ISSN 1294-8322

Dialogues in

clinical
neuroscience e
Posttraumatic Stress Disorder

2000 Volume 2 · No. 1

 Dialogues

Editor-in-chief
Jean-Paul MACHER, MD, Rouffach, France

Editorial Board
Manfred ACKENHEIL, MD, München, Germany
Cesar CARVAJAL, MD, Santiago de Chile, Chile
Marc-Antoine CROCQ, MD, Rouffach, France
Michael DAVIDSON, MD, Tel Hashomer, Israel
Margret R. HOEHE, MD, Berlin, Germany
Barry D. LEBOWITZ, PhD, Rockville, Md, USA
Deborah J. MORRIS-ROSENDAHL, PhD, Johannesburg, South Africa
Rajesh M. PARIKH, MD, Bombay, India
David RUBINOW, MD, Bethesda, Md, USA
Pierre SCHULZ, MD, Chêne-Bourg, Switzerland
Carol A. TAMMINGA, MD, Baltimore, Md, USA

Publication Director / Directeur de la Publication

Jean-Philippe SETA, MD, Neuilly-sur-Seine, France
 Editorial

D ear Colleagues,
Although the main features of posttraumatic stress disorder (PTSD) were identified as early as the first half
of the 20th century in victims of psychological trauma of the two world wars—albeit under different names, such
as shell shock or war neurosis—it is a relative newcomer in the history of psychiatry as a diagnostic entity, having
only made its way into the 3rd edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1980.
This explains why so many key issues, such as prevalence, pathogenesis, mechanisms, and treatment, remain unre-
solved to this day. Some of these are pointed out below, but the reader will surely be able to think of more:
• The prevalence of PTSD in the general population—hence the number of people liable to benefit from
treatment—is debated. The chances of escaping war trauma are reasonably fair in countries spared open
conflicts or civil war, but criminal violence, rape, child abuse, and traffic or industrial accidents are constant
threats almost everywhere, explaining why some community-based studies show prevalence figures as high
as 15%.
• PTSD should be distinguished from the acute stress reaction immediately following traumatization, as
some patients will spontaneously recover. Does this mean that, given a strong enough stressor, nobody is
immune to PTSD, or are some persons in effect more vulnerable to the disorder?
• What of the paradox that trauma caused by an exogenous stressor elicits neurochemical stigmata in the
brain just like an endogenous disorder, and that the resulting symptoms respond to biological treatment?
• What of the possible integration of PTSD into a broader diagnostic framework, in view of the resemblance
between PTSD and other disorders characterized by paroxysms of anxiety? Can the beneficial effect of
antidepressant drug treatment be taken as confirmation of the similarities between PTSD and panic attacks,
social phobias, generalized anxiety, and obsessive-compulsive disorder?
Turning to matters of more immediate practical concern, the mainstay of the management of PTSD currently
consists in the association of cognitive and behavioral psychotherapy and antidepressant drug treatment. Howev-
er, despite evidence that antidepressants are effective, many patients evolve toward chronicity. Double-blind stud-
ies with antidepressants in this indication are comparatively scarce in the literature. Studies with monoamine oxi-
dase inhibitors and tricyclics are now old, and recent ones, complying with current methodological standards, mostly
concern specific serotonin reuptake inhibitors. Drug trials are fraught with various problems, paramount among
which are duration—which must be typically up to 12 weeks—and the filtering out of the effects of potential drug
candidates on comorbid depression. Sertraline was the first compound approved for use in PTSD by the US FDA’s
Psychopharmacologic Drug Advisory Committee, in October 1999, even though studies failed to demonstrate its
efficacy in all general population samples or in the context of combat-induced PTSD. Thus, the challenge remains


to discover new drugs for the treatment of both PTSD-specific symptoms and other acute anxiety disorders.

Dialogues in Clinical Neuroscience is now entering its second year, and we are excited at the encouraging
response expressed so far by our readers. It is our sincere hope that you should contribute to the further develop-
ment of the journal, and we look forward to receiving your criticisms, questions, comments, letters, and articles.

Yours sincerely,
Jean-Paul Macher, MD Marc-Antoine Crocq, MD
1
Dialogues in Clinical Neuroscience is a quarterly publication that aims to
serve as an interface between clinical neuropsychiatry and the neuro-
sciences by providing state-of-the-art information and original insights into
relevant clinical, biological, and therapeutic aspects. Each issue addresses a
specific topic, and also publishes free contributions in the field of neuro-
science as well as other non–topic-related material.

EDITORIAL OFFICES
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Secretariat and submission of manuscripts

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Fax: +33 3 89 78 51 24 / E-mail: macrocq@forenap.asso.fr

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2
 Contents
Page

01 Editorial
Jean-Paul Macher, Marc-Antoine Crocq

05 In this issue
Marc-Antoine Crocq

07 State of the art

Posttraumatic stress disorder and the nature of trauma
Bessel van der Kolk

23 Basic research
Neurobiological findings in posttraumatic stress disorder: a review
Kumar Vedantham, Alain Brunet, Thomas C. Neylan,
Daniel S. Weiss, Charles R. Marmar,
31 Ethical aspects of research on psychological trauma
Dan J. Stein, Allen Herman, Debra Kaminer,
Solomon Rataemane, Soraya Seedat, Ronald C. Kessler,
David Williams

37 Pharmacological aspects
Update on the epidemiology, diagnosis, and treatment of
posttraumatic stress disorder
Joseph Zohar, Daniella Amital, Heidi D. Cropp,
Gadi Cohen-Rappaport, Yaffa Zinger, Yehuda Sasson

44 Posters & images in neuroscience

An overview of the Peritraumatic Distress Scale
Alain Brunet

47 Clinical research
From shell shock and war neurosis to posttraumatic stress
disorder: a history of psychotraumatology
Marc-Antoine Crocq, Louis Crocq
57 Lifelong posttraumatic stress disorder:
evidence from aging Holocaust survivors
Yoram Barak, Henry Szor
63 After the MV Estonia ferry disaster. A Swedish nationwide
survey of the relatives of the MV Estonia victims
Kristina Brandänge, J. Petter Gustavsson
71 A social interaction model for war traumatization. Self-process-
es and postwar recovery in Bosnia in subjects with PTSD and
other psychological disorders
Willi Heinz Butollo

ISSUE COORDINATED BY: Marc-Antoine CROCQ

3
Contributors
Bessel van der Kolk Kristina Brandänge, MD

Author affiliations: Human Resources Author affiliations: Psychiatric Clinic,

Institute, Trauma Clinic, Brookline, Mass, Ersta Hospital, Stockholm, Sweden
USA

Kumar Vedantham, MD

Author affiliations: Department of Psy-

chiatry, University of California, San Marc-Antoine Crocq, MD
Francisco; and Department of Veterans
Affairs, Medical Center, San Francisco,
Calif, USA
Author affiliations: FORENAP – Institute
for Research in Neuroscience and Neu-
ropsychiatry, Rouffach, France

Dan J. Stein

Author affiliations: MRC Research Unit

on Anxiety Disorders, University of Stel-
lenbosch, Cape Town, South Africa

Yoram Barak, MD

Author affiliations: Author affiliations:

Joseph Zohar, MD The Psychogeriatric Department, Abar-
banel Mental Health Center, Bat Yam;
and the Sackler Faculty of Medicine, Tel
Aviv University, Israel
Author affiliations: The Chaim Sheba
Medical Center, Division of Psychiatry
Tel-Hashomer, Israel (Joseph Zohar,
Daniella Amital, Heidi D. Cropp, Gadi
Cohen-Rappaport, Yaffa Zinger, Yehuda
Sasson); and The Sackler Faculty of Med-
icine, Tel Aviv University, Ramat Aviv,
Israel (Joseph Zohar, Yaffa Zinger).

Alain Brunet, MD Willi Heinz Butollo, MD

Author affiliations: University of Cali- Author affiliations: Chair of Clinical Psy-

fornia, San Francisco and Department chology and Psychotherapy, Department
of Veterans Affairs Medical Center, San of Psychology, Ludwigs-Maximilians Uni-
Francisco, USA versity, Munich, Germany

4
In this issue ...
Posttraumatic stress disorder and the nature of trauma
Bessel Van der Kolk
on pages 7 to 22
An alternative title for this brilliant “state of the art” article might have
been “A Century of Posttraumatic Stress Disorder.” Bessel van der
Kolk expertly recounts a hundred years of evolving concepts, from the
first stirrings of the understanding of psychological trauma, with
Charcot, Janet, Freud, and Breuer, past the fledgling diagnostic entity
of “war neuroses,” with Kardiner, to the full-blown diagnostic con-
struct of PTSD as defined in DSM-III and beyond. The emphasis given
to the recent input of the psychobiology of trauma, hormonal
responses, neuroimaging, and psychopharmacology confirms that our
“vision” of PTSD is a never-ending process…
Neurobiological findings in posttraumatic stress
disorder: a review
Kumar Vedantham, Alain Brunet, Thomas C. Neylan, Daniel S. Weiss,
Charles R. Marmar
on pages 23 to 29
This comprehensive review article takes us through the maze of the
truly mindboggling developments that have transformed the under-
standing of PTSD in recent years. Particularly important are the find-
ings concerning noradrenergic axis function, neuroendrocrine
responses, and neuroanatomic changes that occur in PTSD. A clear
view of the biological consequences of this disorder is of paramount
interest, if only because it is a prerequisite for discovering better treat-
ments.
Ethical aspects of research on psychological trauma
Dan J. Stein, Allen Herman, Debra Kaminer, Solomon Rataemane,
Soraya Seedat, Ronald C. Kessler, David Williams
on pages 31 to 36
Ethics—the sine qua non of psychiatric research—is never absent from
the numerous consensus conferences that have been organized in
recent years. The nature of trauma and the propensity for victims to
reexperience it pose critical questions in terms of therapeutic strate-
gies and the need for clinical research in this field. The recent changes
in South Africa gave psychiatrists a concrete opportunity to explore
these issues. Stein and colleagues’ trailblazing experience is a model
for further developments.
Update on the epidemiology, diagnosis, and treatment
of posttraumatic stress disorder
Joseph Zohar, Daniella Amital, Heidi D. Cropp, Gadi Cohen-
Rappaport, Yaffa Zinger, Yehuda Sasson
on pages 37 to 43
In this update, the authors attribute the continuing underdiagnosis
and undertreatment of PTSD to lack of awareness of the prevalence of
the disorder. After recalling the high frequency of traumatic events in
the general population and the main diagnostic features of PTSD, the
authors look at current therapeutic strategies, stressing the benefits of
a combined and psychopharmacological approach in view of the psy-
chobiological features of the disorder.
5
From shell shock and war neurosis to posttraumatic
stress disorder: a history of psychotraumatology
Marc-Antoine Crocq, Louis Crocq
on pages 47 to 55
The twentieth century will go down in history as a century of aston-
ishing technical prowess, but also as the century of wars. Sadly, the
many conflicts of the past hundred years have offered an unequalled
study ground for the psychological consequences of trauma.
Interspersed with historical and literary sidelights from biblical times to
the present day, this article explains how the steady rise of violence in
so many countries and cultures has meant that psychotraumatology
has now escaped from the confines of military psychiatry, and that
PTSD is being increasingly diagnosed in civilian populations.
Lifelong posttraumatic stress disorder: evidence from
aging Holocaust survivors
Yoram Barak, Henry Szor
on pages 57 to 62
The horrors of the Second World War, particularly those perpetrated
by the Nazis, have surpassed anything humanity has had the misfor-
tune to experience. After more than fifty years, the consequences of
the unclosed psychological wounds of one of the worst traumas ever
inflicted on human beings continue to haunt survivors even into old
age. This is made plain by the findings of a study carried out in elder-
ly Holocaust survivors, which led the authors to the poignant conclu-
sion that, for many, “memory is a lifelong burden.”
After the MV Estonia ferry disaster. A Swedish nation-
wide survey of the relatives of the MV Estonia victims
Kristina Brandänge, J. Petter Gustavsson
on pages 63 to 69
Major disasters, such as the sinking of the Estonia ferry in the Baltic
sea six years ago, exemplify how difficult it is for health authorities to
prepare adequate contingency plans. This disaster, like others of its
type, was compounded by the fact that the victims included not only
the survivors themselves, but also their relatives. The experience of the
Ersta Clinic in Stockholm reported in this article gives a first-hand
account of the problems encountered by Swedish psychiatrists as they
set out to help survivors and relatives cope with the aftermath of the
catastrophe.
A social interaction model for war traumatization.
Self-processes and postwar recovery in Bosnia in
subjects with PTSD and other psychological disorders
Willi Heinz Butollo
on pages 71 to 81
The war in Bosnia lays claim to the dubious honor of concluding this
“century of wars.” This article describes the multiple forms of trauma
and ensuing psychological disorders, including PTSD, suffered by Bos-
nian soldiers and civilians, and which exacted a particularly tragic toll
on children. From his experience in the field, the author draws up the
outlines of a social interaction model for war traumatization, centered
on the concept of loss of interpersonal trust, and shows how such a
model may help in developing more effective therapeutic strategies.
Marc-Antoine Crocq, MD
 World Psychiatric Association

Prix
JEAN DELAY
Awarded to:
David Paul Goldberg
In 1999, for the first time, the World Psychiatric
Association has awarded the Jean Delay prize.
This prize is intended as a reward for contributions
that forge links between clinical, biological, and
social aspects of psychiatry, or between psy-
chotherapy and pharmacotherapy.
The international jury, under the presidency of Prof
Norman Sartorius, has selected Sir David Paul
Goldberg, who was awarded a prize of $ 40000
during the opening ceremony of the XIth World
Congress of Psychiatry (Hamburg, Germany,
August 6-11,1999).

The next Jean Delay prize will be

awarded during the XIIth World
Congress of Psychiatry (Yokohama,
Japan, August 2002). Applications
or nominations of applicants,
including a cover letter and a
description of the work presented,
should be send to:
WPA Secretariat 2nd “Jean Delay prize”
International Center for Mental Health
Mount Sinai School of Medicine / CUNY
5th Avenue & 100th Street
Box 1093
New York, NY 10029-6574
USA

