Annu. Rev. Psychol. 2003. 54:229–52
Copyright c ? 2003 by Annual Reviews. All rights reserved
First published online as a Review in Advance on August 6, 2002
PROGRESS AND CONTROVERSY IN THE STUDY
OF POSTTRAUMATIC STRESS DISORDER
Richard J. McNally
Department of Psychology, Harvard University, 33 Kirkland Street, Cambridge,
Massachusetts 02138; e-mail: firstname.lastname@example.org
PTSD, trauma, memory, childhood sexual abuse, repression, Vietnam
controversy as well as progress. This article concerns the evidence bearing on the most
problems with the dose-response model of PTSD, distortion in the recollection of
stressor, risk factors for PTSD, possible brain-damaging effects of stress hormones,
recovered memories of childhood sexual abuse, and the politics of trauma.
Research on posttraumatic stress disorder (PTSD) has been notable for
INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229
THE EMERGENCE OF POSTTRAUMATIC
STRESS DISORDER . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 230
CONCEPTUAL BRACKET CREEP IN THE
DEFINITION OF TRAUMA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231
PROBLEMS WITH THE DOSE-RESPONSE MODEL
OF POSTTRAUMATIC STRESS DISORDER . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 232
DISTORTION IN THE RECOLLECTION OF TRAUMA . . . . . . . . . . . . . . . . . . . . . 233
THE SPECTER OF THE “PHONY COMBAT VET” . . . . . . . . . . . . . . . . . . . . . . . . . 234
GUILT, SHAME, AND TRAUMA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
RISK FACTORS FOR POSTTRAUMATIC
STRESS DISORDER . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
DOES TRAUMATIC STRESS DAMAGE THE BRAIN? . . . . . . . . . . . . . . . . . . . . . . 239
RECOVERED MEMORIES OF SEXUAL ABUSE . . . . . . . . . . . . . . . . . . . . . . . . . . 241
THE POLITICS OF TRAUMA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245
Research on anxiety disorders has increased dramatically since the early 1980s
(Norton et al. 1995). The scientific literature is now vast, defying ready mastery,
and even the finest, most ambitious works of scholarship are unavoidably synoptic
about these syndromes, but with progress comes controversy, and the field has had
(PTSD). My purpose is to examine the evidence bearing on the most contentious
issues in the field of traumatic stress studies.
THE EMERGENCE OF POSTTRAUMATIC
Military psychiatrists have always recognized that horrific events could trigger
acute stress symptoms in previously well-adjusted individuals (Shephard 2001)
but most doctors believed these reactions subsided soon after the soldier left the
battlefield (Wilson 1994). This conventional wisdom changed in the wake of the
Vietnam War. Antiwar psychiatrists, such as Robert Lifton, argued that many
veterans continued to suffer severe stress symptoms long after having returned
home (Scott 1990). Other veterans, they said, appeared well adjusted upon return
to civilian life, only to develop a delayed stress syndrome months or years later.
Because there was no place in the existing diagnostic system for either a chronic
stress syndrome or a delayed one, these psychiatrists lobbied for inclusion of
“post-Vietnam syndrome” in the forthcoming third edition of the Diagnostic and
believed that certain features of this war—such as difficulty telling friend from
foe, atrocities, and unclear military goals—made it especially likely that it would
produce long-lasting psychiatric illness.
Members of the DSM-III task force were reluctant to endorse a diagnosis tied
specifically to a historical event. Yet they eventually relented when veterans’ ad-
vocates persuaded them that the same stress syndrome occurred in survivors of
other traumatic events, such as rape, natural disaster, or confinement in a con-
centration camp. Converging clinical evidence, pointing to a common syndromic
consequence of trauma, clinched the inclusion of PTSD in DSM-III.
Ironically, historical scholarship has now confirmed that psychiatric casualties
was only 12 cases per 1000 men. In contrast, the rate of psychiatric breakdown
a former member of Vietnam Veterans Against the War, has argued that advocates
for the PTSD diagnosis inappropriately medicalized political dissent when they
conceptualized the problems of veterans as a form of mental illness (Lembcke
1998, pp. 101–26).
In any event, the DSM-III defined PTSD as a syndrome erupting in response
to a “stressor that would evoke significant symptoms of distress in almost every-
one” (APA 1980, p. 238). The diagnosis comprised three symptom clusters. The
re-experiencing cluster included recurrent intrusive thoughts about the trauma,
traumatic nightmares, and “flashbacks.” The numbing cluster included feelings of
detachment from others, loss of interest in activities, and constricted affect. The
third cluster included miscellaneous symptoms such as exaggerated startle, sleep
disturbance, and memory impairment or trouble concentrating.
The ratification of PTSD as a formal psychiatric disorder triggered an outpour-
ing of research on trauma and motivated the founding of the International Society
for Traumatic Stress Studies and the establishment of scholarly journals devoted
to the topic (e.g., Journal of Traumatic Stress, launched in 1988). The field has
been enriched by the efforts of clinical scientists specializing in trauma, and their
findings have placed into sharp relief several contentious issues.
