PTSD

Editors: Sadock, Benjamin J.; Sadock, Virginia A.; Ruiz, Pedro

Title: Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition

Copyright 2009 Lippincott Williams & Wilkins

> Table of Contents > Volume II > 28 - Special Areas of Interest > 28.9 - Posttraumatic Stress
Disorder

28.9

Posttraumatic Stress Disorder

Richard J. McNally Ph.D.

Introduction

Posttraumatic stress disorder (PTSD) is an anxiety disorder comprising three clusters of

symptoms that can develop following a person's exposure to a traumatic event.

PTSD is unusual among the syndromes listed in the text revision of the fourth edition of the
Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) in that one of its criteria
specifies an etiological event: Exposure to a traumatic stressor (Table 28.9-1). Unlike the other
anxiety disorders, whose focus of concern is threats looming in the future (e.g., impending heart
attack in panic disorder; concern about embarrassment during a forthcoming speech for social
anxiety disorder), the central focus in PTSD concerns preoccupation with threats that occurred in
the past. Hence, PTSD is a disorder driven by pathogenic memories of past danger.

Definition

The DSM-IV-TR defines PTSD as follows:

The essential feature of Posttraumatic Stress Disorder is the development of characteristic

symptoms following exposure to an extreme traumatic stressor involving direct personal
experience of an event that involves actual or threatened death or serious injury, or other threat to
one's physical integrity; or witnessing an event that involves death, injury, or a threat to the
physical integrity of another person; or learning about unexpected or violent death, serious harm,
or threat of death or injury experienced by a family member or other close associate (Criterion
A1). The person's response to the event must involve intense fear, helplessness, or horror (or in
children, the response must involve disorganized or agitated behavior) (Criterion A2). The
characteristic symptoms resulting from the exposure to the extreme trauma include persistent
reexperiencing of the traumatic event (Criterion B), persistent avoidance of stimuli associated
with the trauma and numbing of general responsiveness (Criterion C), and persistent symptoms
of increased arousal (Criterion D). The full symptom picture must be present for more than 1
month (Criterion E), and the disturbance must cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning (Criterion F).

PTSD is unusual among the DSM-IV-TR syndromes, in that its diagnostic criteria specify an
etiological event: Exposure to a traumatic stressor.

History

Clinicians have long known that traumatic events can produce psychiatric symptoms in many
people. During World Wars I and II, they had described stress-related syndromes such as shell
shock and battle fatigue. Most doctors believed, however, that these reactions dissipated soon
after the soldier left the battlefield, unless he had pre-existing vulnerability or psychopathology.

The Political History of PTSD

The psychiatric consequences of the Vietnam War altered this traditional view. During the war,
psychiatric casualties were uncommon compared to previous wars. The rate of breakdown was
only 12 per

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1,000 men, whereas the rate was 37 per 1,000 during the Korean conflict, and it got as high as
101 per 1,000 during World War II. Moreover, among the psychiatric casualties occurring in
Vietnam, only 3.5 percent had a diagnosis of combat exhaustion.

In striking contrast to the low rate of mental disorder during the war, many individuals returning
from Vietnam began experiencing serious and persistent problems after re-entering civilian life.
Prominent antiwar psychiatrists concluded that the Vietnam War had produced a new kind of
stress disorder, one with a delayed onset and a chronic course. Moreover, instead of viewing
troubled veterans as suffering from pre-existing conditions merely exacerbated by the war, these
psychiatrists became convinced that the war alone was the causal culprit.

During the late 1970s, these doctors joined forces with leaders of Vietnam veterans'
organizations to lobby the American Psychiatric Association (APA) for the inclusion of a post-
Vietnam syndrome diagnosis in the forthcoming DSM-III. Their chief concerns were to ensure
that troubled veterans were eligible to receive treatment from the Veterans Administration (VA)
and service-connected disability payments for their war-related psychiatric problems. The DSM-
II contained no single stress-related diagnosis that could accommodate a profile of delayed
symptoms. Because Congress lists the disorders for which the VA provides compensation, the
absence of a relevant diagnosis disqualified veterans suffering from post-Vietnam syndrome
from receiving treatment and disability payments. Moreover, the VA pays only for conditions
whose onset begins either during the individual's military service or within 1 year after the
individual leaves the military.

The DSM-III task force was initially skeptical of the lobbyists' arguments for this new diagnosis.
Some task force members thought that the problems of veterans were already covered by
combinations of several traditional diagnoses. Moreover, the task force was endeavoring to
develop a descriptive diagnostic system that was relatively free of often-controversial etiological
assumptions. Yet etiology was at the very core of the post-Vietnam syndrome, and the etiological
event was confined to a specific period in history at that.

The eventual success of these lobbying efforts required a change in strategy. Rather than
claiming that the syndrome was unique to Vietnam veterans, advocates for the diagnosis made
common cause with clinical researchers who had worked with victims of rape, natural disaster,
and the Holocaust. A consensus emerged among these professionals that any terrifying, life-
threatening event occurring outside the boundary of everyday experience could produce a
chronic syndrome akin to that suffered by the traumatized Vietnam veteran. A key member of the
DSM-III task force agreed with this view, noting how she had witnessed strikingly similar
symptoms in her patients who had suffered from extreme burns. Advocates dropped the term
post-Vietnam syndrome and replaced it with posttraumatic stress disorder.

When PTSD entered the DSM-III in 1980, Congress listed it as a disorder compensable by the
VA. Moreover, because DSM-III stipulated that PTSD could have a delayed onset, the
requirement that a disorder had to emerge no later than 1 year after the individual left the military
was dropped. Not only did these political developments enable Vietnam veterans whose
symptoms emerged long after their return to civilian life to get treatment and disability payments,
but it also permitted troubled veterans from previous wars to secure these benefits. In 2003, for
example, the VA paid approximately $121 million each month to compensate 193,859 veterans
diagnosed with service-connected PTSD.

Early History of Trauma Syndromes

If trauma, shorn of its historical and cultural context, can produce a universal psychobiological
syndrome, then perhaps PTSD would be detectable across cultures and across time. If so, then
the suspicion that PTSD was merely a socially constructed artifact of the antiwar movement
would be refuted. Hence, to buttress the medical legitimacy

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of PTSD, scholars began to recognize its symptoms not only among the shell shock and battle
fatigue victims of World Wars I and II, respectively, but also in characters such as Hotspur in
Shakespeare's Henry IV, Part I and Achilles in Homer's Iliad. Skeptics wondered whether these
claims were anything more than an anachronistic imposition of contemporary notions onto the
long-dead victims of the distant past.

However, some symptoms often do resurface repeatedly in trauma survivors across cultures and
time, lending credence to the claim that the diagnosis identified at least something universal
about the human response to life-threatening horror. Among these symptoms were nightmares,
anxiety, exaggerated startle response, and disturbing memories.

On the other hand, scholarship has identified differences as well. Shell shock victims in World
War I displayed a range of symptoms suggestive of neurological disease, including (hysterical)
paralysis, tremor, difficulty walking, and inability to speak, that have seldom been seen since.
Troubled veterans of the Persian Gulf War complained of a bewildering array of medically
unexplained symptoms suggestive of toxic exposure.

One recent study of British military medical archives revealed that reports of flashbacks were
nearly nonexistent among psychiatric casualties of the Boer War and World War I. These
symptoms only began to appear frequently in medical archives from much later conflicts, such as
the Falkland Islands War. This study suggested that re-experiencing trauma as vivid sensory
memories may be a new form of suffering unique to a cinematic age. On the other hand, it is
possible that shell shock victims experienced such phenomena but did not express it the doctors.
The absence of evidence is not necessarily evidence of absence.