This prize is supported by a grant from SERVIER

State of the art
Posttraumatic stress disorder
and the nature of trauma
Bessel van der Kolk, MD
The role of psychological trauma (eg, rape, physical
assaults, torture, motor vehicle accidents) as an etiologi-
cal factor in mental disorders, anticipated as early as the
19th century by Janet, Freud, and Breuer, and more
specifically during World War I and II by Kardiner, was
“rediscovered” some 20 years ago in the wake of the psy-
chological traumas inflicted by the Vietnam war and the
discussion “in the open” of sexual abuse and rape by the
women's liberation movement. 1980 marked a major
turning point, with the incorporation of the diagnostic
construct of posttraumatic stress disorder (PTSD) into the
3rd edition of the Diagnostic and Statistical Manual of
Mental Disorders (DSM-III) and the definition of its main
diagnostic criteria (reexperiencing of the traumatic
event, avoidance of stimuli associated with the trauma,
and symptoms of increased arousal). Initially described as
resulting from a onetime severe traumatic incident, PTSD
has now been shown to be triggered by chronic multiple
traumas as well. This “state-of-the-art” article discusses
past and current understanding of the disorder, with par-
ticular emphasis on the recent explosive developments in
neuroimaging and other fields of the neurosciences that
have highlighted the complex interrelationships between
the psychological, psychiatric, biological, and neuro-
anatomical components of the disorder, and opened up
entirely new therapeutic perspectives on how to help the
victims of trauma overcome their past.
7
T he human response to psychological trauma is
one of the most important public health problems in the
world. Traumatic events such as family and social vio-
lence, rapes and assaults, disasters, wars, accidents and
predatory violence confront people with such horror and
threat that it may temporarily or permanently alter their
capacity to cope, their biological threat perception, and
their concepts of themselves. Traumatized individuals
frequently develop posttraumatic stress disorder (PTSD),
a disorder in which the memory of the traumatic event
comes to dominate the victims’ consciousness, depleting
their lives of meaning and pleasure.1 Trauma does not
only affect psychological functioning: for example, a
study of almost 10 000 patients in a medical setting2
reported that persons with histories of severe child mal-
treatment showed a 4 to 12 times greater risk for devel-
oping alcoholism, depression, drug abuse, and suicide
attempts, a 2 to 4 times greater risk for smoking, ≥50 sex
partners, and sexually transmitted disease, a 1.4 to 1.6
times greater risk for physical inactivity and obesity, and
a 1.6 to 2.9 times greater risk for ischemic heart disease,
cancer, chronic lung disease, skeletal fractures, hepatitis,
stroke, diabetes, and liver disease.
Prevalence
Traumatic events are very common in most societies,
though prevalence has been best studied in industrial-
ized societies, particularly in the USA. Kessler et al3
Keywords: posttraumatic stress disorder; stress; history of medicine; dissociation;
premorbid personality; neuroimaging; DESNOS (disorders of extreme stress not oth-
erwise specified); hippocampus; amygdala; neurohormone; SSRI (selective serotonin
reuptake inhibitor); emotional processing; EMDR (eye movement desensitization
and reprocessing)
Author affiliations: Professor of Psychiatry, Boston University School of Med-
icine, Boston, Mass, USA
Address for correspondence: Prof Bessel van der Kolk, Trauma Center, 227
Babcock Street, Brookline, MA 02446, USA
(e-mail: bvanderk@traumacenter.org)
State of the art
found that in the USA at least 15% of the population
reported to have been molested, physically attacked,
raped, or been involved in combat. Men are physically
assaulted more often than women (11.1% vs 10.3%),
while women report higher rates of sexual assault (7.3%
vs 1.3%). Half of all victims of violence in the US are
under age 25; 29% of all forcible rapes occur before the
age of eleven. Among US adolescents aged 12 to 17,
8% are estimated to have been victims of serious sexual
assault; 17% victims of serious physical assault; and 40%
have witnessed serious violence.4 Twenty-two percent of
rapes are perpetrated by strangers, whereas husbands
and boyfriends are responsible for 19%, and other rela-
tives account for 38%. Men sustain twice as many severe
injuries than women do. For women and children, but
not for men, trauma that results from violence within
intimate relationships is a much more serious problem
than traumatic events inflicted by strangers or accidents:
in 1994, 62% of the almost 3 million attacks on women
in the USA were by persons whom they knew, while
63% of the almost 4 million assaults on males were by
strangers. Four out of five assaults on children are at
the hands of their own parents. Over a third of the vic-
tims of domestic assault experienced serious injury,
compared with a quarter of victims of stranger assault.5
This illustrates that an assault by someone “known” is
not less serious than assault by a stranger. Domestic
abuse and child abuse are closely related: in homes
where spousal abuse occurs, children are abused at a
rate 1500% higher than the national average (National
Victim Center, 1993).6
Selected abbreviations and acronyms
ASR abnormal startle response
CRH corticotropin-releasing hormone
DESNOS Disorders of Extreme Stress Not Otherwise Specified
EMDR eye movement desensitization and reprocessing
HPA hypothalamo-pituitary-adrenocortical (axis)
mCPP meta-chlorophenylpiperazine
MHPG 3-methoxy-4-hydroxyphenylglycol
NE norepinephrine
PTSD posttraumatic stress disorder
SSRI selective serotonin reuptake inhibitor
8
Many people experience horrendous events without
seeming to develop lasting effects of their traumatiza-
tion. The most common effects of traumatization are
included in the symptom picture described in the diag-
nosis of PTSD. However, depression, increased aggres-
sion against self and others, depersonalization, dissocia-
tion, compulsive behavioral repetition of traumatic
scenarios, as well as a decline in family and occupational
functioning, may occur without victims meeting full-
blown criteria for PTSD. The most common causes of
PTSD in men are combat and being a witness of death
or severe injury, while sexual molestation and rape are
the most common causes of PTSD in women. The capac-
ity of these events to produce PTSD varied significantly,
ranging from 56% in patients who regain consciousness
in the middle of surgical procedures, to 48.4% of female
rape victims, and 10.7% of men witnessing death or seri-
ous injury. Women have twice the risk of developing
PTSD following a trauma than men do.
The symptomatology of
the trauma response
When people are faced with life-threatening or other
traumatic experiences, they primarily focus on survival
and self-protection. They experience a mixture of numb-
ness, withdrawal, confusion, shock, and speechless terror.
Some victims try to cope by taking action, while others
dissociate. Neither response absolutely prevents the sub-
sequent development of PTSD, though problem-focused
coping reduces the chance of developing PTSD, while
dissociation during a traumatic event is an important
predictor for the development of subsequent PTSD.7
The longer the traumatic experience lasts, the more
likely the victim is to react with dissociation.
When the traumatic event is the result of an attack by a
family member on whom victims also depend for eco-
nomic and other forms of security, as occurs in victims of
intrafamilial abuse, victims are prone to respond to
assaults with increased dependence and with a paralysis
in their decisionmaking processes. Thus, some aspects
of how people respond to trauma are quite predictable,
but individual, situational, and social factors play a major
role in the shaping the symptomatology.
Rape victims, as well as children and women abused by
male partners, often develop long-term reactions that
include fear, anxiety, fatigue, sleep and eating distur-
bances, intense startle reactions, and physical complaints.
PTSD and the nature of trauma - van der Kolk
They often continue to dissociate in the face of threat,
suffer from profound feelings of helplessness and have
difficulty planning effective action. This makes them vul-
nerable to develop “emotion-focused coping,” a coping
style in which the goal is to alter one’s emotional state,
rather than the circumstances that give rise to those
emotional states. This emotion-focused coping accounts
for the fact that people who develop PTSD are vulnera-
ble to engage in alcohol and substance abuse. Between a
quarter and half of all patients who seek substance
abuse treatment suffer from a comorbid PTSD diagno-
sis. The relationship between substance abuse and PTSD
is reciprocal: drug abuse leads to assault, and, recipro-
cally, assault leads to substance use.
Diagnostic issues
In 1980, the diagnosis of PTSD was constructed for
inclusion in the Diagnostic and Statistical Manual of
Mental Disorders, 3rd edition (DSM-III) in order to cap-
ture the psychopathology associated with traumatiza-
tion in adults. Over the years, numerous studies have
demonstrated that the diagnostic construct of PTSD is
clinically relevant to individuals who have suffered sin-
gle incident traumas such as rape, physical assaults, tor-
ture, and motor vehicle accidents. However, it has also
become clear that in clinical settings most treatment-
seeking patients have been exposed to a range of differ-
ent traumatic events over their life span, and suffer from
a variety of psychological problems, only some of which
are covered in the definition of PTSD. These include
affect dysregulation, aggression against self and others,
amnesia and dissociation, somatization, depression, dis-
trust, shame, and self-hatred. These other problems can
either be conceptualized as comorbid conditions, or as
part of a spectrum of trauma-related problems, that
occur depending on the age at which the trauma
occurred, the relationship to the agent responsible for
the trauma, social support received, and the duration of
the traumatic experience(s).
The diagnosis of PTSD is characterized by three major
elements:
• The repeated reliving of memories of the traumatic expe-
rience. These tend to involve intense sensory and visual
memories of the event, which are often accompanied
by extreme physiological and psychological distress,
and sometimes by a feeling of emotional numbing,
9
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
during which there usually is no physiological arousal.
These intrusive memories may occur spontaneously
or can be triggered by a range of real and symbolic
stimuli.
• Avoidance of reminders of the trauma, as well as of
emotional numbing, detachment, and emotional blunt-
ing, often coexist with intrusive recollections. This is
associated with an inability to experience joy and plea-
sure, and with a general withdrawal from engagement
with life. Over time, these features may become the
dominant symptoms of PTSD.
• A pattern of increased arousal is the third element of
PTSD. This is expressed by hypervigilance, irritability,
memory and concentration problems, sleep distur-
bances, and an exaggerated startle response. In the
more chronic forms of the disorder, this pattern of
hyperarousal and the avoidance may be the dominant
clinical features. Hyperarousal causes traumatized peo-
ple to become easily distressed by unexpected stim-
uli. Their tendency to be triggered into reliving trau-
matic memories illustrates how their perceptions
become excessively focused on the involuntary seeking
out of the similarities between the present and their
traumatic past. As a consequence, many neutral expe-
riences become reinterpreted as being associated with
the traumatic past.
Secondary effects of developing PTSD
Once people develop PTSD, the recurrent unbidden
reliving of the trauma in visual images, emotional states,
or nightmares produces a constant reexposure to the
terror of the trauma. In contrast to the actual trauma,
which had a beginning, middle, and end, the symptoms
of PTSD take on a timeless character. The traumatic
intrusions themselves are horrifying: they interfere with
dealing with the past, while distracting from being able
to attend to the present. This unpredictable exposure to
unbidden memories of the trauma usually leads to a
variety of (usually maladaptive) avoidance maneuvers,
ranging from avoidance of people or actions that remind
them of the trauma, to drug and alcohol abuse, to emo-
tional withdrawal from friends or activities that used to
be potential sources of solace. Problems with attention
and concentration keep them from being engaged with
their surroundings with zest and energy. Uncomplicated
activities like reading, conversing, and watching televi-
sion require extra effort. This loss of ability to focus, in
State of the art
turn, often leads to problems with taking one thing at a
time and gets in the way of organizing one’s life to get it
back on track.
Disorders of extreme stress (DESNOS)
The DSM-IV Field Trial8 demonstrated that it was not
the prevalence of PTSD symptoms themselves, but
depression, outbursts of anger, self-destructive behav-
iors, and feelings of shame, self-blame, and distrust that
distinguished a treatment-seeking sample from a non-
treatment seeking community sample with PTSD. The
majority of people who seek treatment for trauma-
related problems have histories of multiple traumas. One
recent treatment-seeking sample9 suffered from a variety
of other psychological problems, which in most cases
were the chief presenting complaints, in addition to their
PTSD symptoms: 77% suffered from behavioral impul-
sivity, affective lability, and aggression against self and
others, 84% suffered from depersonalization and other
dissociative symptoms, 75% were plagued by chronic
feelings of shame, self-blame, and feeling permanently
damaged, and 83% complained of being unable to nego-
tiate satisfactory relationships with others. These prob-
lems contribute significantly to impairment and disabil-
ity above and beyond the PTSD symptoms.10-12 Focusing
exclusively either on PTSD, or on the depression, disso-
ciation and character pathology prevent adequate
assessment and treatment of traumatized populations.
As part of the DSM-IV Field Trial, members of the
PTSD task force delineated a syndrome of psychological
problems that have been shown to be frequently associ-
ated with histories of prolonged and severe interper-
sonal abuse. They called this “Complex PTSD,” or “Dis-
orders of Extreme Stress Not Otherwise Specified
(DESNOS).”8,13 This delineated a complex of symptoms
associated with early interpersonal trauma: (i) alter-
ations in the regulation of affective impulses, including
difficulty with modulation of anger and being self-
destructive; (ii) alterations in attention and conscious-
ness leading to amnesias and dissociative episodes and
depersonalizations; (iii) alterations in self-perception,
such as a chronic sense of guilt and responsibility, chron-
ically feeling ashamed; (iv) alterations in relationship to
others, such as not being able to trust, not being able to
feel intimate with people; (v) somatization—the prob-
lem of feeling symptoms on a somatic level for which no
medical explanations can be found; and (vi) alterations
10
in systems of meaning. These are now listed in the DSM
under “Associated Features of PTSD.”
The DSM-IV Field Trial of PTSD found that DESNOS
had a high construct validity.14 The earlier the onset of
the trauma, and the longer the duration, the more likely
people were to suffer from a high degree of all the symp-
toms that make up the DESNOS diagnosis.8,15-17 These
studies showed that interpersonal trauma, especially
childhood abuse, predicts a high risk for developing
DESNOS. Patients with DESNOS are high utilizers of
crisis psychiatric care16 and are usually refractory to con-
ventional PTSD treatment.17 Recent studies18 showed
that these patients may react adversely to current stan-
dard PTSD treatments and that effective treatment
needs to focus self-regulatory deficits rather than “pro-
cessing the trauma.”
PTSD has become a common diagnosis for people who
become patients in psychiatric hospitals. An examina-
tion of the records of the 384 000 Medicaid recipients in
Massachusetts in 1997/9819 revealed that PTSD, together
with depression, was the most common psychiatric diag-
nosis. However, patients with a PTSD diagnosis spent
10 times as much time in the hospital than patients with
the diagnosis of depression only. It is inconceivable that
the 22 800 Medicaid recipients in Massachusetts who
were admitted to psychiatric hospitals and diagnosed as
suffering from PTSD were admitted following a one-
time traumatic incident, such as a rape or motor vehicle
accident. Most likely, they suffered from a complex con-
stellation of symptoms. However, since the long-term
psychiatric impact of chronic, multiple traumas receives
the same diagnosis (PTSD) as would the effects of a
onetime incident, this diagnosis fails to capture how con-
voluted the psychiatric problems of these patients are,
and how complex their treatment is.
Historical background
Awareness of the role of psychological trauma as a con-
tributory factor in psychiatric disturbances has waxed and
waned throughout the past century.The study of the trau-
matic origins of emotional distress started during the last
decades of the 19th century. At the Hôpital de la
Salpêtrière in Paris, Jean Martin Charcot (1887)20 first pro-
posed that the symptoms of what was then called “hys-
terical” patients had their origins in histories of trauma. In
his first four books, Charcot’s student Pierre Janet
described 591 patients, 257 of whom had a traumatic origin
PTSD and the nature of trauma - van der Kolk
of their psychopathology.21,22 Janet was the first to propose
that during traumatic events people experience “vehe-
ment emotions,” which interferes with the integration of
the overwhelming experience. Instead, the traumatic mem-
ories (and the actions related to them) are split off (disso-
ciated) from everyday consciousness and from voluntary
control: they are “unable to make the recital which we call
narrative memory, and yet they remain confronted by
(the) difficult situation.”23 Janet described how the memo-
ries of these traumas tended to return not as stories of
what had happened: they were reenacted in the form of
intense emotional reactions, aggressive behavior, physical
pain, and bodily states that could all be understood as the
return of elements of the traumatic experience.
Janet first observed that traumatized patients seemed
to react to reminders of the trauma with responses that
had been relevant to the original threat, but that cur-
rently had no adaptive value. Upon exposure to
reminders, the trauma was reactivated in the form of
images, feelings, and physical sensations related to the
trauma.21 He proposed that when patients fail to inte-
grate the traumatic experience into the totality of their
personal awareness, they seem to develop problems
assimilating new experiences as well. It is . . . as if their
personality has definitely stopped at a certain point, and
cannot enlarge any more by the addition or assimila-
tion of new elements.”23 “All (traumatized) patients seem
to have had the evolution of their lives checked; they
are attached to an insurmountable obstacle.”24 Janet pro-
posed that the efforts to keep the fragmented traumatic
memories out of conscious awareness eroded the psy-
chological energy of these patients. This, in turn, inter-
fered with the capacity to engage in focused action and
to learn from experience. Unless the dissociated ele-
ments of the trauma were integrated into personal con-
sciousness, the patient was likely to experience a slow
decline in personal and occupational functioning.25
As a young physician, during the 1880s, Sigmund Freud
did two clinical rotations at the Salpêtrière in Paris.
Upon his return to Vienna he attached himself to an
older internist, Jospeh Breuer, with whom he started to
carefully study the symptoms of “hysterical” patients,
and the origins of their symptoms, which were often
characterized by marked motoric and sensory abnor-
malities. They summarized their first set of findings in a
paper entitled On the Physical Mechanisms of Hysterical
Phenomena.26 Because of the astuteness of their obser-
vations it is useful to quote part of their account:
11
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
The ... memory of the trauma ... acts like a foreign body
which long after its entry must be regarded as an agent
that is still at work. At first sight it seems extraordinary
that events experienced so long ago should continue to
operate so intensely—that their recollection should not
be liable to the wearing away process to which, after all,
we see all our memories succumb. The following consid-
erations may perhaps make this a little more intelligi-
ble. The fading of a memory or the losing of its affect
depends on various factors. The most important of these
is whether there has been an energetic reaction to the
event that provokes an affect. By “reaction” we under-
stand the whole class of voluntary and involuntary
reflexes . . . in which . . . the affects are discharged. If this
reaction takes place to a sufficient amount a large part of
the affect disappears as a result. . . . If a reaction is sup-
pressed [the affect] stays attached to the memory. The
injured person’s reaction to the trauma only exercises a
complete “cathartic” effect if it is an adequate reaction—
as, for instance, revenge. . . . Abreaction, however, is not
the only method of dealing with the situation that is
open to a normal person who has experienced a psychi-
cal trauma. But language serves as a substitute for action:
with its help, an affect can be “abreacted” almost as
effectively. . . . If there is no such reaction, in either deeds
or words, any recollection of the event retains its affec-
tive tone. . . . A memory of such a trauma, even if it has
not been abreacted, enters the great complex of associa-
tions, it comes alongside other experiences, which may
contradict it, and is subjected to rectification by other
ideas. . . . In this way a normal person is able to bring
about the disappearance of the accompanying affect
through the process of association. . . . It may therefore be
said that the ideas which have become pathological have
persisted with such freshness and affective strength
because they have been denied the normal wearing-away
processes by means of abreaction and reproduction in
states of uninhibited association (italicized in original).
We have become convinced that the splitting of con-
sciousness . . . under the form of “double conscience” is
present to a rudimentary degree in every hysteria and
that a tendency to dissociation, and with it, the emer-
gence of abnormal states of consciousness, is the basic
phenomenon of this neurosis . . . in this view we concur
with Janet . . . we must, however, mention another
remarkable fact . . . namely, that these memories, unlike
the memories of the rest of their lives, are not at the
patients’ disposal. On the contrary, these experiences are
State of the art
completely absent from the patient’s memory when they
are in a normal psychical state, or are only present in a
highly summary form…. (1893, pp 7-11).26
Over time, Freud came to disbelieve the reality of his
patients' tales of trauma. In his Autobiographical Study
(1925),27 he wrote:
I believed these stories and consequently supposed that
I had discovered the roots of the subsequent neurosis....
If the reader feels inclined to shake his head at my
credulity, I cannot altogether blame him. I was at last
obliged to recognize that these scenes of seduction had
never taken place, and that they were only fantasies
which my patients had made up (p 34).27
However, like Janet before him, Freud kept being fasci-
nated with the issue of patients’ apparent compulsion
to arrange their lives in such a way that they would
repeat their trauma over and over again. Freud pro-
posed that the compulsion to repeat was a function of
repression: because the memory is repressed the patient
“is obliged to repeat the repressed material as a con-
temporary experience, instead of . . . remembering it as
something belonging to the past” (p 18).28
In Beyond the Pleasure Principle (1920),28 Freud
described how patients suffering from traumatic neu-
roses often experienced a lack of conscious preoccupa-
tion with the memories of their accident. He postulated
that “perhaps they are more concerned with NOT think-
ing of it.” Yet, it appeared that Freud also was concerned
with not thinking about the horrible real-life experiences
that can destroy people’s capacity to function. He did so
by focusing on his patients’ intrapsychic reality: interest
in personal meaning making crowded out interest in the
external reality that had given rise to these meaning sys-
tems. Psychiatry, as a discipline, came to follow Freud in
his explorations of how the normal human psyche func-
tioned: real-life trauma was ignored in favor of fantasy.
Little attention was paid to the further exploration of
“traumatic neuroses” until the outbreak of the second
World War, when Abram Kardiner wrote up his experi-
ences of treating World War I veterans in The Traumatic
Neuroses of War (1941).29 In this book, this psychoana-
lyst emphasized the psychobiological nature of trau-
matic stress. He noted that sufferers from “traumatic
neuroses” develop an enduring vigilance for and sensi-
tivity to environmental threat, and stated that “. . . the
nucleus of the neurosis is a physioneurosis. This is pre-
sent on the battlefield and during the entire process of
organization; it outlives every intermediary accom-
12
modative device, and persists in the chronic forms. The
traumatic syndrome is ever present and unchanged.” He
described extreme physiological arousal in these
patients: they suffered from sensitivity to temperature,
pain, and sudden tactile stimuli:
These patients cannot stand being slapped on the back
abruptly; they cannot tolerate a misstep or a stumble. From
a physiologic point of view, there exists a lowering of the
threshold of stimulation; and, from a psychological point of
view a state of readiness for fright reactions (p 95). 29
Central in Kardiner’s thinking, as it had been for Janet
and Freud, is that fact that:
The subject acts as if the original traumatic situation were
still in existence and engages in protective devices which
failed on the original occasion. This means in effect that
his conception of the outer world and his conception of
himself have been permanently altered” (p 82). 29
At the end of the second World War, Kardiner lamented
that:
. . . these conditions [traumatic neuroses] are not sub-
ject to continuous study . . . but only to periodic efforts
which cannot be characterized as very diligent. Though
not true in psychiatry generally, it is a deplorable fact
that each investigator who undertakes to study [trau-
matic neuroses] considers it his sacred obligation to start
from scratch and work at the problem as if no one has
ever done anything with it before.” 30
This proved to be true for the subsequent 30 years until
the issue of traumatic neuroses was rediscovered in the
wake of the Vietnam war and the emergence of the
women’s movement. When the importance of trauma
was rediscovered, starting around 1978, many of the early
formulations that had long since been forgotten proved
to be remarkably accurate. However, progress in under-
standing the function of attachment in shaping the indi-
vidual and rapid developments in the neurosciences gave
a new shape to these old insights.
The psychobiology of trauma
During the past two decades, important advances have
been made in the understanding of the nature and treat-
ment of PTSD. Probably the most important progress has
been in the areas of the neurobiological underpinnings
and treatment. Modern research has come to elucidate
the degree to which PTSD is, indeed, a “physioneurosis,”
a mental disorder based on the persistence of biological
emergency responses.
PTSD and the nature of trauma - van der Kolk
In order to understand how trauma affects psychobio-
logical activity it is useful to briefly revisit some basic
tenets of neurobiology. Paul McLean31 defined the brain
as a detecting, amplifying, and analyzing device for main-
taining us in our internal and external environment.
These functions range from the visceral regulation of
oxygen intake and temperature balance to the catego-
rization of incoming information necessary for making
complex, long-term decisions affecting both individual
and social systems. In the course of evolution, the human
brain has developed three interdependent “subanalyz-
ers,” each with different anatomical and neurochemical
substrates: (i) the brainstem and hypothalamus, which
are primarily associated with the regulation of internal
homeostasis; (ii) the limbic system, which is in charge
of maintaining the balance between the internal world
and external reality; and (iii) the neocortex, which is
responsible for analyzing and interacting with the exter-
nal world.
It is generally thought that the circuitry of the brain-
stem and hypothalamus is mostly innate and stable, that
the limbic system contains both innate circuitry and cir-
cuitry modifiable by experience, and that the structure of
the neocortex is most affected by environmental input.32
If that is true, trauma would be expected to leave its
most profound changes on neocortical functions, and
least affect basic regulatory functions. However, while
this may be true of the ordinary stress response, trauma,
stress that overwhelms the organism, seems to affect
people over a wide range of biological functioning,
involving a large variety of brain structures and neuro-
transmitter systems.
The interrelation between
regulatory functions
The brainstem, hypothalamus, limbic system, and neo-
cortex in concert monitor relations with the outside
world and assess what is new, dangerous, or gratifying. To
accomplish this assessment, the brain needs to take in
new sensory information, categorize its importance, and
integrate it with previously stored knowledge. Most
importantly, it needs to determine what is significant,
and filter out irrelevant information. After the meaning
of an incoming signal has been categorized, the brain
(usually unconsciously) needs to “formulate” an appro-
priate plan of action, while attending to both short-term
and long-term consequences. This evaluation then needs
13
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
to lead to the initiation of an appropriate response,
which needs to be terminated once the challenge is
gone.32,33 Moreover, in order to remain in a state of rela-
tive stability, people need to learn to engage in sustained
activities without being distracted by irrelevant stimuli.
The organism needs to learn from experience and be
able to entertain a range of alternatives without becom-
ing disorganized, or acting upon them. In order to do
this, they need to learn to discriminate between rele-
vant and irrelevant stimuli, and to only select what is
appropriate for achieving one’s goals. Much of evolu-
tion of the human brain has consisted in developing the
capacity to form highly complex mental images and col-
laborative social relationships that allow complex
thought in the context of social systems. In order for this
to be successful, the organism needs to integrate its own
immediate self-interest with a capacity to adhere to com-
plex social rules.34 People with PTSD usually have seri-
ous problems in carrying out a host of these functions.
The degree of impairment is determined not only by the
severity of their PTSD symptomatology, but also by the
age at which the trauma occurred, the length of time
that the traumatic event lasted, and the degree of social
support that the individual received.
A century ago, the philosopher and psychologist William
James (brother of the novelist Henry James)35 noted that
the power of one’s intellect is determined by one’s per-
ceptual processing style. The ability to comprehend
(grasp, hold together, take hold of—from the Latin cum-
prendere) depends on stimulus sampling and the for-
mation of schematic representations of reality.36 There
seem to be qualitatively significant differences between
the ways people with PTSD sample and categorize expe-
rience, and the ways in which nontraumatized people
do so.37,38 Failure to comprehend the experience (in other
words, dissociation) plays a critical role in making a
stressful experience traumatic.39
The apparent uniqueness
of traumatic memories
A century of study of traumatic memories shows that: (i)
they are primarily imprinted in sensory and emotional
modes, though a semantic representation of the memory
may coexist with sensory flashbacks40; (ii) these sensory
experiences often remain stable over time and unaltered
by other life experiences1,41 (iii) they may return, trig-
gered by reminders, at any time during a person’s life
State of the art
with a vividness as if the subject were having the expe-
rience all over again (DSM IV); and (iv) these sensory
imprints tend to occur in a mental state in which vic-
tims may be unable to precisely articulate what they are
feeling and thinking.42,43
While transformation of memories of day-to-day experi-
ences is the norm, the flashbacks and other sensory reex-
periences of PTSD seem not to be updated or attached
to other experiences. Triggered by a reminder, the past
can be relived with an immediate sensory and emotional
intensity that makes victims feel as if the event were
occurring all over again. Patients with PTSD seem to
remain embedded in their trauma as a contemporary
experience and often become “fixated on the trauma.”29
While most patients with PTSD construct a narrative of
their trauma over time, it is characteristic of PTSD that
sensory elements of the trauma itself continue to intrude
as flashbacks and nightmares, altered states of con-
sciousness in which the trauma is relived, unintegrated
with an overall sense of self. Because traumatic memories
are so fragmented, it seems reasonable to postulate that
extreme emotional arousal leads to a failure of the cen-
tral nervous system (CNS) to synthesize the sensations
related to the trauma into an integrated whole.
The availability of neuroimaging studies of patients with
PTSD has provided an opportunity to determine which
brain structures are affected by traumatic experiences
and, hence, how these structures are mobilized differ-
ently in response to traumatic reminders, compared with
their response to neutral stimuli. This has facilitated a
rapid increase in our understanding of the potential
mechanisms of PTSD and promoted the exploration of
new therapeutic techniques.
Psychophysiological effects of trauma
One of the principal contributions of trauma research to
psychiatry has been the clarification that the develop-
ment of a chronic trauma-based disorder is qualitatively
different from a simple exaggeration of the normal stress
response.44 It also has become clear that PTSD is not an
issue of simple conditioning: many people who do not
suffer from PTSD, but who have been exposed to an
extreme stressor, will again become distressed when they
are once again confronted with the tragedy. Pitman45 has
pointed out that the critical issue in PTSD is that the
stimuli that cause people to overreact may not be con-
ditional enough: a variety of triggers not directly related
14
to the traumatic experience may come to precipitate
extreme reactions.
Abnormal psychophysiological reactions in PTSD occur
on two very different levels: (i) in response to specific
reminders of the trauma; and (ii) in response to intense,
but neutral stimuli, such as loud noises, signifying a loss
of stimulus discrimination.
Conditional responses to specific stimuli—kindling
PTSD sufferers experience heightened physiological
arousal in response to sounds, images, and thoughts
related to specific traumatic incidents. A large number of
studies have confirmed that people with PTSD, but not
controls who did not develop PTSD, respond to such
reminders with significant increases in heart rate, skin
conductance, and blood pressure.46-48 The highly elevated
autonomic responses to reminders of traumatic experi-
ences that happened years, and sometimes decades, ago
illustrate the intensity and timelessness with which these
memories continue to affect current experience.45 Post
and his colleagues49,50 have shown that life events play a
critical role in the first episodes of major affective dis-
orders, but become less pertinent in precipitating subse-
quent occurrences. This capacity of triggers with dimin-
ishing strength to produce the same response over time
is called kindling.
Medications that decrease autonomic arousal, such as
-adrenergic blockers and benzodiazepines, tend to
decrease traumatic intrusions, while drugs that stimu-
late autonomic arousal may precipitate visual images
and affect states associated with prior traumatic experi-
ences in people with PTSD, but not in controls. For
example, in patients with PTSD, the injection of drugs
such as lactate51,52 and yohimbine53 tends to precipitate
panic attacks, flashbacks (exact reliving experiences) of
earlier trauma, or both. In our own laboratory, approxi-
mately 20% of PTSD subjects responded with a flash-
back of a traumatic experience when they were pre-
sented with acoustic startle stimuli.
Hyperarousal to intense, but neutral stimuli—loss of
stimulus discrimination
Excessive stimulation of the CNS at the time of the
trauma may result in permanent neuronal changes that
have a negative effect on learning, habituation, and stim-
ulus discrimination. These neuronal changes do not
PTSD and the nature of trauma - van der Kolk
depend on actual exposure to reminders of the trauma
for expression. The abnormal startle response (ASR)
characteristic of PTSD54 is one example of this phenom-
enon. Several studies have demonstrated abnormalities
in habituation to the ASR in PTSD.55,56 Interestingly, peo-
ple who previously met criteria for PTSD, but no longer
do so now, continue to show failure of habituation of
the ASR (van der Kolk et al, unpublished data; Pitman
et al, unpublished data).
The failure to habituate to acoustic startle suggests that
traumatized people have difficulty evaluating sensory
stimuli and mobilizing appropriate levels of physiologi-
cal arousal.57 Thus, the problems that people with PTSD
have with properly integrating memories of the trauma
and their getting mired in a continuous reliving of the
past is mirrored physiologically in the misinterpretation
of innocuous stimuli as potential threats. To compen-
sate, they tend to shut down. However, the price for
shutting down is decreased involvement in ordinary,
everyday life.
The hormonal response in posttraumatic
stress disorder
In a well-functioning organism, stress produces rapid
and pronounced hormonal responses. However, chronic
and persistent stress inhibits the effectiveness of the
stress response and induces desensitization.58 PTSD
develops following exposure to events that overwhelm
the individual’s capacity to reestablish homeostasis.
Instead of returning to baseline, there is a progressive
kindling of the individual’s stress response. Initially, only
intense stress is accompanied by the release of endoge-
nous, stress-responsive neurohormones, such as corti-
sol, epinephrine and norepinephrine (NE), vasopressin,
oxytocin, and endogenous opioids. In PTSD, even minor
reminders of the trauma may precipitate a full-blown
neuroendocrine stress reaction: it permanently alters
how an organism deals with its environment on a day-
to-day basis, and it interferes with how it copes with
subsequent acute stress.
While acute stress activates the hypothalamo-pituitary-
adrenocortical (HPA) axis and increases glucocorticoid
levels, organisms adapt to chronic stress by activating a
negative feedback loop that results in: (i) decreased
resting glucocorticoid levels in chronically stressed
organisms59; (ii) decreased glucocorticoid secretion in
response to subsequent stress60,61; and (iii) increased con-
15
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
centration of glucocorticoid receptors in the hip-
pocampus.62 Corticotropin-releasing hormone (CRH),
produced by the hypothalamus, controls the secretion of
adrenocorticotrophic hormone from the pituitary. It has
substantial anxiogenic properties and has become the
focus of intense interest in recent years.
Yehuda and associates (see review by Yehuda, 199763)
have comprehensively examined the HPA axis in PTSD,
the neuroendocrine system controlling the stress hor-
mone cortisol. Despite the fact that one would predict
high cortisol as part of the stress response, the avail-
able evidence has consistently demonstrated low lev-
els of serum cortisol. Careful examination of this issue
has demonstrated that people with PTSD suffer from a
disorder of the circadian cortisol modulation. Numerous
studies have now demonstrated that the administration
of low-dose dexamethasone results in supersuppression
of cortisol release in patients with PTSD, but not in
other disorders. Yehuda has suggested that increased
concentration of glucocorticoid receptors could facili-
tate a stronger glucocorticoid negative feedback, result-
ing in a more sensitive HPA axis and a faster recovery
from acute stress.61
In a study by Resnick et al,64 the investigators collected
blood samples from 20 acute rape victims and measured
their cortisol response in the emergency room. Three
months later, a prior trauma history was taken, and the
subjects were evaluated for the presence of PTSD. Vic-
tims with a prior history of sexual abuse were signifi-
cantly more likely to have developed PTSD 3 months
following the rape than rape victims who did not
develop PTSD. Cortisol levels shortly after the rape
were correlated with histories of prior assaults: the
mean initial cortisol level of individuals with a prior
assault history was 15 µg/dL compared to 30 µg/dL in
individuals without. These findings can be interpreted to
mean either that prior exposure to traumatic events
results in a blunted cortisol response to subsequent
trauma, or in a quicker return of cortisol to baseline
following stress.
Yehuda63 has proposed that cortisol basically functions
as an “antistress” hormone, shutting off the other bio-
logical reactions that were initiated by the stress
response. Simultaneous activation of catecholamines and
glucocorticoids stimulates active coping behaviors, while
increased arousal in the presence of low glucocorticoid
levels would provoke undifferentiated fight or flight
reactions.
State of the art
Catecholamines
Release of norepinephrine also plays an important role in
the acute stress response. It leads to increased glucose
metabolism and heightened awareness and concentration.
Increased NE is correlated with heightened emotional
arousal and mediated by right amygdala activation. Emo-
tional arousal correlates with accuracy of recall and the
consolidation of emotional memory.65 Neuroendocrine
studies of Vietnam veterans with PTSD have found good
evidence for chronically increased sympathetic nervous
system activity in PTSD.66 This leads to compensatory
downregulation of adrenergic receptors.67 Southwick et al68
used yohimbine injections (0.4 mg/kg) to study noradren-
ergic neuronal dysregulation in Vietnam veterans with
PTSD. Subjects responded with substantially larger
increases in plasma 3-methoxy-4-hydroxyphenylglycol
(MHPG) than controls.Yohimbine precipitated significant
increases in all PTSD symptoms, as well as panic attacks in
70% of subjects and flashbacks in 40% (for a more exten-
sive discussions of catecholamines in PTSD, see Marburg69).
Other neurotransmitter abnormalities
While the role of serotonin in PTSD has received less sys-
tematic attention than the corticosteroids, the potential
importance of serotonin in PTSD is illustrated by the fact
that inescapably shocked animals are found to have
decreased CNS serotonin levels70 and that serotonin reup-
take blockers are singularly effective pharmacological agents
in the treatment of PTSD. Decreased serotonin in humans
has repeatedly been correlated with impulsivity and aggres-
sion.71-73 The literature tends to readily assume that these
relationships are based on genetic traits. However, studies of
impulsive, aggressive, and suicidal patients seem to find at
least as robust an association between those behaviors and
histories of childhood trauma (eg, refs 74-76). In order to test
serotonergic contributions to trauma-related symptomatol-
ogy, Southwick et al77 administered meta-chlorophenylpiper-
azine (mCPP), a serotonin (5-HT) agonist, to 26 Vietnam
veterans with PTSD.Thirty-one percent of the subjects expe-
rienced a panic attack, and 27% a flashback. These figures
are comparable to the effects of the injection of yohimbine,
which acts solely on the noradrenergic system. There was
almost no overlap between the subjects who had these reac-
tions to mCPP and those who did on yohimbine. This sug-
gests that multiple neurotransmitters are involved in these
complex PTSD symptoms.
16
Trauma and the central nervous system
The disintegration of experience
In a series of studies, we have demonstrated that traumatic
memories initially have few narrative elements: when
PTSD patients have their flashbacks, the trauma is relived
as isolated sensory, emotional, and motoric imprints of the
trauma, without a storyline.We have shown this in victims
of childhood abuse,40 assaults and accidents in adulthood,78
and in patients who gained awareness during surgical pro-
cedures.79 These studies support Janet’s 1889 observations21
and confirm the notion that what makes memories trau-
matic is a failure of the central nervous system to synthesize
the sensations related to the traumatic memory into an
integrated semantic memory. Sensory elements of the expe-
rience are registered separately and are often retrieved
without the patient appreciating the context to which this
sensation or emotion refers.
These observations lead to the notion that in PTSD the
brain’s natural ability to integrate experience breaks down.
A variety of CNS structures have been implicated in these
integrative processes: (i) the parietal lobes are thought to
integrate information between different cortical associa-
tion areas80; (ii) the hippocampus is thought to create a
cognitive map that allows for the categorization of expe-
rience and its connection with other autobiographical
information81; (iii) the corpus callosum allows for the trans-
fer of information by both hemispheres,82 integrating emo-
tional and cognitive aspects of the experience; (iv) the cin-
gulate gyrus is thought to play the role of both an amplifier
and a filter that helps integrate the emotional and cogni-
tive components of the mind83; and (v) the dorsolateral
frontal cortex, which is where sensations and impulses are
“held in mind” and compared with previous information
to plan appropriate actions. The frontal lobes, in general,
are thought to function as a “supervisory system” for the
integration of experience.84 Recent neuroimaging studies
of patients with PTSD have suggested a role for most of
these structures in the neurobiology of PTSD.
Neuroimaging studies in PTSD
As of 1999, there have been seven published studies uti-
lizing neuroimaging of patients with PTSD.85-91 Four stud-
ies have used magnetic resonance imaging (MRI) to
measure hippocampal volume in individuals with PTSD,
and three studies have used positron emission tomogra-
PTSD and the nature of trauma - van der Kolk
phy (PET)85,88,91 to measure differential activation of the
CNS in response to traumatic and nontraumatic scripts
in patients with PTSD.
Hippocampal volume
Three different studies have shown that people with
chronic PTSD have decreased hippocampal volumes, rang-
ing from 8%87,92 to 26%.86 The fact that the only prospective
study of acutely traumatized individuals, Shalev et al (ref 93
and personal communication, 1999) failed to find a corre-
lation between hippocampal volume and PTSD severity
suggests that this hippocampal shrinkage is a function of
chronicity. Recent research suggests that the hippocampal
changes may not be irreversible.94-96 However, work of She-
line97 strongly suggests some irreversible shrinkage of hip-
pocampus in recurrent depression. In animals, decreased
hippocampal functioning has been shown to cause behav-
ioral disinhibition98 and makes animals more likely to
define incoming stimuli in the direction of emergency
(fight/flight) responses. If the same is true for humans, this
might contribute to the problems of PTSD patients with
“taking in” and processing arousing information, and to
learn from such experiences. The decreased size of the
hippocampus might play a role in the ongoing dissociation
and misinterpretation of information in the direction of
threat.Their altered biology would make them vulnerable
to react to newly arousing stimuli as a threat, and to react
with aggression, or withdrawal, depending on their pre-
morbid personality.99
Symptom provocation studies
Rauch, van der Kolk, and colleagues85 conducted a PET
scan study of patients with PTSD in which they were
exposed to vivid, detailed narratives of their own trau-
matic experiences. During exposure to the script of their
traumatic experiences these subjects demonstrated
heightened activity only in the right hemisphere, specif-
ically, in the areas that are most involved in emotional
arousal—the amygdala, insula, and the medial temporal
lobe. During exposure to their traumatic scripts there
was a significant decrease in activation of the left infe-
rior frontal area—Broca’s area—which is thought to be
responsible for translating personal experiences into
communicable language. Shin et al’s study,91 utilizing a
slightly different paradigm, essentially confirmed these
findings in a different trauma population. In another
17
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
study, Lanius et al (submitted) exposed 6 subjects with
PTSD and 6 controls to a traumatic script and measured
their responses with functional magnetic resonance
imaging (fMRI) scans, and consistently found decreased
activation of the thalamus and of the dorsolateral pre-
frontal cortex in PTSD patients during exposure to their
trauma scripts.
These early neuroimaging studies of patients with PTSD
present us with a range of surprising findings that force
us to reevaluate our previous concepts of the patho-
physiology of PTSD. Of the various findings, increased
activation of the amygdala in response to traumatic
scripts is the least surprising. After all, it has been well
established that the amygdala is centrally involved in
the interpretation of the emotional valence of the
incoming information and that confrontation with
feared stimuli activates the amygdala and related struc-
tures.100 Exposure to traumatic scripts frequently pro-
vokes autonomic activation of patients with PTSD (eg,
refs 48 and 101), and this is likely mediated by activation
of the amygdala and related structures. It is well under-
stood that the information evaluated by the amygdala is
passed on to areas in the brainstem that control auto-
nomic and neurohormonal response systems. By way of
these connections, the amygdala transforms sensory
stimuli into emotional and hormonal signals, thereby
initiating and controlling emotional responses.
High levels of stimulation of the amygdala can also inter-
fere with hippocampal functioning.102,103 Thus, extreme
emotional arousal may prevent the proper evaluation
and categorization of experience by interfering with hip-
pocampal functions. It is possible that, when this occurs,
sensory imprints of experience are stored in memory, but
because the hippocampus is prevented from fulfilling its
integrative function, these various imprints are not com-
bined into a unified whole.104 The experience is laid down,
and later retrieved, as isolated images, bodily sensations,
smells, and sounds that feel alien and separate from other
life experiences. Decreased hippocampal functioning is
likely to interfere with the localization of incoming infor-
mation in time and space and cause continued fragmen-
tation of experience. The recent findings of decreased
dorsolateral frontal cortex activation would further pro-
vide a neurobiological explanation why people with
PTSD plunge into reexperiencing their trauma with lim-
ited consciousness that they are simply remembering ele-
ments of experiences belonging to the past. In our pilot
study, using single photon emission computed tomogra-
State of the art
phy (SPECT) as an outcome measure of eye movement
desensitization and reprocessing (EMDR) treatment,
subjects had increased activation of the dorsolateral pre-
frontal cortex following effective treatment.
Hemispheric lateralization
The finding of hemispheric lateralization in subjects
exposed to their personalized trauma scripts indicates
that there is differential hemispheric involvement in the
processing of traumatic memories. This may have impor-
tant implications for the understanding of the nature of
PTSD. The right hemisphere, which developmentally
comes “on-line” earlier than the left hemisphere, is
involved in the expression and comprehension of global,
nonverbal emotional communication (tone of voice,
facial expression, visual/ spatial communication), and
allows for a dynamic and holistic integration across sen-
sory modalities.105 This hemisphere is particularly inte-
grated with the amygdala, which assigns emotional sig-
nificance to incoming stimuli and helps regulate the
autonomic and hormonal responses to that information.
While it is exquisitely sensitive to emotional nuances, it
has, at best, a rudimentary capacity to think or commu-
nicate analytically, to employ syntax, or to reason.106,107
In contrast, the left hemisphere, which mediates verbal
communication and organizes problem-solving tasks into
a well-ordered set of operations and processes informa-
tion in a sequential fashion,107 seems to be less active in
PTSD. It is in the area of categorization and labeling of
internal states that people with PTSD seem to have par-
ticular problems.108,109 It is conceivable that failure of left
hemisphere function during states of extreme arousal is
responsible for the derealization and depersonalization
reported in acute PTSD.7,110
New directions for treatment
For over a century, it has been understood that trau-
matic experiences can leave indelible emotional memo-
ries. Contemporary studies of how the amygdala is acti-
vated by extreme experiences dovetail with the
laboratory observation that “emotional memory may be
forever.”111 The accumulated body of research suggests
that patients with PTSD suffer from impaired cortical
control over subcortical areas responsible for learning,
habituation, and stimulus discrimination. The concept
of indelible subcortical emotional responses, held in
18
check to varying degrees by cortical and hippocampal
activity, has led to the speculation that delayed-onset
PTSD may be the expression of subcortically mediated
emotional responses that escape cortical, and possibly
hippocampal, inhibitory control.1,45,112
The early neuroimaging studies of PTSD showed that,
during exposure to a traumatic script, there was decreased
Broca’s area functioning and increased activation of the
right hemisphere. This would imply that it is difficult for
traumatized individuals to verbalize precisely what they
are experiencing, particularly when they become emo-
tionally aroused. They may experience physiological
arousal and fragments of memories may be activated, but
they often seem to be too hyperaroused or hypoaroused
to be able to “process” and communicate what they are
experiencing. A relative decrease in left hemispheric rep-
resentation provides an explanation for why traumatic
memories are experienced as timeless and ego-alien: the
part of the brain necessary for generating sequences and
for the cognitive analysis of experience is not functioning
properly. Our research85 can be interpreted as showing
that during activation of a traumatic memory, the brain is
“having” its experience. The person may feel, see, or hear
the sensory elements of the traumatic experience, but he
or she may be physiologically prevented from being able
to translate this experience into communicable language.
When they are having their traumatic recall, victims may
suffer from speechless terror in which they may be liter-
ally “out of touch with their feelings.” Physiologically, they
may respond as if they were being traumatized again.
Particularly when victims experience depersonalization
and derealization, they cannot “own” what is happening,
and thus cannot take steps to do anything about it.
In order to help traumatized individuals process their
traumatic memories, it is critical that they gain enough