CONCEPTUAL BRACKET CREEP IN THE
DEFINITION OF TRAUMA
PTSD is unusual among DSM syndromes in that the diagnostic criteria specify an
rape, and earthquakes as the kind of event capable of causing the disorder. How-
ever, DSM-IV defines traumatic exposure as “the person experienced, witnessed,
or was confronted with an event or events that involved actual or threatened death
or serious injury, or a threat to the physical integrity of self or others,” and which
evoked “intense fear, helplessness, or horror” (APA 1994, pp. 427–28, emphasis
the definition of a traumatic stressor. For example, a person who merely learns
about someone else being threatened with harm qualifies as having been exposed
to trauma and is therefore eligible for a PTSD diagnosis (assuming fulfillment of
By broadening the definition of traumatic stressor, DSM-IV codifies a kind of
conceptual bracket creep. No longer must one be the direct (or even vicarious)
recipient of trauma; merely being horrified by what has happened to others now
distinct from being subjected to artillery bombardment for days on end while hud-
dled in a muddy trench. Yet prevailing nosologic practice brackets both kinds of
underlying symptomatic expression.
Noting that a traumatic stressor need not be life-threatening, Avina &
O’Donohue (2002) have recently argued that repeatedly overhearing jokes in the
workplace may qualify as a stressor that triggers PTSD. PTSD induced by re-
peated exposure to sexual jokes and, of course, other more serious forms of sex-
ual harassment in the workplace provides the justification for lawsuits to secure
Overhearing obnoxious sexual jokes in the workplace may provide a legal basis
for litigation, but it seems unlikely to produce the same psychobiological state of
PTSD as violent rape.
Conceptual bracket creep was strikingly evident in the recent national survey
2001 terrorist attacks (Schuster et al. 2001). After interviewing a representative
sample of 560 adults throughout the United States, Schuster et al. concluded that
44% of Americans “had substantial symptoms of stress” (p. 1507), ominously
adding that the psychological effects of terrorism “are unlikely to disappear soon”
(p. 1511) and that “clinicians should anticipate that even people far from the
attacks will have trauma-related symptoms” (p. 1512). This research team asked
respondents whether they had experienced any of five symptoms “since Tuesday”
(i.e., September 11, 2001). Respondents were asked to rate each symptom on a
five-point scale ranging from one (“not at all”) to five (“extremely”). A person
qualified as “substantially stressed” if he or she assigned a rating of at least four
bit” of anger at Osama bin Laden qualified as substantially stressed. As Wakefield
reactions by failing to discriminate between genuine symptoms of disorder and
normal distress reactions.
PROBLEMS WITH THE DOSE-RESPONSE MODEL
OF POSTTRAUMATIC STRESS DISORDER
Pavlovian fear conditioning (e.g., Keane et al. 1985b). Hence, traumatic stressors
of fear. Accordingly, they believe that a laboratory rat’s reaction to inescapable
shock exacerbates a rat’s conditioned fear, so should increasing severity of trauma
exacerbate a victim’s PTSD symptoms.
Some studies are consistent with this prediction. For example, a greater propor-
tion of World War II combat veterans who had been tortured by the Japanese as
prisoners of war (POWs) have current PTSD (70%) than do those who had never
been captured and tortured (18%) (Sutker et al. 1993). Ex-servicemen wounded
in Vietnam are two to three times more likely to have PTSD than are those who
returned unharmed (Kulka et al. 1990, p. 54). Proximity to the epicenter of an
earthquake predicted severity of PTSD symptoms (Pynoos et al. 1993), and the
higher the rate of wounds and fatalities within a combat unit, the higher the rate
of psychiatric casualties (Jones & Wessely 2001).
Bowman 1997, 1999). The relationship between dosage of trauma and resultant
psychopathology is far from straightforward. For example, objective measures of
(and other) accidents (Schnyder et al. 2001), and the number of torture episodes is
(Ba¸ soˇ glu et al. 1994). Of course, the relationship between dose and response
might be nonlinear (Harvey & Yehuda 1999). That is, if PTSD symptoms reach
near maximum severity after a certain dosage of exposure, further exposure might
not add much to existing levels of psychiatric impairment. For example, a person
who is tortured twice may have more symptoms than someone who had never
been tortured. Yet a person who has been tortured a dozen times may be no more
dose-response model in nonlinear terms, any pattern between dose and symptoms
would be interpretable as confirming the model (except, of course, a linear one).
DISTORTION IN THE RECOLLECTION OF TRAUMA
Data are not the only source of trouble for the dose-response model of traumatic
stress. It is plagued by serious measurement difficulties as well. The animal con-
ditioning laboratory provides the conceptual basis for the model, but calibrating
stressor magnitude in trauma studies is vastly more complicated than in Pavlovian
conditioning experiments. Laboratory stressors are measurable in purely physical
of shocks). Yet in the trauma field, researchers usually rely on the retrospective
self-reports of the survivors themselves as the sole basis for measuring stressor
magnitude. This practice presupposes that psychiatrically distressed individuals
can furnish reliable, objective accounts untarnished by clinical state. Scientists
have recently shown just how unwarranted this presupposition is.