The Paradigm Shift in the Concept of PTSD

The original view was that PTSD was a normal response to an abnormal stressor. Destigmatizing
victims, this view placed the causal burden squarely on the trauma, directing attention away from
any differences among people in their vulnerability to develop the illness following exposure to
trauma. Indeed, for many years, research on risk factors for PTSD was de facto taboo. The
prevailing ideology in the field regarded any such research as blaming the victim for his or her
plight.

Yet by the 1990s, it became obvious that most people exposed to qualifying traumatic events did
not succumb to PTSD. Transient symptoms of acute distress were common, but PTSD was not.
Once PTSD was securely ensconced in the DSM, traumatologists began to study why some
trauma victims developed PTSD, whereas others did not. The result of this work was a paradigm
shift in the conceptualization of PTSD. No longer was it a normal response to an abnormal
stressor; it was now viewed as a psychopathological response to an extreme stressor. Clinical
researchers completely inverted the original paradigm without missing a beat.

Comparative Nosology
The concept of PTSD evolved from DSM-III to DSM-III-R to DSM-IV-TR. Space
considerations preclude a comprehensive account of this process. Hence, differences between
DSM-III and DSM-IV-TR are stressed.

Pros and Cons of the Changes in Symptom Criteria

Most of the symptom criteria have survived largely intact since 1980. Factor-analytic studies
affirmed that symptoms tended to cluster into the three groupings of re-experiencing,
avoidance/numbing, and increased arousal (i.e., Criteria B, C, and D). Nonspecific physiological
arousal, one of the original miscellaneous D criteria, was reconceptualized as a specific
physiological reactivity to reminders of the trauma and moved to the re-experiencing cluster.
Another original D criterion, memory and concentration problems, was divided; concentration
problems remained among the D criteria, and general memory difficulty was replaced with the
ambiguous symptom of difficulty recalling an important aspect of the trauma, a C criterion.

Criterion C3 has caused much confusion in the field. The text refers to this symptom as
amnesia, conceptualizing it as a kind of cognitive avoidance. Some clinicians have misread it
as supporting the notion that people can repress parts of their traumatic memories, presumably
because recalling these parts would be too disturbing for the person.

However, the mind does not operate like a video recorder, encoding every aspect of our sensory
experience. Therefore, memory for any eventtraumatic or otherwisewill be incomplete.
People exposed to traumatic events, especially ones that unfold very quickly (e.g., an armed
robbery), often focus their attention and encode certain aspects of the event (e.g., the robber's
gun) at the expense of other aspects (e.g., the robber's face). Hence, a failure to recall an
important aspect of the event (e.g., the robber's face) may result from a failure to encode that
feature rather than an inability to recall it (i.e., amnesia). This symptom is seldom endorsed by
trauma survivors anyway, and its ambiguous character suggests it should be omitted from DSM-
V.

Guilt about surviving a trauma when others did not or guilt about what one had to do in order to
survive has been a prominent feature of combat-related PTSD. It appeared in DSM-III but has
been absent since DSM-III-R. A sense of foreshortened future was first noticed in traumatized
children and has been included as a numbing symptom since DSM-III-R.

Criteria Designed to Distinguish Normal from Pathological Responses to Trauma

Criterion E specifies that symptoms must be present for at least 1 month, and Criterion F was
included in DSM-IV-TR to ensure that symptoms were of sufficient clinical importance to
qualify as disordered. To meet Criterion F, symptoms must either produce significant distress or
impairment in social, occupational, or other domain of functioning. Lacking a laboratory test for
PTSD akin to a bacterial culture, psychiatry must use other means to distinguish normal
emotional responses to horror from pathological ones signifying PTSD. The duration and
impairment criteria are designed to accomplish this aim, but even these requirements are not
without their limitations. For example, intense grief responses may be highly impairing, yet they
need not signal a dysfunction in an evolved psychobiological mechanism governing emotion
regulation.

Conceptual Bracket Creep in the Definition of Trauma

The most important changes have occurred in the concept of trauma itself, as embodied in
Criterion A. In DSM-III, published in 1980, Criterion A was defined as the Existence of a
recognizable stressor that would evoke significant symptoms of distress in almost everyone.
The text elaborated that the psychologically traumatic event is one that is generally outside the
range of usual human experience, and it provided the following exemplars: Rape, assault,
military combat, floods, earthquakes, automobile accidents causing serious physical injury, large
fires, airplane crashes, bombing, torture, and confinement

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to a death camp. DSM-III also provided examples of stressors that would not qualify for
Criterion A, such as simple bereavement, marital conflict, chronic illness, or business losses.

The definition of trauma is much broader in DSM-IV-TR than in DSM-III, and the notion that
the stressor must be outside the range of usual human experience was dropped as being
ambiguous (i.e., whose usual experience?). In fact, the definition of trauma has undergone a kind
of conceptual bracket creep ever since DSM-III. No longer must one be the direct recipient or
even witness of trauma; merely learning about a threat to others now qualifies. For example,
researchers assessed adults for PTSD symptoms throughout the United States following the
widely televised terrorist attacks of September 11, 2001. Subjects who understandably reacted
with horror and helplessness were deemed to have been exposed to a Criterion A trauma in that
they were confronted with a threat to the well-being of others, strangers in this case.
Researchers estimated that about 4 percent of the U.S. population even outside the attacked cities
developed apparent PTSD, caused by a kind of virtual trauma. Hence, people who react with
horror hearing about the serious misfortunes of others now qualify as trauma survivors and are
thus eligible for the PTSD diagnosis.

In one epidemiological study, 89.6 percent of adults qualified as trauma survivors, although only
12 percent of those exposed to trauma developed PTSD. In fact, researchers have found that
broadening the concept of trauma increased the life events qualifying as traumatic by nearly 60
percent.

To be sure, DSM-IV-TR also stipulates that a person must react with intense fear, horror, or
helplessness to qualify fully for Criterion A. Unfortunately, this stipulation conflates the person's
initial response to the stressor with the stimulus event that provokes the reaction.
The primary motivation for bracket creep was to ensure that people exposed to stressors
previously deemed subtraumatic would qualify for PTSD if sufficient symptoms were present.
Moreover, some scholars regard concerns about bracket creep as overblown. After all, a trauma-
exposed person must still fulfill symptomatic, duration, and impairment criteria before a
diagnosis of PTSD can be assigned. Bracket creep alone does not entail an inflated prevalence of
PTSD.

Nevertheless, conceptual bracket creep does create problems for the diagnosis. First, expanding
the concept of trauma makes it difficult to elucidate the psychobiological mechanisms mediating
symptom expression because it increases the heterogeneity among those qualifying for the
diagnosis. For example, people living in Montana who reacted with horror to televised coverage
of the September 11 terrorist attacks are unlikely to have much in common with people who
survived Auschwitz. Yet both now count as trauma survivors under DSM-IV-TR.

Second, the more we broaden the concept of trauma, the less plausibly we can impute causal
significance to the stressor itself and the more we must emphasize vulnerability factors in the
etiological account. The original definition of trauma placed the causal burden squarely on the
trauma. Risk factors for succumbing to PTSD were usually ignored entirely or thrust into the
causal background. However, diagnosing PTSD in those exposed to noncanonical stressors
woven into the fabric of everyday life produces a backgroundforeground inversion whereby risk
factors move into the causal foreground whereas the stressor recedes into the background.
Shifting the causal burden so far away from the stressor, however, undermines the very rationale
for having the diagnosis of PTSD in the first place.