distance from their sensory imprints and trauma-related
emotions so that they can observe and analyze these
sensations and emotions without becoming hyper-
aroused or engaging in avoidance maneuvers. The sero-
tonin reuptake blockers seem to be able to accomplish
exactly that. Studies in our laboratory have shown that
selective serotonin reuptake inhibitors (SSRIs) can help
PTSD patients gain emotional distance from traumatic
stimuli and make sense of their traumatic intrusions.113
The apparently relative decrease in left hemisphere acti-
vation while reexperiencing the trauma suggests that it is
important to help people with PTSD find a language in
which they can come to understand and communicate
PTSD and the nature of trauma - van der Kolk
their experiences. It is possible that some of the newer
body-oriented therapies, dialectical behavior therapy, or
EMDR may yield benefits that traditional insight-ori-
ented therapies lack.
Making meaning of the traumatic experience usually is
not enough. Traumatized individuals need to have expe-
riences that directly contradict the emotional helpless-
ness and physical paralysis that accompany traumatic
experiences. In many people with PTSD, such helpless-
ness and paralysis become a habitual way of responding
to stressful stimuli, further weakening their feelings of
control over their destiny. The critical steps in treating
PTSD can be summarized as follows (for more details
see ref 114):
• Safety. When people’s own resources are inadequate to
deal with threat, they need to rely on others to provide
them with safety and care. After having been trauma-
tized, it is critical that the victim reestablishes contact
with his or her natural social support system. If this
system is inadequate to ensure the safety of the
patient, institutional resources need to be mobilized
the help the patient find a place to recover.
• Anxiety management. After the patient’s safety has
been assured, there may be a need for a variety of psy-
chological interventions. Patients need to learn to
name the problems they face, and learn to formulate
appropriate solutions. Assault victims must learn to
distinguish between the real-life threats, and the haunt-
ing, irrational fears that are part of the disorder PTSD.
If anxiety dominates, victims need to be helped to
strengthen their coping skills. Practical anxiety man-
agement skills training may include deep muscle relax-
ation, breathing control, role-playing, covert model-
ing, thought stopping, and guided self-dialogue.
• Emotional processing. In order to put the event(s) in
perspective, the victim needs to reexperience the event
without feeling helpless. Traditionally, following
Freud’s notion that words can substitute for action to
resolve a trauma (1893),115 this has been done by help-
ing people to talk about their entire experience.13,64,116
They are asked to articulate what they think hap-
pened, and what led up to it; their own contributions to
what happened, their thoughts and fantasies during
the event, what was the worst part of it, and their reac-
tions to the event in detail, including how it has
affected their perceptions of themselves and others.
Such exposure therapy is thought to promote symp-
tom reduction by allowing patients to realize that: (i)
19
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
remembering the trauma is not equivalent to experi-
encing it again; (ii) that the experience had a begin-
ning, middle, and end, and that the event now belongs
to one’s personal history.
In recent years, a variety of new techniques have been
developed that have the potential of desensitizing
patients with PTSD without requiring them to fully
engage in a verbal reliving of the traumatic experience.
Of these treatments, EMDR has been best studied.117
Although traditional exposure therapy can be very help-
ful in overcoming traumatic intrusions, it needs to be
applied with care. Some patients, on recalling their
trauma, may become flooded with both the traumatic
memories and memories of previously forgotten trau-
mas. Increased activation of traumatic memories may
be associated with increased shame, guilt, aggression,
and increase in alcohol and drug use.
Conclusions
The rediscovery of trauma as an etiological factor in
mental disorders is only about 20 years old. During this
time, there has been an explosion of knowledge about
how experience shapes the central nervous system, and
the formation of the self. Developments in the neuro-
sciences have started to make significant contributions
to our understanding of how the brain is shaped by
experience, and how life itself continues to transform
the ways biology is organized. The study of trauma has
probably been the single most fertile area within the
disciplines of psychiatry and psychology in helping to
develop a deeper understanding of the interrelation-
ships between emotional, cognitive, social, and biologi-
cal forces that shape human development. Starting with
PTSD in adults, but expanding into early attachment
and coping with overwhelming experiences in child-
hood, our field has discovered how certain experiences
can “set” psychological expectations and biological
selectivity. Research in these areas has opened up
entirely new insights in how extreme experiences
throughout the life cycle can have profound effects on
memory, affect regulation, biological stress modulation,
and interpersonal relatedness. These findings, in the
context of the development of a range of new therapy
approaches, are beginning to open up entirely new per-
spectives on how traumatized individuals can be helped
to overcome their past. ❏
State of the art
El trastorno de estrés postraumático y las
características del trauma
El papel del trauma psíquico (ej. violación, asalto, tor-
tura, accidentes de vehículos motorizados) como un
factor etiológico en los trastornos mentales fue antici-
pado por Charcot, Freud y Breuer en el siglo XIX, y
luego más específicamente durante la I Guerra Mun-
dial por Kardiner. Hace 20 años este papel etiológico
fue “redescubierto” en el contexto de los traumas psi-
cológicos producidos por la guerra de Vietnam y tam-
bién a raíz de la discusión pública que ha realizado el
movimiento de liberación de la mujer sobre el abuso
sexual y las violaciones. El año 1980 marcó un hito
importante ya que se incorporó el constructo diagnós-
tico del trastorno de estrés postraumático (TEPT) en
la tercera edición del Manual Diagnóstico y Estadís-
tico de los Trastornos Mentales (DSM-III) y se defi-
nieron sus principales criterios diagnósticos (re-expe-
rimentar el acontecimiento traumático, evitación de
estímulos asociados con el trauma y síntomas de hiper-
alerta). Inicialmente se describió que el TEPT se pro-
ducía por un acontecimiento traumático aislado; sin
embargo, actualmente se ha observado que el TEPT
puede ser gatillado también por múltiples traumas
crónicos. Este artículo que constituye una puesta al día
sobre el TEPT discute las comprensiones pasadas y
las actuales acerca de este trastorno, con especial énfa-
sis en el explosivo desarrollo reciente de las técnicas de
neuroimágenes y otros campos de las neurociencias.
Estos estudios han iluminado las complejas interrrela-
ciones entre los componentes psicológicos, psiquiátri-
cos, biológicos y neuroanatómicos de este cuadro, y
han abierto perspectivas totalmente novedosas acerca
de la formo de ayudar a las víctimas de traumas para
superar el pasado.
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Basic research
Neurobiological findings
in posttraumatic stress disorder: a review
Kumar Vedantham, MD; Alain Brunet, PhD; Thomas C. Neylan, MD; Daniel
S. Weiss, PhD; Charles R. Marmar, MD
Since posttraumatic stress disorder (PTSD) was first
recognized as a psychiatric disorder, it has generated
a great deal of scientific interest. Recent studies on
the neurobiology of PTSD provide evidence that PTSD
is biologically distinct from other types of traumatic
and nontraumatic stress responses. This paper reviews
three important directions of neurobiological
research in PTSD: noradrenergic axis changes and
associated alterations in autonomic responsivity, neu-
roendocrine changes involving the hypothalamic-pitu-
itary-adrenocortical (HPA) axis, and neuroanatomic
changes involving the hippocampus. Each section
reviews the salient aspects of preclinical research on
the biology of stress and their bearing on the under-
standing of PTSD, and summarizes prominent find-
ings from clinical biological studies of PTSD. Tenta-
tive models that integrate current findings from the
clinical study of PTSD are reviewed. To conclude, the
important methodological and empirical issues that
need to be addressed by future studies are indicated.
Address for correspondence: Kumar Vedantham, Department of Psychiatry,
University of California, SFVAMC Psychiatry Service (116P), 4150 Clement
Street, San Francisco CA 94121-1545, USA
(e-mail: kumar@itsa.ucsf.edu)
Keywords: noradrenergic; neuroendocrine; neuroanatomic; stress; mental dis-
order
23
S ince posttraumatic stress disorder (PTSD)
was first recognized as a psychiatric disorder in the
Diagnostic and Statistical Manual of Mental Disorders,
3rd edition (DSM-III) in 1980,1 it has generated
tremendous scientific and public interest. Research on
PTSD has only served to elucidate the great complex-
ity of this disorder. While early theoreticians viewed
PTSD as part of the continuum of normal stress
responses, recent studies indicate that the biological
patterns seen in PTSD are different from biological
responses to nontraumatic stress.2 Researchers have
made important advances in characterizing the neuro-
biological features of PTSD and distinguishing biolog-
ical features associated with PTSD from patterns asso-
ciated with other types of reactions to traumatic and
nontraumatic stressors. This paper reviews three impor-
tant directions of neurobiological research in PTSD:
noradrenergic axis changes and associated alterations
in autonomic responsivity, neuroendocrine changes
involving the hypothalamic-pituitary-adrenal (HPA)
axis, and neuroanatomic changes involving the hip-
pocampus.
Noradrenergic axis function in PTSD
To react appropriately to danger, both animals and
humans must rapidly marshal a complex set of behav-
ioral responses. The locus ceruleus (LC), which is
located in the dorsal pons, plays a crucial role in acti-
vating central and peripheral nervous system responses
to threat. Through its broad connections with cortical
structures, the hippocampus, hypothalamus, amygdala,
Author affiliations: Department of Psychiatry, University of California, San
Francisco; and Department of Veterans Affairs, Medical Center, San Fran-
cisco, Calif, USA. Kumar Vedantham acknowledges fellowship support from
the Program for Minority Research Training in Psychiatry (PMRTP), which is
funded by the National Institute of Mental Health and administered by the
American Psychiatric Association. Alain Brunet acknowledges financial sup-
port from the Fonds de Recherche en Santé du Québec
Basic research
Selected abbreviations and acronyms
ACTH adrenocorticotropic hormone
CRH corticotropin-releasing hormone
HPA hypothalamic-pituitary-adrenocortical (axis)
LC locus ceruleus
MRSI magnetic resonance spectroscopy imaging
NE norepinephrine
PTSD posttraumatic stress disorder
and spinal cord, the LC organizes affective, cognitive,
and motor responses to acute stressors.3 Activation of
LC neurons leads to secretion of norepinephrine (NE),
which recruits the multiple pathways involved in mod-
ulating behavioral responses to acute stressors. For
example, upon receiving electrical stimulation to their
locus ceruleus, restrained monkeys will immediately
wake up and exhibit behaviors such as head and body
turning, eye scanning, tongue movement, hair pulling,
and escape struggling. These behavioral responses are
similar to those elicited when they are threatened in
their natural environment.4
The noradrenergic system also modulates cognitive and
behavioral adaptations to chronic stressors. Repeated
exposure to a stressful stimulus leads to increased NE
secretion and facilitates the process of behavioral stress
sensitization, whereby the animal develops a height-
ened behavioral response to further presentations of
the same stimulus. Exposure to severe and repeated
stress depletes brain NE concentrations and leads to
behavioral changes such as decreased exploration in a
plus-maze novelty task, decreased appetite, and deficits
in previously well-learned behavioral tasks.5 Such
behavioral changes induced by chronic stress have
been characterized by the term “learned helplessness.”6
These animal models differ from PTSD in that the
development of stress sensitization and learned help-
lessness requires repeated exposure to stressful stimuli,
while PTSD can develop after only a single exposure to
traumatic stress. Despite this important difference,
stress sensitization and learned helplessness models
are useful in explaining behavioral changes associated
with PTSD, such as heightened reactions to trauma-
related stimuli and decreased interest in usual-life
activities.7
Through its reciprocal connections with the amygdala,
the LC/NE axis also mediates classically conditioned
24
fear responses in animals. In this model, the repeated
pairing of a neutral stimulus such as a bright light with
a noxious stimulus, such as an electrical shock, even-
tually results in a conditioned fear response to the
previously neutral stimulus when it is presented
alone. 8 Reactivation of the neuronal connections
between the LC and amygdala that are established
during acute stress exposure may explain the failure
of animals to extinguish stress-related associations.
Conditioned fear patterns may underlie features of
PTSD such as heightened arousal responses to ordi-
nary noises and increased avoidance behaviors, while
failure of extinction may subserve persistent alarm
reactions to reminders of past trauma.
Research on noradrenergic function in PTSD includes
hormone- and receptor-binding assays, assessment of
autonomic reactivity, and pharmacological probes
involving central 2-adrenergic receptor agonists. One
method to assess noradrenergic function in PTSD has
been to measure plasma NE levels or levels of NE
metabolites in 24-hour urine collections. Studies have
found increased urinary concentrations of NE among
hospitalized PTSD patients compared with hospital-
ized patients with other mental disorders. 9 Similar
findings have been reported in sexually abused chil-
dren compared with healthy controls.10 Other investi-
gators have noted decreases in the density of platelet
cell  2-adrenergic receptors in combat veterans with
PTSD and in traumatized children.11,12 Reduction of
these NE-binding receptors may indicate an adaptive
downregulation in response to chronically elevated
plasma NE levels.
Since the noradrenergic axis also modulates periph-
eral autonomic responses, investigators have also
assessed noradrenergic function in PTSD by compar-
ing autonomic responses in PTSD subjects and con-
trols. Autonomic measures in these studies have
included heart rate, systolic and diastolic blood pres-
sure, and galvanic skin responses. While early stud-
ies13,14 noted baseline autonomic differences between
combat veterans with PTSD and non-PTSD controls,
later studies15-17 did not replicate these findings. This
may be due to the fact that earlier studies did not con-
trol for the effects of anticipatory anxiety and study
demand characteristics.18,19 Studies that have compared
autonomic responses in PTSD and non-PTSD sub-
jects to stressful but nontraumatic stimuli such as hav-
ing to perform arithmetic calculations 20,21 or watch
Neurobiological findings in PTSD - Vedantham et al
unpleasant films16,22 have not identified autonomic dif-
ferences between PTSD subjects and controls. Thus,
there is little evidence to suggest that PTSD involves
changes in resting autonomic function or in auto-
nomic responsivity to nontraumatic stimuli.
In contrast to these negative findings, there is com-
pelling evidence to indicate that individuals with
PTSD exhibit an increased autonomic responsivity to
trauma-related stimuli. Compared with trauma-
exposed controls, PTSD subjects exhibit greater auto-
nomic arousal to trauma-related stimuli such as audio-
tapes of combat sounds,13,14,23 videotapes of war zone
scenes,16,24 and trauma-related smells.25 Pitman et al22
noted increased autonomic arousal in PTSD subjects
using a script-driven imagery technique in which
trauma survivors listened to their own trauma narra-
tive while viewing trauma-related slides. These find-
ings prompted a multisite Veterans Affairs Coopera-
tive Study to evaluate the diagnostic utility of
psychophysiological assessments in Vietnam combat
veterans with PTSD. 21 This study included three
groups: veterans with current PTSD (n=778), veter-
ans with lifetime but not current PTSD (n=181), and
veterans who never had PTSD (n=369). Using physi-
ological variables alone, researchers correctly classi-
fied 67% of the current PTSD group and a similar
percentage of the non-PTSD group. Collectively, these
studies suggest that increased autonomic reactivity to
traumatic stimuli is an important feature of many
individuals with PTSD.
Investigators have also examined noradrenergic axis
activity in PTSD using pharmacologic probes such as
yohimbine, which activates noradrenergic neurons in
the LC region by blocking inhibitory  2-adrenergic
autoreceptors at the presynaptic terminal. 26 South-
wick et al27 found that after receiving yohimbine, a
subset of PTSD patients not only exhibited physio-
logical arousal such as increased heart rate and blood
pressure, but also developed severe anxiety symptoms
including acute panic attacks and increased PTSD
symptoms such as intrusive thoughts, flashbacks, and
emotional numbing.Yohimbine did not elicit similar
responses in trauma-exposed controls without PTSD.
Morgan et al28 demonstrated that yohimbine infusion
enhanced acoustic startle responses in combat veter-
ans with PTSD, but did not affect startle responses in
combat veterans without PTSD. Consistent with psy-
chophysiologic findings, these result further support
25
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
the hypothesis that increased noradrenergic respon-
sivity is a core biological feature of PTSD.
Neuroendocrine changes in PTSD
Baseline neuroendocrine changes
In addition to activating the noradrenergic system,
exposure to acute stress elicits important neuroen-
docrine changes that are modulated by the HPA axis. In
response to acute stress, corticotropin-releasing hor-
mone (CRH) is released from nuclei in the hypothala-
mus, amygdala, and cortex.29 CRH is a 41–amino-acid
peptide that is transported to the anterior lobe of the
pituitary gland where it stimulates pituitary secretion of
adrenocorticotropic hormone (ACTH). ACTH enters
the systemic circulation and binds to cells in the adrenal
cortex, thereby stimulating the secretion of cortisol.
Cortisol is the primary stress hormone. Cortisol binds to
the type I and type II glucocorticoid receptors that are
present on cell membranes and activates a cascade of
physiologic stress responses involving altered metabo-
lism, increased cellular uptake of glucose, modulation of
immune activity, and induction of hepatic enzymes. This
has been reviewed by Michelson et al.30 Cortisol also
blocks further secretion of CRH and ACTH, thereby
curtailing the acute stress response once the stress is
over. This is a crucial function of cortisol, since uncon-
trolled activation of acute stress hormones can signifi-
cantly harm host tissue. There is clear evidence from
animal studies that persistent activation of the HPA
axis by chronic and repetitive stress can have deleteri-
ous effects such as the acceleration of aging, disruption
of reproductive function, immunosuppression, and
reduced ability to fight cancers: these findings have
been reviewed by Johnson et al.31
Noting that increased HPA axis activity is associated
with chronic stress in preclinical studies, investigators
initially predicted that individuals with PTSD would
have elevated plasma cortisol levels and would fail to
suppress cortisol levels after being administered dexa-
methasone.32-34 However, evidence indicates that HPA
axis patterns in PTSD are quite different from patterns
seen in studies of chronic nontraumatic stress. Mason
and colleagues32 first noted that veteran inpatients with
PTSD had lower 24-hour urinary cortisol levels than
other psychiatric inpatients. This finding has been repli-
cated in studies involving both psychiatric35,36 and
Basic research
healthy35,37-39 controls and in other trauma-exposed pop-
ulations such as holocaust survivors,39 rape victims,34,40
and adolescents exposed to a natural disaster.41 This
literature has been reviewed in detail by Yehuda.42
However, not all studies have obtained similar find-
ings.11 Differences in study results may reflect differ-
ences in study settings, different assay techniques, and
patient differences such as inpatient versus outpatient
status, obesity, substance abuse, use of medications, and
comorbid illnesses.43 Associated research has examined
diurnal fluctuations in plasma cortisol levels in PTSD.
Two studies have found that cortisol release in PTSD
patients is comparable to that of healthy subjects dur-
ing the daytime (7 AM to 7 PM), but significantly lower
during the late evening and early morning, leading to
wider diurnal fluctuations in the PTSD group.36,44 Other
studies have examined target receptor alterations in
PTSD and have identified increased glucocorticoid
receptors on lymphocyte cell membranes in PTSD sub-
jects compared with controls.45-48 Collectively, these
studies indicate that basal cortisol secretion is altered
in PTSD.
Changes in dynamic
neuroendocrine responses
To evaluate the dynamic responsivity of the HPA axis
in PTSD, investigators have used exogenous hormones
that stimulate or inhibit the HPA axis at a specific
locus. A well-established paradigm involves measuring
ACTH and cortisol levels after administering dexa-
methasone.
• Dexamethasone is a synthetic glucocorticoid that
mimics the negative feedback effects of cortisol on
the HPA axis. It inhibits ACTH release from the pitu-
itary gland, which subsequently leads to a decrease in
serum cortisol levels. Four studies have reported that,
in response to dexamethasone, individuals with
PTSD demonstrate a more robust suppression of
ACTH and cortisol release that normal controls.48-50
This contrasts with the nonsuppression of cortisol
levels seen in almost half of all depressed patients
after dexamethasone administration.51
• Other studies have measured ACTH and cortisol lev-
els after infusing CRH, which stimulates the pituitary
gland to release ACTH. Two studies found decreased
ACTH responses to CRH infusion in adult PTSD
26
subjects compared with controls,49,52 while another
study10 found no differences in ACTH response to
CRH infusion in sample of adolescent girls.
• Finally, metyrapone, which blocks the synthesis of cor-
tisol in the adrenal gland, has been used to examine
hypothalamic and pituitary responses to decrease cor-
tisol in PTSD. One study found that PTSD patients
show larger increases in ACTH levels following
metyrapone administration that do normal controls.53
These findings led Yehuda and colleagues42 to propose
that PTSD may involve an HPA axis that is character-
ized by enhanced sensitivity to feedback inhibition.
According to this model, individuals with PTSD expe-
rience chronic and recurrent stress events that lead to
increased secretion of CRH. Pituitary sensitivity to
CRH decreases the need to compensate for increased
CRH release, as reflected by blunted ACTH responses
to CRH infusion. To protect against the toxic effects
of elevated cortisol, the HPA axis in PTSD becomes
increasingly sensitized to feedback inhibition from cor-
tisol through upregulation of glucocorticoid receptors
and other mechanisms. This is evidenced by low base-
line ACTH and cortisol levels and robust suppression
of ACTH and cortisol release after dexamethasone
administration. By tightly controlling cortisol secretion
and responding aggressively to acute rises in cortisol
levels, the neuroendocrine system may serve to buffer
vulnerable neuronal structures such as the hippocam-
pus from cellular toxicity induced by elevated serum
cortisol levels.54,55
Neuroanatomic changes in PTSD
While evidence that severe stress can affect noradren-
ergic and neuroendocrine function has been well-estab-
lished, recent animal studies have identified important
neurotic effects of stress-mediated increases in gluco-
corticoid levels. One neuroanatomical structure that
appears to be particularly susceptible to stress-induced
damage is the hippocampus, which is involved in learn-
ing and memory circuits. Studies of monkeys exposed
to the stressors of disrupted attachment found damage
to cells in the hippocampal region56; similar patterns of
cell damage could be induced by implanting glucocor-
ticoids directly into the hippocampus.57 This suggests
that elevated glucocorticoid levels, such as might occur
acutely during exposure to traumatic stress, could lead
Neurobiological findings in PTSD - Vedantham et al
to hippocampal damage. Other studies examining
stress-induced hippocampal damage in mice have iden-
tified important memory deficits that are correlated
with the extent of hippocampal damage,58 suggesting
that structural damage to the hippocampus may also be
associated with functional memory deficits.
These findings have led investigators to hypothesize
that PTSD may be associated with hippocampal
changes resulting from either the acute neurotoxic
effects of elevated serum cortisol during exposure to
traumatic stress or the gradual deterioration result-
ing from glucocorticoid-mediated effects of chronic
stress. Using magnetic resonance imaging (MRI) tech-
niques to measure hippocampal volume, Bremner et
al59 compared hippocampal size in 26 male Vietnam
combat veterans with PTSD and 22 healthy controls,
and found a statistically significant 8% reduction in
right hippocampal volume in the PTSD group. How-
ever, this difference was not associated with PTSD
symptoms or combat exposure. Gurvits and col-
leagues60 compared hippocampal volumes in veterans
with PTSD (n=7) and matched controls (n=7). The
PTSD group showed bilateral reductions in hip-
pocampal size (26% on the left, 22% on the right),
which remained significant after controlling for age,
brain volume, drinking history, and combat exposure.
Total hippocampal size was negatively correlated with
combat exposure (r=-0.72, P=0.003) and number of
PTSD symptoms (r=-0.78, P=0.001), but only weakly
associated with memory performance. Examining a
different population, Bremner et al61 compared hip-
pocampal volumes in adult child abuse survivors with
PTSD (n=17) versus healthy controls (n=17) and
found a statistically significant 12% reduction in left
hippocampal size in the PTSD group after control-
ling for alcohol use, age, and educational status. How-
ever, hippocampal volume was not associated with
memory deficits, number of PTSD symptoms, or expo-
sure. Finally, Stein et al62 examined hippocampal vol-
umes in 21 female survivors of childhood sexual abuse
with PTSD and 21 nonvictimized controls, and noted
a statistically significant 5% reduction in left hip-
pocampal size in the abused group. Combining MRI
measurements with proton magnetic resonance spec-
27
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
troscopy (MRSI), Schuff et al 63 observed a 6%
decrease in right hippocampal volume which was
associated with an 18% decrease in hippocampal
activity as measured by the ratio of N-acetyl aspar-
tate signal activity to that of choline and creatinine.
Their results suggest that utilizing MRSI measure-
ment may enhance our ability to detect subtle hip-
pocampal changes in PTSD. While the above studies
included only adults, De Bellis et al64 compared hip-
pocampal size in 43 abused children with PTSD and 61
matched controls, and found no corresponding
decrease in hippocampal volume in the PTSD group.
Collectively, these studies provide preliminary evi-
dence that changes in hippocampal size and function
may be an important feature of chronic PTSD.
Conclusion and future directions
The findings reviewed in this paper provide tantalizing
new insights into PTSD and offer the promise of a richer
understanding of this complex disorder. However, for
these findings to be truly meaningful, important empirical
questions need to be addressed. Most studies have
employed a cross-sectional design and included PTSD
subjects who suffer from comorbid disorders such as
major depression or alcohol abuse. This makes it difficult
to identify whether a biological finding associated with
PTSD represents a premorbid condition, reflects the
impact of a comorbid disorder, or actually results from
PTSD.There is a need for prospective longitudinal studies
to measure biological variables prior to the onset of
PTSD and track their change across time. Furthermore,
animal models of PTSD have primarily examined bio-
logical responses that develop over days to weeks: find-
ings from such animal models may be less applicable to a
disorder such as PTSD, which develops over a period of
months to years. Improved animal paradigms are needed
to anchor future research in the biology of PTSD.65
Another critical issue is to determine which biological
responses in PTSD are similar to biological stress
responses in other populations, and which biological pat-
terns are uniquely associated with PTSD. Exciting
research lies ahead and promises to advance our scientific
understanding of this major public health challenge. ❏
Basic research
Hallazgos neurobiológicos en el
trastorno de estrés postraumático:
una revisión
Desde que fue reconocido por primera vez el trastorno
de estrés postraumático (TEPT) como una patología
psiquiátrica, se ha generado bastante interés científico.
Estudios recientes acerca de la neurobiología del TEPT
aportan evidencias que el TEPT es biológicamente dis-
tinto de otros tipos de respuestas de estrés traumático o
no traumático. Este artículo revisa tres importantes líne-
as de la investigación neurobiológica en el TEPT: a)
cambios en el eje noradrenérgico y alteraciones asocia-
das a la respuesta autonómica, b) cambios neuroendo-
crinos en el eje hipotálamo-hipófisis-adrenal (HHA) y
c) cambios neuroanatómicos que afectan al hipocampo.
Cada sección revisa los aspectos más destacados de la
investigación preclínica en la biología del estrés y su
relación con la comprensión del TEPT, y resume los
hallazgos principales de los estudios clínico biológicos
del TEPT. También se revisan algunos modelos tentati-
vos que integran los hallazgos actuales de los estudios
clínicos del TEPT. Para concluir, se mencionan los
temas importantes metodológicos y empíricos que
requieren ser abordados en futuros estudios.
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Basic research
Ethical aspects of research
on psychological trauma
Dan J. Stein, MB; Allen Herman, MD, PhD; Debra Kaminer, MA;
Solomon Rataemane, MB; Soraya Seedat, MB;
Ronald C. Kessler, PhD; David Williams, PhD, MPH
Research in the area of psychological trauma raises
a number of complex ethical issues. These include
questions about unjustified medicalization of suf-
fering, retraumatization of survivors, the morality
of also investigating perpetrators of trauma, and
neglecting to provide appropriate intervention.
We discuss some of these issues against the back-
drop of a study of trauma in South Africa, and the
recent work of the Truth and Reconciliation Com-
mission in that country.
In the early part of the twentieth century, sci-
ence was seen by its practitioners and by professional
philosophers as a value-free enterprise.1,2 By careful
observation of the phenomena of the world, and by rig-
orous analysis of their relationships, the laws of nature
Author affiliations: MRC Research Unit on Anxiety Disorders, University of
Stellenbosch, Cape Town, South Africa (Dan J. Stein, Debra Kaminer, Soraya
Seedat); Faculty of Public Health, Medical University of South Africa,
Medunsa, South Africa (Allen Herman); Dept of Psychiatry, University of the
Orange Free State, Bloemfontein, South Africa (Solomon Rataemane); Dept
of Health Care Policy, Harvard University Medical School, Boston, Mass, USA
(Ronald C. Kessler); and Institute for Social Research, University of Michigan,
Ann Arbor, Mich, USA (David Williams)
31
would be gradually deciphered and science would res-
olutely advance. Such advances would, in turn, pave the
way for general progress in human affairs.
As the century grew older, however, and theoretical
physics provided the foundation for the practicalities
and horrors of such phenomena as atomic warfare, the
line between science and values blurred. Many twenti-
eth-century philosophers have since portrayed science
as simply one way of understanding the world, one
more game with its own particular rules, no more accu-
rate or appropriate than any other.1,2
Medical science has perhaps the advantage of often
appearing intrinsically valuable. Diseases, almost by
definition, involve harmful effects3,4; thus research that
leads to their defeat would seem valuable. When the
costs of research (eg, the adverse effects of a new drug)
potentially outweigh the benefits (eg, the therapeutic
effects of the same agent), however, ethical issues obvi-
ously become more apparent. Other important ethical
issues include those of informed consent, confidential-
ity and privacy protection, and disclosure of results.5,6
In the field of psychological trauma and posttraumatic
trauma, controversy is not uncommon, and questions
about the ethics of research on trauma are no less sub-
ject to debate. In this paper, we discuss some of the
ethical questions that surround work in this area, ques-
tions which have been inspired by some of our work in
South Africa on trauma, posttraumatic stress disorder
(PTSD), and the recent proceedings of the South
African Truth and Reconciliation Commission (TRC).
Address for correspondence: Prof Dan J. Stein, Director MRC Research Unit
on Anxiety Disorders, Cape Town, PO Box 19063, Tygerberg 7505, South
Africa
(e-mail: DJS2@GERGA.SUN.AC.ZA)
Keywords: posttraumatic stress disorder; psychological trauma; testimony psy-
chotherapy; retraumatization; apartheid; human rights violation; ethics; transfer-
ence; countertransference
Basic research
Background
Before moving on to discussing ethical issues per se, it
may be helpful to provide some general background
on South Africa and the TRC. In 1994, after decades
of political struggle, the apartheid regime of the
Nationalist Party was replaced by a democratically
elected government in which the African National
Congress held the majority of seats. In response to
the gross violations of human rights in the past, the
new government passed the Promotion of National
Unity and Reconcilation Act. This act was a negoti-
ated settlement between the old and new regimes, and
at its heart was a move away from the concept of ret-
ributive justice for past crimes (as in the Nuremberg
trials), and towards a prudential focus on the com-
mon good.7-9
The act provided for a Truth and Reconciliation
Commission, which would: (i) provide survivors a
chance to relate the violations that they had suf-
fered and recommend reparations where indicated;
and (ii) provide perpetrators with the opportunity to
receive amnesty if they gave full disclosure of facts
related to politically motivated acts. By establish-
ing “as complete a picture as possible of the nature,
causes, and extent of gross violations of human
rights,” the act aimed “to promote national unity
and reconciliation in a spirit of understanding which
transcends the conflicts and divisions of the past.”
For medical practitioners and researchers, a whole
series of questions immediately springs to mind: What,
if any, was the impact of gross human rights violations
on health? Did the TRC have a therapeutic effect for
survivors who gave testimony, or were they retrauma-
tized? Was the effect of the TRC on the nation as a
whole beneficial or not?10
Medical research was, of course, not at the head of the
TRC's agenda and, unfortunately, there was no
prospective attempt to investigate such questions. Nev-
ertheless, we recently obtained funding to study a
cross-sectional probability sample of South Africans
with the aim of assessing exposure to trauma, post-
traumatic psychiatric symptoms, and attitudes toward
the TRC. In formulating this study, a range of different
ethical issues were raised by investigators and by focus
groups comprised of participant–observers (eg, peo-
ple who had themselves suffered gross human rights
violations). We review some of these here.
32
Is it justifiable to medicalize suffering?
There is of course an enormous amount of literature doc-
umenting a relationship between psychosocial adversity
and stress, and medical and psychiatric disorders.11,12 It
would seem incumbent upon clinicians to recognize these
relationships, and use this knowledge to help motivate for
appropriate changes to improve health. Certainly, in the
South African context, during the time of apartheid, it
was common for progressive clinicians and researchers to
argue that the oppressive political system exacerbated
the prevalence and severity of medical and psychiatric
disorders,13 and that a democratic dispensation would
ultimately result in improved health for all.
On the other hand, there is also a body of literature that
adopts a critical stance towards the medicalization of a
range of phenomena including sexual deviance, violent
behavior, and even stress.14,15 This work argues that the
use of medical terms and constructs in such areas com-
prises an inappropriate extension of the health profes-
sions, and undermines recognition of the sociopolitical
nature of these phenomena. In writing about the suffer-
ing of individuals who lived through the Cultural Revo-
lution in China, Kleinman,16 a leading medical anthro-
pologist, writes that “To interpret such problems,
because of the bodily idioms that frequently accompany
them, solely as illness is to medicalize (and thereby triv-
ialize and distort) their significance.”
The entity of posttraumatic stress disorder (PTSD) itself
exemplifies some of these issues. Some might empha-
size the “normality” of posttraumatic stress responses;
these are in some ways ordinary responses to extraordi-
nary events. Similarly, there is a body of work that argues
that the diagnosis of PTSD, is merely the medicaliza-
tion of a sociopolitical arena. Young,17,18 for example, has
argued that the use of notions of stress reproduces con-
ventional knowledge about individual vulnerability
(rather than emphasizing resilience and the need for
sociopolitical change), and that the construct of PTSD
should be seen primarily as a cultural product. On the
other hand, there is a growing body of data that shows
that only a minority of those exposed to trauma go on to
develop PTSD, and that PTSD is mediated by specific
psychobiological dysfunctions, indicating that this con-
dition is best characterized as a medical disorder.19
It may be possible to reach a compromise between
these dichotomous viewpoints.20 After all, medical dis-
orders involve psychobiological dysfunctions, but also
Ethical aspects of research on psychological trauma - Stein et al
occur within sociocultural contexts that may contribute
to their pathogenesis and mold the experience of suf-
fering from symptoms. Similarly, it is important to
appreciate and investigate both the particular cognitive
and biological dysfunctions that characterize PTSD and
the social factors that affect vulnerability and resilience,
and that influence its course, experience, and outcome.
Indeed, in good clinical and epidemiological research it
is precisely this kind of complex interplay that is the
focus of the work. Scientific data can, for example, be
used to justify medical resources for those who suffer
from psychiatric symptoms, without losing sight of the
resilience people show in the face of adverse circum-
stances and the need for appropriate sociopolitical
interventions.
Do trauma interviews retraumatize
the individual?
In one model of the mind, favored by early psychoana-
lysts, psychopathology results when suppressed impulses
appear in a disguised form. In this model, expression of
these impulses resolves the unconscious conflict, and is
therefore cathartic. Indeed, many programs for the treat-
ment of PTSD insist that patients verbalize their past
traumas, explaining that this articulation is in and of
itself therapeutic.21 Pennebaker and colleagues have
published a series of studies suggesting that disclosure of
trauma, even if only in writing, is therapeutic.22,23 Rela-
tively simple interviews in Holocaust survivors,24 as well
as more complex forms of “testimony psychotherapy,”25
have been found beneficial.
Later psychodynamic models of the mind, however, have
emphasized the importance of the relationships on
which psychopathology and psychotherapy are based.
Certainly, therapeutic reprocessing of traumatic experi-
ence is more complex than simply talking about past
trauma; there is also a need for restructuring of the emo-
tional memories and acquisition of new and adaptive
responses.26,27 Similarly, testimony is arguably effective
only within certain contexts; talking about trauma may
only be useful at a particular time for a particular indi-
vidual, and it may be countertherapeutic to encourage
the traumatized person to relate his or her story when
time and/or context are inappropriate.
Debate about the value of the TRC exemplifies some of
these issues. On the one hand, there were many anec-
dotal reports that those who testified before the TRC
33
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
found this a healing experience.28 The historical signif-
icance of the event possibly facilitated a therapeutic
process. On the other hand, it should be pointed out
that there were also significant negative aspects,
including sometimes having to face cross-examination,
not receiving long-term psychological care, and not
receiving reparations in a timely fashion. Certainly, we
would warn that people who suffer from PTSD may
require a great deal more than merely the one-off
opportunity to testify about their experience.29
In the research setting, interviews about psychologi-
cal trauma typically comprise ratings scales and
structured interviews. In our anecdotal experience,
research subjects who complete realms of self-rat-
ing scales often have ambivalent feelings, experienc-
ing many of these as inapplicable or inaccurate.
Structured interviews, for their part, are often expe-
rienced as supportive (and rarely as traumatic). An
interesting recent study provides empirical confir-
mation of this positive experience in a study of child-
hood victimization.30 Nevertheless, it has been noted
that a minority of subjects in epidemiological sur-
veys do report distress, suggesting that intended
respondents should be warned of this.31,32 The experi-
ence that the research subject has of the research
interviewer (the research transference!) is likely
determined by multiple factors, including whether
the subject views the research as important, the rap-
port established with the interviewer, and the extent
to which the subject feels adequately heard and
appreciated.
Such considerations reinforce the necessity for
researchers to liaise closely with the community in
order to clearly convey the aims of the research, and
its potential risks and benefits. In terms of a modern
understanding of trauma responses, which incorpo-
rates an appreciation of both the underlying dys-
functional psychobiology of disorders such as PTSD,
as well as of the experience of suffering in the after-
math of trauma, the research interview (perhaps
particularly if it is part of a broader effort to archive
trauma histories 25) provides the opportunity for a
supportive, meaningful experience of giving testi-
mony about the past. At the same time, it should be
recognized that in order to help those with signifi-
cant psychosocial stressors, or medical disorders
such as PTSD, a research interview alone will be
insufficient.
Basic research
What about investigating perpetrators?
A number of people in our focus groups have felt that
the most important group of people in the country are
survivors. Why concentrate, they ask, on such questions
as the motivation and psychological status of perpetra-
tors? Clearly, the most important victims of the horrors
of apartheid are the survivors of gross human rights vio-
lations. Such people surely deserve the bulk of clinical
care and research attention.
At times, however, it can be problematic to draw an
overly simplistic distinction between survivor and per-
petrator. For one thing, it turns out that people who are
survivors are at times also perpetrators.28 During the lib-
eration struggle in South Africa, for example, victims of
apartheid at times perpetrated tremendous violence
against alleged traitors. Conversely, for example, soldiers
and policemen (white and black) who were recruited
against their will were arguably both perpetrators (fight-
ing against liberation forces) and victims (at times
coerced or tortured into their roles).
These phenomena, although somewhat unusual, are per-
haps reminiscent of the object-relations perspective that
emphasizes the prevention of splitting of idealized
“good” and devalued “bad” objects, and working
towards integration of mental representations. Such a
perspective could be useful in several areas of trauma
practice and research. For example, in the clinic, in work-
ing with disorders such as borderline personality disor-
der, which may be characterized by significant rage and
aggression, it is useful to appreciate that many patients
with this disorder have significant histories of childhood
trauma.
From a research perspective, much remains unknown
about perpetrators, and work in this area may in theory
ultimately prove of practical importance. In the after-
math of the second World War, writers were motivated
to tackle such issues as the concept of the authoritarian
personality.33 While more recent research has continued
to investigate antisocial personality disorder, there
appears to be a relative dearth of information about
“ordinary” perpetrators, and about the sociocultural and
psychobiological factors that may be relevant to pre-
venting perpetration in the future.34
At the same time, of course, there is an immense gap
between the average victim of apartheid and the average
perpetrator of gross human rights violations in South
Africa, and this must be clearly acknowledged. Ulti-
34
mately, the pain and suffering of the survivor does and
should remain paramount. It is important to emphasize,
as have many authors who have undertaken research
on perpetrators, that understanding perpetration by no
means implies condoning it.34,35
Failure to provide intervention
Is it morally justifiable to spend resources on a study of
people who have experienced gross human rights viola-
tions without subsequently receiving just recompense?
Providing an assessment of needs is assuredly an impor-
tant first step in directing resources towards survivors of
human rights violations. However, in the South African
setting, although the TRC has already documented the
existence of past violations, it has so far failed to deliver
the bulk of reparations. Is there an acceptable rationale
for spending more money in order to demonstrate past
trauma and current gaps in medical services?
We would argue that it is erroneous to draw too quick a
distinction between science and research as value-free
and processes such as the TRC as sociopolitical. Research
on trauma and posttraumatic responses may be invalu-
able in making a statement about the need for appropri-
ate resources for traumatized subjects. The TRC certainly
reached a similar conclusion (about the need for addi-
tional resources for traumatized South Africans), but it
did not provide detailed clinical and disability data that
would indicate the extent of resources necessary.
Thus, there would appear to be a crucial need to demon-
strate the extent of trauma and consequent psy-
chopathology in South Africa, and to use these data as
the basis for developing appropriate interventions. It is
important to document not only suffering but also
resilience to trauma. Similarly, there are a range of path-
ways to health; in South Africa these likely include the
use of traditional healers and participation in religious
communities. Given that medical resources are limited in
many parts of South Africa, the use of nonmedical
resources may be crucially helpful. Patients with PTSD
do, however, deserve referral to appropriate medical
services.
Interviewing traumatized people raises a range of
thoughts and feelings for research interviewers (the
research countertransference!). This may include guilt
at having been spared trauma oneself, frustration at not
being able to provide more help, and feeling that one is
taking advantage of research subjects in order to
Ethical aspects of research on psychological trauma - Stein et al
advance one's own professional career. Again, the expe-
rience of the interviewer is determined by multiple fac-
tors, including whether they view the research as impor-
tant, the rapport established with the interviewee, and
the extent to which they feel they are able to provide
help (such as a medical referral).
In short, in the area of trauma, research interviews
should not be idealized as providing a form of brief psy-
chotherapy, but nor should they be demonized as being
intrusive or as an inadequate substitute for treatment. It
would seem reasonable to provide interviewees with a
token gift in order to show the researcher's gratitude. In
higher socioeconomic groups a similar token may be
seen as insufficient in some ways; it certainly cannot rec-
ompense the interviewee adequately for their time and
effort. In lower socioeconomic groups, however, too
large a token might however be construed as a bribe
and may lead to distortion of data.
Aspectos éticos de la investigación en el
trauma psicológico
La investigación en el área del trauma psicológico
genera diversas cuestiones éticas complejas. Estos
aspectos éticos incluyen reflexiones acerca de la
justificación de la medicalización del sufrimiento, de la
nueva exposición al trauma por la que tienen que pasar
los pacientes, de los aspectos morales de quienes
investigan a los que han provocado algún trauma y
también del rechazo que puede presentarse para
proporcionar intervenciones apropiadas en víctimas de
traumas. Se discuten algunos de estos temas en el
contexto de un estudio de trauma realizado en
Sudáfrica y del reciente trabajo de la Comisión de
Verdad y Reconciliación en ese país.
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1. Bhaskar R. The Possibility of Naturalism: A Philosophical Critique of the Con-
temporary Human Sciences. Sussex, UK: Harvester Press; 1979.
2. Keat R, Urry J. Social Science as Theory. 2nd ed. London, UK: Routledge and
Kegan Paul; 1982.
3. Reznek L. The Nature of Disease. London, UK: Routledge and Kegan Paul;
1987.
4. Wakefield JC. Disorder as harmful dysfunction: a conceptual critique of
DSM-III-R's definition of mental disorder. Psychol Rev. 1992;99:232-247.
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Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
Conclusion
We tend to agree with the critic who argued that while
the TRC may not have provided “truth and reconcilia-
tion,” it was beneficial insofar as it fostered “knowledge
and acknowledgment.”36 Similarly, while research on psy-
chological trauma may of course have significant short-
comings, it is welcome since it fosters awareness of
trauma and facilitates appropriate intervention. Indeed,
good medical research involves good clinical principles
and fosters good clinical practices, and so the endeavors
of trauma researcher and clinician go hand in hand. ❏
This work was supported by the MRC Research Unit on Anxiety Disorders
(Prof Stein) and by an NIMH Grant R01 MH59575 (Dr Williams).
Aspects éthiques de la recherche sur les
traumatismes psychologiques
La recherche dans le domaine des traumatismes psy-
chologiques génère un certain nombre de questions
éthiques complexes : celles concernant la médicalisation
injustifiée des survivants souffrants et exposés à nou-
veau au traumatisme, celles relatives aux implications
morales de la conduite de recherches sur les auteurs de
sévices, celles, enfin, liées à la négligence à apporter des
mesures adaptées. Nous discutons certains de ces pro-
blèmes dans le contexte d'une étude de traumatismes
survenus en Afrique du Sud, et sur les travaux récents de
la Truth and Reconciliation (Commission pour la Vérité
et la Réconciliation) dans ce pays.
5. Wear S, Engelhardt HT, Wildes KW. Informed Consent: Patient Autonomy
and Clinician Beneficence Within Health Care. Washington, DC: Georgetown
University Press; 1998.
6. Coughlin SS. Ethics and Epidemiology. Oxford, UK: Oxford University Press;
1996.
7. Boraine A, Levy J. The Healing of a Nation? Cape Town, South Africa:
IDASA; 1995.
8. Boraine A, Levy J, Scheffer R. Dealing with the Past: Truth and Reconciliation
in South Africa. 2nd ed. Cape Town, South Africa: IDASA; 1997.
9. Asmal K, Asmal L, Roberts RS. Reconciliation Through Truth: A reckoning of
Apartheid's Criminal Governance. Cape Town, South Africa: David Philip; 1996.
Basic research
10. Stein DJ. Psychiatric aspects of the Truth and Reconciliation Commission
in South Africa. Br J Psychiatry. 1998;173:455-458.
11. Cooper CL. Handbook of Stress, Medicine, and Health. CRC Press; 1995.
12. Dohrenwend BP. Adversity, Stress and Psychopathology. Oxford, UK: Oxford
University Press; 1998.
13. Swartz L. Culture and Mental Health: A Southern African View. Cape Town,
South Africa: Oxford University Press; 1998.
14. Conrad P, Schneider J. Deviance and Medicalization: From Badness to Sick-
ness. St Louis, Mo: Mosby; 1980.
15. Wright P, Treacher A, eds. The Problem of Medical Knowledge: Examining
the Social Construction of Medicine. Edinburgh, UK: Edinburgh University
Press; 1982.
16. Kleinman A. Suffering and its professional transformation: toward an
ethnography of interpersonal experience. Cult Med Psychiatry. 1991;15:275-
301.
17. Young A. The discourse on stress and the reproduction of convention-
al knowledge. Soc Sci Med [Med Anthropol]. 1980;14B:133-146.
18. Young A. The Harmony of Illusions: Inventing Post-Traumatic Stress Dis-
order. Princeton, NJ: Princeton University Press; 1995.
19. Yehuda R, McFarlane AC. Conflict between current knowledge about
posttraumatic stress disorder and its original conceptual basis. Am J Psychi-
atry. 1995;152:1705-1713.
20. Stein DJ. Philosophy and the DSM-III. Compr Psychiatry. 1991;32:404-415.
21. Shay J. Achilles in Vietnam: Combat Trauma and the Undoing of Character.
New York, NY: Athaneum; 1993.
22. Pennebaker JW, Susman JR. Disclosure of traumas and psychosomatic
processes. Soc Sci Med. 1988;26:327-332.
23. Esterling BA, L'Abate L, Murray EJ, Pennebaker JW. Empirical founda-
36
tions for writing in prevention and psychotherapy: mental and physical
health outcomes. Clin Psychol Rev. 1999;19:79-96.
24. Pennebaker JW, Barger SD, Tiebout J. Disclosure of traumas and health
among Holocaust survivors. Psychosom Med. 1989;51:577-589.
25. Weine SM, Kulenovic AD, Pavkovic I, Gibbons R. Testimony psychother-
apy in Bosnian refugees: a pilot study. Am J Psychiatry. 1998;155:1720-1726.
26. Foa EB, Rothbaum BO. Treating the Trauma of Rape: Cognitive-Behavioral
Therapy for PTSD. New York, NY: Guilford; 1998.
27. Littrell J. Is the experience of painful emotion therapeutic? Clin Psychol
Rev. 1998;18:71-102.
28. Stein DJ, Swartz L, Walaza N, et al. Mental health beyond the Truth and
Reconciliation Commission. MRC (South Africa) Policy Brief. 1998;5:1-2.
29. Stein DJ, Bouwer C, Schmidt A, Allan A. Posttraumatic stress disorder
and the Truth and Reconciliation Commission [letter]. South Afr Med J.
1997;87:763.
30. Neuman E, Walker EA, Gefland A. Assessing the ethical costs and ben-
efits of trauma-focused research. Gen Hosp Psychiatry. 1999;21:187-196.
31. Henderson AS, Jorm AF. Do mental health surveys disturb? Psychol Med.
1990;20:721-724.
32. Jorm AF, Henderson AS, Scott R, et al. Do mental health surveys disturb?
Further evidence. Psychol Med. 1994;24:233-237.
33. Adorno TW, Frenkel-Brunswick E, Levinson DJ, Sanford RN. The Author-
itarian Personality. New York, NY: Harper; 1950.
34. Baumeister RF. Evil: Inside Human Violence and Cruelty. New York, NY: WH
Freeman; 1997.
35. Rosenbaum R. Explaining Hitler. New York, NY: Random House; 1998.
36. Ash TG. True Confessions. New York Review of Books. 1997;July 17:33-38.
Pharmacological aspects
Update on the epidemiology, diagnosis, and
treatment of posttraumatic stress disorder
Joseph Zohar, MD; Daniella Amital, MD; Heidi D. Cropp, BA;
Gadi Cohen-Rappaport, MD; Yaffa Zinger, MSc; Yehuda Sasson, MD