Several studies show that a survivor’s current clinical state affects how he or
she remembers the traumatic experience. Longitudinal studies on staff present at
a fatal shooting at an elementary school (Schwarz et al. 1993), Gulf War veterans
(Southwick et al. 1997), automobile accident survivors (Harvey & Bryant 2000),
and former military peacekeepers who had served in Somalia (Roemer et al. 1998)
researchers obtained self-reports of traumatic events on two occasions. The more
the traumatic experience to have been. For example, Southwick et al. found that
88% of Gulf War veterans remembered their traumatic events differently at time
two than how they had originally reported them two years earlier. Seventy-percent
recalled a traumatic event at time two that they had not mentioned at time one (one
month after the war), whereas 46% failed to mention a traumatic event at time two
that they had mentioned at time one. The severity of PTSD symptoms at time two
significantly predicted the number of traumatic events mentioned at time two that
were not mentioned at time one. Southwick et al. (1997) concluded that veterans
with higher PTSD scores “tend to amplify their memory for traumatic events over
time” (p. 176).
It is unlikely that the trauma survivors in these studies were lying. Rather,
traumatic memories, like all autobiographical memories, are reconstructed from
retrieval, including clinical state, affects how these recollections occur. Although
scientists, who study fear conditioning in rats, once believed that emotional mem-
ories are indelible (LeDoux et al. 1989), they have recently discovered that even
these memories are subject to alteration (Morrison et al. 2002). What is true for
rats is even more true for people. Although people retain traumatic memories very
well, even recollections of the most horrific events are not immune to alteration of
time (McNally 2003).
THE SPECTER OF THE “PHONY COMBAT VET”
The aforementioned studies concern benign memory distortion, not dishonesty,
but two other issues have come to the fore in the trauma field that pose greater
problems than mere “normal” memory change. One problem concerns deliberate
sis (Frueh et al. 2000). As many as 94% of veterans with PTSD apply for financial
compensation for their illness (McGrath & Frueh 2002), and the incentive to do so
is strong, especially for those with limited occupational opportunities (Mossman
1994). A veteran who obtains a service-connected disability rating of 100% for
PTSD can earn more than $36,000 per year, tax-free and indexed to inflation, for
life (Burkett & Whitley 1998, p. 236). The financial loss is substantial should they
ever recover from PTSD. This incentive structure does not mean that most PTSD
veterans are malingerers. However, the ease of faking symptoms and the incen-
tives for doing so should worry researchers, who need to ensure that subjects in
their studies really do have the disorder. This problem is not confined to Vietnam
veterans. The risk of malingered PTSD arises in civil suits following accidents in
civilian life as well (e.g., Rosen 1995).
The second problem concerns men who claim to be suffering from combat-
related PTSD but who either never saw combat, never served in Vietnam, or never
served in the military at all. In their award-winning book, Stolen Valor, Vietnam
veteran B.G. Burkett and investigative journalist Glenna Whitley thoroughly doc-
umented seemingly countless cases of “phony combat vets” (Burkett & Whitley
1998). By obtaining military records, via the Freedom of Information Act, of men
whose names had appeared in public (e.g., leaders of veterans’ organizations, the
actor Brian Dennehy), Burkett & Whitley discovered much fraud. Some alleged
of the American Ex-POW Association, they discovered that nearly 30% of those
claiming to have been held captive by the North Vietnamese were never POWs
(Burkett & Whitley 1998, pp. 502–3). The men investigated by Burkett & Whitley
to trauma itself. Burkett & Whitley estimated that about 75% of those “receiving
PTSD compensation are pretenders” (Burkett & Whitley 1998, p. 279).
Given that a vast amount of what we know about PTSD is based on the reports
of Vietnam veterans, clinical researchers need to attend to the issues raised by
Burkett & Whitley. They recommend obtaining military records directly from the
National Personnel Records Center in St. Louis to verify self-reports of combat
exposure rather than merely relying on a photocopy of the DD-214 furnished by
the veteran himself. The DD-214 is a military transcript, issued to each veteran
upon his discharge. It lists his military occupational specialty, receipt of awards
(e.g., Combat Infantryman’s Badge, Purple Heart), and dates of service. At most,
PTSD researchers have usually required only that the veteran furnish a photocopy
of his DD-214 as proof of combat exposure, but there are two problems with this
procedure. First, one can easily forge combat-related items on the DD-214 by, for
example, typing “Purple Heart” on the form. Second, the clerk-typists responsible
for completing these forms when a soldier was discharged sometimes failed to
include relevant items on the DD-214. Hence, DD-214s may either overestimate
or underestimate combat exposure. A veteran’s complete military file is much less
vulnerable to these validity problems.
to a persistent urban legend in the traumatic stress field, the fire that erupted in the
National Personnel Records Center on July 12, 1973 did not destroy the files of
Vietnam veterans (Stender & Walker 1974). Not only were the damaged records
those of men who served before the Vietnam era, but government archivists were
able to reconstruct 94% of them by relying on microfilm and archives stored
their top-secret, covert operations from their record. In reality, details of the covert
mission will be redacted, leaving only the dates of the mission and the phrase
“Classified Assignment.” However, the special training requisite for membership
in elite units assigned to covert operations (e.g., the Green Berets) is not redacted
(Burkett & Whitley 1998, pp. 285–86).