Third, by viewing increasingly more of contemporary life through the lens of trauma, we may
overmedicalize normal emotional responses to stressors and may undercut resilience in the face
of adversity. If nearly every unpleasant event qualifies as a trauma, provided that the person
reacts with fear, horror, or helplessness, then trauma morphs into a trope for misfortune in
modern life and loses whatever meaning it originally had.

Epidemiology

According to the National Comorbidity Survey Replication, 6.8 percent of Americans develop
PTSD at some point in their lives. The lifetime prevalence rate is 9.7 percent in women and 3.6
percent in men. In fact, most epidemiological studies indicate that about 8 to 12 percent of the
U.S. population will develop PTSD at some point in their lives (lifetime prevalence) and that
between 1 and 3 percent will have the disorder in any given year (annual prevalence).

The conditional risk for PTSD refers to the proportion of individuals exposed to trauma who
succumb to the disorder. Clearly, this varies depending on how broadly one defines trauma. If the
concept is confined to the most horrific, personal encounters with life-threatening events, the
proportion will be higher than if it is defined broadly.
In addition, estimates of conditional risk vary depending on whether researchers ask respondents
about their reaction to a traumatic event randomly selected from among several the respondent
has experienced or whether they ask about reactions to the respondents' worse experience. For
example, a study of Detroit-area subjects indicated that the conditional probability of lifetime
PTSD was 13 percent among trauma-exposed women and 6 percent among trauma-exposed men
when researchers randomly selected a reference trauma event. These estimates rose to 18 percent
among women and 10 percent among men when they asked about reactions to the respondent's
most traumatic experience.

Epidemiologists have consistently found that the prevalence of PTSD is at least twice as great in
women as in men, despite the fact that men are exposed to more Criterion A traumatic events
than are women. Some scholars have endeavored to explain the sex difference in PTSD
prevalence by arguing that women are more often exposed to traumatic events (e.g., rape) that
are inherently more pathogenic than the ones to which men are typically exposed (e.g., combat).
However, a recent meta-analysis failed to confirm this hypothesis. Controlling for the type of
trauma (e.g., rape) did not eliminate the sex difference in PTSD. It remains unclear why women
develop PTSD more often than men in response to the same type of trauma.

The National Vietnam Veterans Readjustment Study (NVVRS) is the most influential
epidemiological study done on PTSD among war veterans. According to this study, 30.9 percent
of men developed full-blown PTSD after having served in the war, and an additional 22.5
percent developed partial PTSD, falling just short of qualifying for the disorder. The NVVRS
researchers reported that 15.2 percent still had PTSD when the study was conducted in the late
1980s.

Many specialists in the history of military psychiatry have expressed puzzlement at the
extraordinarily high rate of PTSD. Given that only about 15 percent of the men who served in
Vietnam had a direct combat role, it is surprising that the NVVRS estimated the lifetime
prevalence of PTSD as greater than 30 percent. Of course, the approximately 15 percent of men
who had served in a combat support role (e.g., medical corpsmen) also were at increased risk for
exposure to traumatic events. However, being at risk for exposure to trauma is not equivalent to
being exposed to trauma, and being exposed to trauma is not equivalent to developing PTSD.

In response to growing concerns that the original NVVRS team had overestimated the
prevalence of PTSD, one research team reanalyzed the data after doing three things, each
designed to ensure that cases identified as having PTSD really did qualify. First, they excluded
subjects who had developed PTSD either before or after the war (i.e., had onsets unrelated to the
war). Second, they excluded cases whose retrospective reports of war-related trauma could not
be corroborated

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by archival sources. Third, they used scores on the Global Assessment of Functioning scale to
ascertain whether a given veteran had more than minimal functional impairment.

These adjustments resulted in the prevalence of PTSD dropping by 40 percent (i.e., lifetime,
from 30.9 percent to 18.7 percent; current, from 15.2 percent to 9.1 percent). A slightly more
stringent definition of impairment produced a 65 percent drop in prevalence, resulting in a then-
current (late 1980s) estimate of 5.4 percent. Clearly, how one defines and measures PTSD
greatly affects estimates of its prevalence.

Recent civilian studies also show that how one defines caseness can affect prevalence estimates.
In two independent epidemiological studies, a requirement that symptoms result in impairment
lowered the prevalence of PTSD in men by 33 percent and 44 percent and in women by 25
percent and 30 percent, respectively.

The wars in Iraq and Afghanistan have reignited interest in risk for PTSD among those exposed
to combat. Among these veterans seeking health care from the VA, 13 percent have received a
diagnosis of PTSD.

Epidemiological estimates of PTSD vary widely. Using questionnaires, one research team
reported that 12.6 percent of men serving in combat units in Iraq qualified for PTSD, whereas
6.2 percent of their counterparts who had fought in Afghanistan did so. Yet another study
revealed a rate of probable PTSD of only 6 percent in British combat troops that had served in
Iraq, and another British study revealed that mental health had improved among elite troops after
they had served in Iraq. In a prospective longitudinal study of Dutch veterans of Iraq, researchers
found that whereas 21 percent of veterans met criteria for PTSD, as determined by questionnaire,
only 4 percent met criteria for war-related PTSD as defined by clinical interview.

Etiology

Characteristics of the Traumatic Stressor

Stressors of human design, such as rape and violent assault, are usually more pathogenic than
either accidental trauma or natural disaster. Sudden, unexpected, and life-threatening events are
especially pathogenic, as are those involving exposure to grotesque death.

Some studies imply a doseresponse effect whereby the likelihood of PTSD increases as a
function of stressor magnitude. Hence, a near-fatal automobile accident is more likely to result in
PTSD than a fender bender. However, valid testing of the doseresponse hypothesis can be
difficult if the measurement of stressor magnitude rests on the retrospective self-report of
victims. Studies on veterans and civilians indicate that the more symptomatic victims are
currently, the more likely they are to recall the trauma as worse than they had originally
described it to be. This recall bias can inadvertently inflate the apparent strength of the dose
response effect.

Risk Factors

Unlike risk for most psychiatric disorders, risk for PTSD entails two steps: Risk for exposure to
traumatic events, and risk for PTSD among those exposed to traumatic events. With regard to the
former, some people are more likely than others to get in harm's way. Risk factors for being
exposed to trauma include having less than a college education, being male, having a history of
childhood conduct problems, having a family history of psychiatric illness, being more
extroverted, and being more neurotic. A prospective study confirmed that elevated extroversion
and elevated neuroticism heightened risk for exposure to trauma and indicated that black subjects
were at greater risk than white ones.

Among those exposed to trauma, risk factors for PTSD include being female, neuroticism, lower
social support, lower intelligence quotient (IQ), pre-existing psychiatric illness (especially mood
and anxiety disorders), family history of mood, anxiety, or substance abuse disorders, and
neurological soft signs (e.g., nonspecific abnormalities in central nervous function).

Certain variables, such as low social support, have been assessed after individuals have
developed PTSD. Accordingly, it can be unclear whether acute PTSD symptoms alienated
potential sources of support or whether lack of support impeded resolution of these symptoms, or
both. One recent study indicated that diminished social support appears to be primarily a
consequence of posttraumatic symptoms.

Some researchers have reported that previous exposure to trauma heightens the risk for PTSD in
response to exposure to subsequent traumatic events. That is, exposure to trauma sensitizes the
person for later succumbing to PTSD (i.e., lowering the threshold for subsequent breakdown).
Unfortunately, in these studies researchers failed to assess whether victims had developed PTSD
in response to their earlier trauma. Indeed, recent work has shown that previous exposure to
trauma heightens the risk for PTSD in response to subsequent trauma only if the person develops
full-blown PTSD in response to the earlier trauma. That is, these data imply that early trauma per
se does not heighten the risk for PTSD in response to later trauma.