bat situations and that it is a “normal” response to

a traumatic situation, have contributed to poor
recognition of this disorder. The misconception
regarding combat and PTSD is reflected in the his-
tory of the names given to the disorder—“shell
shock,” “soldier’s heart,” “combat neurosis,” and
“operational fatigue.” However, in the late 1980s, it

P
osttraumatic stress disorder (PTSD) is a
maladaptive response to a traumatic event, which is
currently underdiagnosed and undertreated. It is
probable that several myths that surround PTSD,
for example, that it is almost solely related to com-
was realized that PTSD is related to all types of
traumatic events, including rape, physical attack,
severe automobile accidents, and natural or human-
made disasters. Consequently, the terms for the dis-
order were changed to “traumatic neurosis” and
later to “posttraumatic stress disorder,” and the
defined spectrum of events related to PTSD was
expanded accordingly. 1,2

Posttraumatic stress disorder (PTSD) is a maladaptive, pathological response to a traumatic event, which is cur-
rently underdiagnosed and undertreated. This results in part from a lack of awareness regarding the prevalence
of the disorder. It has been estimated that at least one third of the general population will be exposed to severe
trauma throughout their lifetime, out of which approximately 10% to 20% develop PTSD. A prevalence of 3%
to 6% of PTSD in the general population, found in several studies, corresponds well with these figures. Both the
type of trauma and the personal characteristics of the individual involved are associated with the probability
of developing PTSD. The Diagnostic and Statistical Manual of Mental Disorders, 4th ed (DSM-IV) gives four diag-
nostic criteria: (i) exposure and emotional response to a traumatic event; (ii) reexperiencing; (iii) avoidance; and
(iv) increased physiological arousal, along with severe impairment in occupational, social, and interpersonal func-
tioning. The rate of comorbidity with other mental disorders is high, particularly for major depression, anxiety
disorders, and substance abuse. Different types of psychological intervention, including cognitive-behavioral
therapy and a host of pharmacological interventions, have been tried. Selective serotonin reuptake inhibitors
(SSRIs) are currently the most widely researched agents with consistent, though modest, therapeutic effects.
Other compounds, such as tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs) have also
been found to be effective, although their use is limited due to side effects. PTSD is a psychobiological phe-
nomenon in response to psychological trauma, which represents maladaptive neurobiological dysregulation and
psychological dysfunction, and awaits further recognition and research.

Keywords: posttraumatic stress disorder; epidemiology; comorbidity; treatment; Author affiliations: The Chaim Sheba Medical Center, Division of Psychiatry Tel-
SSRI; tricyclic antidepressant; MAOI; augmentation treatment Hashomer, Israel (Joseph Zohar, Daniella Amital, Heidi D. Cropp, Gadi Cohen-
Rappaport, Yaffa Zinger, Yehuda Sasson); and The Sackler Faculty of Medicine,
Tel Aviv University, Ramat Aviv, Israel (Joseph Zohar, Yaffa Zinger).
Address for correspondence: Prof Joseph Zohar, Division of Psychiatry, The
Chaim Sheba Medical Center, Tel Hashomer 552621, Israel
(e-mail: jzohar@post.tau.ac.il)

37
Pharmacological aspects
Selected abbreviations and acronyms
CBT cognitive-behavioral treatment
5-HT 5-hydroxytryptamine (serotonin)
MAOI monoamine oxidase inhibitor
NCS National Comorbidity Survey
PTSD posttraumatic stress disorder
SSRI serotonin selective reuptake inhibitor
TCA tricyclic antidepressant
Interpretation of symptoms, which we would now con-
sider indicating a diagnosis of PTSD, as a “normal
response” to traumatic events has further impeded
progress in the field. Based on extensive epidemiological
studies, it is becoming increasingly clear that the vast
majority of individuals who are exposed to a traumatic
event will later adapt and continue with their lives. Only
a small percentage, which partially depends on the sever-
ity and the duration of the trauma and partially on addi-
tional factors, will develop a pathological fixation on the
traumatic event, ie, PTSD.
According to the 4th edition of the Diagnostic and Sta-
tistical Manual of Mental Disorders (DSM-IV), there are
three subtypes of PTSD: (i) acute; (ii) chronic; and (iii)
with delayed onset. These subtypes are defined according
to when the symptoms appear in relation to the key trau-
matic event and their duration, although all subsets
require a minimum duration of 1 month. Symptom dura-
tion of less than 3 months that appear within 6 months of
the trauma is diagnosed as acute-form PTSD. Chronic
PTSD corresponds to duration of symptoms of more
than 3 months, and delayed-onset PTSD corresponds to
an onset of at least 6 months after initial traumatic expo-
sure (and may begin up to several decades later).
Epidemiology
It has been estimated that at least one third of the pop-
ulation will be exposed to a severe trauma during their
lifetime.3,4 Since 10% to 20% of individuals exposed to
severe trauma will develop PTSD,5 according to this fig-
ure, the prevalence of PTSD in the general population
will range from 3% to 6%. This estimation has been con-
firmed in several studies carried out in the United
States,4, 6,7 but not in others.8,9
38
The type and magnitude of the trauma on the one hand,
and the characteristics of the individual on the other,
are all factors associated with the probability of devel-
oping PTSD. Personal characteristics that have been
associated with higher risk of developing PTSD include
high neuroticism scores,6 preexisting depression and anx-
iety8 (especially social phobia), early history of adver-
sity, and exposure to traumatic events in childhood
(childhood separation from parents, childhood abuse,
sexual assault, and parental divorce in early childhood).6
It also seems that, at least in relation to assaultive vio-
lence, the female gender is associated with higher risk.8
Other predictors include socioeconomic status: individ-
uals from lower socioeconomic levels may be more
prone to develop PTSD.6
The association between the type of trauma and the dif-
ferential risk of developing PTSD has been investigated
in a number of epidemiological studies. Kessler et al,6
in data deriving from 5877 persons 15 to 54 years of age
from the larger National Comorbidity Survey (NCS) of
8098, found that PTSD was associated with 65% of rape
cases in males (although the number of times this par-
ticular event occurred was very small) and with 49.5% of
rape cases in women, with 38.8% of combat-related
events, and with 21.3% of women who were faced with
criminal assault. Breslau et al4 also report that the high-
est risks of developing PTSD following civilian trau-
matic events were associated with rape (49.0% ±12.2%),
followed by being badly beaten up (31.9%± 8.6%), and
other kinds of sexual assault (23.7%±10.8%).
Definition and diagnosis of PTSD
The diagnostic criteria for PTSD are listed in both the
DSM-IV and the International Classification of Dis-
eases, 10th revision (ICD-10). The criteria are essen-
tially the same, with the exception that no time require-
ment is stipulated in the ICD-10. As the authors believe
that the element of time is critical in this disorder, the
DSM-IV seems to be a more appropriate diagnostic
system, and, indeed, has been applied much more
widely in studies.
There are four main diagnostic criteria, or characteristic
features, of PTSD. These are: exposure to a traumatic
event, reexperiencing, avoidance, and increased arousal.
According to the DSM-IV, only extreme traumatic stres-
sors, in contrast with general stressful experiences, have
been linked etiologically to PTSD. Such traumatic events
Epidemiology, diagnosis, and treatment of PTSD - Zohar et al
are defined as situations in which “the person experi-
enced, witnessed, or was confronted with an event or
events that involved actual or threatened death or seri-
ous injury, or a threat to the physical integrity of self or
others …” (DSM-IV, p 427). As per this definition, very
severe humiliation, or any other type of disappointment
or intense stress, does not fulfill the criteria for a trau-
matic event. On the other hand, it has been recognized
in the DSM-IV that an individual does not need to be
exposed to a trauma that is “outside the range of usual
human experience,” as previously defined by DSM-III.
Moreover, the DSM-IV has added an important element
to the diagnosis: the emotional response, which is char-
acterized as “intense fear, helplessness, or horror”; DSM-
IV, p 428), and hence, the diagnostic criteria in DSM-IV
is more stringent in this regard.
The second feature of PTSD is reexperiencing (Criterion
B). The PTSD patient is emotionally stuck in the trau-
matic event, even many years after it has occurred, and
constantly reexperiencing it in various ways: flashbacks;
stressful recollections; recurrent, distressing dreams; act-
ing or feeling as if the traumatic event were reoccurring
or experiencing intense psychological distress or physi-
ological reactivity following exposure to internal or
external cues that symbolize or resemble the event.
An additional maladaptive mechanism used by patients
diagnosed with other anxiety disorders, including patients
with PTSD, is avoidance.Avoidance is listed as Criterion C
in the DSM-IV’s definition of PTSD. Patients with PTSD
attempt to avoid any stimuli associated even in a periph-
eral way with the trauma, including smells, feelings,
thoughts, activities, places, or people. This avoidance often
expresses itself as “emotional anesthesia,” ie, “markedly
diminished interest or participation in significant activi-
ties,” “feeling of detachment,” a “restricted range of
affect,” and a “sense of a foreshortened future.” Some-
times amnestic or dissociative symptoms (which may also
be interpreted as avoidance) appear in response to the
extreme reexperiencing, and are thought of as another
maladaptive mechanism that originally evolves to buffer
the individual from painful recollections.
The fourth feature of PTSD (Criterion D) is increased
arousal. Patients are constantly “on alert,” have diffi-
culty in falling or staying asleep, suffer from irritability
or outbursts of anger, have difficulty concentrating, and
experience hypervigilance and exaggerated startle
response. For many of the patients and their families,
this group of symptoms is particularly difficult as the
39
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
families need to maintain a very calm environment while
the patients are concerned about losing control.
An additional criterion relates to the functional impair-
ment of the symptoms, described as causing severe impair-
ment in social, occupational, and family areas of life.
Comorbidity with other mental disorders is prevalent
in PTSD. A recent epidemiologic survey indicated that
approximately 80% of PTSD patients meet criteria for
at least one other psychiatric diagnosis.3,10 The most com-
mon disorders experienced concurrently with PTSD
found in the US National Comorbidity study are major
depression (48.5 in women and 47.9 in men), other anx-
iety disorders (more than one third), and substance
abuse (found in one third of women and half of all
men).6 Depression seems to be a common disorder
found in comorbidity with PTSD as evidenced by addi-
tional studies of different populations.11,12 Since symp-
toms such as guilt, ruminations, decreased concentra-
tion, anxiety, and outbursts of anger are parts of other,
more familiar disorders, the diagnosis of PTSD may be
overlooked. Many times such patients may be misdiag-
nosed with depression, sleep disturbance, personality
disorder, substance abuse, malingering, or even schizo-
phrenia.4,5
Two studies of psychotic female inpatients demonstrate
this point. These studies indicate that patients with a his-
tory of childhood sexual abuse were more likely to have
intrusive, avoidant/numbing, and hyperarousal symp-
toms than their nonabused counterparts; a full 66% of
these women met the diagnosis for PTSD, but had never
been diagnosed.13,14
It has further been suggested that the high levels of
comorbidity may point to the possibility of several dif-
ferent subgroups of PTSD.15-17 An example of such a
grouping is development of psychological or behavioral
problems before, concurrent with, or after exposure to
the traumatic stressor.16 An alternative approach sug-
gests that the picture may be more complex, that asso-
ciated psychiatric disorders are not purely comorbid,
but “interwoven with the PTSD.”17
Treatment approaches
Treatment can either be applied to “seal over” the dis-
tress of the patient or do exactly the opposite, to
“uncover the pain,” which can then facilitate resolution
of the traumatic experience in conjunction with psycho-
logically oriented therapy.18 Accordingly, it has been
Pharmacological aspects
noted that serotonin selective reuptake inhibitors
(SSRIs) and tricyclic antidepressants (TCAs) are use-
ful in helping the patient to “put their fears away,” while
cognitive-behavioral treatment (CBT) helps patients via
stress inoculation, training, and exposure19,20 to better
cope with the traumatic event.
Psychological treatment
The effect of different courses of psychological treat-
ment are only beginning to be systematically reviewed.
A combined approach to treatment is generally consid-
ered to be beneficial, especially in the acute stages.21
CBTs are the most developed, and have been most rig-
orously tested; they include a variety of treatments such
as exposure procedures, cognitive restructuring proce-
dures, and anxiety management programs (for a review,
see Foa and Meadows20). Further methodologically
sound research is needed to follow up on the encourag-
ing preliminary research.
Psychopharmacological treatment
The aim of pharmacotherapy is to reduce symptoms of
intrusion and generalization of the trauma, lower the
degree of avoidance and numbing behavior, reduce
hyperarousal, and decrease impulsivity and dissociative
symptoms.22
While attempting pharmacological intervention for
patients with PTSD, careful listing of the main symp-
toms is advisable, and the therapeutic effect of medica-
tions should be evaluated according to the specific
changes in those symptoms. In addition, patients should
be made aware that it may take as long as 10 weeks, or
even longer, to attain the maximal beneficial response.
Emerging data indicate that antidepressant medications
may have more prominent roles in the treatment of this
disorder, namely, selective serotonin reuptake inhibitors
(SSRIs), tricyclic antidepressants (TCAs), and monoamine
oxidase inhibitors (MAOIs).
Serotonin selective reuptake inhibitors (SSRIs)
SSRIs are currently the most widely investigated agents,
and have been studied in several large, multinational,
double-blind, placebo-controlled studies. Based on stud-
ies with sertraline and fluoxetine, and on additional pos-
40
itive open studies with other SSRIs, namely fluvoxamine
and paroxetine, it is becoming increasingly clear that
SSRIs are effective in the treatment of PTSD. More-
over, the symptomatic changes are related to the core
symptoms of PTSD and not merely to unspecified
changes. The doses used in these studies were 40 mg for
fluoxetine, 100 to 150 mg for sertraline, 150 to 300 mg for
fluvoxamine, and a mean dose of 40 mg for paroxetine.
Tricyclic antidepressants (TCAs)
Two double-blind studies with amitriptyline and
imipramine showed these drugs to be superior to
placebo in PTSD by a difference of 35% in number of
improved patients.23-25 Doses used were 150 to 250 mg
of amitriptyline and a mean dose of 225 mg for
imipramine. However, as PTSD patients have low tol-
erance for side effects (related to their hyperarousal
cluster of symptoms), TCAs have not been widely used
in PTSD. It is of interest to note that there appears to
be an inverse relationship between the intensity of
exposure to trauma and the success of treatment with
TCAs.
Monoamine oxidase inhibitors (MAOIs)
In a study that compared imipramine with phenelzine, at
a mean dose of 68 mg, and placebo,23 a better rate of
improvement was demonstrated in the phenelzine group
(68%) than in the placebo group (28%). Moreover,
phenelzine-treated patients showed better treatment
retention than those treated with imipramine (7.4 weeks
vs 5.6 weeks for imipramine and 5.5 weeks for placebo)
and also improved more on globally assessed symptoms
(phenelzine: 44%; imipramine: 25%; placebo: 28%).23
However, it is important to note the attendant risks,
namely, hypertensive crisis, if the dietary restrictions
(low tyramine diet) associated with this medication are
not kept. In a disorder where impulsiveness and the
abuse of alcohol are often present these risks may be
even higher.
If the patient is not responding, or if the response is
partial, one possibility is to switch from one group of
medication to another, eg, switching from SSRIs to
another group, such as TCAs or MAOIs, or else, to
make a switch within the same group, eg, switching from
one SSRI (or one TCA) to another.
Epidemiology, diagnosis, and treatment of PTSD - Zohar et al
Although the available data are very limited, another
alternative may be to switch from SSRIs to nefazodone,
since the side-effect profile of this medication is very
favorable and its mode of action quite different. Nefa-
zodone potently antagonizes 5-HT2 receptors while also
inhibiting both serotonin and norepinephrine reuptake.
The recommended dose for depression is 200 mg twice a
day, which would probably be suitable for PTSD as well,
providing double-blind studies are able to demonstrate
the efficacy in this condition.
Benzodiazepines
Regarding the available evidence on benzodiazepines,
this group of drugs to have limited efficacy in the treat-
ment of PTSD. Braun et al26 found no significant differ-
ence between alprazolam and placebo in a group of 10
patients who had treatment-resistant illness.
Propranolol has been administered in open studies of
children and adults and was found to improve PTSD
symptoms in most of the studies. The role of propra-
nolol is still unclear and needs to be further examined in
double-blind studies.
Augmentation therapies in PTSD
Although little is known about augmentation strategies
in PTSD, one possible approach to treating an individ-
ual who is partly responsive or nonresponsive to treat-
ment is in accordance with the symptomatic approach,
ie, if the patient is suffering from an outburst of anger,
mood stabilizers such as lithium, carbamezapine, or val-
proic acid might be added.27,28 If anxiety and irritability
are present, a buspirone augmentation is an option to
be considered.29
Another possibility for augmentation is for a patient
who is very agitated. In such cases, small doses of
antipsychotics might be administered. The case for the
addition of antipsychotics is even stronger if a concur-
rence of psychosis and PTSD is present. Indeed, there
are several case reports demonstrating the efficacy of
thioridazine, olanzapine, risperidone, and clozapine.30
Buspirone, a 5-HT1A agonist, and clonidine have been
administered either alone or as augmenting agents in
PTSD. As buspirone may be associated with decrease
of anxiety, it may be administered either as an aug-
menting agent for SSRIs or TCAs, or as a stand-alone
drug (10-20 mg, three times daily).
41
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
Clonidine has been reported in open studies to be effec-
tive in ameliorating PTSD symptoms, especially the
depression component. Although it has also been used
as an augmenting agent for imipramine, double-blind
studies are needed in order to substantiate this claim.
There are a number of case reports with antidepres-
sants such as trazodone, venlafaxine, and bupropion,
which in very limited cases under open conditions were
reported to be of benefit in improving PTSD symp-
toms. The doses used were 300 mg for trazodone, 250
mg for venlafaxine, and 300 mg for bupropion.
Duration of treatment
Very little is known regarding maintenance treatment
of the disorder. It seems, though, that there is a spon-
taneous decrease in the symptoms of PTSD in the first
6 months following the trauma, which continues up to 4
or 5 years. From this standpoint, one should take into
account this spontaneous recovery when applying psy-
chopharmacological intervention during the first 5
years after the trauma, ie, a gradual down-titration of
the dose is called for in order to evaluate whether the
medication is really needed.
The same basic rules about discontinuation of medica-
tion in other anxiety disorders apply here as well,
namely, slow and gradual discontinuation, every 6
weeks or so. The down-titration of medication should
be in very small doses. Only if by the end of this period
there is no sign of symptom exacerbation may the
patient proceed to the next titration. In cases of dete-
rioration, a return to the previous dose seems logical,
although evidence to confirm this is lacking.
For patients who have exceeded the 4- to 5-year period,
it seems that long-term administration of medication is
often needed, although there is still the possibility of
spontaneous remission, as long as 10 years following
the trauma.
A special consideration for long-term maintenance
treatment of patients with PTSD is in relation to spe-
cific dates in the year that may be associated with an
exacerbation of PTSD symptoms, such as the anniver-
sary of the trauma, or memorial days for veterans with
PTSD. During these periods, specific close monitor-
ing may be appropriate, with the possible addition of
nonbenzodiazepine hypnotics and anxiolytics, or alter-
natively, preparing the patient by increasing the dose of
medication that was used throughout the year.
Pharmacological aspects
Conclusion
The prevalence of PTSD ranges from 1.5% to 6% in
different studies of different populations. The disorder
has severe consequences on the quality of life, not only
of the individuals afflicted, but also for their families
and significant others. Although it is a prevalent and
severe disorder, PTSD is currently underdiagnosed, and
consequently undertreated.
The diagnostic criteria for PTSD are comprised of four
components: the trauma (including the immediate
emotional response); reexperiencing; avoidance
(including “emotional anesthesia”); and hyperarousal.
In order to identify PTSD patients, specific questions
REFERENCES
1. American Psychiatric Association. Diagnostic and Statistical Manual of Men-
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2. American Psychiatric Association. Diagnostic and Statistical Manual of Men-
tal Disorders. 4th ed. Washington, DC: American Psychiatric Press; 1994.
3. Solomon SD, Davidson JRT. Trauma, prevalence, impairment, service use,
and cost. J Clin Psychiatry. 1997;58:5-11.
4. Breslau N, Kessler, RC, Chilcoat HD, Schultz LR, Davis GC, Andreski P. Trau-
ma and posttraumatic stress disorder in the community: the 1996 Detroit
Area Survey of Trauma. Arch Gen Psychiatry. 1998;55:626-632.
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traumatic stress disorder in an urban population of young adults. Arch Gen
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post-traumatic stress disorder in the community: prevalence, risk factors
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ty sample of older adolescents. J Am Acad Child Adolesc Psychiatry.
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10. Brady KT. Posttraumatic stress disorder and comorbidity: recognizing
the many faces of PTSD. J Clin Psychiatry. 1997;58 (suppl 9):12-15.
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and depression. An analysis of comorbidity. Br J Psychiatry. 1997;170:479-482.
12. North CD, Smith EM, Spitznagel EL. Posttraumatic stress disorder in sur-
vivors of a mass shooting. Am J Psychiatry. 1994;151:82-88.
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ior of chronically hospitalized psychotic women. Am J Psychiatry.
1987;144:1474-1476.
14. Craine LS, Henson CB, Colliver JA, et al. Prevalence of a history of sexu-
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Community Psychiatry. 1988;39:300-304.
42
addressing these points need to be included in every
mental status examination, especially if elements of
depression, anxiety, oubursts of anger, or drug or alco-
hol abuse are present, as they often appear to be seque-
lae of PTSD.
Treatment should take a broad approach, addressing
familial and occupational issues as well. Currently, SSRIs
are emerging as the pharmacological treatment of choice
for this disorder, as demonstrated in large double-blind,
placebo-controlled, multicenter studies.
However, the effect size, though significant, is modest.
Clearly, more research and better therapeutic interven-
tions are called for in this unique disorder, which, as
per the definition, point to the external stressor as the
cause. ❑
15. Friedman MJ. Posttraumatic stress disorder. J Clin Psychiatry.
1997;58(suppl 9):33-36.
16. Keane TM, Kaloupek, DG. Comorbid psychiatric disorders in PTSD. Impli-
cations for research. Ann NY Acad Sci. 1997;821:24-34.
17. Deering CG, Glover SG, Ready D, Eddleman HC, Alarcon RD. Unique pat-
terns of comorbidity in posttraumatic stress disorder from different sources
of trauma. Compr Psychiatry. 1996;37:336-346.
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19. Foa EB, Rothbaum BO, Riggs DS, Murdock TB. Treatment of posttrau-
matic stress disorder in rape victims: a comparison between cognitive-behav-
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20. Foa EB, Meadows EA. Psychosocial treatments for posttraumatic stress
disorder: a critical review. Annu Rev Psychol. 1997;48:449-480.
21. Sutherland SM, Davidson JR. Pharmacotherapy for post-traumatic stress
disorder. Psychiatr Clin North Am. 1994;17:409-423.
22. Davidson MD, Jonathan RT. Biological therapies for posttraumatic stress
disorder: an overview. J Clin Psychiatry. 1997;58:29-32.
23. Kosten TR, Frank JB, Dan E, et al. Pharmacotherapy for posttraumatic
stress disorder using phenelzine or imipramine. J Nerv Ment Dis.
1991;179:336-370.
24. Davidson JRT, Kudler H, Saunders WB, et al. Predicting response to
amitriptyline in posttraumatic stress disorder. Am J Psychiatry. 1993;150:1024-
1029.
25. Davidson J, Kudler H, Smith R, et al. Treatment of posttraumatic stress dis-
order with amitriptyline and placebo. Arch Gen Psychiatry. 1990;47:259-266.
26. Braun P, Greenberg D, Dasberg H, et al. Core symptoms of posttrau-
matic stress disorder unimproved by alprazolam treatment. J Clin Psychiatry.
1990;51:236-238.
27. Lipper S, Hammett EB, Davidson JRT, et al. Preliminary study of carba-
mazepine in posttraumatic stress disorder. Psychosomatics. 1986;27:849-854.
28. Fesler FA. Valproate in combat-related posttraumatic stress disorder.
J Clin Psychiatry. 1991;52:361-364.
29. Fichtner CG, Crayton JW, Buspirone in combat-related posttraumatic
stress disorder. J Clin Psychiatry. 1994;57:66-72.
30. Katz RJ, Loh MH, Arbus P, et al. Pharmacotherapy of posttraumatic
stress disorder with a novel psychotropic. Anxiety. 1995;1:169-172.
Epidemiology, diagnosis, and treatment of PTSD - Zohar et al
Puesta al día en la epidemiología, el
diagnóstico y el tratamiento del
trastorno de estrés postraumático
El trastorno de estrés postraumático (TEPT) es una
respuesta patológica, que traduce una mala adapta-
ción frente a un acontecimiento traumático. Este cua-
dro está actualmente subdiagnosticado y subtratado.
Esto se debe en parte a una falta de conciencia acerca
de la prevalencia de este trastorno. Se ha estimado que
al menos un tercio de la población general estará
expuesta a un trauma severo en algún momento de su
vida, y de ellos aproximadamente un 10% a 20%
desarrollará un TEPT. En diversos estudios en pobla-
ción general se ha encontrado una prevalencia entre
el 3% y el 6% de TEPT, lo que se corresponde bien
con el marco de referencia antes enunciado. Tanto el
tipo de trauma, como las características personales
del individuo afectado se asocian con la probabilidad
de desarrollar un TEPT. El Manual Diagnóstico y
Estadístico de los Trastornos Mentales en su cuarta
edición (DSM-IV) determina cuatro criterios diag-
nósticos para el TEPT: a) exposición y respuesta
emocional al acontecimiento traumático, b) re-experi-
mentar el acontecimiento, c) conductas de evitación y
d) aumento de la activación fisiológica. Todos estos
criterios se traducen en un severo deterioro del fun-
cionamiento ocupacional, social e interpersonal. La
frecuencia de comorbilidad con otros trastornos men-
tales es alta, especialmente con depresión mayor, tras-
tornos de ansiedad y abuso de sustancias. Se han
ensayado diferentes tipos de intervenciones psicológi-
cas incluyendo terapia cognitivo conductual y varia-
dos tratamientos farmacológicos. Los inhibidores
selectivos de la recaptación de serotonina (ISRS) han
sido los fármacos más ampliamente investigados y se
ha encontrado que sus efectos terapéuticos, aunque
modestos, son consistentes. Otros medicamentos
como los antidepresivos tricíclicos (AT) y los inhibi-
dores de la mono amino oxidasa (IMAO) han
demostrado ser efectivos, pero su uso está limitado
por los efectos secundarios indeseables. El TEPT
constituye un fenómeno psicobiológico, en respuesta
al trauma psicológico, que representa una disregula-
ción neurobiológica de mala adaptación y una dis-
función psicológica que requiere de mayor reconoci-
miento e investigación en el futuro.
43
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
Mise au point sur l'épidémiologie, le
diagnostic et le traitement de l’état de
stress post-traumatique
L’état de stress post-traumatique (ESPT) correspond
à une réponse inadaptée et pathologique à un événe-
ment traumatisant. Ce trouble est actuellement sous-
diagnostiqué et sous-traité, en partie en raison d’une
mauvaise appréciation de sa prévalence. On a estimé
qu’au moins le tiers de la population générale sera
exposée à un traumatisme sévère au cours de sa vie et
que 10 à 20% de cette population développera un
ESPT. Plusieurs études ont trouvé une prévalence de
3 à 6% d’ESPT dans la population générale, ce qui
correspond bien à ce schéma. Le type du traumatisme
et les caractéristiques personnelles du sujet impliqué
sont corrélés à la probabilité de développer un ESPT.
La 4e édition du Manuel Diagnostique et Statistique
des Troubles Mentaux (DSM-IV) définit quatre cri-
tères diagnostiques : l’exposition et la réponse émo-
tionnelle à un événement traumatisant ; la réexpérien-
ce ; l’évitement et l’hyperactivité neurovégétative, ainsi
qu’une altération sévère des activités professionnelles,
sociales et interpersonnelles. Le taux de comorbidité
avec d’autres troubles mentaux est élevé, particulière-
ment en ce qui concerne les dépressions majeures, les
troubles anxieux et l’usage de substances toxiques.
Différents types d’aides psychologiques, y compris la
thérapie cognitivo-comportementale et un grand
nombre de traitements médicamenteux ont été essayés.
Les inhibiteurs de la recapture de la sérotonine (IRS)
sont actuellement les médicaments faisant l'objet des
recherches les plus nombreuses, car ils ont des effets
thérapeutiques constants, bien que modestes. D’autres
composés, tels que les antidépresseurs tricycliques et
les inhibiteurs de la monoamine oxydase (IMAO), se
sont aussi montrés actifs, bien que leur utilisation soit
limitée par leurs effets secondaires. L'ESPT, phéno-
mène psychobiologique en réponse à un traumatisme
psychologique qui correspond à une dysrégulation
neurobiologique inadaptée et à un dysfonctionnement
psychologique, nécessite donc de faire l'objet d'une
meilleure identification et d'une recherche accrue.
Posters & images in neuroscience
An overview of the Peritraumatic Distress Scale
Posttraumatic stress disorder (PTSD) occurs when significant intrusion, avoidance, and
hyperarousal symptoms are manifest for at least 1 month following exposure to a traumatic
event, with at least 1 month elapsed between the event and the diagnosis (Diagnostic and
Statistical Manual of Mental Disorders, 4th edition, 1994 [DSM-IV]).1 However, such
symptoms are not necessarily manifest in the immediate aftermath of the trauma,2 nor does
their initial presence strongly predict who will develop PTSD.3 One immediate response to
trauma which has been convincingly linked to PTSD symptoms is peritraumatic dissociation.4
In this poster, we briefly introduce a new scale assessing immediate responses distinct from
peritraumatic dissociation, and we examine its power to predict PTSD symptoms.

