as beginning school,
leaving home, getting married, becoming a parent, failing to achieve occupational
goals, having the last child leave home, and retiring, are often associated with
adjustment disorders.
Psychodynamic Factors
Pivotal to understanding adjustment disorders is an understanding of three factors: the
nature of the stressor, the conscious and unconscious meanings of the stressor, and the
patient’s preexisting vulnerability. A concurrent personality disorder or organic
impairment may make a person vulnerable to adjustment disorders. Vulnerability is also
associated with the loss of a parent during infancy or being reared in a dysfunctional
family. Actual or perceived support from key relationships can affect behavioral and
emotional responses to stressors.
Several psychoanalytic researchers have pointed out that the same stress can produce
a range of responses in various persons. Throughout his life, Sigmund Freud remained
interested in why the stresses of ordinary life produce illness in some and not in others,
why an illness takes a particular form, and why some experiences and not others
predispose a person to psychopathology. He gave considerable weight to constitutional
factors and viewed them as interacting with a person’s life experiences to produce
fixation.
Psychoanalytic research has emphasized the role of the mother and the rearing
environment in a person’s later capacity to respond to stress. Particularly important
was Donald Winnicott’s concept of the good-enough mother, a person who adapts to the
infant’s needs and provides sufficient support to enable the growing child to tolerate the
frustrations in life.
Clinicians must undertake a detailed exploration of a patient’s experience of the
stressor. Certain patients commonly place all the blame on a particular event when a
less obvious event may have had more significant psychological meaning for the
patient. Current events may reawaken past traumas or disappointments from childhood,
so patients should be encouraged to think about how the current situation relates to
similar past events.
Throughout early development, each child develops a unique set of defense
mechanisms to deal with stressful events. Because of greater amounts of trauma or
greater constitutional vulnerability, some children have less mature defensive
constellations than other children. This disadvantage may cause them as adults to react
with substantially impaired functioning when they are faced with a loss, a divorce, or a
financial setback; those who have developed mature defense mechanisms are less
vulnerable and bounce back more quickly from the stressor. Resilience is also crucially
determined by the nature of children’s early relationships with their parents. Studies of
trauma repeatedly indicate that supportive, nurturing relationships prevent traumatic
incidents from causing permanent psychological damage.
Psychodynamic clinicians must consider the relation between a stressor and the
human developmental life cycle. When adolescents leave home for college, for example,
they are at high developmental risk for reacting with a temporary symptomatic picture.
Similarly, if the young person who leaves home is the last child in the family, the
parents may be particularly vulnerable to a reaction of adjustment disorder. Moreover,
middle-aged persons who are confronting their own mortality may be especially
sensitive to the effects of loss or death.
Family and Genetic Factors
Some studies suggest that certain persons appear to be at increased risk both for the
occurrence of these adverse life events and for the development of pathology once they
occur. Findings from a study of more than 2,000 twin pairs indicate that life events and
stressors are modestly correlated in twin pairs, with monozygotic twins showing greater
concordance than dizygotic twins. Family environmental and genetic factors each
accounted for approximately 20 percent of the variance in that study. Another twin
study that examined genetic contributions to the development of PTSD symptoms (not
necessarily at the level of full disorder and, therefore, relevant to adjustment disorders)
also concluded that the likelihood of developing symptoms in response to traumatic life
events is partially under genetic control.
DIAGNOSIS AND CLINICAL FEATURES
Although by definition adjustment disorders follow a stressor, the symptoms do not
necessarily begin immediately. Up to 3 months may elapse between a stressor and the
development of symptoms. Symptoms do not always subside as soon as the stressor
ceases; if the stressor continues, the disorder may be chronic. The disorder can occur at
any age, and its symptoms vary considerably, with depressive, anxious, and mixed
features most common in adults. Physical symptoms, which are most common in
children and the elderly, can occur in any age group. Manifestations may also include
assaultive behavior and reckless driving, excessive drinking, defaulting on legal
responsibilities, withdrawal, vegetative signs, insomnia, and suicidal behavior.