Burkett & Whitley believe that many studies of combat-related PTSD are con-
trauma. They are especially critical of the National Vietnam Veterans Readjust-
ment Study (NVVRS), an epidemiologic survey that yielded a lifetime PTSD
prevalence rate of 30.9% among men who had served in Vietnam (Kulka et al.
1990). This rate of PTSD is astonishingly high, given that only 15% of the men
who served in Vietnam were assigned to combat units (Dean 1997, p. 209). To
be sure, men with noncombat military occupational specialties (e.g., truck driver)
sometimes got in harm’s way and developed PTSD. But even after we allow for
the ambushed truck drivers and other trauma-exposed noncombatants, explaining
the 30.9% PTSD prevalence rate is not easy.
According to Burkett & Whitely (1998), the NVVRS is fatally flawed because
the research team failed to verify, via military records, the self-reported traumatic
events of the subjects. The NVVRS researchers will likely have an opportunity
to correct this oversight: A multimillion-dollar follow-up of the PTSD veterans
is in the works. One can only hope that researchers will verify reports of combat
exposure this time, thereby addressing Burkett & Whitley’s critique empirically.
The most important psychophysiologic study ever done on PTSD also required
only that veterans furnish a copy of their DD-214 as evidence of trauma exposure
the country, Keane et al. examined psychophysiologic reactivity to personalized,
audiotaped scripts describing actual combat events in 778 veterans with PTSD,
181 veterans with past PTSD, and 369 veterans with no history of PTSD. Relative
to combat veterans who never had PTSD, those with the disorder exhibited greater
heart rate, skin conductance, electromyographic activity (facial muscle), and di-
astolic blood pressure during autobiographical combat scripts. Similar findings
occurred during a standardized audiovisual combat presentation. Those with past
PTSD tended to fall midway between the other groups with regard to physiologic
(a) Psychophysiologic assessment may fail to detect true cases of PTSD, perhaps
because a subgroup of patients is biologically nonreactive to traumatic reminders,
large group of nonreactive subjects may have contained veterans who either exag-
gerated their symptoms or fabricated their histories of combat. Without consulting
the veteran’s military file, it is impossible to rule out any of these possibilities. If
corroborated cases of combat-related PTSD would likely result in even stronger
psychophysiologic differences between PTSD and non-PTSD groups than Keane
et al. had originally reported.
vets might have slipped into my information-processing experiments on PTSD
(McNally 1998). Following Burkett & Whitley’s suggestion, I obtained military
records from the National Personnel Records Center for 34 of my PTSD subjects.
The archival data confirmed that all were genuine Vietnam veterans. No subject,
stationed at Fort Riley, Kansas. Although the richness of the archival record varied
across subjects, evidence of combat exposure was clear for most of them. The
absence of phony vets in this small pilot study suggests that men who volunteer
for research studies are from a different pool than those who have caught the
attention of Burkett & Whitley. Indeed, Burkett & Whitley typically investigated
men whose public statements and actions seemed suspicious. Nevertheless, the
integrity of the PTSD database is at issue here, and researchers should attempt to
verify combat experience by consulting military archives whenever possible.
GUILT, SHAME, AND TRAUMA
shame, not just fear. Among Vietnam veterans, commission of atrocities predicts
1987). Even among those qualifying for a PTSD diagnosis, commission of atroc-
ities (or at least passive exposure to them) predicts severity of PTSD symptoms
et al. 1992).
underscores the moral complexity of trauma, but it exposes another limitation of
the animal conditioning model of PTSD. Although some scholars have attempted
to conceptualize atrocity involvement as a high-magnitude stressor for the perpe-
trator (March 1993), this gambit obscures important issues by reversing the roles
of victim and victimizer. Unlike fear, which can be experienced by rats, guilt and
shame are complex emotions emergent only in animals possessing a sense of self.
As Kagan (1998) has observed, one cannot “model” guilt in the rodent condition-
ing laboratory without distorting the meaning of guilt beyond recognition. Only
human beings capable of cognitive self-representation can experience complex
self-referent emotions like shame and guilt. Pavlovian animal-conditioning mod-
els that reduce trauma to its biological basis cannot capture this uniquely human
aspect of trauma.
Of course, committing atrocities can produce PTSD only if these actions vio-
late the person’s sense of right and wrong. Brutal acts that are not interpreted as
violating one’s moral code will not produce PTSD, regardless of how atrocious
they appear to others. Osama bin Laden, for example, is unlikely to develop PTSD
as a result of his orchestrating the attacks on the World Trade Center.
RISK FACTORS FOR POSTTRAUMATIC
has been exposed to traumatic stressors, but only a minority ever develops PTSD.
The National Comorbidity Survey revealed that 60.7% of a random sample of
American adults had been exposed to traumatic events, but only 8.2% of the men
and 20.4% of the women had ever developed the disorder (Kessler et al. 1995).