Methods Results and discussion

Participants
Six hundred officers were recruited from the police
departments of New York, NY, and Oakland and San
Jose, Calif, USA. Fifty-two percent of the sample was
Caucasian. Eighty percent were male. The mean age was
36.50 years (standard deviation [SD] = 6.96). Years in the
police force averaged 12.37 (SD= 6.78). Most participants
(85%) were living with a partner. Number of exposure
to critical incidents ranged from 2 to 670 (mean
[M] = 171.27, SD = 130.93).5 The incident selected for
completing the questionnaires had occurred on average
6.50 (SD =5.11) years ago.A reimbursement of $100 was
provided for participation in the study.
Instruments
The Peritraumatic Distress Scale (PDS) was used to
assess emotional, cognitive, and physical reactions occur-
ring during a critical incident and immediately after.6 Dis-
sociation at the time of the incident was measured with
the Peritraumatic Dissociative Experience Questionnaire
(PDEQ).7 The Impact of Event Scale–Revised (IES-R)
was used to measure PTSD symptoms in the last 7 days.8
The Mississippi Scale (MCS) was used to measure PTSD
and associated symptoms since the critical incident.9
Statistical analyses
We conducted a Cronbach alpha reliability analysis and
an oblique principal factor analysis with Promax rota-
tion on the items of the PDS. Two series of hierarchical
multiple regression analyses were conducted using
sociodemographics (gender, ethnicity, years of service),
exposure, the PDEQ and PDS as predictors of either
the MCS or the IES-R.
The PDS scores ranged from 0.10 to 3.57 and the mean was
1.37 (SD=0.56).The distribution of scores approached nor-
mality and was deemed suitable for parametric analyses.
The scale was internally consistent (=0.80) and showed
strong convergent validity with the PDEQ, r(599)=0.55,
P<0.001.
The PDS factor solution is presented in Table I. Items
defining factor 1 included dysphoric emotions such as
helplessness, sadness and grief, frustration and anger,
and horror. Factor 2 was mostly defined by items related
to loss of safety and arousal, such as being afraid, think-
ing one might die, and having intense bodily reactions
(sweating, shaking, heart-pounding). Items loading on
factor 3 were related to the loss of positive beliefs about
the self and others, such as thinking that one had done
all he or she could during the critical incident, not feel-
ing prepared by one’s experience, and not believing that
others understood. We labeled the factors negative emo-
tions, perceived life threat and bodily arousal, and
appraisal. Those factors had eigenvalues of 3.32, 2.53,
and 2.02, respectively. The sum of the communality esti-
mates was 7.58, explaining 38% of the total variance and
93% of trace. Intercorrelations among the PDS factors
were low, ranging from -0.25 to 0.12 (P<0.05). The low
PDS factor intercorrelation coupled with correlations
of 0.17 to 0.42 (P<0.001) with the outcome measures
(IES-R and MCS) suggest that various forms of peri-
traumatic distress, as captured by the PDS, can lead to
the development of PTSD symptoms.
Two stepwise regression analyses (not fully reported
here) were conducted. In predicting the MCS and IES-R,
demographic and exposure variables explained very lit-
tle variance (3%). The PDEQ, entered in the second

44
step, explained 20% and 16% of unique variance on the
MCS and IES-R, respectively. Entering the PDS in step
3 explained 11% and 8% unique variance on the MCS
and IES-R, respectively. We repeated this set of analyses
with the inclusion order of the PDEQ and PDS reversed.
Entered in the second step, the PDS explained 29% and
17% of unique variance on the MCS and IES-R, respec-
tively. Entered in the third step, the PDEQ explained 3%
of unique variance on both the MCS and the IES-R.
The items and factors of the PDS provide insight as to
what some of the salient peritraumatic dimensions may
be, in addition to peritraumatic dissociation. In this
study, the PDS explained a significant amount of vari-
ance over and above peritraumatic dissociation which is
currently considered among the most powerful predic-
tors of PTSD symptoms.3 Test-retest data for the PDS is
currently being gathered as well as data from individu-
als not working in the police. In future, it would be use-
ful to investigate prospectively the power of the PDS in
predicting PTSD diagnosis rather than symptoms, as
well as other trauma-related disorders.

REFERENCES
1. Diagnostic and Statistical Manual
Factor loadings of Mental Disorders. 4th ed. Wash-
ington, DC: American Psychiatric
1 2 3 Association; 1994. 2. Malt UF, Kar-
Item Negative Perceived Appraisal Commu- lehagen S, Hoff H, et al. The effect of
major railway accidents on the psy-
M (SD) emotions life threat nality chological health of train drives. 1.
Acute psychological responses to
Abbreviated item description accident. J Psychosom Res.
1993;37:793-805. 3. Shalev AY, Peri
T, Canetti L, Schreiber S. Predictors
1. Felt helpless to do more 1.7 (1.4) 0.73 0.07 -0.19 0.53 of PTSD in injured trauma survivors:
a prospective study. Am J Psychiatry.
2. Felt confident that all was being done 2.1 (1.3) -0.23 -0.14 0.55 0.32 1996;153:219-225. 4. Marmar CR,
Weiss DS, Metzler TJ. Peritraumatic
3. Felt sadness and grief 2.0 (1.5) 0.72 0.23 -0.05 0.61 dissociation and posttraumatic stress
4. Felt frustrated or angry that I did not do more 2.1 (1.5) 0.74 0.10 -0.17 0.55 disorder. In: Bremner JD, Marmar CR,
eds. Trauma, Memory and Dissocia-
5. Felt afraid for my safety 1.4 (1.6) 0.13 0.74 -0.02 0.58 tion. Washington, DC: American Psy-
chiatric Press; 1998. 5. Brunet A,
6. Felt prepared by my experience 1.7 (1.3) -0.32 -0.05 0.47 0.27 Weiss D, Best SR, Liberman A, Fagan
J, Marmar CR. Assessing Recurring
7. Felt guilty not more was done 1.0 (1.3) 0.59 0.22 -0.32 0.40 Traumatic Exposure: The Critical Inci-
8. Felt others were sympathetic 2.1 (1.3) -0.21 -0.02 0.54 0.42 dent History Questionnaire. Paper
presented at the International Soci-
9. Felt others understood my experience 1.7 (1.2) -0.06 -0.09 0.58 0.36 ety for Traumatic Stress Studies,
Washington, DC. November 21,
10. Felt ashamed of my emotions 0.4 (1.0) 0.37 0.29 -0.29 0.24 1998. 6. Brunet A, Weiss DS, Metzler
11. Felt I did all I could 2.4 (1.3) -0.32 -0.01 0.54 0.34 TJ, Best S, Fagan J, Marmar CR. Post-
traumatic Stress Response in Police
12. Was upset by other people’s action 1.1 (1.4) 0.22 0.22 -0.36 0.18 Officers: The Predictive Power of Per-
itraumatic Reactions. Paper pre-
13. Worried about the safety of others 1.7 (1.6) 0.09 0.54 -0.14 0.34 sented at the International Society
for Traumatic Stress Studies, Miami,
14. Was about to lose control over emotions 0.7 (1.1) 0.54 0.30 -0.30 0.38 Fla. November 15, 1999. 7. Marmar
15. Difficulty controlling bowel and bladder 0.1 (0.4) 0.16 0.26 -0.14 0.10 CR, Weiss DS, Metzler TJ. The Peri-
traumatic Dissociative Experiences
16. Felt like it would never end 0.8 (1.2) 0.27 0.56 -0.18 0.37 Questionnaire. In: Wilson JP, Keane
TM, eds. Assessing Psychological
17. Was horrified 1.4 (1.5) 0.57 0.06 -0.12 0.33 Trauma and PTSD: A Handbook for
18. Had physical reactions 1.5 (1.4) 0.27 0.59 -0.05 0.41 Practitioners. New York, NY: Guilford
Press; 1997. 8. Weiss DS, Marmar CR.
19. Felt I might pass out 0.2 (0.8) 0.24 0.36 -0.16 0.18 The Impact of Event Scale. Revised.
In: Wilson JP, Keane TM, eds. Assess-
20. Thought I might die 0.7 (1.3) 0.09 0.67 -0.06 0.48 ing Psychological Trauma and PTSD:
A practitioner’s Handbook. New
York, NY: Guilford Press; 1997:399-
Note. Item scores range from 0 (not at all true) to 4 (completely true). The PDS is scored by computing 411. 9. Keane TM, Fairbank JA, Cad-
dell JM, Zimering RT, Taylor KL, Mora
the mean of the 20 items, with items 2, 6, 8, 9, and 11 being reversed for scoring. Items loading above C. Clinical evaluation of a measure
0.5 are in red. to assess combat exposure. Psycho-
logical Assessment: A journal of Con-
sulting and Clinical Psychology.
1989;1:53-55.

Table I.
The PDS factor solution. Poster by: Alain Brunet, PhD;
Daniel S. Weiss, PhD; Thomas J. Metzler, MA; Suzanne R. Best, PhD; Jeffrey Fagan, PhD;
Kumar Vedantham, MD; Charles R. Marmar, MD
USCF Department of Psychiatry, DVAMC Psychiatry Service (116P), 4150 Clement Street
San Francisco, CA 94121-1545, USA