How victims respond during a trauma may predict whether they later develop PTSD. Of course,
researchers are seldom present to record these peritraumatic responses, and so they must ask
hours, days, or even years later how victims had responded as the trauma was unfolding.
Retrospective accounts of certain peritraumatic dissociative responses, such as feeling
disconnected from one's body or feeling as if events were occurring in slow motion, predict later
PTSD.

How victims appraise their responses to trauma may also influence whether they develop PTSD.
Certain negative interpretations of one's acute responses can predict whether someone develops
PTSD. For example, if trauma victims interpret their exaggerated startle responses and
nightmares as indicative of personal weakness or if they misconstrue flashbacks as indicative of
impending psychosis, they at increased risk for failing to recover from the acute effects of
trauma.

These findings, however, pose an interpretive problem. Researchers have conceptualized

peritraumatic responses and negative symptom appraisals as independent variables predictive of
the dependent variable of PTSD. Yet these phenomena are themselves features of the very
outcome that researchers are trying to predict.

As the foregoing review makes clear, most research on risk factors for PTSD focuses on personal
vulnerability factors. Yet interpersonal variables, such as group cohesion and morale among
combat units, may figure prominently as factors affecting whether individuals suffer psychiatric
breakdown after exposure to trauma.

Genetics

Scientists have investigated genetic influence on PTSD symptoms. One research group studied
2,092 male monozygotic (MZ) twin pairs who had served in the Vietnam War. There were 715
pairs in which one member had served in Vietnam, whereas the other member had served
elsewhere. The researchers found that the rate of PTSD was 16.8 percent in cotwins who had
served in Vietnam and 5.0 percent in their cotwins who had served elsewhere.

In a subsequent study, this research team studied 4,042 male Vietnam era MZ and dizygotic (DZ)
twin pairs to determine the relative contributions of heredity, shared environment, and unique
environment to variance in PTSD symptoms. They found that MZ twins were more concordant
for combat exposure than were DZ twins.

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Controlling for extent of combat exposure, they found that between 13 and 30 percent of the
variance in re-experiencing symptoms was associated with genetic variation. Heritability
estimates for avoidance symptoms and arousal symptoms ranged from 30 to 34 percent and from
28 to 32 percent, respectively. Measures of shared childhood and adolescent environment (e.g.,
family socioeconomic status) were unrelated to variance in PTSD symptoms. These data indicate
that as much as one third of the variance in PTSD symptoms is associated with genetic variance,
whereas the remainder is chiefly associated with unique environmental experiences (e.g., intense
combat).

Other research has likewise pointed to genetic influence on vulnerability for PTSD. One research
team administered IQ and other neurocognitive tests to MZ twin pairs. They tested four groups:
Men who had developed PTSD after fighting in Vietnam; their identical twins who had neither
been exposed to combat nor had PTSD; Vietnam combat veterans who had not developed PTSD;
their identical twins who had neither been exposed to combat nor had PTSD. The findings were
consistent: On almost everyone test, combat veterans with PTSD and their identical twins
performed very similarly, and both groups performed in the normal range. However, these
subjects did worse than did the healthy combat veterans and their cotwins. This study points to
several conclusions. First, trauma exposureat least among military personnelhas little or no
effect on measures of IQ and other tests of neurocognitive functioning. Second, the striking
similarity in the test scores between cotwins implies genetic influence on cognitive performance.
Third, because the PTSD group scored within the normal range on all but one test, above-
average cognitive ability seems to protect against PTSD among those exposed to trauma. These
findings dovetail with earlier research showing that the mean IQ of healthy combat veterans was
118, whereas the mean IQ of PTSD subjects was 105.

Other data further implicate increased cognitive ability as protective against PTSD. One
epidemiological research group obtained the IQ scores of 6-year-old children living in either the
suburbs or in the inner city. The researchers interviewed these youngsters when they were 17
years of age, assessing them for exposure to trauma and for PTSD. Relative to those with
average or low IQ scores, adolescents whose IQ at age 6 years was greater than 115 had been
exposed to less trauma, and, when they had been exposed to trauma, were less likely to have
developed PTSD. Children with below-average IQ and average IQ were at similar risk for PTSD,
thereby implying that higher IQ buffers against PTSD rather than lower IQ increasing risk for
PTSD.

Diagnosis and Clinical Features

Unlike many syndromes in DSM-IV-TR, the diagnostic criteria for PTSD do not constitute a
laundry list of symptoms. Instead, they possess an inner logic characterized by theoretically
meaningful functional interrelations. That is, exposure to a trauma establishes a pathogenic
memory manifested in Criterion B as re-experiencing symptoms of intrusive recollections,
sensory flashbacks, nightmares, and psychophysiologic reactivity to reminders. Recurrent
intrusions of the memory, in turn, motivate responses of victims to avoid stimuli likely to trigger
these involuntary rememberings of trauma, as embodied in the C criteria. Finally, symptoms of
increased arousal (D criteria) may result from either the direct consequences of traumatic fear
conditioning or from recurrent re-experiencing symptoms. It is the memory of the traumatic
stressor that unites the otherwise disparate symptoms of PTSD into a coherent syndrome. Hence,
we cannot dispense with Criterion A without dissolving the conceptual integrity of the diagnosis.

There are distinct ways in which a person may be haunted by memories of trauma. A victim
might suffer from repetitive, intrusive thoughts about the trauma, such as Why did this have to
happen to me? or suffer from repetitive, intrusive thoughts of the trauma, such as vivid, sensory
flashbacks of the event. Of interest, the concept of flashback itself has varied since DSM-III.
Early descriptions of flashbacks often concerned behavioral sequences of varying lengths of time
in which trauma survivors, often combat veterans, acted as if the trauma were recurring. Today,
however, flashbacks often denote a nonbehavioral, passive reinstatement of the sensory
impressions present during the trauma (e.g., the smell of dead bodies, the sight of blood, the
sound of screeching tires).

Criterion B4 and B5 are closely linked. Hence, a rape victim who experiences tachycardia,
trembling, and hyperventilation on encountering someone who resembles her assailant is very
likely to experience subjective distress as well. Criterion B2 refer to distressing dreams of the
event, and these sometimes produce the illusion of instant replays of the trauma.

The C criteria can be divided into symptoms that reflect deliberate attempts to avoid stimuli
likely to trigger disturbing recollections of the trauma and symptoms that reflect numbing of
emotional responsiveness. For example, war veterans may avoid Fourth of July celebrations,
where they are likely to hear firecrackers reminiscent of gunfire, or they may avoid media
coverage of current wars or geographical locales (e.g., tropical regions) similar to those where
they had fought. Whether numbing symptoms reflect unconscious avoidance is controversial.
Numbing may instead result from neurobiological emotional exhaustion resulting from the
heightened arousal, especially that consequent to re-experiencing episodes.

The D criteria are nonspecific manifestations of heightened arousal, as exemplified by war

veterans who startle at a backfiring car, who explode with rage at the slightest frustration, and
whose hypervigilance compels them to scan their immediate environment for hostile intruders.

Some researchers have suggested that PTSD is best construed dimensionally rather than
categorically. According to this view, PTSD merely represents the endpoint of a stress response
continuum, whereas partial PTSD would represent a subsyndromic degree of severity somewhere
between no or mild response and full-blown PTSD. Recent work, however, suggests that
impairment correlates do not smoothly vary as a function of increasing symptoms; those victims
who meet full criteria for PTSD are markedly more impaired than those who merely qualify for
partial PTSD, a finding more congenial to a categorical rather than a dimensional construal of the
illness.