Among the survivors (nearly all injured) of the Oklahoma City terrorist bombing,
only 34.3% developed PTSD (North et al. 1999).
have endeavored to identify risk factors that predict the emergence of the disor-
der among those exposed to trauma (Brewin et al. 2000, Yehuda 1999, Yehuda
& McFarlane 1995). Risk factor research offends some people, who mistakenly
believe that it entails blaming the victim. Yet discovering risk factors is essential
for understanding PTSD just as it is for heart disease and other conditions. The
alternative to research is ignorance, and ignorance provides an unreliable basis for
treatment and prevention of any illness, including PTSD.
the disorder. For example, Vietnam veterans with PTSD report lower levels of so-
cial support than do those without the disorder (e.g., Keane et al. 1985a). It is
the acute stress symptoms? Or do these symptoms alienate possible sources of
social support? Or are both processes operative? However, some variables, identi-
fied cross-sectionally, are unlikely to be consequences of the illness, and therefore
may constitute risk factors. Among these are lower intelligence (McNally & Shin
1995; Vasterling et al. 1997, 2002), neurological soft signs (nonspecific behav-
ioral indicators of central nervous system impairment) (Gurvits et al. 2000), and
neuroticism (Breslau et al. 1991, McFarlane 1989). Other apparent risk factors,
albeit ascertained via retrospective self-reports, are unstable family during child-
hood (King et al. 1996), preexisting mood or anxiety disorder (Breslau et al. 1991,
Smith et al. 1990), and a family history of anxiety or mood disorder (Breslau
et al. 1991, Davidson et al. 1985). Individuals who developed PTSD in response
to trauma during adulthood have reported having been sexually (Engel et al. 1993,
Nishith et al. 2000) or physically (Bremner et al. 1993) abused during childhood.
Prospective studies designed to identify risk factors for PTSD are scarce. How-
ever, researchers have used archival data that predates exposure to trauma as a
means of identifying variables that predict PTSD among the trauma-exposed.
(i.e., Hypochondriasis, Masculinity-Femininity, Psychopathic Deviate, Paranoia)
predicted PTSD symptoms. Using predeployment military testing data, Bramsen
et al. (2000) found that negativistic personality traits predicted PTSD symptoms
among Dutch peacekeepers who were stationed in the former Yugoslavia.
Macklin et al. (1998) obtained predeployment intelligence test scores for
Vietnam combat veterans. The mean predeployment IQ for those who later de-
veloped PTSD fell within the normal range (M=106.3), whereas the mean pre-
deployment IQ for those who did not develop PTSD was well above average
(M=119.0). Lower intelligence predicted current severity of PTSD symptoms,
even after Macklin et al. statistically controlled for extent of combat exposure.
PTSD symptom severity was unrelated to differences between precombat and
current intelligence, thereby indicating that lower intelligence increases risk for
PTSD, rather than PTSD lowering current IQ scores. Stated differently, above-
average cognitive ability may enhance a soldier’s ability to cope with stressors,
thereby buffering him against developing PTSD.
Silva et al. (2000) likewise found that IQ was the best predictor of resilience
against PTSD among inner city trauma-exposed children and adolescents. These
children had been exposed to diverse traumatic events including witnessing rob-
beries, being in fires, and experiencing physical or sexual abuse. Among those
with above average intelligence, 67% had neither PTSD nor subthreshold PTSD,
or PTSD symptoms.
that predict later PTSD. These studies are not truly prospective because measure-
ment occurs after trauma exposure, but they are prospective in the sense that
measurement occurs before the person has had time to develop the disorder. Some
studies have shown that peritraumatic dissociation predicts PTSD. Time distortion
and feelings of unreality did so among trauma-exposed Israeli citizens (Shalev
et al. 1996), and time distortion and a sense of bodily distortion predicted PTSD
among French citizens exposed to violent crimes (Birmes et al. 2001). Emotional
numbing, depersonalization, motor restlessness, and a sense of reliving the trauma
predicted PTSD among survivors of automobile accidents in Australia (Harvey
& Bryant 1998). Dissociative symptoms—most commonly a sense of time slow-
ing down or speeding up—increased the risk of PTSD by nearly a factor of five
among American motor vehicle accident survivors (Ursano et al. 1999). Finally,
elevated heart rate among civilian trauma survivors, assessed in the emergency
room, predicted subsequent PTSD (Shalev et al. 1998).
DOES TRAUMATIC STRESS DAMAGE THE BRAIN?
Glucocorticoids—cortisol in primates—are released as part of the fight-flight re-
sponse. Although these stress hormones adaptively facilitate defense in the short
term, prolonged glucocorticoid exposure produces hippocampal atrophy, at least
of trauma survivors. The stress of having chronic PTSD might also wear away at
the hippocampus (Bremner 2001).
Consistent with this hypothesis, several magnetic resonance imaging (MRI)
those of matched control subjects. In one study Vietnam combat veterans with
PTSD had significantly smaller (by 8%) right hippocampi than nonveteran control
subjects (Bremner et al. 1995), and in another, those with PTSD had significantly
smaller left (by 26%) and right (by 22%) hippocampi than a combined group of
Vietnam combat veterans and healthy nonveteran control subjects (Gurvits et al.
Smaller hippocampi are not confined to veterans with combat-related PTSD.
Adult PTSD sufferers with histories of childhood physical or sexual abuse have
(Bremner et al. 1997). Women with childhood sexual abuse histories, most quali-
fying for PTSD, had significantly smaller (4.9%) left hippocampi than nonabused
control subjects (Stein et al. 1997).