45
Clinical research
From shell shock and war neurosis
to posttraumatic stress disorder: a history
of psychotraumatology
Marc-Antoine Crocq, MD; Louis Crocq, MD
The term posttraumatic stress disorder (PTSD) has
become a household name since its first appearance
in 1980 in the third edition of the Diagnostic and
Statistical Manual of Mental Disorders (DSM-III) pub-
lished by the American Psychiatric Association. In the
collective mind, this diagnosis is associated with the
legacy of the Vietnam War disaster. Earlier conflicts
had given birth to terms, such as “soldier's heart,”
“shell shock,” and “war neurosis.” The latter diag-
nosis was equivalent to the névrose de guerre and
Kriegsneurose of French and German scientific liter-
ature. This article describes how the immediate and
chronic consequences of psychological trauma made
their way into medical literature, and how concepts
of diagnosis and treatment evolved over time.
Keywords: posttraumatic stress disorder; shell shock; psychotraumatology; litera-
ture; history of medicine
Author affiliations: FORENAP – Institute for Research in Neuroscience and
Neuropsychiatry, Rouffach, France (Marc-Antoine Crocq); and Cellule d’Ur-
gence Médico-Psychologique, SAMU de Paris, Hôpital Necker, Paris France
(Louis Crocq)
Address for correspondence: Centre hospitalier, FORENAP, BP 29, 68250
Rouffach, France
(e-mail: macrocq@forenap.asso.fr)
47
Epics and classics
M ankind's earliest literature tells us that a signif-
icant proportion of military casualties are psychological,
and that witnessing death can leave chronic psychological
symptoms. As we are reminded in Deuteronomy 20:1-9,
military leaders have long been aware that many soldiers
must be removed from the frontline because of nervous
breakdown, which is often contagious:
When thou goest out to battle against thine enemies,
and seest horses, and chariots, and a people more than
thou . . . the officers shall say, What man is there that is
fearful and fainthearted? Let him go and return unto
his house, lest his brethren's heart faint as well as his
heart. (King Jame's Version)
Mankind's first major epic, the tale of Gilgamesh, gives
us explicit descriptions of both love and posttraumatic
symptoms, suggesting that the latter are also part of
human fundamental experience. After Gilgamesh loses
his friend Enkidu, he experiences symptoms of grief, as
one may expect. But after this phase of mourning, he
races from place to place in panic, realizing that he too
must die. This confrontation with death changed his per-
sonality. The first case of chronic mental symptoms
caused by sudden fright in the battlefield is reported in
the account of the battle of Marathon by Herodotus,
written in 440 BC (History, Book VI, transl. George
Rawlinson):
A strange prodigy likewise happened at this fight.
Epizelus, the son of Cuphagoras, an Athenian, was in the
thick of the fray, and behaving himself as a brave man
should, when suddenly he was stricken with blindness,
without blow of sword or dart; and this blindness con-
tinued thenceforth during the whole of his afterlife. The
Clinical research
following is the account which he himself, as I have
heard, gave of the matter: he said that a gigantic war-
rior, with a huge beard, which shaded all his shield, stood
over against him; but the ghostly semblance passed him
by, and slew the man at his side. Such, as I understand,
was the tale which Epizelus told.
It is noteworthy that the symptoms are not caused by a
physical wound, but by fright and the vision of a killed
comrade, and that they persist over the years. The loss of
sight has the primary benefit of blotting out the vision of
danger, and the secondary benefit of procuring support
and care. Frightening battle dreams are mentioned by
Hippocrates (460?–377 BC), and in Lucretius' poem, De
Rerum Natura, written in 50 BC (Book IV, transl. William
Ellery Leonard):
The minds of mortals … often in sleep will do and dare
the same . . . Kings take the towns by storm, succumb to
capture, battle on the field, raise a wild cry as if their
throats were cut even then and there. And many wrestle
on and groan with pains, and fill all regions round with
mighty cries and wild, as if then gnawed by fangs of pan-
ther or of lion fierce.
This text shows very vividly the emotional and behav-
ioral reexperiencing of a battle in sleep. Besides Greco-
Latin classics, old Icelandic literature gives us an exam-
ple of recurring nightmares after battle: the Gísli
Súrsson Saga tells us that the hero dreams so frequently
of battle scenes that he dreads obscurity and cannot
stay alone at night.
Jean Froissart (1337?–1400/01) was the most represen-
tative chronicler of the Hundred Years' War between
England and France. He sojourned in 1388 at the court
of Gaston Phoebus, Comte de Foix, and narrated the
case of the Comte's brother, Pierre de Béarn, who could
not sleep near his wife and children, because of his habit
of getting up at night and seizing a sword to fight oneiric
enemies. The fact that soldiers are awakened by fright-
ening dreams in which they reexperience past battles is
a common theme in classical literature, as, for instance,
Mercutio's account of Queen Mab in Shakespeare's
Romeo and Juliet (I, iv):
Sometime she driveth o’er a soldier’s neck,
And then dreams he of cutting foreign throats,
Of breaches, ambuscadoes, Spanish blades,
Of healths five fathom deep; and then anon
Drums in his ear, at which he starts and wakes,
And being thus frighted, swears a prayer or two,
And sleeps again.
48
Etiologic hypotheses were put forward by army physi-
cians during the French Revolutionary wars (1792-1800)
and the Napoleonic wars (1800-1815). They had observed
that soldiers collapsed into protracted stupor after shells
brushed past them, although they emerged physically
unscathed. This led to the description of the “vent du
boulet” syndrome, where subjects were frightened by the
wind of passage of a cannonball. The eerie sound of
incoming shells was vividly described by Goethe, in his
memoirs of the cannonade at the battle of Valmy in 17921
“The sound is quite strange, as if it were made up of the
spinning of a top, the boiling of water, and the whistling
of a bird.” In the same text, Goethe gives an account of
the feelings of derealization and depersonalization
induced by this frightening environment:
I could soon realize that something unusual was hap-
pening in me . . . as if you were in a very hot place, and at
the same time impregnated with that heat until you
blended completely with the element surrounding you.
Your eyes can still see with the same acuity and sharp-
ness, but it is as if the world had put on a reddish-brown
hue that makes the objects and the situation still more
scary . . . I had the impression that everything was being
consumed by this fire . . . this situation is one of the most
unpleasant that you can experience.
The dawn of modern psychiatry
The psychiatrist Pinel is often depicted as freeing the
insane from their chains; in his treatise entitled Noso-
graphie Philosophique (1798), he described the case of
the philosopher Pascal who almost drowned in the Seine
when the horses drawing his carriage bolted. During the
remaining eight years of his life, Pascal had recurring
dreams of a precipice on his left side and would place a
chair there to prevent falling off his bed. His personality
changed, and he became more apprehensive, scrupulous,
withdrawn, and depressive. From his experience with
patients shocked by the events and wars of the French
Revolution, Pinel wrote the first precise descriptions of
war neuroses—which he called “cardiorespiratory neu-
rosis”—and acute stuporous posttraumatic states—
which he called “idiotism.”
The Industrial Revolution and the introduction of steam-
driven machinery were to give rise to the first civilian
man-made disasters and cases of PTSD outside the bat-
tlefield. The public's imagination was struck by the first
spectacular railway disasters, and physicians at the time
From shell shock and war neurosis to PTSD - Crocq and Crocq
were puzzled by the psychological symptoms displayed by
survivors. Very soon, a controversy pitted the proponents
of the organic theory, according to which the mental
symptoms were caused by microscopic lesions of the
spine or brain (hence the names “railway spine” and “rail-
way brain”), against those who held that emotional shock
was the essential cause and that the symptoms were hys-
terical in nature. This controversy was to last until World
War I. It seems that the first mention of the term “trau-
matic neurosis” dates from that time: it was the title given
in 1884 by the German physician Hermann Oppenheim2
to his book containing a description of 42 cases caused by
railway or workplace accidents. This new diagnosis was
vehemently criticized by Charcot who maintained that
these cases were only forms of hysteria, neurasthenia, or
hystero-neurasthenia.3 After Charcot's death in 1893, the
term traumatic neurosis made its way into French-lan-
guage psychiatry: witness the Belgian psychiatrist Jean
Crocq4 who in 1896 reported 28 cases caused by railway
accidents. It is at the time of Charcot's famous Tuesday's
lectures that Janet (1889) and Freud (1893) discovered
traumatic hysteria with all its correlates: the dissociation
caused by trauma, the pathogenic role of forgotten mem-
ories, and “cathartic” treatment.This was a first glimpse of
what would later be known as the unconscious.
The Russian-Japanese war (1904-5) was marked by the
siege of Port Arthur and the naval battle of Tsushima. It
was probably during this conflict that post-battle psy-
chiatric symptoms were recognized for the first time as
such by both doctors and military command. Russian
psychiatrists—notably Avtocratov, who was in charge of
a 50-bed psychiatric clearing hospital at Harbin in
Manchuria—are credited with being the first to develop
forward psychiatric treatment. This approach may have
been a response to the difficulty of evacuating casualties
over huge distances at a time when the Trans-Siberian
Railway was not yet completed. Whatever the initial rea-
son, forward treatment worked, and would again be con-
firmed as the best method during succeeding conflicts.
The number of Russian psychiatric casualties was much
larger than expected (1500 in 1904 and 2000 in 1905)
and the Red Cross Society of Russia was asked to assist.
The German physician Honigman served in this body,
and he was the first to coin the term “war neurosis”
[Kriegsneurose] in 1907 for what was previously called
“combat hysteria” and “combat neurasthenia”; also, he
stressed the similarity between these cases and those
reported by Oppenheim after railway accidents. 5
49
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
World War I
World War I (WWI) was the first modern war fought
with massive industrial means. This dubious distinction is
also, to a lesser degree, shared by the American Civil
War. In any event, WWI is certainly the period in history
when “modern” warfare coincided with a “scientific”
psychiatry that endeavored to define diagnostic entities
as we understand them today. The role played by WWI
in advancing the knowledge of psychotraumatology in
European psychiatry may be compared to that of WWII
and the Vietnam War in American psychiatry.
The mental distress of WWI soldiers was repeatedly
described in literary autobiographies by English, Ger-
man, and French authors such as Robert Graves (Good-
bye to All That, 1929), Ernst Jünger (In Stahlgewittern
[Storm of Steel], 1920), or Henri Barbusse (Le Feu,
1916). Jünger wrote: “The state takes away our respon-
sibility but cannot ease our grief, we have to carry it
alone and it reaches deep within our dreams.”
Shell shock
Psychiatric casualties were reported very early in the
war, in numbers that no-one had anticipated. The French
physician Milian reported four cases of “battle hypnosis”
following military actions in 1914.6 The well-known Ger-
man psychiatrist Robert Gaupp reported in 1917:
The big artillery battles of December 1914 . . . filled our
hospitals with a large number of unscathed soldiers and
officers presenting with mental disturbances. From then
on, that number grew at a constantly increasing rate. At
first, these soldiers were hospitalized with the others . . .
but soon we had to open special psychiatric hospitals for
them. Now, psychiatric patients make up by far the
largest category in our armed forces . . . The main causes
are the fright and anxiety brought about by the explosion
of enemy shells and mines, and seeing maimed or dead
comrades . . . The resulting symptoms are states of sud-
den muteness, deafness . . . general tremor, inability to
stand or walk, episodes of loss of consciousness, and con-
vulsions.7
In his review of 88 cases of mental disorder in 1915, the
French psychiatrist Régis had expressed a very similar
opinion about the etiological role of witnessing the hor-
rible death of comrades: “20% only presented with a
physical wound, but in all cases fright, emotional shock,
and seeing maimed comrades had been a major factor.”
Clinical research
The clinical picture of war neuroses differed only slightly
in the two World Wars.
In the British military, patients presenting with various
mental disorders resulting from combat stress were orig-
inally diagnosed as cases of shell shock, before this diag-
nosis was discouraged in an attempt to limit the number
of cases. It is not known when the term began to be used.
According to Merskey,8 the first mention may be a story
published in the Times on February 6, 1915, indicating
that the War Office was arranging to send soldiers suf-
fering from “shock” to be treated in special wards at the
National Hospital for the Paralyzed and Epileptic, in
Queen Square. Also in February 1915, the term shell
shock was used by Charles Myers in an article in The
Lancet to describe three soldiers suffering from “loss of
memory, vision, smell, and taste.”9,10 Myers reported on
three patients, admitted to a hospital in Le Touquet dur-
ing the early phase of the war, between November 1914
and January 1915. These patients had been shocked by
shells exploding in their immediate vicinity and pre-
sented with remarkably similar symptoms. According to
Myers, these cases bore a close relation to “hysteria.”
The first two patients were transferred to England for
further treatment after a couple of weeks (the third was
still being treated in Le Touquet when the article was
published). As we shall see below, these patients might
not have been evacuated to the peaceful surroundings of
their home country had they sustained their wounds a
year later.
Forward treatment
Indeed, the experience of the first war months and the
unexpected large influx of psychiatric casualties led to a
change in treatment approaches. The evacuation of psy-
chiatric casualties to the rear became less systematic as
the experience of the remaining war years convinced
psychiatrists that treatment should be carried out near
the frontline, and that evacuation only led to chronic
disability. It was noticed that soldiers treated in a front-
line hospital, benefiting from the emotional support of
their comrades, had a high likelihood of returning to
their unit, whereas those who were evacuated often
showed a poor prognosis, with chronic symptoms that
ultimately led to discharge from the military. Also, it was
discovered that prognosis was better if the convalesc-
ing soldiers remained in the setting of the military hier-
archy, rather than in a more relaxed hospital environ-
50
ment. Thus, by the end of 1916, evacuations became rare
and patients were treated instead in forward centers,
staffed by noncommissioned officers (NCOs), within
hearing distance of the frontline guns and with the
expectation of prompt recovery.11 Treatment in the for-
ward area (psychiatrie de l'avant) became the standard
treatment, along with the five key principles summa-
rized in 1917 by the American physician Thomas W.
Salmon,12 chief consultant in psychiatry with the Amer-
ican Expeditionary Forces in France: immediacy, prox-
imity, expectancy, simplicity, and centrality. Immediacy
meant treating as early as possible, before acute stress
was succeeded by a latent period that often heralded
the development of chronic symptoms; proximity meant
treating the patient near the frontline, within hearing
distance of the battle din, instead of evacuating him to
the peaceful atmosphere of the rear, which he would,
understandably, never wish to leave; expectancy referred
to the positive expectation of a prompt cure, which was
instilled into the patient by means of a persuasive psy-
chotherapy; simplicity was the use of simple treatment
means such as rest, sleep, and a practical psychotherapy
that avoided exploring civilian and childhood traumas;
finally, centrality was a coherent organization to regu-
late the flow of psychiatric casualties from the forward
area to the rear, and a coherent therapeutic doctrine
adopted by all medical personnel. Salmon's principles
were discovered independently and applied universally
by all warring sides; only to be forgotten, and rediscov-
ered again, during World War II.
Among the many treatment applied to stress disorders,
one was much used during WWI, and scarcely at all dur-
ing WWII: the application of electrical current, also called
faradization.This was probably because motor symptoms,
such as tremor, paralysis, contractions, limping, or fixed
postures, were common during WWI, and rare in WWII.
Faradization was criticized in post-war Austria; Wagner-
Jauregg—a professor of psychiatry in Vienna who was
awarded a Nobel prize in 1928—was even accused of
excessive cruelty in the administration of this treatment
and had to appear before an investigation committee, in
which Sigmund Freud had the more enviable role of tes-
tifying as an expert.13 A most radical description of elec-
trotherapy was published in 1916 by Fritz Kaufmann,14
in which he explained how war neuroses could be treated
in one session only by combining suggestion, authority,
and steadfast application of electricity until the symptoms
subsided—a form of fight at outrance.
From shell shock and war neurosis to PTSD - Crocq and Crocq
Concussion, fright, or malingering?
Etiology was a controversial question that was reflected
by the choice of terms: shell shock or war neurosis?
Soma or psyche? The now obsolete term shell shock,
harking back to the vent du boulet of the Napoleonic
wars, implied a somatic etiology, such as microscopic
brain lesions due to a vascular, meningeal, white or gray
matter concussion. Other diagnoses were also used to
express the belief that the cause was more an emotional
stressor, rather that a physical concussion. Such diag-
noses were, for instance, war neurasthenia and war psy-
choneurosis, in France.
Emil Kraepelin (1856–1926), without doubt one of the
most influential psychiatrists of our times, wrote about
his experience with war neuroses during WWI in his
autobiography, published posthumously in German in
198315:
[As early as 1917], the question of war neuroses was
raised. We alienists all agreed that we should try to limit
an excessively liberal granting of compensations which
might lead to a sharp rise in the number of cases and
claims . . . the fact that all kinds of more or less severe
psychiatric symptoms could lead to a lengthy stay in a
hospital, or even to a discharge from the military with a
generous disability pension, had disastrous conse-
quences. This was compounded by the population's feel-
ing of pity for the seemingly severely ill “war-shakers”
[Kriegszitterer], who drew attention to themselves on
street corners and used to be generously rewarded. In
such circumstances, the number of those who believed
that a “nervous shock,” or, especially, having been buried
alive, entitled them to discharge and continuous support,
increased dramatically.
Kraepelin's comments typify the controversies that
raged at the time: (i) were the mental symptoms nothing
more than malingering, with the clear objective of get-
ting away from the frontline? Some 346 British and
Commonwealth soldiers were actually shot on the
orders of military command and this number certainly
included soldiers suffering from acute stress disorder
who walked around dazed or confused and were
accused of desertion or cowardice; (ii) Did posttrau-
matic symptoms have pathoanatomical explanations?
For instance, were they produced by a concussion of the
brain or strained nerve fibers, as had been hypothesized
in previous decades for the “railway spine” resulting
from train accidents? (iii) A third explanation was a psy-
51
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
chological origin—in that case, was the psychological
cause limited to the overwhelming fright constituting
the trauma, or was it necessary to delve further into the
patient's previous personality? The cases of war neuro-
sis observed during WWI were indeed a challenge to
psychoanalytical theories; it was simply unbelievable
that all cases were caused by childhood traumas and it
had to be admitted that psychological symptoms could
be produced by recent traumas. Freud had postulated
that dreams were a wish fulfillment. Not until 1920, in an
address at an international congress of psychoanalysts,
did he allow one exception: the case of traumatic
dreams, dreams that recall recent accidents or childhood
traumas. And even this turned out to be no real excep-
tion at all: Freud eventually understood traumatic
dreams as fitting into his wish-fulfillment theory of
dreams in that they embodied the wish to master the
trauma by working it through.16
World War II
A dreadful invention of WWII was the concept “total
war,” with the systematic targeting of civilian popula-
tions, as exemplified by the millions of deaths caused by
the Holocaust, the air raids on cities to break the morale
of civilian populations, and the atomic bombs dropped
over Hiroshima and Nagasaki. Despite WWI, most
armies were once again unprepared for the great num-
ber of psychiatric casualties and psychiatrists were often
viewed as a useless burden, as exemplified by a memo-
randum addressed by Winston Churchill to the Lord
President of the Council in December, 1942, in the fol-
lowing terms17:
I am sure it would be sensible to restrict as much as pos-
sible the work of these gentlemen [psychologists and
psychiatrists] . . . it is very wrong to disturb large numbers
of healthy, normal men and women by asking the kind of
odd questions in which the psychiatrists specialize.
American psychiatry
American psychiatrists made a major contribution to
the study of combat psychiatry during WWII. In Psy-
chiatry in a Troubled World, William C. Menninger18
shows how the lessons of WWI seemed at first to have
been entirely forgotten by the American military: “dur-
ing the initial battles in Africa, psychiatric casualties
were sent back to base hospitals, often hundreds of miles
Clinical research
from the front. Only 5% of these were able to return to
duty.” As explained by Jones,19 American planners, under
the guidance of Harry Stack Sullivan, had believed that
potential psychiatric casualties could be screened out
prior to being drafted. Correspondingly, no psychiatrists
were assigned to combat divisions and no provision for
special psychiatric treatment units at the field army level
or communications zone had been made. The principles
of forward treatment were rediscovered during the
North Africa campaign in 1943. Advised by the psychia-
trist Frederick Hanson, Omar N. Bradley issued a direc-
tive on 26 April 1943, which established a holding period
of 7 days for psychiatric patients at the 9th Evacuation
Hospital, and for the first time the term “exhaustion”
was prescribed as initial diagnosis for all combat psy-
chiatric cases.20 This word was chosen because it was
thought to convey the least implication of neuropsychi-
atric disturbance. Beginning in 1943, treatment in the
forward area similar to that in WWI was the rule, with
the result that between 50% to 70% of psychiatric casu-
alties were able to return to duty. Here again, the sheer
number of psychiatric casualties was staggering. For the
total overseas forces in 1944, admissions for wounded
numbered approximately 86 per 1000 men per year, and
the neuropsychiatric rate was 43 per 1000 per year.
In 1941, the first year of the war for the United States,
Abram Kardiner—famous for having been analyzed by
Freud himself—published a book based on his treatment
of WWI veterans at Veterans Hospital No. 81 between
1922 and 1925.21 In the light of the experience with
WWII soldiers, Kardiner published a revised edition of
his book at the end of the war.22 He wrote that “the real
lesson of WWI and the chronic cases was that this syn-
drome must be treated immediately to prevent consoli-
dation of the neurosis into its chronic and often
intractable forms.” He identified traumatic neurosis as a
“physioneurosis,” thereby stressing the concomitance of
somatic and psychological symptoms. Kardiner devel-
oped his own concept of the “effective ego” and he pos-
tulated that “ego contraction” was a major mechanism.
Posttraumatic psychiatric symptoms in military personnel
fighting in WWII were reported as early as 1945 by the
American psychiatrists Grinker and Spiegel.23 Their
book—Men under Stress—is an excellent reflection of
psychiatric thinking of the time; it remained a classic
treatise on war psychiatry because of its detailed descrip-
tion of 65 clinical cases, its reference to psychoanalytical
theories, and the description of cathartic treatment by
52
“narcosynthesis” using barbiturates. Grinker and Spiegel
distinguished acute “reactions to combat” from delayed
“reactions after combat.” The latter included “war neu-
roses,” designated by the euphemism “operational
fatigue” syndrome in the Air Force. Other chronic con-
sequences of combat included passive-dependent states,
psychosomatic states, guilt and depression, aggressive
and hostile reactions, and psychotic-like states.
European studies
Long-lasting psychological disorders were not tolerated
in the German military during WWII, and official doc-
trine held that it was more important to eliminate weak
or degenerate elements rather than allow them to poi-
son the national community. Interviews we conducted
with Alsatian veterans who had been forcibly drafted
into the Wehrmacht taught us that soldiers who had suf-
fered acute combat stress (such as being buried under a
bunker hit by a bomb) were given some form of psy-
chological assistance soon after rescue; they were typi-
cally sent to a forward area first aid station (Verbands-
platz) where they received milk and chocolate and were
allowed to rest. The Soviet army evolved its own system
of forward treatment, under the responsibility of the
unit's political (ie, morale) officer.24 A look at the text-
book of psychiatry published by Gurevich and
Sereyskiy25 in Moscow immediately after the war in
1946, at the height of Stalin's power, shows the existence
of a specific diagnostic label to classify posttraumatic
disorders. The authors describe the “affective shock reac-
tions” (affektivno-shokovye reaktsii), a subtype of psy-
chogenic reactions, that are observed after wartime
events, earthquakes, or railway accidents; these are char-
acterized by acute (a few days) and subchronic (a few
months) symptoms. These Russian authors tended to
emphasize cardiovascular and vasomotor symptoms,
which reminds us of Da Costa's “irritable heart” in
American Civil War soldiers. The literature on Holo-
caust and concentration camp survivors is too abundant
to be summarized here. The best known of all the early
works studying concentration camp survivors is proba-
bly the article published by Eitinger.26
In contrast to WWI, the course of symptoms over
decades and their chronic nature were extensively stud-
ied in WWII survivors. For instance, in 1988, we stud-
ied27 a group of French civilians living in the Alsace-
Lorraine region who were conscripted into the German
From shell shock and war neurosis to PTSD - Crocq and Crocq
army and later held in captivity in Russia. This popula-
tion of Alsace-Lorraine was interesting because it was
bilingual, French and German, and had cultural roots in
both heritages. The analysis of 525 questionnaires
showed that, after over four decades, 82% still experi-
enced intrusive recollections and nightmares of their
wartime captivity; 73% actively attempted to avoid
thoughts or feelings associated with the trauma; 71%
reported a foreshortened sense of the future; and
nearly 40% reported survivor guilt. Beyond PTSD,
these survivors from Alsace-Lorraine also suffered last-
ing personality changes. We believe that an aggravating
factor was the fact that these individuals returned
home uncelebrated, embittered, psychologically iso-
lated, and that they were caught in a web of psycho-
logical ambiguity. They had fought in the German army
against their will and under the threat of their families
being deported, and were considered unreliable by the
Germans. They were surprised to be treated as Ger-
man soldiers upon their capture by the Soviet army.
They were repatriated to a new post-war social envi-
ronment in a French society that was itself plagued by
the guilt of its early surrender to the Nazis, and they
felt misunderstood by some of their countrymen who
criticized their incorporation into the German military
as a form of treason.
The Vietnam war
During the Vietnam war, the principles of treating psy-
chiatric casualties in the forward area were successfully
applied, with a correspondingly low level of acute psy-
chiatric casualties (11.5 per 1000 men per year). In con-
trast, the incidence of alcoholism and drug abuse was
high. Similarly, the late and delayed effects of combat
exposure in the form of PTSD were a significant source
of suffering and disability among veterans in the United
States. An estimated 700 000 Vietnam veterans—almost
a quarter of all soldiers sent to Vietnam from 1964 to
1973—required some form of psychological help. The
prevalence of delayed and chronic PTSD, in spite of the
careful prevention of psychiatric casualties in Vietnam
itself, was a rude awakening. Trying to explain this para-
dox called for new hypotheses, for instance, that PTSD
might be a common form of psychiatric casualty in “low-
53
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
level” warfare.28 Similar profiles had been observed in
the French post-colonial wars in Indochina and Alge-
ria.29 This post-Vietnam syndrome, increasingly diag-
nosed in veterans in the seventies, ultimately led to the
adoption of PTSD as a diagnostic category in 1980 in
DSM-III. It seems puzzling that no such category existed
in DSM-II, which had even abandoned the former
DSM-I category of so-called “gross stress reaction,”
when it was published in 1968, the year of the Commu-
nist Tet Offensive in Vietnam.
Retrospect
There is currently a measure of consensus on the diag-
nosis and phenomenological description of PTSD, which
is recognized as a specific syndrome in individuals who
have experienced a major traumatic event. Most modern
textbooks concur in describing this syndrome as com-
prising three groups of symptoms: (i) the recurrent and
distressing reexperiencing of the event in dreams,
thoughts, or flashbacks; (ii) emotional numbing and
avoidance of stimuli reminiscent of the trauma; (iii) and
a permanent state of increased arousal. The first symp-
toms of PTSD are often delayed and they are separated
from the trauma by a latency period; however, once
installed, the disorder tends to follow a chronic course
and the symptoms do not abate with time. DSM-IV30 has
the merit of clearly distinguishing PTSD, a chronic syn-
drome, from acute stress disorder, which is short-lived
and appears soon after the trauma. We tend to abusively
interpret the literature of previous decades as if today's
diagnostic categories had always existed. However, a
clear distinction between acute stress disorder and
chronic PTSD is usually lacking in previous works. Also,
there was little attempt to predict the risk of developing
PTSD. Providing the trauma is severe enough, most indi-
viduals will go on to develop PTSD. However, one puz-
zling question is that many survivors seemingly do not
develop symptoms even after a severe stressor.31 Like-
wise, the historical literature on PTSD offers few clues
concerning effective treatment, once the symptoms have
become chronic. The practice of forward treatment aim-
ing to prevent the development of chronic disorders may
have inspired today's psychological debriefing of disas-
ter victims. ❑
Clinical research
Desde el “corazón de soldado” y la
“neurosis de guerra” al trastorno de
estrés postraumático: una historia del
trauma psíquico
La denominación de trastorno de estrés postraumático
ha sido ampliamente reconocida desde su primera apa-
rición en 1980 en la tercera edición del Manual
Diagnóstico y Estadístico de los Trastornos Mentales
(DSM-III) publicado por la Asociación Psiquiátrica
Americana. Para la población general este diagnóstico
se asocia con el desastroso legado de la Guerra de
Vietnam. Una serie de conflictos bélicos anteriores han
dado origen a otras denominaciones de esta patología
como: “corazón de soldado”, shock de la explosión y
neurosis de guerra. Este último diagnóstico corresponde
a la névrose de guerre y Kriegsneurose de la literatura
científica francesa y alemana respectivamente. Este artí-
culo describe la forma en que las consecuencias –agudas
y crónicas- del trauma psíquico hicieron su aparición en
la literatura médica y cómo han evolucionado los con-
ceptos diagnósticos a lo largo del tiempo.
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Taschenbuch Verlag; 1998:X,234. (der Ton ist wundersam genug, als wär' er
zusammengesetzt aus dem Brummen des Kreisels, dem Butteln des Wassers
und dem Pfeifen eines Vogels . . . konnt' ich jedoch bald bemerken, daß
etwas Ungewöhnliches in mir vorgehe . . . es schien, als wäre man an einem
sehr heißen Orte, und zugleich von derselben Hitze völlig durchdrungen,
so daß man sich mit demselben Element, in welchem man sich befindet,
vollkommen gleich fühlt. Die Augen verlieren nichts an ihrer Stärke, noch
Deutlichkeit; aber es ist doch, als wenn die Welt einen braunrötlichen Ton
hätte, der den Zustand sowie die Gegenstände noch apprehensiver macht
. . . mir schien vielmehr alles in jener Glut verschlungen zu sein . . . Es gehört
übrigens dieser Zustand unter die am wenigsten wünschenswerten).
2. Oppenheim H. Die Traumatischen Neurosen. 2nd ed. Berlin, Germany:
Hirschwald; 1892.
3. Crocq L. Les Traumatismes Psychiques de Guerre. Paris, France: Odile Jacob;
1999.
4. Crocq J. Les Névroses Traumatiques. Étude Pathogénique et Clinique. Brus-
sels, Belgium: H. Lamertin; 1896.
5. Ellis PS. The origins of the war neuroses. Part I. J R Nav Med Serv.
1984;70:168-177.
6. Milian G. L'hypnose des batailles. Paris Med. 1915;(2 Jan):265-270.
7. Ulrich B, Ziemann B. Frontalltag im Ersten Weltkrieg. Wahn und Wirklichkeit.
Frankfurt, Germany: Fischer; 1994:102-103.
8. Merskey H. Post-traumatic stress disorder and shell shock—clinical sec-
tion. In: Berrios GE, Porter R, eds. A History of Clinical Psychiatry. London, UK:
The Athlone Press; 1995:490-500.
9. Myers CM. Contributions to the study of shell shock. Lancet. 1915;13:316-320.
10. Brown EM. Post-traumatic stress disorder and shell shock—social sec-
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The Athlone Press; 1995:501-508.
54
Du shell shock et de la névrose de guerre
à l'état de stress post-traumatique:
une histoire de la psychotraumatologie
Depuis sa première apparition dans la troisième édi-
tion du Manuel Statistique et Diagnostique des
Troubles Mentaux (DSM-III) publiée par
l’American Psychiatric Association, la dénomination
“état de stress post-traumatique” est largement
reconnue. Ce diagnostic évoque immédiatement la
guerre du Vietnam et les séquelles qu’elle a engen-
drées. Lors de conflits plus anciens, d’autres dénomi-
nations ont été utilisées telles que “cœur de soldat “
“shell shock”, ainsi que des termes “névrose de guer-
re” et “kriegsneurose” dans la littérature scientifique
française et allemande. Cet article retrace l’historique
de la description, dans la littérature médicale, des
conséquences immédiates et chroniques de ces trau-
matismes psychologiques et l’évolution dans le
temps des conceptions diagnostiques et thérapeu-
tiques.
11. Winter D. Death's Men. Soldiers of the Great War. London, UK: Allen Lane;
1978:136.
12. Salmon TW. Care and treatment of mental diseases and war neuroses
(shell shock) in the British army. Mental Hygiene. 1917;1:509-547.
13. Eissler KR. Freud und Wagner-Jauregg vor der Kommission zur Erhebung Mil-
itärischer Pflichtverletzungen. Vienna, Austria: Löcker Verlag; 1979.
14. Kaufmann F. Die planmäßige Heilung komplizierter psychogener Bewe-
gungsstörungen bei Soldaten in einer Sitzung. In: Feldärtz Beilage Münch
Med Wochenschr. 1916;63:802ff.
15. Kraepelin E. Lebenserinnerung. Berlin, Germany: Springer Verlag;
1983:189.
16. Freud S. Supplements to the Theory of Dreams. London, UK: Standard Edi-
tion; 1920;XVIII:4-5.
17. Ahrenfeldt RH. Psychiatry in the British army in the second World War. New
York, NY: Columbia University Press; 1958:26.
18. Menninger WC. Psychiatry in a Troubled World. New York, NY: Macmillan;
1948.
19. Jones FD, ed. War psychiatry. Textbook of Military Medicine. Walter Reed
Army Medical Center, Washington DC: Office of the Surgeon General USA;
1995.
20. Glass AJ. Neuropsychiatry in World War II. Vol II. Overseas Theaters. Wash-
ington DC: Office of the Surgeon General, Dept of the Army; 1973.
21. Kardiner A. The traumatic neuroses of war. Psychosomatic Medicine
Monograph II III. Menasha, Wis: George Banta Publishing Company; 1941.
22. Kardiner A, Spiegel H. War Stress and Neurotic Illness. New York, NY: Paul
B. Hoeber Inc; 1947.
23. Grinker RR, Spiegel JP. Men Under Stress. Philadelphia, Pa: Blakiston;
1945.
24. Gabriel R. Soviet Military Psychiatry: The Theory and Practice of Coping With
Battle Stress. Westport, Conn: Greenwood Press; 1986:33–37.
25. Gurevich MO, Sereyskiy M Ya. Uchebnik Psikhiatrii. Moscow, Russia: Med-
giz; 1946:376-377.
From shell shock and war neurosis to PTSD - Crocq and Crocq
26. Eitinger L. Pathology of the concentration camp syndrome. Arch Gen Psy-
chiatry. 1961;5:79-87.
27. Crocq MA, Macher JP, Barros-Beck J, Rosenberg SJ, Duval F. Post-trau-
matic stress disorder in World War II prisoners of war from Alsace-Lorraine
who survived captivity in the USSR. In: Wilson JP, Raphael B, eds. The Inter-
national Handbook of Traumatic Stress Syndromes. Stress and Coping Series. New
York, NY: Plenum Press; 1992:(chap 21):253-261.
28. Belenky G (ed). Contemporary Studies in Combat Psychiatry. Westport,
55
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
Conn: Greenwood Press; 1987:4.
29. Crocq L, Crocq MA, Barrois C, Belenky G, Jones FD. Low-intensity com-
bat psychiatry casualties. In: Pichot P, Berner P, eds. Psychiatry, the State of the
Art. New York, NY: Plenum Press; 1985;6:545-550.
30. American Psychiatric Association. Diagnostic and Statistical Manual of Men-
tal Disorders, 4th ed. Washington DC: American Psychiatric Association; 1994.
31. Turner S. Place of pharmacotherapy in post-traumatic stress disorder.
Lancet. 1999;354:1404-1405.
Clinical research
Lifelong posttraumatic stress disorder:
evidence from aging Holocaust survivors
Yoram Barak, MD; Henry Szor, MD
Despite the fact that 50 years have passed since the
Nazi regime and the Holocaust, the psychic seque-
lae are far from being overcome. The majority of
Holocaust survivors and World War II veterans still
list their experiences as the “most significant stres-
sors” of their lives. The literature provides ample
evidence that posttraumatic stress disorder among
survivors persists into old age. However, there is still
a need to define the differences in frequency, clini-
cal presentation, severity, and comorbid conditions
among aging Holocaust survivors. Age at the time
of trauma, cumulative lifetime stress, and physical
illness are reported to have a positive association
with more severe posttraumatic symptomatology.
The presence of comorbid Axis I psychiatric disor-
ders (Diagnostic and Statistical Manual [DSM]), has
been the focus of research by our group, demon-
strating that their interaction with earlier trauma
leads to a course of chronic, debilitating disease.
Despite reactivation of traumatic symptoms during
aging and continuous mental suffering, the majori-
ty of Holocaust survivors show good instrumental
coping and preserved functioning.
Keywords: PTSD; Holocaust; aging; reactivation; chronicity
Author affiliations: The Psychogeriatric Department, Abarbanel Mental
Health Center, Bat Yam; and the Sackler Faculty of Medicine, Tel Aviv Uni-
versity, Israel
Address for correspondence: Dr Yoram Barak, Head, Psychogeriatric Depart-
ment, Abarbanel Mental Health Center, Bat Yam 59100, Israel
(e-mail: mdybarak@netvision.net.il)
57
R esearch into posttraumatic psychiatric mor-
bidity has a long history. Since the first descriptions of
“soldiers’ heart” syndrome in the American Civil War,
wars, natural catastrophes, mass fires and accidents, rape
abuse, and torture have all added to our understanding
of the effects of trauma on the human psyche.1-4 Despite
the accumulating data and the magnitude of human suf-
fering, the unique diagnostic categorization of posttrau-
matic stress disorder (PTSD) is a “latecomer” in formal
psychiatric classification systems.
Two factors have delayed the progress in diagnosis and
understanding of PTSD: (i) the attribution of this disor-
der to combat-related events; and (ii) the tendency to
view the symptoms developing after a trauma as “nor-
mal response.” Thus, in the first half of this century, the
psychiatric approach to trauma has varied widely.5 After
World War II (WWII), the American Psychiatric Asso-
ciation included “gross stress reaction” in the first edi-
tion of the Diagnostic and Statistical Manual (DSM).
Surprisingly, this entity was dropped from DSM-II and
only the advent of DSM-IV in 1994 separated acute
stress disorder from PTSD. In addition, DSM-IV offers
as specifiers the definitions of “acute” or “chronic” to
describe the course of the disorder, as well “with delayed
onset” to acknowledge appearance of the disorder 6
months (or later) after exposure to the trauma. It is
important to note that the current classification also
relinquishes the emphasis of the uniqueness of the trau-
matic event and conceptualizes PTSD as common to
many different types of events. In these events, the indi-
vidual experiences, witnesses, or is confronted with death
or serious injury, and responds with intense fear, help-
lessness, or horror.3,6
Despite the refinement and operationalization of diag-
nostic criteria for PTSD, relatively little is known about
the course of the disorder. In the March 1999 issue of the
American Journal of Psychiatry, three published studies
used longitudinal designs to address both the acute and
chronic effects of trauma.7-9 The study by Koren and col-
leagues,9 in conjunction with retrospective studies of the
Clinical research
Selected abbreviations and acronyms
IES Impact of Event Scale
PTSD posttraumatic stress disorder
R-PTSD Revised Posttraumatic Stress Disorder (inventory)
SCID Schizophrenia Clinical Interview for Diagnosis
WWII World War II
natural history of PTSD10 seem to emphasize that the
course of PTSD is one of an increase in symptoms in
the early phase (1 to 3 months after trauma), followed
by a plateau. Is this “plateau” phase lifelong? Do PTSD
symptoms remain severe and disabling throughout the
life cycle? Are maturation, aging, and reintegration into
society factors that affect the course of PTSD?
Veterans of WWII and Holocaust survivors offer a
unique opportunity to evaluate the course of PTSD
through the life cycle of people who have been subjected
to extreme and massive psychic trauma in their youth.
The majority of Holocaust survivors and more than half
of WWII veterans interviewed 50 years after the war
spontaneously listed it as the “most significant stressor”
of their life.11 With the aging of veterans and survivors,
reports of reactivation of PTSD have been published.12
Physical ill health, retirement, loneliness, comorbid psy-
chiatric illness, anniversaries, reunions, and use of alcohol
and psychotropic medication are all factors implicated in
the exacerbation of both arousal and reexperiencing
symptoms of PTSD.12-15 For many WWII veterans, PTSD
has lasted 50 years,15 although masking of intrusive
symptoms in midlife was usual.12 The rates of active
PTSD reported among the veterans range from 12.4%14
to 45%.13 It is noteworthy that veterans who suffer from
comorbid psychiatric conditions report no significant
reduction in symptoms over the preceding 10 years.13
The Holocaust was the most traumatic experience to
occur in the 20th century. Most of the survivors are now
elderly and for them, aging is a phase of severe crisis.16
Psychiatrists and other health professionals can facili-
tate the voicing of the suffering of people who spent
their lives in the persistent shadows of the Holocaust.
Indeed, in the last decade, many studies have focused
on the long-term consequences of this massive trauma-
tization.17 Among the particularities of survivor suffering
were: being outlawed, discrimination, defamation, total
absence of rights, loss of individuality, life-threatening
over a long period of time, torture, physical hardships, ill
58
health, being uprooted, few or no survivors in the family
and elsewhere, lack of graves for victims, and the real-
ization at the end of WWII that language, culture, and
home are lost forever.18 In later life, when friends are
gone, the need to share with others becomes urgent; to
bear witness is vital.19
In 1997, Sadavoy20 reviewed the late-life effects as
reported in studies of Holocaust survivors and WWII
veterans. He concluded that survivor syndromes indeed
persist into old age, that Holocaust survivors as a group
have adapted well to instrumental aspects of life, but
that there is a deficiency of treatment studies in this
population. The Traumatic Stress Studies Program at the
Mount Sinai School of Medicine, New York,21-24 provides
more specific data, as do several research groups in
Israel.16,25-29 Converging lines of research demonstrate
that aging Holocaust survivors are in a sense a “fragile”
group. Cumulative trauma, recent stress, and lack of
social support increase the probability of retraumatiza-
tion in old age.21,24,29 Nevertheless, it is surprising that
using DSM criteria to diagnose present PTSD in aging
Holocaust survivors, the reported rates in controlled
studies are 46% to 55.5%.22,30 Major comorbid psychi-
atric illness was excluded from these studies. This may be
a significant drawback, as depressive and dissociative
features, as well as markers of the adrenocortical
(steroidal) pathway, are notably abnormal in nontreat-
ment-seeking survivors.23,24 Increased risk of suicide,
depression, chronicity of schizophrenia, and develop-
ment of late-life paranoia have all been reported in
aging Holocaust survivors.16 Thus, there is a need to
study the presence of comorbid PTSD in the minority of
survivors who suffer from psychiatric disease. This may
aid in understanding the complex relationship between
massive psychic trauma and the course of PTSD in sub-
jects who have been under close observation by mental
health professionals most of their lives.
The present study was conducted to evaluate the pres-
ence of “active” PTSD in a group of aging Holocaust sur-
vivors who were either repeatedly hospitalized, or spent
most of their lives in long-stay psychiatric institutions.
Subjects
At the end of WWII, nearly 500 000 Jews survived the
Holocaust. Of these, approximately 300 000 immigrated
to Israel in two main periods: shortly after the estab-
lishment of the State of Israel, and between 1989 and
PTSD among Holocaust survivors - Barak and Szor
1992 when large groups of Jews immigrated from the
former USSR.28 It is estimated that 200 000 survivors
are now living in Israel, most of whom are now elderly.
In the 1950s, nearly 2000 Holocaust survivors were
repeatedly or chronically hospitalized in psychiatric hos-
pitals in Israel. The most common diagnosis then was
that of schizophrenia. In 1998, there were 700 such
patients hospitalized in long-stay wards. The Abarbanel
Mental Health Center is Israel’s largest academic psy-
chiatric center. The center’s psychogeriatric division con-
sists of three wards encompassing 110 inpatient beds.
From January to June 1998, for the purpose of the pre-
sent study, all aging Holocaust survivors were inter-
viewed.
Holocaust survivors were defined as subjects that were
in Eastern or Western Europe under the Nazi regime
during the years 1933 to 1945. Inclusion criteria for the
study were: (i) age ≥65 years; (ii) being a Holocaust sur-
vivor. Exclusion criteria were: (i) DSM-IV diagnosis of
dementia; (ii) inability (cognitive impairment or lan-
guage difficulties) to endorse the Impact of Event Scale
(IES)31; and (iii) patient’s refusal to participate in the
study.
Methods
All patients had previously been diagnosed according
to DSM-IV criteria as part of an ongoing study project
(the data relevant to this project are detailed in refer-
ence 16). For purposes of the present study, the IES31
and revised PTSD inventory (R-PTSD)32 were used.
The IES comprises two subscales describing and quan-
tifying intrusive and avoidance experiences. The R-
PTSD inventory is based on endorsement (by the inter-
viewing researcher) of DSM criteria for the presence of
PTSD. Both these instruments were previously used and
validated in studies of Holocaust survivors and trauma
victims.32,33
Data are presented as means ± standard deviation (SD)
and ranges. We used these simple statistical measures as
the aim of the study was to present a descriptive audit.
Results
During the period January to June 1998, 93 Holocaust
survivors were being treated at the Abarbanel Mental
Health Center psychogeriatric wards. Of these, 32 did
not fulfill the criteria of the study, and were excluded. All
59
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
61 participating patients underwent a semistructured
interview. After the interview all endorsed the IES.
Our series comprised 41 women and 20 men. Mean age
for the group was 77.1 years (± 6.8; range 65-91). The
majority of subjects were in Eastern Europe during the
Nazi regime (43 of 61; 70.5%). Axis I (DSM) psychiatric
diagnoses for the group were as follows: 32 of 61
(52.5%) schizophrenia, 17 of 61 (27.9%) affective disor-
ders, and 12 of 61 (19.6%) other psychotic disorders.
The R-PTSD inventory facilitated diagnosis of comorbid
PTSD in 91.8% of patients (56 of 61). As previously
shown, the inventory correlated well with the Schizo-
phrenia Clinical Interview for Diagnosis (SCID). Thus,
comorbid PTSD can be said to be reliably diagnosed in
the overwhelming majority of subjects in the present
study. The IES results demonstrated a significant differ-
ence between intrusive and avoidance symptoms. While
both subscales were scored as significantly higher than
the reported means for the normal population, intru-
sions were scored as notably more prominent than
avoidance. Mean intrusion score was 42.7±4.1 (range 36-
51) and mean avoidance score was 29.7±3.4 (range 27-
31); P<0.01 [paired Student t-test]). The IES scores in
the present study are in the range of a previous study of
elderly subjects suffering from PTSD reported by our
group.33
Discussion
Our sample represents a unique group of elderly Holo-
caust survivors who show a high comorbidity of chronic
PTSD (91.8%), with psychotic disorders more than 50
years after the experience of the massive psychic trauma
of the Holocaust.
The occurrence of chronic PTSD of such magnitude for
an extremely prolonged period is striking. It is signifi-
cantly higher than the rate reported for war veterans,
ranging from 12.4%14 to 45%.13 This difference may be
related to the unique nature of the Holocaust trauma,
combining dehumanization, confrontation with death,
and massive loss for a prolonged period.21 Beal15 demon-
strated that the co-occurrence of imprisonment in addi-
tion to the experience of combat led to a higher inci-
dence of PTSD and other psychological symptoms,
compared to combat experience alone. Furthermore,
Kidson et al13 show that the specific nature of the trau-
matic experience, such as taking of casualties, or the
experience of combat stress, resulted in more pro-
Clinical research
nounced severity, and was significantly associated with
the occurrence of PTSD in WWII veterans. Thus, the spe-
cific nature of the traumatic experience may influence
the occurrence of PTSD and its persistence over time.
Beyond this aspect, the coexistence of a severe psychotic
disorder in our series of patients seems to be decisive. As
demonstrated by Kidson et al,13 even minor pathologies,
such as anxiety and depressive disorders, were more
common in war veterans with PTSD. Therefore, this
seems to suggest that the severity of the coexistent psy-
chiatric morbidity, such as schizophrenia, may explain
the high incidence of chronic PTSD present for such a
prolonged period.
It is difficult to say whether the occurrence of PTSD in
our group represents lifelong suffering, beginning close
to the end of the traumatic experience and persisting
for more than 50 years, or whether it represents a phase
of symptomatic reactivation occurring in WWII veterans
in their old age, as demonstrated by Macleod.12
The exposure to trauma puts into effect mechanisms of
coping (directed towards the environment), as well as
defense mechanisms (directed towards traumatic mem-
ory and its psychic repercussions). It is generally
acknowledged that most Holocaust survivors have suc-
ceeded in mobilizing effective skills for coping, mani-
festing themselves by recreating families and adapting to
social roles. However, the impact of the Holocaust on
ego functions led to the activation of defense mecha-
nisms, mostly of splitting and ensuing encapsulation,
numbing, and avoidance. As in psychosis, the coexistence
60
of psychosis in our patients led to processes of fragmen-
tation of the ego, thus impairing the exercise of these
ego functions. Again, this may have been a decisive fac-
tor in the occurrence of active PTSD symptomatology.
Furthermore, the primary process (psychosis) may have
uncovered the core memories of the traumatic experi-
ence and prevented the possibility of masking. One of
our patients only described a cannibalistic experience
during extreme starvation in the Theresienstadt con-
centration camp when in the manic-psychotic phase of
his bipolar disorder. While euthymic or depressed, he
was unable to recall or recollect this experience. Our
sample demonstrates a relative preponderance of intru-
sive symptomatology versus avoidant features. This find-
ing may also be related to the disorganizing effect of
psychosis on the ego.34
Conclusion
Our findings show that the comorbidity of psychosis and
PTSD in Holocaust survivors leads to a lifelong debili-
tating illness. Nonpsychotic survivors usually succeeded
in achieving a sense of integrity through “historicizing”
their memories35 (establishing a continuity between
early, positive pre-Holocaust memories, through trau-
matic memories during the Holocaust and memories of
reestablishing the fabric of life in the post-Holocaust
period). In contrast, the psychotic survivors were unable
to reach this equilibrium and, for them, memory is a life-
long burden. ❏
PTSD among Holocaust survivors - Barak and Szor
Trastorno de estrés postraumático
crónico: resultados en sujetos mayores
de 65 años sobrevivientes del
Holocausto
A pesar que han transcurrido 50 años desde el régimen
nazi y del Holocausto, las secuelas psíquicas aun no han
sido superadas. La mayoría de los sobrevivientes del
Holocausto y los veteranos de la II Guerra Mundial toda-
vía relatan sus experiencias como los “factores estresantes
más significativos de sus vidas”. La literatura ofrece una
amplia evidencia acerca de la persistencia del trastorno de
estrés postraumático entre los sobrevivientes a lo largo de
los años. Sin embargo, aun existe la necesidad de definir
las diferencias en cuanto a frecuencia, presentación clíni-
ca, severidad y comorbilidad entre los sobrevivientes –de
edad avanzada- del Holocausto. Se ha informado que la
edad en que ocurrió la experiencia traumática, la acumu-
lación de factores estresantes a lo largo de la vida y la
enfermedad física presentan una asociación positiva con
la sintomatología postraumática más severa. La presen-
cia de algún trastorno psiquiátrico del eje I (del Manual
Diagnóstico y Estadístico, DSM) ha sido el foco de inves-
tigación de nuestro grupo y se ha demostrado que la inte-
racción con traumas precoces conduce a una enfermedad
de curso crónico y debilitante. A pesar de la reactivación
de síntomas traumáticos durante el envejecimiento y el
continuo sufrimiento mental, la mayoría de los sobrevi-
vientes del Holocausto muestran una adecuada adapta-
ción y un buen funcionamiento en la vida diaria.
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32. Solomon Z, Benbenishty R, Neria Y, et al. Assessment of PTSD: valida-
tion of the revised PTSD inventory. Isr J Psychiatr Relat Sci. 1993;30:110-115.
33. Barak Y, Achiron A, Rotstein Z, Elizur A, Noy S. Stress associated with
asbestosis: the trauma of waiting for death. Psycho-Oncology. 1998;7:126-128.
34. Searles HF. The fear of change. In: Searles HF, ed. Collected Papers on
Schizophrenia and Related Subjects. International Psychoanalytic Library, Lon-
don, UK: Hogarth Press; 1965:164-183.
35. Auerhahn NC, Laub D. Annihilation and restoration: post-traumatic
memory as pathway and obstacle to recovery. Int Rev Psychoanal.
1984;11:327-344.
Clinical research
After the MV Estonia ferry disaster
A Swedish nationwide survey of the relatives
of the MV Estonia victims
Kristina Brandänge, MD; J. Petter Gustavsson, PhD
Just after midnight on the 28th of September 1994,
the Estonian-flagged ro-ro passenger ferry MV
Estonia was shipwrecked on its route between
Tallinn and Stockholm. Out of about 1000 persons
on board only 137 survived. This paper describes the
work that the Psychiatric Clinic at Ersta Hospital per-
formed with the relatives of the MV Estonia victims
after the disaster. In addition, we present data from
seven consecutive Swedish nationwide surveys
based on a questionnaire, which started as a corre-
spondence between the hospital and the relatives
of the Estonia victims. Findings concerning the care
relatives received and issues regarding their collab-
oration with the decisionmaking authorities are
presented. The importance of inviting the relatives
to participate in discussions concerning the Estonia
victims is stressed.
Keywords: disaster at sea; grief response; coping; relative; survivor; posttraumat-
ic stress disorder
Author affiliations: Psychiatric Clinic, Ersta Hospital, Stockholm, Sweden
(Kristina Brandänge); Department of Nursing, Karolinska Institute, Stock-
holm, Sweden (J. Petter Gustavsson)
Address for correspondence: Kristina Brandänge, MD, Psychiatric Clinic,
Ersta Hospital, PO Box 4622, SE-11691 Stockholm, Sweden.
(e-mail: kristina.brandange@ersta.se)
63
The Estonia ferry disaster
O n September 27, 1994, the Estonian-flagged ro-
ro passenger ferry MV Estonia departed from Tallinn,
Estonia en route to Stockholm, Sweden. Just after mid-
night the ship capsized and sank near Utö, an island off
the coast of Finland. There were about 1000 people on
board and of these, only 137 survived.1 Many were left
afloat in 11°C water for around 6 to 7 hours before being
rescued. Those who survived saw many fellow passen-
gers die during the long, cold night. According to the
Accident Investigation Commission, 17 countries were
represented on board. The majority of the passengers
were Swedish (n=552). Of the 552 Swedish passengers,
51 were rescued, 40 bodies were recovered, and 461 are
still missing.1
Sweden had not been involved in a war for almost 200
years and had been spared from major catastrophes. The
sinking of the Estonia was the first major disaster in mod-
ern-day Sweden. The hospitals in the Stockholm area had
received previous training in disaster emergency service
that included examples of just such an incident occurring
in the Baltic Sea. Now for the first time the extensive psy-
chosocial preparations that had been made in Stockholm
would be put to use in helping those affected.
The Prime Minister, who was soon to leave office, made
an announcement immediately following the incident
promising that no effort would be spared to try to
recover the remaining bodies. For his part, two days after
the disaster, the Prime Minister–elect added, during a
television interview, that efforts would also be made to
salvage the ship.
However, on December 15, 1994, the Swedish govern-
ment decided not to salvage the MV Estonia. The deci-
sion was based on the standpoints and conclusions of the
National Maritime Administration and of the Ethics
Committee appointed by the government. The Ethics
Clinical research
Committee came to the conclusion that the vessel should
be sealed and covered with concrete. On March 2, 1995,
the government entrusted the National Maritime Admin-
istration to purchase the concrete and have the MV Esto-
nia covered. The process of covering the ship was already
under way when the government, on February 11, 1999,
decided that the project should be discontinued.
The government decided on September 18, 1997 to
appoint an Analysis Group whose responsibility would
be to review the public actions that had been taken in
connection with the Estonia disaster. The Analysis
Group submitted a report to the government on Novem-
ber 12, 1998, in which they recommended that efforts
should be made to recover and identify the deceased.2
On February 11, 1999 the government decided not to
follow these recommendations.3
The Ersta Psychiatric Clinic
The Ersta Psychiatric Clinic is specifically devoted to
treating hospital personnel, its first responsibility
being to hospital personnel from Stockholm County
Council area. The Psychiatric Clinic is part of Ersta
Hospital, which is owned by the Ersta Deaconess
Society, a nonprofit association in close connection
with the Church of Sweden. It has 40 employees,
which makes it the smallest psychiatric clinic in Stock-
holm. Because Ersta does not belong to Stockholm
County Council, Ersta Hospital was the only emer-
gency hospital that had not received disaster emer-
gency training.
What can we at Ersta do to help the victims? This ques-
tion was to be often raised on the day of the catastrophe
and the following days. As Ersta Hospital was not part of
the emergency plan, the answer was obvious. Ersta should
continue with its habitual health care activities and let
the other hospitals concentrate on helping the victims.
During the first days, the Psychiatric Clinic at Ersta Hos-
pital kept on with the daily psychiatric workload as
planned. However, just two days after the catastrophe,
relatives of the Estonia passengers started to call. A com-
pany, many employees of which had been on board the
Estonia, also called the clinic asking if we could do some-
thing to help since the crisis groups in Stockholm were
being shut down. Ersta learned that 7 of the 9 hospitals in
Stockholm had shut down their Estonia crisis groups
because so few people had contacted them. Only the two
university hospitals, Huddinge Hospital and Karolinska
64
Hospital in Stockholm, intended to keep their crisis
groups going, at least for the following two days.
The following day, Sweden’s largest morning newspaper
carried an article about the distraught relative of a victim
who had been turned away after showing up at a crisis
center in Stockholm. Ersta got in touch with the crisis
centers at Huddinge and Karolinska, asking them if they
were going to start groups for the relatives. We could pic-
ture what would happen when all of the crisis groups
had shut down and the relatives’ reactions began to mul-
tiply. After several enquiries, we learned that Huddinge
and Karolinska had no intention of starting groups for
relatives, leaving it up to Ersta to take the initiative.
The weeks after the Estonia disaster
The Sunday after the Estonia catastrophe, the decision
was made to notify the relatives of the new crisis groups
that were being set up at Ersta Hospital. An official
memorial service was to be broadcast on the media
throughout Sweden, and the Dean of the Church was
asked to read a message to the relatives. However,
instead, the message was distributed by hand to the per-
sons attending the memorial service. The message wasn’t
typed very well and part of it was in longhand. We had
not intended for the relatives to receive the message in
that manner, especially under such tragic circumstances.
But in this way, a small paragraph was published in the
morning papers informing those interested that they could
either call Ersta or, 1 week after the disaster, go to the
clinic, where information about the crisis groups for rela-
tives would be available. During the first couple of days, the
clinic didn’t receive any phone calls. However, the third
day, the phones began to ring. Many callers said they would
like to come and take part in the crisis groups for relatives,
but expressed concern about the presence of television
and newspaper reporters, asking us to guarantee that the
press would not be there.Accordingly, we asked the news-
papers and television networks to show understanding, and
posted a note to that effect at the entrance to the clinic.
Over 120 relatives attended the meeting that evening.
Besides giving information on crisis groups for relatives and
asking them to write down their requests, some practical
post-disaster information was given by a lawyer, an insur-
ance company representative, and the police. The entire
room was like an open wound of grief, despair, and rage.A
petition from some relatives to demand the salvaging of
Estonia was passed around, which many signed.
After the MV Estonia ferry disaster - Brandänge and Gustavsson
Eleven crisis groups were subsequently organized,
including one just for children and teenagers, and one
for the relatives of survivors. During the months when
the groups met regularly, group leaders met every week
for guidance and supervision. More and more relatives
continued to contact Ersta. In order to meet the infor-
mation needs and requests, Ersta began holding open
house for the relatives twice a week. Ersta also held sev-
eral large meetings with invited speakers, mainly to deal
with financial and legal matters as well as general issues.
The relatives kept asking us to do even more to help.
Although our small clinic could not handle more groups
or meetings at that time, it was difficult to turn down
the requests from the relatives and survivors. That is
when the idea of a questionnaire came up.
The Ersta questionnaire
How the questionnaire evolved
One of the guest speakers at earlier training seminars,
Dagfinn Winje, a psychologist from Norway, had used
questionnaires during a major disaster in 1988.4,5 He
explained how this had had definite therapeutic results
for the participants. This questionnaire was based on two
classic inventories, the Symptom Checklist (SCL-90).6
and the Impact of Event Scale (IES).7 The same inven-
tories were used after a ferry accident that took place in
Sweden in 1990. On the basis of these two inventories, a
new questionnaire was put together at Ersta.
The questionnaire study was not intended as a research
project, but as a part of Ersta’s work with the relatives.
The main purpose was to be of real help to them. How-
ever, when the first completed questionnaires came
back, they included much more information than just
answers to the structured items. The relatives added per-
sonal comments, other information, and sometimes
included letters describing their present situation. Many
relatives living in rural areas pointed out that this was
the first time anyone had asked them about how they
had been feeling since the catastrophe. The question-
naire study that had started as a simple correspondence
with the relatives took on far greater proportions than
had been anticipated. Distribution and processing of the
questionnaires started posing considerable financial
problems for Ersta, the smallest psychiatric clinic in
Stockholm. To date, Ersta has received funds for eight
questionnaires.
65
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
This paper discusses the care the relatives received and
issues regarding their collaboration with the decision-
making authorities. Most of these items were presented
as visual analog scales, with a numbered response format
(ranging between 1 and 10) below. For ease of presen-
tation, answers to the questionnaire were divided into
three categories (yes, no, don't know). Moreover, only
the answers from the relatives (and not from the sur-
vivors) are presented. The surveys were approved by
the Ethics Committee of Huddinge Hospital.
The participants
The first questionnaire was sent out just before Christ-
mas, 1994, ie, 3 months after the disaster. To insure that
the questionnaire would not arrive without warning,
Peter Nobel, a lawyer and the government-appointed
representative for the Estonia victims, announced the
questionnaire’s arrival in a letter that was sent to the
relatives. Since then, six more surveys have been con-
ducted, 6, 12, 18, 24, 30, and 36 months after the ferry dis-
aster.
The first four questionnaires were sent only to the rela-
tives of the deceased and the survivors who had lost a
relative in the disaster. However, the survivors who had
not lost a relative expressed their frustration at being
left out. So, a letter was written to all survivors irrespec-
tive of whether or not they had lost a relative, asking if
they wished to participate in the survey. The answer
being yes, the survivors were included starting with the
fifth questionnaire.
To date, 879 relatives have completed the question-
naires, representing 89% of the MV Estonia’s Swedish
victims. The typical MV Estonia passenger was a male
between 34 and 44 years old, which implied that
bereaved relatives could include a spouse/partner, par-
ents, children, and siblings. Thus, different kinds of
bereaved relatives may exist for each victim, as indi-
cated in Figure 1 (see next page). The relationships
shown are those that the deceased had with the persons
who replied to the questionnaire. Thus, child or chil-
dren denotes that the respondent had lost one or more
children and parent or parents indicates the loss of one
or two parents. The relationships stated by the rela-
tives who responded to the questionnaires tally with
those in the official police report listing 577 relatives.
The largest group, both in the official police report and
in our survey, was that of persons who had lost their
Clinical research
Child/children Parent/s Partner Sibling/s Other Negative +/- Positive
100 60
90
50
80
70 40
60