Pathology and Laboratory Examination

Cognitive Aspects of PTSD

Psychopathologists have used both self-report and laboratory methods to investigate the
cognitive aspects of PTSD. A longitudinal study of community subjects who provided one
traumatic memory and one positive memory from the same period in their lives documented that
vividness and emotional intensity of positive memories tended to wane over the course of several
years, and their accuracyor rather the consistency of description relative to the original
description at baselinelikewise diminished. In contrast, the decline in vividness, emotional
intensity, and accuracy (consistency) was far less pronounced for traumatic memories.
Some researchers have found that victims with PTSD provide narratives of their trauma that are
more disorganized than narratives of nontraumatic events and more disorganized than the trauma
narratives

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of victims without PTSD. The degree of disorganization in trauma narratives has sometimes
predicted the severity of PTSD symptoms. Others, however, have failed to replicate this finding.
Hence, it remains unclear how often fragmentation in narrative memory is associated with
PTSD.

Trauma survivors, especially those with PTSD, exhibit difficulty retrieving specific memories
from their past in response to simple cue words. So, when asked to recall a specific personal
memory in response to the word happy, they tend to retrieve overgeneral memories denoting
either an extended period from their past (e.g., I was happy as a child) or a categorical memory
(e.g., I'm happy when I'm playing golf). In contrast, healthy control subjects seldom have
difficulty with this task, easily recalling a specific episode (e.g., I was happy on the day I got
married). Difficulty retrieving specific memories from one's past is associated with difficulty
envisioning one's future, difficulty solving problems, and difficulty recovering from depression.
Recent work suggests that overgeneral memory retrieval style results from limitations in working
memory capacity and difficulties in controlling the focus of attention. Whether these problems
result from PTSD or serve as risk factors is unknown.

Patients with PTSD complain about involuntary recollection of traumatic memories, suggesting
difficulties of attentional control. Psychologists have confirmed these complaints via objective
laboratory methods, such as the emotional Stroop paradigm. In the original Stroop task, subjects
are shown words, such as red and green, that are either printed in ink colors that match the
content of the word (e.g., red printed in red ink) or not (e.g., red printed in green ink). When
color word and ink color match, subjects easily name the colors of the ink. However, when they
conflict, subjects experience involuntary activation of the meaning of the word, as evinced by
delayed naming of the word's color.

In the emotional Stroop paradigm, subjects are asked to view words that vary in emotional
significance and to name the colors in which the words appear while ignoring the meaning of the
words. When the meaning of a word involuntarily intrudes, capturing the subject's attention
despite the subject's effect to attend to the word's color, the subject's color-naming response is
slowed down (i.e., Stroop interference). If information related to trauma is involuntarily
accessed in PTSD and difficult to inhibit, subjects with the disorder should exhibit slower color
naming of trauma words relative to other words and relative to trauma-exposed people without
PTSD.
Most experiments have confirmed the prediction of heightened Stroop interference for trauma
words in PTSD. For example, in one experiment, Vietnam veterans with PTSD, relative to
veterans without PTSD, took longer to name the colors of words related to the war (e.g.,
firefight) than to name the colors of other negative words (e.g., filthy), positive words (e.g.,
friendship), or neutral words (e.g., concrete). Similar findings have emerged for subjects whose
PTSD stemmed from rape, shipwrecks, automobile accidents, and childhood sexual abuse. Rape
victims who have recovered from their PTSD following cognitivebehavioral therapy do not
exhibit Stroop interference for trauma words. Professional actors informed about how PTSD
patients respond in this task were unable to simulate the effect. Instead of selectively slowing
their color-naming responses to trauma words, they were slower overall in their color naming,
including to control words unrelated to trauma. This study implies that the emotional Stroop
paradigm might be useful in forensic settings in which assessors need to discriminate genuine
PTSD cases from malingerers. The emotional Stroop studies illustrate how experimental
psychology methods may be used to investigate intrusive cognition in ways that do not rely on
the patient's introspective self-report.

Biological Research on PTSD

Researchers have investigated the neural mechanisms mediating the emotional Stroop effect in
PTSD. In a positron emission tomography (PET) study, researchers found that women with
PTSD linked to childhood sexual abuse, relative to victims without PTSD, had less anterior
cingulate activation during the emotional Stroop task. The groups were indistinguishable in terms
of anterior cingulate activation while they were performing the standard Stroop task. Therefore,
the activation deficit in the PTSD group was confined to the processing of trauma-related
information.

In a functional magnetic resonance imaging (fMRI) experiment, scientists discovered that

Vietnam veterans with PTSD exhibited attenuated rostral anterior cingulate activation when
exposed to war-related words in the emotional counting Stroop test. In this task, subjects view
displays consisting of one through four copies of a word that varies in emotional valence (e.g.,
firefight, firefight, firefight). They must quickly count the number of copies (in this case, three)
and push a key corresponding to this number. To the extent that their attention is involuntarily
captured by the emotional meaning of the words, their response will be slowed.

The aforementioned studies incorporating both cognitive and neuroimaging methods provided
evidence consistent with a pathophysiologic model of PTSD that highlights dysfunction in the
medial prefrontal cortex (PFC) and amygdala. The medial PFC includes medial frontal gyrus,
anterior cingulate cortex (ACC), and subcallosal cortex. The PFC's downward projections inhibit
activation of amygdala, thereby explaining why an intact PFC is essential for the extinction of
conditioned fear responses. Intrusive recollections of trauma, accompanied by heightened
physiologic arousal, are consistent with a hypoactive medial PFC, a hyperresponsive amygdala,
or both.
Prefrontal Cortical Abnormalities

Other studies provided further evidence of this pathophysiologic model. An fMRI study revealed
that PTSD subjects exhibited heightened amygdala responses and attenuated medial PFC
responses to photographs of fearful versus happy facial expressions. Indeed, signal changes in
the amygdala and symptom severity were negatively correlated with signal changes in the medial
PFC. These findings are consistent with data showing that briefly presented and backwardly
masked (subliminal) fearful faces triggered increased amygdalar responses in PTSD subjects.
Furthermore, PTSD patients have exhibited diminished medial prefrontal/anterior cingulate
activation while listening to audiotaped scripts of their traumatic experiences.

In additional to these functional abnormalities in PTSD, structural ones have been detected as
well. Researchers have also observed smaller ACC volumes in subjects with PTSD relative to
trauma victims without PTSD. Furthermore, smaller ACC volume has been associated with
more-severe symptoms in some studies, and in one of them, most subjects had recovered from
PTSD, thereby implying that diminished ACC volume may be a vulnerability factor for PTSD
among those exposed to trauma.

Hippocampal Volume

Basic animal research shows that stress hormones, such as the glucocorticoid corticosterone
(cortisol in humans), may produce atrophy in the hippocampus, a brain structure essential for
autobiographical memory. Given that PTSD is a stress disorder, might those with the disorder
also be characterized by hippocampal atrophy? Using MRI methods, researchers found that
Vietnam veterans with PTSD had

P.2657

smaller hippocampi than did nonveteran control subjects. Another study documented small
hippocampi among combat veterans with PTSD, but not among healthy combat veterans. Other
studies have likewise documented small hippocampi among adults whose PTSD was associated
with sexual and physical abuse during childhood.

Although these findings are consistent with the hypothesis that traumatic stress shrinks the
hippocampus of PTSD patients, there are reasons to question this interpretation. First, although
cortisol is the presumed neurotoxic agent in hippocampal atrophy, levels of this stress hormone
are usually in the low-normal to average range for people with PTSD.