The clinical presentations of adjustment disorder can vary widely. DSM-5 lists six
adjustment disorders, including an unspecified category (Table 11.2-1).
Table 11.2-1
DSM-5 Diagnostic Criteria for Adjustment Disorders
Adjustment Disorder with Depressed Mood
In adjustment disorder with depressed mood, the predominant manifestations are
depressed mood, tearfulness, and hopelessness. This type must be distinguished from
major depressive disorder and uncomplicated bereavement. Adolescents with this type
of adjustment disorder are at increased risk for major depressive disorder in young
adulthood.
Adjustment Disorder with Anxiety
Symptoms of anxiety, such as palpitations, jitteriness, and agitation, are present in
adjustment disorder with anxiety, which must be differentiated from anxiety disorders.
Adjustment Disorder with Mixed Anxiety and Depressed Mood
In adjustment disorder with mixed anxiety and depressed mood, patients exhibit features
of both anxiety and depression that do not meet the criteria for an already established
anxiety disorder or depressive disorder.
A 48-year-old married woman, in good health, with no previous psychiatric
difficulties, presented to the emergency room reporting that she had overdosed on a
handful of antihistamines shortly before she arrived. She described her problems as
having started 2 months earlier, soon after her husband unexpectedly requested a
divorce. She felt betrayed after having devoted much of her 20-year marriage to being
a wife, mother, and homemaker. She was sad and tearful at times, and she
occasionally had difficulty sleeping. Otherwise, she had no vegetative symptoms and
enjoyed time with family and friends. She felt desperate and suicidal after she realized
that “he no longer loved me.” After crisis intervention in the emergency setting, she
responded well to individual psychotherapy over a 3-month period. She occasionally
required benzodiazepines for anxiety during the period of treatment. By the time of
discharge, she had returned to her baseline function. She came to terms with the
possibility of life after divorce and was exploring her best options under the
circumstances. (Courtesy of Jeffrey W. Katzman, M.D., and Cynthia M. A. Geppert,
M.D., Ph.D., M.P.H.)
Adjustment Disorder with Disturbance of Conduct
In adjustment disorder with disturbance of conduct, the predominant manifestation
involves conduct in which the rights of others are violated or age-appropriate societal
norms and rules are disregarded. Examples of behavior in this category are truancy,
vandalism, reckless driving, and fighting. The category must be differentiated from
conduct disorder and antisocial personality disorder.
Adjustment Disorder with Mixed Disturbance of Emotions and Conduct
A combination of disturbances of emotions and of conduct sometimes occurs. Clinicians
are encouraged to try to make one or the other diagnosis in the interest of clarity.
Adjustment Disorder Unspecified
Adjustment disorder unspecified is a residual category for atypical maladaptive
reactions to stress. Examples include inappropriate responses to the diagnosis of
physical illness, such as massive denial, severe noncompliance with treatment, and
social withdrawal, without significant depressed or anxious mood.
DIFFERENTIAL DIAGNOSIS
Although uncomplicated bereavement often produces temporarily impaired social and
occupational functioning, the person’s dysfunction remains within the expectable
bounds of a reaction to the loss of a loved one and, thus, is not considered adjustment
disorder. See Section 34.1 for a further discussion of bereavement.
Other disorders from which adjustment disorder must be differentiated include major
depressive disorder, brief psychotic disorder, generalized anxiety disorder, somatic
symptom disorder, substance-related disorder, conduct disorder, and PTSD. These
diagnoses should be given precedence in all cases that meet their criteria, even in the
presence of a stressor or group of stressors that served as a precipitant. Patients with an
adjustment disorder are impaired in social or occupational functioning and show
symptoms beyond the normal and expectable reaction to the stressor. Because no
absolute criteria help to distinguish an adjustment disorder from another condition,
clinical judgment is necessary. Some patients may meet the criteria for both an
adjustment disorder and a personality disorder. If the adjustment disorder follows a
physical illness, the clinician must make sure that the symptoms are not a continuation
or another manifestation of the illness or its treatment.