%
%

50 30
40
20
30
20 10
10
0 0
3 6 12 18 24 30 36 3 6 12 18 24 30 36
Months after the disaster Months after the disaster

Figure 1. Relatives’ relationship to the deceased, as indicated Figure 2. Ratings by relatives of their experience of the help
by the relatives in each of the seven questionnaires. and care they received after the disaster.

parents. The second largest group were those who had

lost a spouse/partner. The third largest group were
Yes Don't know No
those who had lost a child or children, followed by
60
those who had lost siblings. The remaining groups
included grandparents, in-laws, and cousins. Respon- 50
dents who suffered multiple losses (for example, who
had lost both a husband and children) are included in 40
the 6% to 8% denoted as other in Figure 1.
%

30

Results 20

Figure 2 shows how the relatives rated the care they 10

received. The ratings were classed into 3 categories
(negative, positive, and in-between). In each survey,
there were more people who judged the care they
received as negative than those who regarded it as pos-
itive. Remarkably, the group that rated the care as pos-
itive decreased after the first year. Up until the first-
year anniversary of the sinking of the Estonia they had
a more positive outlook in regard to the help they
received. Thereafter, care tended to be increasingly
rated as negative. In addition, many participants com-
plained that the help they received ended too soon.
Another item in the questionnaire asked if subjects
would still like to receive help (Figure 3). Yes replies
eventually decreased in number, but 3 years after the
catastrophe, still slightly more than 20% of the rela-
tives wanted to continue receiving help. Those who
were unsure (don’t know) showed a tendency to
increase and numbered 30% after the third year.
0
3 6 12 18 24 30 36
Months after the disaster
Figure 3. Relatives’ answers to the question of whether they
would like to continue receiving help.
Opinions were split, among the relatives, about how to
deal with the bodies of the victims and to dispose of
the ship. The relatives have sometimes felt themselves
to be overlooked by the decisionmakers and claim that
no one listened to them. For us, at Ersta, it was very
important that all opinions and all feelings in this mat-
ter should be allowed to be voiced. We did not agree
that the relatives should not be asked to express their
opinions and wishes. We thought it important for them
to feel involved, to be seen and heard, even though
everybody's wishes could not be fulfilled.

66
After the MV Estonia ferry disaster - Brandänge and Gustavsson Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000

No Don't know Yes No Don't know Yes

100 100
90 90
80 80
70 70
60 60
%

%
50 50
40 40
30 30
20 20
10 10
0 0
3 12 18 24 30 36 18 24 30 36
Months after the disaster Months after the disaster

Figure 4. Relatives’ answers to the question: Do you think that Figure 5. Relatives’ opinions on whether the MV Estonia should
the authorities, before coming to a decision on December 15, be covered with concrete or not.
1994, should have consulted the victims' relatives regarding
the salvaging matter?

Yes Don't know No

Figure 4 shows the responses to the question: Do you 100
think that the authorities, before coming to a decision on 90
December 15, 1994, should have consulted the victims' 80
relatives regarding the salvaging of the Estonia? This
70
question was not included in the first questionnaire,
60
which only contained questions relating to health and
%

50
disaster emergency relief. The majority of the relatives
40
clearly wished the government had asked them for their
30
opinion, and, as can bee seen in Figure 4, there was a
20
noticeable increase of yes-answers with time.
10
Figure 5 relates to the question of whether the Estonia
0
should be covered with concrete or not. According to
18 24 30 36
public authorities, this was the wish of the overwhelming Months after the disaster
majority of the relatives. However, replies concerning
this point in the questionnaire 18 months after the dis- Figure 6. Percentage of relatives who reported that they felt
aster show a clear majority of no-answers. This question overlooked by the government.
has evoked the most frequent written comments in the
questionnaires.
The relatives who claimed to have been overlooked by Comments
the government make up over 80% of the total group
(Figure 6). This figure may have changed since the This is the first paper assessing the results of our ques-
appointment by the government, 36 months after the dis- tionnaire study. Future papers will discuss the psychi-
aster, of an Analysis Group to investigate the manage- atric symptoms developed by the relatives and how the
ment of disaster emergency relief. This group gave rise tragedy affected quality of life self-ratings. Preliminary
to high expectations among the relatives. In November results indicate that psychiatric symptoms were corre-
1998, a report from that investigation group concluded lated with the type of familial relationship, ie, that they
that the bodies should be retrieved and buried in Swedish depended on whether the bereaved relative was a par-
soil.2 However, the government rejected the proposition.3 ent, partner, sibling, or child.8 Other publications avail-

67
Clinical research
able in English about the MV Estonia disaster include questionnaire was completed, the matter of salvaging
the report from the Joint Accident Investigation Com- was included. In the third questionnaire, the matter of
mission,1 a research report describing the psychiatric sta- covering the Estonia with concrete appeared for the first
tus among the Swedish survivors 3 months after the dis- time. To date, seven questionnaires have been distrib-
aster,9 as well as a chapter in a book by a Finnish uted and at least two more are planned.
psychologist describing the work of the Finnish Disaster
Victims Identification Team.10 Conclusion
Certain limitations of the present study should be noted.
No thorough investigation was performed in order to We would like to conclude this paper with a poem that
draw a comprehensive list of each victim’s close rela- a relative, a young man, sent in connection with the
tives. When a catastrophe occurs, there is always a ques- questionnaire. We want to show that the questionnaire
tion of who, among the victims’ relatives feels close or study is not just important in terms of figures and charts,
not. We have allowed the relatives to decide for them- but that it also provided an opportunity for relatives
selves on this point, ie, whether they wished to partici- and survivors to give vent to deep-felt emotions.
pate in the survey or not. Contact with the families was
established partly through the intervention programs I miss my mother.
held at Ersta Hospital, but mainly through a letter sent I wish she were alive again,
to all relatives who had been listed by the Swedish gov- If only for a day.
ernment. Further analyses will be done to identify and One hour, a few minutes,
evaluate possible selection biases. If only for a day.
When the first questionnaire was sent out three or four To say good-bye.
days before Christmas 1994, Ersta expected to receive To thank her for everything she has given me.
many angry phone calls. Some doubt was expressed
about sending the questionnaire to relatives with whom She gave me life.
no prior contact had been made. It was difficult to imag- Now she has given me her last gifts,
ine what it would be like to receive such a questionnaire Death and great sorrow.
on a tragedy of such proportions so close to Christmas Now I have received life in its entirety.
from a hitherto unknown institution. ❑
Only 1 out of the 758 recipients called to protest about
the procedure, and asked to be sent no further ques-
tionnaires. However, a year later, this person relented
and has since been participating in the study, as well as
this person’s family. Many others called to point out that
the questionnaire did not include the question that was
most important to them, ie, the question of salvaging
the ship. It was explained to the relatives that this ques-
tion should not be asked by Ersta, as we are a hospital
concerned with their health and well-being, and that the
government had already made the decision on Decem-
ber 15, 1994, not to salvage the Estonia. We contacted
the Department of Communications, and tried to
explain how important it was to the relatives that they
be asked their opinion, in spite of the fact that the deci-
sion had already been made. However, it was clear that
the government was not about to consult the relatives
regarding the salvaging issue. In the end, it was decided This study was supported by grants from Stockholm County Council, Folk-
sams, AMF, other companies, private individuals, and from the Swedish gov-
to let the relatives themselves formulate the questions ernment. We thank Sara Göransson and Sam Sundquist for their skillful
that they thought were important. So when the second assistance.

68
After the MV Estonia ferry disaster - Brandänge and Gustavsson
Consecuencias de la catástrofe del ferry
MV Estonia. Una encuesta nacional
sueca en los familiares de las víctimas
del MV Estonia
Unos minutos después de la medianoche del 28 de
septiembre de 1994 el transbordador de bandera
estoniana, el MV Estonia, naufragó en la ruta entre
Tallinn y Estocolmo. Del total de casi 1000 personas a
bordo sólo 137 sobrevivieron. Este artículo describe el
trabajo que la Clínica Psiquiátrica del Hospital de Ersta
llevó a cabo con los familiares de las víctimas del MV
Estonia después de la catástrofe. Además se presentan
los datos basados en siete encuestas consecutivas en que
se utilizó un cuestionario distribuido en toda la nación.
Este cuestionario, que fue concebido inicialmente sólo
como una simple correspondencia entre el hospital y los
familiares de las víctimas, permitió definir otros
aspectos: a) diversos elementos relacionados con la
atención que recibieron los familiares y b) diferentes
temas vinculados con la participación de los familiares
en las decisiones gubernamentales. Se destaca el hecho
que los familiares de las víctimas participen en las
discusiones concernientes a la catástrofe del Estonia.
REFERENCES
1. The Joint Accident Investigation Commission of Estonia Finland and Swe-
den. Final Report on the Capsizing on 28 September 1994 in the Baltic Sea of the
Ro-Ro Passenger Vessel MV Estonia. Helsinki, Finland: Edita; 1997:228.
2. Örn P, Björklund L, Jutterström C, Nordin C, Strömholm S. En Granskning
av Estoniakatastrofen och Dess Följder [An Examination of the Estonia Disaster and
its Consequences]. Stockholm, Sweden: Swedish Government Publications;
1998:284.
3. Örn P, Björklund L, Jutterström C, Nordin C, Strömholm S. Lära av Esto-
nia [Lessons Learned from the Estonia Disaster]. Stockholm, Sweden: Swedish
Government Publications, 1999:228.
4. Winje D. Long-term outcome of trauma in adults: the psychological con-
sequences of a bus accident. J Consult Clin Psychol. 1996;64:1037-1043.
5. Winje D, Ulvik A. Long-term outcome of trauma in children: the psycholog-
ical consequences of a bus accident. J Child Psychol Psychiatr. 1998;39:635-642.
69
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
Après la catastrophe du ferry MV
Estonia: enquête basée sur un
questionnaire national adressé aux
membres des familles des victimes du
MV Estonia
Un peu après minuit, le 28 septembre 1994, le navire
roulier de transport de passagers MV Estonia, battant
pavillon estonien, fit naufrage entre Tallinn et Stock-
holm. Seuls 137 des quelque 1000 passagers ont sur-
vécu. Cet article rapporte les résultats du travail qui a
été réalisé auprès des membres des familles des vic-
times du MV Estonia dans le service de psychiatrie de
l’hôpital de Ersta à la suite de la catastrophe. Des don-
nées fondées sur les résultats d’un questionnaire natio-
nal, qui leur a été adressé à sept reprises après la catas-
trophe, sont rapportées. Ce questionnaire, qui n’était
conçu au départ que comme une simple correspon-
dance entre l’hôpital et les membres des familles des
victimes, a permis de définir plusieurs éléments
concernants les soins qui leur ont été prodigués et de
poser le problème en ce qui concerne leur participa-
tion aux décisions prises par le gouvernement. Cette
étude a permis de souligner l’intérêt de la participation
des membres des familles aux entretiens concernant les
victimes de la catastrophe de l’Estonia.
6. Derogatis LR. The SCL-90 1. Scoring, administration and procedures for
the SCL-90. Baltimore, Md: Johns Hopkins School of Medicine; 1977.
7. Horowitz MJ, Wilner N, Alvarez W. Impact of event scale: a measure of
subjective stress. Psychosom Med. 1979;41:209-218.
8. Gustavsson, JP, Brandänge, K. After the MV Estonia disaster: a longitu-
dinal psychiatric study on bereaved relatives. Paper presented at the 5th
AEP Symposium, November 1999, Strasbourg, France.
9. Eriksson NG, Lundin T. Early traumatic stress reactions among Swedish
survivors of the m/s Estonia disaster. Br J Psychiatry. 1996;169:713-716.
10. Nurmi L. The Estonia disaster: national interventions, outcomes, and per-
sonal impacts. In: Zinner ES, Williams MB, eds. When a Community Weeps: Case
Studies in Group Survivorship. Philadelphia, Pa: Brunner/Mazel; 1999:49-72.
Clinical research
A social interaction model
for war traumatization
Self-processes and postwar recovery in Bosnia in subjects
with PTSD and other psychological disorders
Willi Heinz Butollo, MD

able to physical injury, life-threatening events, or the

Theoretical aspects
The traumatized self
Although true of most conflicts, that which took place
in Bosnia between 1993 and 1995 was characterized by
the fact that a great number of acts of extreme cruelty
were waged specifically against civilians. This implies
that war-related traumatization is not solely attribut-
social consequences of displacement or deportation,
but that loss of interpersonal trust plays a paramount
role as well. Thus, among the many areas that must be
addressed when designing therapeutic methods to deal
with traumatized individuals, particular emphasis
should be placed on self-processes as a representation
of social interactions and the violation/distortion of
these self-processes by the experience of a traumatic
incident.
This concept is in strong support of a more dialectical
approach to the treatment of posttraumatic stress dis-
order (PTSD). Equating self-processes with represen-
tations of social interactions implies that distorted
interactions, which have been shown to develop in the
wake of most traumatic incidents, exert a dramatic
influence on these self-processes. If such is the case,
then therapy must deal in priority with interactional
experiences.
Our treatment approach was originally developed for
patients having experienced a single traumatic event

Traumatization of self-processes as a consequence of acts of war is not only determined by the content and num-
ber of traumatic experiences, but also, to a large extent, by factors related to posttraumatic socioeconomic, envi-
ronmental, and psychosocial interactions. A model is presented to describe posttraumatic adaptation of war-trau-
matized selves according to the characteristics of the individuals' social interactions and the cognitive
representations of those processes. Findings in children (n=816) and adults (n=801) from postwar Bosnia are ana-
lyzed. One of the most traumatic experiences was having a missing relative, particularly a father: not knowing
the fate of a close relative is an ongoing stressor that alters cognitive-emotional processes and reduces self-esteem
and interactional competence, whether in children or in adults. Use of a multiphasic integrative therapy for trau-
matized subjects (MITT) showed promising results in victims of the Bosnian war.