Second, the surge of cortisol release occurring during trauma is integral to the adaptive fight-or-
flight response, and its duration is too brief to cause lasting damage.

Third, people with Cushing's syndrome, an endocrine disorder associated with chronic cortisol
output five times higher than normal, do exhibit hippocampal atrophy. However, once this
disorder is successfully treated, cortisol levels return to normal, and the hippocampus rebounds
to normal size. Hence, atrophy is reversible once cortisol levels return to the normal range.

Fourth, a landmark study of MZ twins indicated that small hippocampi signal vulnerability factor
for PTSD among trauma-exposed people. In this study, Vietnam combat veterans with PTSD
again had smaller hippocampi than Vietnam combat veterans without PTSD. However, the
identical twins of the subjects with PTSD had hippocampi just as small as their ill brothers.
Because the cotwins of the veterans with PTSD had neither seen combat nor developed PTSD,
the most likely explanation for the results was that having small hippocampi is a vulnerability
factor for developing PTSD among those individuals exposed to the trauma of combat.

Psychophysiologic Reactivity to Trauma-Related Cues

Two diagnostic criteria for PTSD are increased psychological distress and physiological
reactivity in response to reminders of the trauma. Researchers have shown that many PTSD
patients do react this way on exposure to trauma-relevant cues in the laboratory.

In one experimental procedure, subjects view an audiovisual presentation comprising a series of

photographs depicting a trauma accompanied by a soundtrack (e.g., combat in Vietnam). They
also view a control presentation involving a neutral event (e.g., a family going shopping). A
variant involves exposing subjects only to an audiotape (e.g., of battle sounds). Using these
methods, researchers found that Vietnam veterans with PTSD express psychological distress and
exhibit greater heart rate increases to the trauma cues than to the neutral ones. Some studies
showed that physiological reactivity extends to increases in blood pressure and in
electromyographic (EMG) activity reflecting muscle tension in the face.

Another procedure, used more frequently, is the script-driven imagery paradigm. Subjects are
first asked to provide a written narrative of their trauma (e.g., firefight in Vietnam), another
stressful event (e.g., a car accident) unrelated to their PTSD, a positive event (e.g., birth of one's
first child), and a neutral event (e.g., mowing the lawn last weekend). Researchers then convert
these narratives into 30-second audiotaped scripts, written in the second person, present tense.
Subjects are asked to listen to the scripts and to recall the memory prompted by each script as
vividly as possible as if it were happening again. Their physiological responses are recorded.

Script-driven imagery studies have shown that combat veterans with PTSD exhibit greater heart
rate, skin conductance responses (sweating on the hand), and facial EMG to their trauma scripts
than to than do healthy combat veterans. This effect is less pronounced when the trauma script
describes a generic combat scene than when it describes a personalized traumatic combat scene.
Psychophysiological reactivity to trauma scripts is not confined to Vietnam veterans with PTSD;
it also occurs in adults with PTSD resulting from childhood sexual abuse, combat in World War
II or the Korean conflict, horrific accidents, and terrorist attacks in Israel. Combat veterans with
anxiety disorders other than PTSD do not exhibit reactivity to their combat scripts, and healthy
combat veterans asked to fake physiological responses to trauma scripts do not match the
reactivity of genuine PTSD cases. On the other hand, one study showed that psychiatrically
healthy individuals who reported having been abducted and traumatized by space aliens revealed
marked physiological reactivity to their trauma scripts. Hence, apparently false memories, if
sufficiently emotionally intense, can incite responses strikingly similar to genuine memories of
trauma in people with PTSD.

An analysis of many studies of script-driven imagery revealed that 57 percent of people

diagnosed with PTSD exhibit physiological reactivity in the script-driven imagery paradigm,
whereas 89 percent of trauma-exposed people without the disorder do not exhibit reactivity. It is
unclear why 43 percent of trauma victims formally diagnosed with the disorder are not reactive.

Exaggerated Startle Responses

Another diagnostic criterion investigated in the laboratory is exaggerated startle response.

Researchers have assessed this response by either measuring the magnitude of the subject's EMG
eyeblink or the magnitude of the subject's heart rate response to a sudden, loud sound. Relative
to healthy combat veterans, those with PTSD exhibit larger EMG eyeblink responses to a sudden
auditory stimulus. Moreover, subjects with PTSD, both civilian and veteran, tend to exhibit
larger EMG magnitudes than do subjects with other anxiety disorders or no disorder. However,
the rate by which EMG responses decline during the course of the laboratory session to repeated
stimulus presentations does not differ between PTSD and non-PTSD groups. That is, there were
no differences in the habituation rate.

Three studies documented enhanced heart rate responses to loud tones in PTSD groups compared
to non-PTSD groups. One of these studies also revealed larger skin conductance responses,
whereas another did not. Finally, skin conductance response magnitudes habituate more slowly
in subjects with PTSD than in subjects without PTSD.

An important recent study involved an attempt to ascertain the etiology of exaggerated startle.
Researchers studied Vietnam veterans with or without PTSD, each of whom had an identical
twin who had not served in the war. The results revealed that only the PTSD group exhibited
heightened heart rate responses to the sudden, loud tones. Because the healthy cotwins of the
PTSD subjects did not exhibit exaggerated startle, the researchers concluded that this response is
a consequence of PTSD rather than indicative of vulnerability to develop PTSD.

Noradrenergic Dysregulation

Exposure to uncontrollable stressors activates the noradrenergic (NA) system, as indicated by the
increased release of norepinephrine (NE) by the brainstem locus coeruleus. Basic science studies
show that animals exposed to chronic uncontrollable stressors exhibit hypersensitivity of the NA
system, and several lines of evidence suggest that this holds for people with PTSD as well.
Indeed, the heightened autonomic
P.2658

arousal noted clinically and in the aforementioned laboratory studies is consistent with this
possibility. Direct supportive evidence comes from yohimbine challenge research involving
Vietnam combat veterans with PTSD and healthy control subjects. Yohimbine is an antagonist at
the -2 autoreceptor. Release of NE activates the autoreceptor, which then attenuates further NE
release, thereby functioning as a brake on NE release. By blocking the autoreceptor, yohimbine
permits NE to surge unimpeded. Researchers found that 70 percent of the PTSD subjects
experienced a yohimbine-induced panic attack, and 40 percent experienced an associated
flashback. Moreover, consistent with the NE dysregulation hypothesis, yohimbine produced
more-pronounced biochemical and cardiovascular effects in PTSD subjects than in control
subjects.

Differential Diagnosis

PTSD cannot be diagnosed in the absence of exposure to a traumatic stressor. Indeed, it is the
memory of trauma that generates and knits together the otherwise disparate symptoms of PTSD,
many of which overlap with other mood and anxiety disorders. Hence, identifying the
etiologically significant trauma is the crucial starting point for differential diagnosis.

The symptoms must persist for at least 1 month following exposure to the stressor, thereby
distinguishing PTSD from acute stress disorder, whose symptoms, by definition, cannot persist
for longer than 1 month. PTSD arises in response to a traumatic stressor, whereas the residual
diagnosis of adjustment disorder is suitable for people who experience anxiety, mood, or other
symptoms following exposure to a subtraumatic stressor. In addition, adjustment is diagnosable
only for individuals whose symptoms last no longer than 1 year after the stressful event.

PTSD comprises two kinds of symptoms: Those that possess intentionality (i.e., aboutness),
and those that do not. Hence, intrusive thoughts, nightmares, and flashbacks possess content
they are about the trauma, and hence possess intentionality. They are expressions of traumatic
memory. Moreover, avoidance of activities and stimuli reminiscent of the trauma possess
derivative intentionality. To avoid is to avoid something, and that something is a stimulus or
activity that evokes the memory of the trauma.