Acute and Posttraumatic Stress Disorders
The presence of a stressor is a requirement in the diagnosis of adjustment disorder,
PTSD, and acute stress disorder. PTSD and acute stress disorder have the nature of the
stressor better characterized and are accompanied by a defined constellation of affective
and autonomic symptoms. In contrast, the stressor in adjustment disorder can be of any
severity, with a wide range of possible symptoms. When the response to an extreme
stressor does not meet the acute stress or posttraumatic disorder threshold, the
adjustment disorder diagnosis would be appropriate. PTSD is discussed fully in Section
11.1.
COURSE AND PROGNOSIS
With appropriate treatment, the overall prognosis of an adjustment disorder is generally
favorable. Most patients return to their previous level of functioning within 3 months.
Some persons (particularly adolescents) who receive a diagnosis of an adjustment
disorder later have mood disorders or substance-related disorders. Adolescents usually
require a longer time to recover than adults.
Research over the past 5 years has disclosed a risk for suicide, especially in adolescent
patients with adjustment disorder, not previously fully appreciated. A recent study of
119 patients with adjustment disorder indicated that 60 percent had documented suicide
attempts in the hospital. Fifty percent had attempted suicide immediately prior to their
hospital admission. Comorbid diagnoses of substance abuse and personality disorder
contributed to the suicide risk profile. A study of the background, pathology, and
treatment-related factors of suicidal adolescents found that those with adjustment
disorder and suicidality were more likely to have made attempts (up to 25 percent), to
exhibit psychomotor restlessness and dysphoric mood, to have experienced a suicide of
another person as a stressor, to have poor psychosocial functioning upon treatment
entry, and to have received prior psychiatric care.
A 16-year-old high school senior experienced rejection in his first serious
relationship. In the weeks after the end of the relationship, he began to exhibit
dysphoric mood accompanied by anxiety and psychomotor agitation. He had received
counseling in junior high school when his parents divorced and he began using alcohol
and marijuana and had been suspended during his freshman year for fighting. A
month after the breakup, he began to tell his parents that life was no longer worth
living without his former girlfriend. Two months later his parents came home from
work and found him hanging in the garage with a note stating he could not go on
alone. (Courtesy of J. W. Katzman, M.D., and C. M. A. Geppert, M.D., Ph.D., M.P.H.)
TREATMENT
Psychotherapy
Psychotherapy remains the treatment of choice for adjustment disorders. Group therapy
can be particularly useful for patients who have had similar stresses—for example, a
group of retired persons or patients having renal dialysis. Individual psychotherapy
offers the opportunity to explore the meaning of the stressor to the patient so that
earlier traumas can be worked through. After successful therapy, patients sometimes
emerge from an adjustment disorder stronger than in the premorbid period, although no
pathology was evident during that period. Because a stressor can be clearly delineated
in adjustment disorders, it is often believed that psychotherapy is not indicated and that
the disorder will remit spontaneously. This viewpoint, however, ignores the fact that
many persons exposed to the same stressor experience different symptoms, and in
adjustment disorders, the response is pathological. Psychotherapy can help persons
adapt to stressors that are not reversible or time limited and can serve as a preventive
intervention if the stressor does remit.
Psychiatrists treating adjustment disorders must be particularly aware of problems of
secondary gain. The illness role may be rewarding to some normally healthy persons
who have had little experience with illness’s capacity to free them from responsibility.
Thus, patients can find therapists’ attention, empathy, and understanding, which are
necessary for success, rewarding in their own right, and therapists may thereby
reinforce patients’ symptoms. Such considerations must be weighed before intensive
psychotherapy is begun; when a secondary gain has already been established, therapy is
difficult. Patients with an adjustment disorder that includes a conduct disturbance may
have difficulties with the law, authorities, or school. Psychiatrists should not attempt to
rescue such patients from the consequences of their actions. Too often, such kindness
only reinforces socially unacceptable means of tension reduction and hinders the
acquisition of insight and subsequent emotional growth. In these cases, family therapy
can help.