Although each of the aforementioned studies is consistent with the hypothesis
that stress produces hippocampal atrophy in PTSD patients, other facts strongly
argue against this interpretation. Rather than being elevated—as the atrophy hy-
pothesis predicts—urinary cortisol levels in people with PTSD are often in the
low-normal range (Mason et al. 1986; Yehuda et al. 1990, 1995). The normal
range is 20–90 µg/day. In early studies PTSD patients usually had lower val-
ues (about 30–40 µg/day) than matched control subjects (about 50–60 µg/day)
(2001) failed to replicate their original finding of low cortisol in PTSD patients.
Ironically, the mean value for these PTSD subjects (61.3 µg/day) was nearly iden-
tical to that of the nonpsychiatric control subjects (62.8 µg/day) in one of their
in PTSD is not maintained at high levels for a sufficiently long period of time to
produce hippocampal atrophy. Short periods of very high levels of cortisol adap-
tively mobilize the person for fight or flight; only if such levels are maintained for
months or years might damage occur.
For example, because of an adrenal tumor, patients with Cushing’s syndrome
and hippocampal atrophy (e.g., 508 µg/day) (Starkman et al. 1992). However,
not only does surgical correction of the tumor normalize cortisol levels, but it
eliminates memory deficits and enables the hippocampus to rebound to its normal
size (Starkman et al. 1999).
stress shrinks the hippocampus of trauma survivors. Bonne et al. (2001) used MRI
gency room. They rescanned them six months later. By this second assessment,
10 of the 37 subjects had developed PTSD. The PTSD and non-PTSD groups did
group remained stable over the course of the 6-month period.
In a landmark study, Gilbertson et al. (2002) may have decisively refuted the
atrophy hypothesis. Using MRI, these researchers measured hippocampal volume
PTSD, whereas his brother did not serve in Vietnam and did not have PTSD. If
be smaller than those of their nontraumatized twin brothers. Although Gilbertson
et al. once again found smaller than average hippocampi in subjects with severe
PTSD, they also found that the hippocampi of nontraumatized twins were just
as small. Not only was PTSD symptom severity negatively correlated with total
severity was just as negatively correlated with the total hippocampal volume of
strongly suggests genetic influence on hippocampal volume. Because the cotwins
had not been exposed to traumatic stress, Gilbertson et al. concluded that small
hippocampi may constitute a preexisting vulnerability factor for PTSD among
the trauma-exposed. These data are consistent with studies showing that PTSD
patients report more neurodevelopmental abnormalities than do trauma-exposed
people without the disorder (Gurvits et al. 2000). Compromised neurocognitive
functioning may impede a person’s ability to cope with traumatic stressors.
RECOVERED MEMORIES OF SEXUAL ABUSE
By far the most contentious issue in the field of traumatic stress concerns the ac-
curacy of recovered memories of childhood sexual abuse (McNally 2003). In their
award-winning book, Brown et al. (1998) asserted that “approximately a third of
Accordingly, because of “massive repression” (Herman & Schatzow 1987,
p. 12), Brown et al. (1998) believe that therapists must often apply special tech-
niques to retrieve memories of trauma that presumably lie at the root of diverse
symptoms. They assert, “Because some victims of sexual abuse will repress their
in retrieving these memories. Indeed, for some victims, hypnosis may provide the
only avenue to the repressed memories” (p. 647).
Not only does hypnosis fail to enhance the accuracy of recollection, but it fosters
the production of false memories that are mistakenly experienced as accurate
(Kihlstrom 1997, Lynn et al. 1997, Steblay & Bothwell 1994).
The controversy concerning repressed and recovered memories of childhood
argue that there is no convincing evidence that people can banish and then recover
memories of horrific experiences (e.g., Pope et al. 1998), whereas others proclaim
“overwhelming scientific support for the existence of repressed or dissociated
memory” (Brown et al. 1998, pp. 538–39). What is most bizarre about this debate
diametrically opposed positions. How is this possible? Anyone who actually reads
the contested studies, however, will immediately realize that the most influential
advocates of the traumatic amnesia position misunderstand much of the science
they cite. I can only provide illustrative examples of their misreadings here; for
further analysis, see McNally (2003) and Piper et al. (2000).
For starters, consider Brown et al.’s (1999) claim that “the burden of proof is
on them [skeptics of repressed memories] to show that repressed memories do
not exist” (p. 125). They have it exactly backwards: The burden of proof lies on
Brown et al. to provide convincing evidence that people can repress and later
recover memories of trauma. For logical reasons, the skeptics cannot prove the
null hypothesis that repression does not occur.
Many studies have shown that people complain about nonspecific memory
impairment following exposure to traumatic events. This is the DSM-III symptom
misunderstand what this symptom means, mistakenly believing that it “typically
includes both hypermnesia and amnesia” (Brown et al. 1999, p. 27). In reality, it
refers to neither; hypermnesia—vivid recollections of the trauma—is, of course,
already covered by the diagnostic criterion of recurrent and intrusive recollections
of the event. DSM-III memory impairment refers to forgetfulness in everyday life
that emerges after exposure to a traumatic event; it does not refer to difficulty
remembering the traumatic event itself (i.e., traumatic amnesia).