The intentional content of the aforementioned symptoms facilitates differential diagnosis by

distinguishing PTSD from other syndromes such as obsessive-compulsive disorder (OCD) and
generalized anxiety disorder. Although each of these three syndromes involves intrusive
cognition, PTSD concerns memorythe intrusion of past stressors into the present. In contrast,
OCD concerns current and future threats, such as intrusive thoughts about possible
contamination. Likewise, generalized anxiety disorder concerns envisioning and worrying about
threats that lie in the future.
Other PTSD symptoms are nonspecific. They lack intentionality but are deemed consequences of
exposure to trauma. These include loss of interest in activities, a sense of foreshortened future,
difficulty in experiencing loving feelings toward others, exaggerated startle response, difficulty
sleeping, difficulty concentrating, difficulty sleeping, and irritability. These symptoms present
two challenges during differential diagnosis. First, the assessor must determine that these
symptoms followed in the wake of trauma rather than predating exposure to trauma. Obviously,
this dating problem is not a problem for intentional symptoms, but it is for nonspecific,
nonintentional ones. Many people have sleep problems, are irritable, and so forth, and one cannot
automatically assume that the presence of these problems signifies PTSD. Indeed, a person
exposed to a trauma who exhibits irritability, difficulty concentrating, and insomnia must not be
assumed to have PTSD symptoms unless these difficulties postdate the trauma. Automatically
interpreting insomnia in a trauma victim as a symptom of PTSD makes no more sense than
calling coughing a symptom of bacterial pneumonia in the absence of a confirming culture.

The other challenge arises when assessors must determine whether apparent PTSD symptoms are
direct consequences of memory for trauma or they signify the presence of another disorder. So,
for example, sleep disturbance, irritability, difficulty envisioning one's future, loss of loving
feelings, and loss of interest in activities are common symptoms of major depressive disordera
condition often comorbid with PTSD. Likewise, other symptoms, such as hypervigilance and
startle, may occur in other anxiety disorders as well.

PTSD seldom occurs by itself. Cases of pure PTSD are extremely rare. Of course, comorbidity is
common throughout psychiatry, especially within clinical settings. For example, researchers
studying Vietnam veterans found that that 84 percent of outpatients as well as inpatients with
PTSD met criteria for comorbid conditions, often alcoholism and antisocial personality. In
another study of help-seeking veterans, researchers diagnosed current major depression, panic
disorder, bipolar disorder, and social phobia more often in among those with PTSD than among
those without PTSD.

Comorbidity is also extremely common in epidemiological samples. In the NVVRS, 98.8 percent
of the men who had a lifetime diagnosis of PTSD also qualified for at least one other mental
disorder, whereas only 40.6 percent of those without PTSD did so. The most common comorbid
disorders were alcohol abuse, depression, and generalized anxiety disorder.

Comorbidity is common in epidemiology studies of civilian PTSD as well. In one study

conducted in the Detroit area, about 80 percent of subjects with PTSD had at least one other
disorder at some point during their lives. In a representative survey of the U.S. population, the
lifetime comorbidity rates were 88.3 percent in men and 79 percent in women with PTSD. Major
depression and alcohol dependence were common comorbid conditions. Retrospectively reported
ages of onset suggested that other anxiety disorders usually predated PTSD, whereas alcohol and
mood disorders usually developed after PTSD.
Course and Prognosis

Immediately following exposure to a traumatic event, many people experience shock,

nightmares, intrusive thoughts about the trauma, and so forth. Indeed, it would be surprising if
severely traumatized people had no emotional reaction whatsoever to horrific events.
Accordingly, a diagnosis of PTSD requires symptoms that persist for at least 1 month following
the trauma.

For most people exposed to trauma, symptoms do wane. For example, in a study of help-seeking
rape victims, researchers found that found that 95 percent met PTSD symptom criteria within 2
weeks of the rape. Yet the proportion of victims who still met symptom criteria at 1, 3, and 6
months after the rape declined to 63.3, 45.9, and 41.7 percent, respectively. Among victims of
nonsexual assault, 64.7 percent met PTSD symptom criteria 1 week after the trauma, whereas the
proportion still meeting criteria at 1, 3, 6, and 9 months after the assault declined to 36.7, 14.6,
11.5, and 0 percent, respectively.

Epidemiological data from the National Comorbidity Study (NCS) indicate that the median time
for PTSD to remit is 36 months for individuals who sought help for any mental health problem
(not necessarily for PTSD, however) and about 64 months for individuals who never sought help
for a mental health problem. Approximately one third of those who qualify for PTSD had a
chronic course.

A recent review of studies concerning delayed-onset PTSD confirmed that symptom onset is
almost never delayed. This is in striking contrast to the original claim in the text of DSM-III that
symptoms

P.2659

often only surface months or years after the trauma. In some rare cases, a person may develop
immediate symptoms but fall just short of meeting full criteria for PTSD. A worsening of
symptoms several months later may result in the person finally qualifying for the diagnosis. At
first glance, this would appear to constitute a delayed onset of the PTSD syndrome, but it is not
as if the person has been wholly asymptomatic during the period following the trauma and prior
to meeting full criteria. For example, in one study of Israeli combat veterans, most cases of
apparent delayed-onset PTSD involved either exacerbation of chronic, subsyndromic symptoms
or delayed help seeking in those with chronic PTSD. For example, some veterans finally met full
criteria for PTSD after receiving notice that they were about to be reactivated for military
service.

An intense controversy has recently erupted concerning what appears to be a massive increase in
very delayed-onset (or at least delayed help-seeking) PTSD among Vietnam veterans. The
number of veterans from this cohort seeking treatment and service-connected disability
compensation for PTSD has skyrocketed. Compensation payments for PTSD increased by 148.8
percent during the years 1999 to 2004. The total number of veterans receiving compensation for
all health problems increased by 12.2 percent, whereas the total number of veterans receiving
compensation for PTSD increased by 79.5 percent.

It is unclear why so many veterans are only now seeking treatment and service-connected
disability for PTSD, decades after the trauma. Multiple factors likely play a role. First, some
aging veterans in straitened financial circumstances may frame any psychological difficulties
they may be having as PTSD related to Vietnam. Service-connected disability compensation
may provide needed financial relief, regardless of whether their psychological problems actually
reflect war-related PTSD. Second, some veterans may have had chronic subsyndromic PTSD
that worsened as they became ready to retire. These symptoms may not have caused problems
during their earlier, busy postmilitary lives. Third, others may have once had PTSD, but have
experienced a resurgence of symptoms, perhaps attributable to the aging of neural structures that
kept symptoms in check. Fourth, some veterans may only now have opted to seek help for their
unremitting PTSD.

Recent work, however, suggests that at least some individuals fabricate trauma histories,
exaggerate symptoms, or both. An investigation of VA patients conducted by the federal Office
of the Inspector General (OIG) indicated that the modal veteran in this recent compensation-
seeking cohort deteriorates psychiatrically despite remaining in treatment but then terminates
treatment after achieving 100 percent service-connected disability. Most of these individuals,
however, continue to receive nonpsychiatric medical care. In another study, however, there was
no association between achievement in 100 percent disability compensation and decline in
mental health visits.