Crisis Intervention
Crisis intervention and case management are short-term treatments aimed at helping
persons with adjustment disorders resolve their situations quickly by supportive
techniques,
suggestion,
reassurance,
environmental
modification,
and
even
hospitalization, if necessary. The frequency and length of visits for crisis support vary
according to patients’ needs; daily sessions may be necessary, sometimes two or three
times each day. Flexibility is essential in this approach.
Pharmacotherapy
No studies have assessed the efficacy of pharmacological interventions in individuals
with adjustment disorder, but it may be reasonable to use medication to treat specific
symptoms for a brief time. The judicious use of medications can help patients with
adjustment disorders, but they should be prescribed for brief periods. Depending on the
type of adjustment disorder, a patient may respond to an antianxiety agent or to an
antidepressant. Patients with severe anxiety bordering on panic can benefit from
anxiolytics such as diazepam (Valium), and those in withdrawn or inhibited states may
be helped by a short course of psychostimulant medication. Antipsychotic drugs may be
used if there are signs of decompensation or impending psychosis. Selective serotonin
reuptake inhibitors have been found useful in treating symptoms of traumatic grief.
Recently, there has been an increase in antidepressant use to augment psychotherapy in
patients with adjustment disorders. Pharmacological intervention in this population is
most often used, however, to augment psychosocial strategies rather than serving as the
primary modality.
REFERENCES
Busch AB, Yoon F, Barry CL, Azzone V, Normand SL, Goldman HH, Huskamp HA. The effects of mental health parity on
spending and utilization for bipolar, major depression, and adjustment disorders. Am J Psychiatry. 2013;170(2):180–187.
Chen PF, Chen CS, Chen CC, Lung FW. Alexithymia as a screening index for male conscripts with adjustment disorder.
Psychiatr Q. 2011;82:139.
Daniels J. The perils of “adjustment disorder” as a diagnostic category. J Humanistic Counsel. 2009;48:77.
Giltaij H, Sterkenburg P, Schuengel C. Psychiatric diagnostic screening of social maladaptive behaviour in children with
mild intellectual disability: Differentiating disordered attachment and pervasive developmental disorder behaviour.
J Intellect Disabil Res. 2013.
Katzman JW, Geppert CMA. Adjustment disorders. In: Sadock BJ, Sadock VA, Ruiz P, eds. Kaplan & Sadock’s
Comprehensive Textbook of Psychiatry. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2009:2187.
Kim-Cohen J, Turkewitz R. Resilience and measured gene-environment interactions. Dev Psychopathol. 2012;24(4):1297–
1306.
Li M, Hales S, Rodin GM. Adjustment disorders. In: Holland JC, Breitbart WS, Jacobsen PB, Lederberg MS, Loscalzo MJ,
McCorkle RS, eds. Psycho-oncology. 2nd ed. New York: Oxford University Press; 2010:303.
Regier DA, Kuhl EA, Kupfer DJ. The DSM-5: Classification and criteria changes. World Psychiatry. 2013;12(2):92–98.
Schuengel C, Schipper JC, Sterkenburg PS, Kef S. Attachment, intellectual disabilities and mental health: Research,
assessment and intervention. J Appl Res Intellect Dis. 2013;26(1):34–46.
Schulze T, Maercker A, Horn AB. Mental health and multimorbidity: psychosocial adjustment as an important process for
quality of life. Gerontology. 2014;60(3):249–254.
Simon NM. Treating complicated grief. JAMA. 2013;310(4):416–423.
Strain JJ, Diefenbache A. The adjustment disorders: The conundrums of the diagnoses. Compr Psychiatry. 2008;49:121.
Strain JJ, Friedman MJ. Considering adjustment disorders as stress response syndromes for DSM-5. Depress Anxiety.
2011;28:818.
Zimmerman M, Martinez JH, Dalrymple K, Chelminski I, Young D. “Subthreshold” depression: Is the distinction between
depressive disorder not otherwise specified and adjustment disorder valid? J Clin Psychiatry. 2013;74(5):470–476.