Brown et al.’s misconstrual is immediately apparent to anyone who reads the
studies they cite in support of traumatic amnesia. For example, 88.2% of the
witnesses to the catastrophic collapse of the Hyatt Regency Hotel skywalks in
Kansas City experienced “repeated recollections” of the disaster, and 27.4% re-
ported “memory difficulties” (Wilkinson 1983). Obviously, these individuals re-
recollections might have interfered with their ability to concentrate and remember
ordinary things in everyday life.
While searching for evidence of traumatic amnesia, Brown et al. sometimes
cite findings attributable to direct physical insult to the brain as relevant to psychic
dren studied after watching lightning strike and kill a playmate had no memory
of the event” (Brown et al. 1998, pp. 609–10). Unfortunately, they fail to mention
that both children had themselves been struck by side flashes from the main light-
ning bolt, knocked unconscious, and nearly killed (Dollinger 1985). Such cases of
obvious organic amnesia are irrelevant to psychogenic, traumatic amnesia.
In yet another example, they cite the work of Wagenaar & Groeneweg (1990)
as evidence that “amnesia for Nazi Holocaust camp experiences has also been re-
camp survivors 40 years after their liberation. These investigators compared the
memory reports of former inmates with the depositions they had provided about
their trauma four decades earlier. After comparing recent recollections with the
original reports, Wagenaar & Groeneweg said that inmates exhibited “a remark-
able degree of remembering” (p. 80) of their Holocaust experiences, all the more
impressive in view of the starvation and head beatings many suffered. “There is no
Camp Erika in great detail, even after 40 years” (p. 84). So, why did Brown et al.
cite this study as indicating amnesia for Holocaust experiences? As it turns out,
several former inmates had forgotten to mention several violent events, plus other
had vividly recalled. But with one exception, each camp survivor remembered
these temporarily forgotten events after having examined their original deposi-
tions. Because autobiographical memory does not operate like a videorecorder, it
is not surprising that some of these elderly individuals did not immediately recall
every traumatic event that happened in the concentration camp.
Most of the studies adduced by Brown et al. in support of the concept of
traumatic amnesia concern sexual abuse, and most suffer from the same fatal flaw.
In the modal study (e.g., Briere & Conte 1993) sexual abuse survivors were asked
whether there was ever a time when they could not remember their abuse. Nearly
60% said “yes.” However, a reported inability to remember one’s abuse implies
unsuccessful retrieval attempts. If survivors were unaware of their abuse, on what
basis would they attempt to recall it in the first place? Obviously, the best way to
make sense out of affirmative replies to this question is to assume that survivors
interpreted the question as asking, “Has there ever been a time when you did not
as being unable to recall it.
In one of the best studies on this topic Williams (1994) and her research team
interviewed 129 women who had been medically evaluated for suspected sexual
survey, the interviewers asked questions about childhood sexual experiences and
Although 38% (n=49) of the women did not mention the index event for which
they had been taken to the hospital many years earlier, most (n=33) of them did
describe other episodes of sexual abuse. However, 16 subjects denied ever having
been sexually abused.
nesia, other explanations are plausible. Some subjects may have been too young
either to understand or remember what had happened to them. Several of the non-
reporters were under 4 years of age when they were assessed for abuse at the
hospital. Hence, ordinary childhood amnesia might have precluded their remem-
bering (or even understanding) what had happened. Also, the 16 nonreporters may
have remembered their abuse, but elected not to mention it to the interviewer. It
would have been helpful if Williams had done a follow-up clarification interview
with subjects who denied ever having been abused to determine whether they had
actually forgotten the event or whether they were merely reluctant to report it.
Femina et al. (1990) did such a study with subjects who had documented histo-
ries of physical abuse. Those subjects who had mentioned this abuse in an earlier
interview but had denied their abuse in a second interview were contacted a third
time. During the third interview they were asked to explain the discrepancy be-
tween the first and second interviews. Each subject then acknowledged having
remembered the abuse during the second interview and admitted to having denied
it for various reasons (e.g., dislike of the interviewer). Without such clarification
interviews to resolve discrepancies between official records and self-report denial
of abuse, it is impossible to distinguish between failure to report abuse and failure
to remember it.
The most intriguing evidence for recovered memories of abuse comes from
case studies in which the events have been independently corroborated (e.g., Cheit
1998, 1999; Schooler et al. 1997). However, explaining even these cases does not
for example, a girl who is fondled by a man and who does not think about this
frightening (or perhaps confusing) episode for many years. As a young woman,
she meets someone who reminds her of the perpetrator, and suddenly remembers
the experience. Such a case would constitute a recovered memory of sexual abuse,
but not repression or amnesia. That is, during the period when she had not thought
not involve any special dissociative mechanism, but they not require therapeutic
efforts to exhume presumptively repressed memories. Indeed, many people who
report recalling memories of abuse after long periods of not thinking about them
do not remember these experiences in psychotherapy (Herman & Harvey 1997,
McNally et al. 2000a). One does not need a “recovered memory therapist” to be
reminded of long forgotten episodes from one’s childhood.