In one especially unsettling study, clinical researchers endeavored to corroborate reports of

trauma exposure conveyed to assessing VA clinicians by consulting each patient's DD-201
personnel file. The subjects were 100 men who had recently sought treatment and often service-
connected disability for PTSD arising from their service in Vietnam; 94 had received the PTSD
diagnosis. The DD-201 provided data consistent with reports of combat trauma in only 41
percent of the cases. The researchers found that 7 percent of the cases had either never served in
Vietnam or had never even been in the military at all. Although no source of data is infallible,
and although some men may have experienced PTSD trauma that failed to be reflected in the
DD-201, epidemiologists, using the DD-201 alone, corroborated 86 percent of the PTSD cases
they studied in the NVVRS. Moreover, many of the uncorroborated cases in the clinical study
had DD-201 files that were inconsistent with self-reported combat trauma. Indeed, the
uncorroborated cases claimed exposure to battlefield atrocities at twice the rate of corroborated
cases, and many of the former cases claimed highly implausible trauma (e.g., a cook who
claimed having been imprisoned in the Hanoi Hilton and whose name was not among the men,
many of them aviators, listed on the POW register).
Some researchers have called for excluding compensation-seeking cases from basic and applied
research studies on PTSD. This guideline, however, would rule out many potential research
subjects; as many as 94 percent of war veterans in the VA system are seeking service-connected
disability for PTSD.

Treatment of PTSD

Early Intervention

In view of the emotional and financial costs of chronic PTSD, it would seem wise to intervene
early to prevent the emergence of a chronic, treatment-refractory illness. Psychological
debriefing is an early intervention method designed to reduce acute distress in trauma survivors
and to prevent subsequent psychiatric morbidity. Usually delivered in a several-hour session
involving either a single trauma survivor or a group of trauma survivors, debriefing entails
educating survivors about common acute stress symptoms in an effort to depathologize and
destigmatize them. Each survivor is then asked to describe his or her experience during the
trauma so that an emotional catharsis occurs. The idea is that bottling up one's feelings and
adopting the posture of the stiff upper lip will likely cause emotional problems down the road.

Most research indicates that victims who undergo psychological debriefing within a few days of
the trauma express positive feelings about the debriefing. However, controlled research has
shown that debriefing either fails to reduce morbidity or impedes natural recovery from the acute
symptoms of trauma. Hence, despite the face validity of the procedure and its congruence with
widely held beliefs (e.g., expressing one's emotions to others is advisable), most experts now
recommend against compelling people to engage in these group cathartic experiences in the
wake of trauma.

Given that the pressure to do somethinganythingin the wake of trauma, mental health
professionals are now advising a screen, watch, and wait policy. The idea is to conduct a brief
symptom survey in the hope of identifying people who are unlikely to recover from the acute
effects of trauma on their own and who therefore may require professional clinical attention soon
afterward. Rather than treating all survivors with a debriefing interventiona procedure wasteful
of time and professional resources and potentially counterproductive screening to identify
those at risk is being recommended. Recent work on screening of veterans returning from Iraq
has been disappointing. Short PTSD symptom assessments have identified veterans who do well
at follow-up and have failed to identify many who later sought help on their own. Given that
most people exposed to trauma will not develop PTSD, most screening procedures will almost
always yield a high false-positive rate, identifying individuals who will not actually need
professional help. The alternative to screening is to treat victims who develop PTSD and to do so
early in the course of the illness.

Psychological Treatment of PTSD

In 2007, the Institute of Medicine (IOM) released a comprehensive study designed to ascertain
what treatments for PTSD had convincing evidential support. The report was requested by the
VA in view of the increasing number of new PTSD cases anticipated to be arriving from the wars
in Iraq and Afghanistan. The committee conducting the review confined its attention to
randomized, controlled trials (RCTs).

P.2660

They located 53 RCTs concerning various psychotherapeutic treatments. However, even these
RCTs varied greatly in methodological quality, and the committee's assessment of their probative
weight was adjusted accordingly.

The largest group of psychotherapy RCTs concerned cognitivebehavior therapy (CBT)

involving exposure to traumatic memories, exposure to avoided stimuli associated with those
memories, or both. The imaginal exposure component requires patients to close their eyes and
imagine the trauma as if it were happening again and to describe aloud the sequence of events
and what they were thinking, feeling, and doing at the time. Repeated imaginal relivings
typically resulted in a decline in self-ratings of distress. Just as watching a frightening movie
again and again results in the loss of its ability to provoke fear, structured, systematic, repeated
imaginal exposure to the feared and avoided memory diminishes its evocative power. Because
many patients avoid stimuli and activities associated with the trauma, therapists have them
gradually confront these situations until their discomfort eases (e.g., driving in increasingly busy
traffic for a patient whose PTSD arose from a motor vehicle accident).

The committee concluded that the evidence is sufficiently strong to indicate the efficacy of
exposure therapies for the treatment of PTSD. Some of the CBT trials also included cognitive
restructuring or provision of coping skills training. Studies, however, have not provided
convincing evidence that the addition of these elements bolsters the efficacy of exposure therapy
per se.

The committee also scrutinized RCTs on eye movement desensitization and reprocessing
(EMDR). EMDR requires patients to evoke the memory of the trauma while simultaneously
moving their eyes back and forth while tracking the moving finger of the therapist. Although
EMDR also involves systematic imaginal exposure, albeit in much shorter, repeated doses than
in the prolonged exposure described in the preceding paragraphs, debate about its distinctiveness
led the IOM committee to evaluate its efficacy separately from conventional exposure therapy.

The committee concluded that the RCT evidence is inadequate to ascertain the efficacy of
EMDR for the treatment of PTSD. The committee members drew similar conclusions about
RCTs emphasizing cognitive restructuring per se and coping skills training. They also concluded
that the evidence is inadequate to determine the efficacy of therapies delivered to groups of
PTSD patients. They did not conclude that these interventions were inefficacious. Rather, they
concluded that the evidential base was too ambiguous to draw any firm conclusions. The
committee stated that RCTs of much better methodological quality are urgently needed. Finally,
the committee noted that most trials concerned civilian PTSD, and they noted that some evidence
seemed to suggest that civilian PTSD is more responsive to treatment than is PTSD among
chronically ill war veterans.

Psychopharmacology

The IOM committee located 37 psychopharmacology RCTs. It concluded that the evidence is
inadequate to ascertain the efficacy of the following medication types for PTSD: Alpha-
adrenergic blockers (e.g., prazosin), anticonvulsants (e.g., topiramate), novel antipsychotics (e.g.,
olanzapine, risperidone), benzodiazepines (e.g., alprazolam), and monoamine oxidase inhibitors
(e.g., phenelzine, brofaromine).

The committee also reached the same conclusion with regard to the selective serotonin reuptake
inhibitors (SSRIs). Although there were 14 RCTs testing the efficacy of these medications (e.g.,
sertraline, fluoxetine, paroxetine, citalopram), 7 studies were only weakly informative because of
interpretive limitations such as high or differential dropout rates across conditions and subpar
handling of missing data. Moreover, the effects of SSRIs were inconsistent: Seven studies
documented a significant effect, whereas the other 7 did not. The committee members identified
the 7 studies with the fewest limitations and found that 2 of 2 studies on veterans were negative,
and 3 of 4 studies on civilians were positive and 1 was negative. Another study comprising a mix
of veteran and civilian patients was positive.

In summary, a form of CBTexposure therapyhas sufficient evidence for efficacy, especially

in civilian PTSD. As for other psychotherapies and medication, the IOM committee regards the
jury as still out.

Suggested Cross-References

The reader is referred to Chapter 14 on anxiety disorders, Chapter 13 on mood disorders, Section
7.3 on signs and symptoms in psychiatry, and Section 9.1 on psychiatric classification.

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