Despite all the furor surrounding people who report recovering memories of
sexual abuse, research on cognitive functioning in these individuals has scarcely
begun. Our group has been conducting studies on four groups of individuals:
adults who report remembering abuse after years of not thinking about it (“recov-
ered memory” group); adults who believe they have been abused, but who have
no conscious memories of trauma (“repressed memory” group); adults who have
always remembered they had been abused (continuous memory group); and adults
memory” and “repressed memory” are in quotes because we were not in a posi-
tion to determine whether these individuals had, in fact, been abused. The terms,
however, describe their phenomenologic experience.)
ory subjects report more symptoms of psychological distress (PTSD and depres-
sion symptoms) than do continuous memory subjects (who resemble controls),
repressed memory subjects (McNally et al. 2000a). Recovered memory subjects
PTSD (McNally 1998), however, including sexually abused children with the dis-
et al. 2000b). Repressed and recovered memory subjects do not exhibit a supe-
rior ability to forget trauma-related words on a directed forgetting task (McNally
memory for material related to abuse. Moreover, childhood sexual abuse survivors
with PTSD actually exhibit impaired ability to forget trauma-related material on
this task (McNally et al. 1998). Recovered memory subjects are more prone to
exhibit false memory effects on the list learning paradigm developed by Deese
(1959) and Roediger & McDermott (1995) than are continuous memory subjects
(Clancy et al. 2000). Subjects who report having been abducted by space aliens
likewise exhibit this false memory effect in the laboratory (Clancy et al. 2002).
THE POLITICS OF TRAUMA
There is never a dull moment in the field of traumatic stress studies. Discover-
ies are continually intermixed with explosive social controversies. For example,
on July 12, 1999, members of the United States Congress unanimously voted to
condemn a scientific article on childhood sexual abuse for its alleged moral and
methodological flaws. The article contained a meta-analysis of 59 studies that had
addressed the long-term psychological correlates of childhood sexual abuse (Rind
et al. 1998). Stunning many people, the meta-analysis revealed that subjects who
had been sexually abused were nearly as well adjusted as their nonabused counter-
childhood sexual abuse. The meta-analysis indicated that childhood sexual abuse
survivors were apparently more resilient than most mental health professionals
(who see only the most traumatized cases) had ever suspected. Rind et al. took
pains to emphasize that harmfulness must not be confused with wrongfulness:
Merely because sexual abuse does not invariably produce long-term psychologi-
cal damage does not make it morally permissible.
Despite this emphasis, the article incited an uproar among many mental health
professionals, talk show hosts, and religious groups. Although scientists had rig-
orously reviewed the manuscript prior to publication, the critics assumed it must
be flawed because it ran counter to prevailing opinion. Hence, they attempted to
debunk it on methodological as well as on moral grounds. Politically conservative
radio personality “Dr. Laura” railed against Rind and his colleagues and against
the American Psychological Association for publishing the article in Psycholog-
ical Bulletin. Condemning it as “junk science at its worst,” (quoted in Lilienfeld
2002a, p. 178), she urged Congress to take formal action against the Association.
Raymond D. Fowler, Chief Executive Officer of the American Psychological As-
sociation, initially defended the scientific quality of Rind et al.’s work and the
integrity of peer review (Garrison & Kobor 2002) but when it became clear that
Congress was about to condemn the APA itself, as well as Rind et al., Fowler
(1999) abruptly reversed himself in a letter written to House Majority Whip, Tom
cations had not been considered during the review process. Fowler also promised
that the APA would “seek independent expert evaluation of the scientific quality”
of Rind et al.’s article, and would encourage “refutations from researchers and
practitioners with expertise in child sexual abuse in an upcoming issue of one of
our premier journals.”
Fowler’s apology did not save Rind and his colleagues from the wrath of
Congress. Passing unanimously, House Congressional Resolution 107 stated that
“Congress condemns and denounces” Rind et al.’s “severely flawed” article (US
House of Representatives 1999). The United States Senate unanimously approved
nation, others saw it as a serious threat to scientific freedom. Many psychologists
were outraged that the APA had capitulated to political pressure (Lilienfeld
Keeping his promise to Congress, Fowler asked the American Association for
article. But after an initial evaluation uncovered “no clear evidence of improper
application of methodology or other questionable practices on the part of the
article’s authors,” the AAAS committee declined to conduct a full-scale review,
noting that it saw no reason to second-guess an article that had already undergone
expert peer review (Lerch 1999). In fact, the AAAS sharply rebuked the critics of
the meta-analytic methods they had attacked.
Reverting to the conventional methods of scholarship, some of the critics who
et al. 2001, Sher & Eisenberg 2002). Ironically, studies on nonclinical populations
appearing since the publication of Rind et al.’s meta-analysis have uncovered
adverse consequences of childhood sexual abuse (Kendler et al. 2000, Nelson
et al. 2002).
In any event, the overriding lesson of this bizarre episode concerns the impor-
tance of maintaining a firewall between science and politics (Hunt 1999). This is
especially true whenever the topic concerns trauma and its consequences.
Preparation of this chapter was supported in part by NIMH grant MH61268
awarded to R.J. McNally.
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