Keywords: traumatized self; posttraumatic stress disorder; loss; integrative trauma

therapy; social interaction and self-processes; cognitive therapy; dialectical therapy Address for correspondence: Prof Willi Heinz Butollo, Chair of Clinical Psy-
chology and Psychotherapy, Department of Psychology, Ludwigs-Maximilians
Author affiliations: Chair of Clinical Psychology and Psychotherapy, Depart- University (Institut für Psychologie), Leopoldstr 13, 80802 Munich, Germany
ment of Psychology, Ludwigs-Maximilians University, Munich, Germany (e-mail: butollo@psy.uni-muenchen.de)

71
Clinical research
Selected abbreviations and acronyms
DSRS Depression Self-Rating Scale
WRTE war-related traumatic experience
PWRS postwar-related stress
MITT multiphasic integrative therapy for traumatized people
PSS Posttraumatic Stress Symptom scale
PTSD posttraumatic stress disorder
SCL-90-R Symptom Checklist 90-R
occurring in a civilian setting, such as an accident or
exposure to violence or sexual assault. It was later
applied to war traumatization in Bosnia, during the war
and in the postwar period. Joint projects were carried
out with workers at the University of Sarajevo to study
the diagnosis of PTSD, empirical treatment, and thera-
peutic processes (for further details, see references 1-7).
The social interaction model
Throughout our lives, we develop models based on our
experience of the world in which we live and of the other
human beings with whom we come into contact. Our
expectations about future experiences and behaviors are
largely influenced by these models, which are constantly
being revised, as new experiences add to previous ones
to gradually evolve and stabilize into a set of models of
reality out of which we somehow “create” our own rep-
resentations of our selves and of the world. The com-
plexity of these models depends on many factors, includ-
ing the sophistication of a given individual's cognitive-
processing system, as reflected in its selection, memory,
and retrieval functions, and probably several other fac-
tors as well. Similar to our representations of the “phys-
ical” world, the configuration of our self-processes is
determined by the experience of interactions between
ourselves (the acting person) and our world.
Phases of posttraumatic adaptation
Under normal conditions, new experiences do not dif-
fer drastically from our expectations, so that we are
able to adapt our models of the world, our self, and the
resulting interactions in a more or less smooth and
gradual way.
In contrast, traumatic experiences are, by definition, far
72
removed from what an individual expects in so-called
normal-life situations, and as a result, cognitive and
emotional functions must adapt in order to restore con-
gruency between the individual's model of the world,
self, and the traumatic experiences that are being inte-
grated. Cognitive and emotional attempts to integrate
traumatic experiences appear to run through different
phases and levels, in which the coping processes vary in
complexity and goals. Strategies that are helpful in the
aftermath of a traumatic incident might be counterpro-
ductive or even harmful at a later stage, and vice versa.
During the acute phase of trauma, the coping process
aims to achieve a general reduction in stress through the
use of “inner” and “outer” (cognitive and behavioral)
strategies such as escape or avoidance. During the later
phases of posttraumatic adaptation, particularly in the
event of failure to deal successfully with the traumatic
experience in its entirety, coping strategies focus on
denial of either the experience as a whole or some of its
aspects, as subjects try to hold on to the remnants of
competence and coherence of the pretraumatic self.8 In
contrast, individuals who feel relatively secure and
strong, who are again able to engage in well-integrated
relationships and have recovered their competence in
dealing with everyday issues, attempt to confront the
memories of the traumatic events emotionally and cog-
nitively, even though the stresses experienced at the
time risk being reawakened in the process. This takes
place through a step by step approach of the sealed
memories of the experiences that were unbearable in
their full extent when the traumatic incident took place.
Unanswered questions
The above considerations give rise to a certain number
of questions. One problem is that the models of post-
traumatic adaptation on which therapeutic concepts are
based are purely theoretical,8 without there being, to
date, any confirmation by empirical evidence: what,
therefore, is the validity of current therapeutic practice?
Another important question relates to the extent of
posttraumatic adaptation: traumatized subjects appear
to be able to integrate their experiences in such a way
that their old models of the world are not completely
shattered, but are replaced by new ones influenced by
the implications of the traumatic experience, ie, they do
not attempt to rigidly restore the old models by ignor-
ing or denying the impact of the traumatic incident.
Self-processes and postwar recovery in Bosnia - Butollo Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000

How is this possible, and which processes are involved?
It is with these questions in mind that we carried out
our studies on Bosnia war victims’ adaptive skills in over-
coming trauma, in the hope of finding some answers.
Studies on war traumatization in Bosnia
Stress in children whose father is missing, separated
from them, or dead
Children from war areas who are displaced or obliged
to seek asylum in foreign countries have to cope with
multiple traumatic experiences, one of the most serious
being the loss of a father, who has either been killed or
is missing.
We carried out a study in the canton of Sarajevo on 816
children and early adolescents (age 10-15 years). The
main goal of the study was to look at the psychological
effects of traumatic experiences caused by the loss of a
father as a consequence of the war.9
This study evaluated the number of traumatic experi-
ences during the war and in the postwar period, and
measured depressive symptoms using Birleson’s
Depression Self-Rating Scale for children (DSRS).10
Four groups of children were defined as follows:
• Missing fathers: Children who lost contact with their
father during the war and had still not received any
information about his fate at the time of the study
(n=201; 106 boys, 95 girls).
• Separation: Children who were separated from their
father during the war, but could be reunited with
him after the war (n=204; 104 boys, 100 girls).
• Killed fathers: Children whose fathers were killed dur-
ing the war; the children had full knowledge of the
fact and circumstances (n=208; 105 boys, 103 girls).
• Controls: Children not having lost or been separat-
ed from their father; all other factors were the same
as in the other groups (n=203; 99 boys, 104 girls).
Table I shows the average number of traumatic experi-
ences other than the loss of a father. The fact the num-
ber of such experiences was significantly higher in the
group with fathers missing is worthy of note.
A potential confounding factor with respect to depres-
sive symptoms was the possibility that a child's lack of
information about a close relative could be a conse-
quence of the chaotic circumstances brought about by
“ethnic cleansing,” the latter being in itself associated

RESULTS OF ANALYSIS OF VARIANCE (4x2) OF THE VARIABLES WAR- AND

POSTWAR-RELATED STRESSFUL/TRAUMATIC EXPERIENCES
Source of variation Stressful/traumatic experiences
WRTE PWRS
F P F P
Groups 87.86 0.000 25.17 0.000
Gender 0.26 0.610 0.09 0.754
2-way interactions group x gender 0.43 0.730 0.46 0.710

MEANS ON THE QUESTIONNAIRE FOR WAR-RELATED TRAUMATIC EVENTS (WRTE)

Subjects whose father was: Missing Separated Killed Controls Mean
Boys 13.50 7.17 9.90 9.16 9.96
Girls 13.58 7.80 9.67 9.24 10.02
Mean 13.54 7.48 9.78 9.20 9.99

MEANS ON THE QUESTIONNAIRE FOR POSTWAR-RELATED STRESSFUL/TRAUMATIC EXPERIENCES (PWRS)

Subjects whose father was: Missing Separated Killed Controls Mean
Boys 2.98 1.69 2.12 1.66 2.12
Girls 2.83 1.90 2.13 1.73 2.13
Mean 2.91 1.79 2.13 1.69 2.13

Table I. War-related traumatic experience (WRTE) and postwar-related stress (PWRS) in children.

73
Clinical research
RESULTS OF ANALYSIS OF VARIANCE (4x2) ON THE VARIABLE OF DEPRESSIVE REACTIONS
CONTROLLED FOR COVARIATES WRTE AND PWRS
Source of variation Depressive reactions
F P
Group 6.72 0.000
Gender 67.90 0.000
2-way interactions
group x gender 0.72 0.538

MEANS ON THE DEPRESSION SELF-RATING SCALE (DSRS) CONTROLLED FOR COVARIATES

Subjects whose father was: Missing Separated Killed Controls Mean

Boys 12.20 9.18 11.28 9.16 10.48
Girls 14.96 11.23 13.72 12.10 12.97
Mean 13.50 10.19 12.49 10.67 11.71

Table II. Depression and losses in children. WRTE, war-related traumatic experience; PWRS, postwar-related stress.

with higher trauma scores. An analysis of covariance
was therefore performed in order to correct for the
confounding effect of this covariate on the variable
“depression.” The main depression scores, adjusted for
covariates, are shown in Table II. The differences
among the groups were highly significant, and, again,
the highest depression scores were found in the chil-
dren with a missing father, with almost as high scores in
children whose father had been killed. These results
highlight the cognitive processes that are triggered in
children who lose a parent through acts of violence or
who are left with no information concerning the fate of
their father, and that uncertainty with respect to family
members was the strongest factor in childhood depres-
sion.
Traumatic and stressful events experienced by adults
with different flight paths
Profile of traumatic events and exposure to stress
In a second study, we looked at the types of stressful
and traumatic events and situations experienced during
and after the war by adults with different flight paths
(returnees, displaced people, and “stayers”).11
The study was carried out in a total sample of 501 sub-
jects consisting of 5 subgroups of returnees, displaced
people, or stayers, from Sarajevo (capital of Bosnia-
Herzegovina) and Banya Luka and Prijedor (northwest
of Sarajevo, now in the Serb Republic). We used a
checklist taken from the first section of the Modified
Posttraumatic Stress Symptom scale (PSS) made up of
130 different traumatic and stressful events. For conve-
nience of evaluation, these 130 items were divided into
10 different event clusters (groups), such as total events
in war zone, expulsion and flight, time spent in concen-
tration camps or temporary shelters, etc, and statistical
evaluation was carried out separately for each event
group (Table III).
One of the most important findings was that the
Sarajevo returnees had about as much exposure to the
war and war events as the two displaced groups from
the Serb Republic. The returnees and displaced people
had spent a great deal of time in temporary shelters and
collective centers (Table IV). Not surprisingly, all sub-
jects had experienced appalling losses. Subjects housed
in collective centers are those experiencing a particu-
larly high level of current stress (see next section). Each
group had a distinctive profile of traumatic events and
other stressors. The Banja Luka stayers seemed to have
been somewhat better off, while the two Sarajevo
groups experienced the highest number of traumatic
events and other stressors. It should be noted that ex-
soldiers were not excluded from the study population.
Correlation with current symptoms
Most of the events and event groups described are
correlated with current psychological distress: the
greater the subjects’ exposure to such events, the

74
Self-processes and postwar recovery in Bosnia - Butollo Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000

worse their current symptoms of distress. We used the
SCL-90-R Symptom Checklist to measure these symp-
toms.12 This checklist records psychologically relevant
symptoms, such as headaches, anxiety, or hearing voic-
es that are not there.12
It should be stressed that the mere presence of a cor-
relation between the occurrence of a given group of
events and the presence of current symptoms does
not necessarily imply that a causal relationship exists.
For instance, it is possible that some groups of events

Sarajevo Sarajevo Prijedor

returnees from displaced or Banja Luka Banja Luka displaced in Group
outside formerly displaced stayers collective mean
ex-Yugoslavia displaced) (n=100) (n=100) centers
(n=104) (n=97) (n=100)
War events: self
Total traumatic events in war zone:
events that happened to the
individual during the war, such as
being shot at, being wounded, being 8.98 12.76 12.28 7.47 10.04 10.68
in a cellar for over 3 weeks, etc.
Witnessing violence to others is
also included
(number of events)

Stressors: expulsion and flight 1.63 3.07 3.27 0.02 3.02 1.97
(number of events)

Other war-related stressors (material

loss, ill-health, displacement) 4.18 4.88 5.17 0.95 4.27 3.68
(number of events)

Length of time in war zone (years) 1.61 2.96 2.65 0.96 1.92 2.01

Stressors: length of time in 4.36 7.27 0.16 0.00 0.37 0.68

concentration camp (months)

Displacement, flight, refuge

Stressors: length of time in 22.36 18.00 0.92 0.00 40.30 14.93
collective center (months)

Stressors: length of time in 39.44 55.53 27.40 0.00 8.72 21.97

temporary accommodation (months)

Stressors: length of time with 3.38 4.40 23.49 0.00 13.86 11.10
no accommodation at all (days)

Stressors: refuge abroad 1.18 0.83 0.02 0.00 0.01 0.31

(number of events)

*The events shown to have the strongest influence on psychological status are italicized.

Table III. War events and displacements.

75
Clinical research
Sarajevo Sarajevo Prijedor
returnees from displaced or Banja Luka Banja Luka displaced in Group
outside formerly displaced stayers collective mean
ex-Yugoslavia displaced) (n=100) (n=100) centers
(n=104) (n=97) (n=100)
Loved ones
Losses of loved ones 2.51 2.79 2.78 1.52 2.26 2.36
(number of people)

Violence, threat ,and injury to 5.29 5.75 5.74 4.00 3.76 4.78
loved ones (number of events)

Total length of separations from 67.28 45.94 30.13 18.77 25.48 37.14
family members (months)

Total length of no information 23.29 23.39 12.14 8.33 17.40 16.32

about family members (months)

Current stress
Stressors: unemployment since 1991
(number of months, plus number 68.57 74.96 57.66 26.10 60.05 56.07
of months no-one in family was employed)

Current stressors: family members 1.89 1.85 2.03 1.15 1.71 1.73
separated or missing (number of people)

Current stressors: accommodation,

health, unemployment, etc 3.68 4.61 6.50 2.15 7.37 4.29
(number of stressors)

*The events shown to have the strongest influence on psychological status are italicized.

Table IV. Vicarious traumatization and losses.

are highly correlated with symptoms just because
they occurred together with other events which them-
selves have a genuine causal relationship with symp-
toms. A regression analysis was therefore carried out
to try to determine the specific effect of each of these
event groups on symptoms, independently of the
influence of the other groups. The event groups char-
acterized by the strongest specific influence on psy-
chological status in this analysis are italicized in
Tables III and IV. Regression analysis showed that
the most psychologically debilitating event groups
were traumatic events sustained during the war and
difficult present-day personal and social circum-
stances. However, this is only a preliminary analysis;
much more work needs to be done, for instance, to
isolate as many of the factors that predict particular
psychological problems as possible.
Psychological profile of non-PTSD sufferers
Psychological adjustment is important not just
because it is an indication of the pain, optimism, etc,
experienced by the citizens of Bosnia-Herzegovina,
but also because it has a major influence on the recon-
struction of the country. To take but one example,
depression is a major obstacle because even the most
talented or resourceful people achieve very little for
themselves or others if they are depressed or hopeless.

76
Self-processes and postwar recovery in Bosnia - Butollo
We therefore sought to identify the specific needs in
terms of psychosocial intervention for each of the
study’s subgroups.
German subjects with no noteworthy psychological his-
tory and German psychiatric inpatients were used as
reference groups, and three additional semirandom
comparison groups of stayers identified by our
Research Institute in Sarajevo in 1998 were included: a
medical treatment group, a psychological treatment
group, and a random group of Sarajevo residents, with
n=100 for each group. Figures 1 and 2 (next page) show
the scores for items as defined by the SCL-90-R check-
list. It is not, at present, completely clear to which extent
the differences in symptom scores found in comparison
with the reference groups is attributable solely to war
and postwar stress, or could reflect, at least in part, cul-
tural differences between Bosnian and German sub-
jects.
Symptom scores in all groups of Bosnian subjects were
significantly higher than in the reference samples, but not,
however, as high as would be expected in psychiatric inpa-
tient populations. Predictably, the Banja Luka stayers had
the fewest symptoms. The subjects with the highest symp-
tom scores were the Prijedor and Banja Luka groups of
persons displaced in camps. In Sarajevo, the returnees had
slightly fewer symptoms than the displaced groups, who
were about as well adjusted as the stayers were in 1998.
Figure 2 shows the same findings in a different way, which
makes it easier to compare the study group profiles with
respect to the reference groups.The profiles of the postwar
Bosnia-Herzegovina groups are very distinctive, showing a
peak for the item “paranoid ideation,” (encompassing sus-
piciousness and the feeling of being isolated), and a lesser
elevation of passive symptoms such as anxiety and depres-
sion, in comparison with aggression, paranoid ideation, and
somatization.
Psychological profile of PTSD sufferers
Alongside the high incidence of general psychological
symptoms in our population of subjects exposed to the
war in Bosnia, there was also a high incidence of PTSD.
This is a serious disorder that has extremely unpleasant
consequences for those affected and significantly alters
their daily functioning at work and in the family.
Figure 3 shows that these subjects had a distinctive psy-
chological profile, characterized by hyperarousal (sleep-
lessness, restlessness), reexperiencing of the events
77
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
(nightmares, flashbacks), and avoidance (trying not to
think or talk about the events, emotional numbing).
It should be noted that, as in Figures 1 and 2, three semi-
random samples of Sarajevo stayers from 1998 were
included in Figure 3 for the purpose of comparison.
Between 10% and 35% of subjects in the nontreatment
group were diagnosed as having PTSD. The differences
observed in terms of incidence of PTSD among the
study groups were much greater than those relating to
general psychological symptoms (see preceding sec-
tion). Unsurprisingly, the subjects exposed to the high-
est level of war stresses showed the highest incidence of
PTSD. However, the displaced subjects placed in col-
lective centers had the highest incidence of PTSD
among the 1999 groups, which could indicate that par-
ticularly difficult social circumstances can significantly
contribute to the maintenance of PTSD. The incidence
of PTSD was higher in older people and women. This
broadly agrees with results in the international litera-
ture on PTSD, although further research is needed to
investigate differential exposure to traumatic events.
The results for general psychological symptoms as mea-
sured by the SCL-90-R checklist are very similar.
Therapeutic implications
Multiphasic integrative therapy for traumatized
people (MITT)
After presenting the theoretical aspects of self-process-
es and posttraumatic adaptation and discussing the find-
ings from our two studies carried out on Bosnian war
victims, we now look at the contribution of what we
have termed a social interaction therapeutic approach
to rebuilding self-processes shattered by traumatic
experiences.This approach is based on enabling patients
to achieve a successful integration of pretraumatic, trau-
matic, and posttraumatic experiences in a mature way.
The social interaction model outlined is, in fact, more a
heuristic guideline than a therapeutic technique as such.
Its role is to help select appropriate therapeutic meth-
ods and techniques during the different phases of post-
traumatic adaptation, and adjust them according to the
speed of the individual’s recovery and the level at which
he or she operates. These include techniques to reduce
characteristic posttraumatic symptoms like intrusion,
hyperarousal, avoidance, depression, feelings of insecu-
rity, cognitive deficits, flashbacks, sleep disturbances,
Clinical research

1.8
1.6
Symptom scale score

1.4
1.2
1.0
0.8
0.6
Psychiatric German inpatients
0.4 Prijedor displaced in collective centers
0.2 Banja Luka displaced or formerly displaced
0 Sarajevo stayers, medical treatment (1998)
n Sarajevo stayers, psychological treatment (1998)
z atio e
at i iv
o m p uls ers Sarajevo stayers, random sample (1998)
S m isord ia
c
- do ob Sarajevo displaced or formerly displaced
ive ph
n

s s a l
sio

se ci Sarajevo returnees from outside ex-Yugoslavia

So
es

Ob
y
pr

t
xie
De

Banja Luka stayers

An

n
sio
es

ty

Normal German population

gr

xie
Ag

an

n
tio
i c

ea
ob

ism
id
Ph

tic
id

ho
no
ra

yc
Pa

Ps

Figure 1. Level of symptoms for each of the nine types of symptoms by group, including comparison with a normal German popula-
tion, a group of psychiatric German inpatients, and three samples of Sarajevo stayers from 1998 (medical treatment, psy-
chological treatment, and random sample).

1.8
Psychiatric German inpatients
1.6 Prijedor displaced in collective centers
(higher score = worse symptoms)

Banja Luka displaced

1.4 or formerly displaced
Symptom scale score

1.2 Sarajevo stayers,

medical treatment (1998)

1.0 Sarajevo stayers,

psychological treatment (1998)

0.8 Sarajevo stayers,

random sample (1998)
0.6 Sarajevo displaced or
formerly displaced
0.4 Sarajevo returnees from
outside ex-Yugoslavia
0.2
Banja Luka stayers

0 Normal German population

Somatization Obsessive- Social Depression Anxiety Aggression Phobic Paranoid Psychoticism

compulsive phobia anxiety ideation
disorders

Figure 2. Alternative view of the general symptom profile of the groups in Figure 1.

78
Self-processes and postwar recovery in Bosnia - Butollo Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000

40
nongovernmental organiza-
tions, and in hospitals. The
35 training was offered in various
Respondents in each group

30 towns in Bosnia to groups of up

to 30 participants. The principal
with PTSD (%)

25 goals of this training were to

20 provide role models for therapy
and technical skills, but we also
15
helped to combat burnout and
10 treat trauma disorders of par-
ticipants whose war-shattered
5
self-processes badly needed
0 support. During this period,
research was not in the fore-
la or

la ed

rs

nt ed

99 s

(1 en rs

(1 en rs
(1 er
la es

ye

at ye

at ye
sp ac

ce lac
sp d

e ay
d

8)

99 t

99 t
os ne

er
via

sta

re ta

re ta
di ce
ce

ce
di pl

pl st
ive sp

front of our work. As a feed-

ug ur

8)

8)
lt os

lt os
ly la

m
ly is

ka

ct di

m o
-Y et

er isp

sa ev

ica jev

ca v
ex o r

Lu

gi je
a

lle or
rm d

aj
rm uk

back for us, as trainers, and for

ed ra

lo ara
co ed
de jev

fo jevo

om ar
fo a L

m Sa
nj
er

in Prij

nd S

ho S
tsi ara

Ba
or nj
ra

the participants, we used the

Ba
S

Sa

SCL-90-R12 checklist to assess

yc
ou

ra

ps
m
fro

the stresses the participants

were exposed to and their reac-
Figure 3. Percentage of respondents with the diagnosis of posttraumatic stress disorder tions to these stresses. Figures 4
(PTSD) by group.
and 5 show some of the results
using group averages (before
bad dreams, dissociation processes, social isolation, and after training sessions). It can be seen that, at the
achievement difficulties, concentration problems, etc. beginning of the two different workshops (in 1994 and
However, as the theoretical model predicts, and our 1995), most of the participants were in a severe state,
empirical data show, social, economic, and educational with a large number of symptoms and scores on the scale
support is important too, and has a synergistic effect on clearly above the clinical norms, and that these scores
the outcome of psychological intervention. had already dramatically changed during the first week
In general, patients, particularly in the posttraumatic of training (Figure 4). The second training session took
phase, show great motivation for therapy provided the place in 1995 in the same group. Figure 5 shows evidence
therapist is ready to work with them on their symptoms. of the stresses of another year of war, with scores even
However, the patient’s motivation often undergoes fluc- higher than at the beginning of the 1994 workshop.
tuations due to the interference of intrusions, avoidance Again, after training, the participants recovered their
patterns, or plain socioeconomic problems, which affect liveliness and optimism, and the extreme values of their
the dialectical (social interactional) aspect and the self- scores were dramatically reduced again.
processes. The social interaction model of the trauma- One could question the usefulness of this type of train-
tized self allows symptom-oriented or psychosocial ther- ing if its results were short-lived. Considering the decay
apy to be more effectively focused, thus helping patients of clinical scores during an ongoing war situation, critics
whose self-processes are shattered by traumatic experi- might be right. However, our data show that the effect
ences to restore self-assertiveness and self-stability. on our Bosnian colleagues’ depression, despair, and fear
This therapeutic approach was used in a series of train- was very positive, at least in the short- and mid-term.
ing programs throughout Bosnia. Actual training started They certainly recovered enough of their former capa-
during the war in 1993 and was continued after the war, bilities, which they in turn were able to apply to their
with the support of UNICEF (the United Nations patients and family, to carry them—at least for a few
Children’s Fund) and Volkswagen-Stiftung. During the weeks or months—through shelling, hunger, life-threat-
war, the training program was offered to local profes- ening events, and expulsion experiences, and—the expe-
sionals and paraprofessionals, who worked in camps, for rience reported as the worst—the daily discovery that

79
Clinical research
Figure 4. Average symptom scores
1.6 Before training (1994) After training (1994) Normal population of trainees before and after train-
ing sessions during the war in
1.4 Bosnia (October 1994).

1.2

1.0
Scale averages

0.8

0.6

0.4

0.2

0
n ve ty on ty lit
y ty n sm
at
io lsi er ivi ssi xie sti xie at
io ici
iz pu ord sit e An o n e ot
at m s e n pr r-h ca id h
m co di ls De ge bi id P yc
So e- na o no
s siv r so An Ph ra
se e Pa
Ob rp
te
In
SCL-90-R - Scales

Figure 5. Average symptom scores

1.6 Before training (1994) After training (1994) Normal population of trainees before and after train-
ing sessions during the war in
1.4 Bosnia (September 1995).

1.2

1.0
Scale averages

0.8

0.6

0.4

0.2

0
n ve ty n ty lit
y ty n
ism
at
io lsi er ivi sio xie sti xie at
io
tic
iz pu ord sit r es An o n e
at m s e n ep r-h ca id c ho
m co di ls D ge bi id Py
So e- na o no
s siv r so An Ph ra
se e Pa
Ob rp
te
In
SCL-90-R - Scales

friends have given up and left the country as refugees to processes. One positive aspect, however, is that persons
take themselves and their families to safer places. who share such experiences tend to develop long-last-
However, our results also show that the training ses- ing bonds and solid friendships. This was verified in
sions should have been offered much more frequently. both the trainers and the trainees in Bosnia. ❑
Traumatic stress, such as that experienced in the wake
of the recent war in Bosnia, seems to exert an imprint- We are grateful to Volkswagen-Stiftung, Hannover, which supported the
ing effect, with devastating consequences on self- studies described in this paper.

80
Self-processes and postwar recovery in Bosnia - Butollo
Un modelo de interacción social para
sujetos que han sufrido traumas de guerra
La imagen de sí mismo y el proceso de recuperación
en sujetos con trastorno de estrés postraumático y
otros trastornos psicológicos con posterioridad a la
guerra de Bosnia
Los problemas de la imagen de sí mismo secundarios a
traumas de guerra no están determinados sólo por las
características y el número de las experiencias traumá-
ticas, sino también –y en gran medida- por la interac-
ción de diversos factores postraumáticos de tipo socio-
económicos, ambientales y psicosociales. Los autores
presentan un modelo que describe la adaptación, que
ocurre con posterioridad al trauma, de la imagen de sí
mismo de sujetos que han sufrido traumas de guerra.
En este modelo se integran las características de las inter-
acciones sociales de los individuos y las representacio-
nes cognitivas de estos procesos. Se analizan los resul-
tados provenientes de 816 niños y 801 adultos que fue-
ron víctimas de la guerra de Bosnia. Una de las expe-
riencias más traumáticas fue la pérdida de algunos de
los padres, particularmente la del padre. El hecho de
desconocer el destino de algún familiar cercano consti-
tuye un factor de estrés permanente que altera los pro-
cesos cognitivo-emocionales, y reduce la autoestima y la
capacidad de reaccionar de manera adecuada, lo que se
observó tanto en niños como en adultos. La utilización
de una terapia multifásica integradora en el tratamien-
to de pacientes que han presentado traumas ha demo-
strado resultados promisorios en víctimas de la guerra
de Bosnia.
REFERENCES
1. Butollo W. Psychotherapy integration for war traumatization—a train-
ing project in central Bosnia. Eur Psychologist. 1996;1:140-146.
2. Butollo W. “Denn traumatisiert sind wir hier alle”: Psychologische Noti-
zen aus Sarajewo. Report Psychologie. 1997;10:766-772.
3. Butollo W. Traumapsychologie und Traumapsychotherapie—Eine Her-
ausforderung für Psychotherapeutische Praxis und Forschung. Psychother
Psychiatr Psychother Med Klin Psychol. 1997;1:23-34.
4. Butollo W. Traumatherapie—Die Bewältigung schwerer posttraumatischer
Störungen. Munich, Germany: CIP—Mediendienst; 1997.
5. Butollo W, Krüsmann M, Hagl M. Leben nach dem Trauma: Über den
therapeutischen Umgang mit dem Entsetzen. Munich, Germany: Pfeiffer Ver-
lag; 1998.
6. Butollo W, Hagl M, Krüsmann M. Kreativität und Destruktion posttraumati-
scher Bewältigung. Forschungsergebnisse und Thesen zum Leben nach dem Trau-
ma. Munich, Germany: Pfeiffer Verlag; 1999.
81
Dialogues in Clinical Neuroscience - Vol 2 . No. 1 . 2000
Un modèle d'interaction sociale pour
les traumatismes de guerre
Image de soi et processus d'adaptation chez des
sujets ayant développé un état de stress post-trauma-
tique et d'autres troubles psychologiques en rapport
avec la guerre en Bosnie
Les troubles de l’image de soi secondaires à des trau-
matismes de guerre sont déterminés non seulement par
la nature et le nombre des événements traumatisants,
mais également, et pour une large part, par l’interaction
d’un certain nombre de facteurs post-traumatiques
socioéconomiques, environnementaux et psychoso-
ciaux. Les auteurs présentent un modèle permettant de
décrire les processus d’adaptation post-traumatique
chez les sujets ayant développé des troubles de l’image
de soi lors de traumatismes de guerre en fonction des
interactions de l’individu avec son environnement
social et de sa représentation cognitive de ces événe-
ments. Les résultats ont été recueillis et analysés chez
816 enfants et 801 adultes victimes de la guerre en
Bosnie. L’un des événements les plus traumatisants est
représenté par la perte d’un parent, en particulier lors-
qu’il s'agit du père. Le fait d’être dans l’ignorance du
sort subi par un parent proche constitue un facteur de
stress permanent à l’origine de troubles cognitifs et
émotionnels avec, en particulier, une diminution de la
confiance en soi et de la capacité de réagir de façon
adéquate, aussi bien chez l’adulte que chez l’enfant.
Une thérapie multiphasique d’intégration a été propo-
sée pour le traitement des victimes de la guerre de
Bosnie et les résultats obtenus semblent prometteurs.
7. Butollo W, Gavranidou M. Intervention bei traumatischen Ereignissen.
In: Oerter R, Hagen CV, Röper G, Noam G, eds. Klinische Entwicklungspsy-
chologie. Weinheim, Germany: Psychologische Verlagsunion; 1999;chap 19.
8. Horowitz MD. Stress-response syndromes. A review of posttraumatic
stress and adjustment disorders. In: Wilson JP, Raphael B, eds. International
Handbook of Traumatic Stress. New York, NY: Plenum Press; 1993:49-60.
9. Butollo W, Zvicdiz S. War-related losses and depression in children. Paper pre-
sented at the German Congress of Psychology (DGfPS), Jena, Germany; 2000.
10. Birleson P, Hudson I, Buchanan DG, Wolff S. Clinical evaluation of a self-
rating scale for depressive disorder in childhood (depression self-rating
scale). J Child Psychol Psychiatry. 1987;28:43-60.
11. Powell S, Rosner R, Butollo W. Flight Paths. Report to the Office of the Fed-
eral Government Commissioner for the Return of Refugees, Reintegration and
Related Reconstruction in Bosnia and Herzegovina, Hans Koschnik; 2000.
12. Derogatis LR. Symptom-Check-Liste (SCL-90-R). In: Collegium Interna-
tionale Psychiatriae Scalarum. Internationale Skalen für Psychiatrie. Weinheim,
Germany: Beltz; 1986.
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Dialogues
 e Contents of latest issues
1999 · Volume 1 · No. 2
Depression in the Elderly
Editorial
Jean-Paul Macher, Marc-Antoine Crocq __________________ 53
In this issue
Barry D. Lebowitz ____________________________________ 56
State of the art
Depression in late life
Barry D. Lebowitz ____________________________________ 57
Posters & images in neuroscience
Charles F. Reynolds III ________________________________ 66
Basic research
Vascular depression: a new view of late-onset depression
George S. Alexopoulos, Martha L. Bruce,
David Silversweig, Balu Kalayam, Emily Stern ____________ 68
Depression in late life: psychiatric-medical comorbidity
Ira R. Katz __________________________________________ 81
Clinical research
Long-term course and outcome of depression in later life
Charles F. Reynolds III __________________________________ 95
Designing an intervention to prevent suicide:
PROSPECT (Prevention of Suicide in Primary
Care Elderly: Collaborative Trial
Martha L. Bruce, Jane L. Pearson ______________________ 100
Pharmacological aspects
Treatment of depression in late life
Lon S. Schneider ______________________________________ 113
Free papers
Exploring the affective toxicity of commonly prescribed
medications in the elderly
David W. Oslin, Thomas R. Ten Have ____________________ 125
Salience of positive and negative affect in the
recognition of depression among elderly persons
Tina L. Harralson, M. Powell Lawton ____________________ 129
1999 · Volume 1 · No. 3
Nosology and Nosography
Editorial
Jean-Paul Macher, Marc-Antoine Crocq __________________ 137
In this issue
Manfred Ackenheil ____________________________________ 140
State of the art
The impact of classification on psychopharmacology
and biological psychiatry
Herman M. van Praag ________________________________ 141
Basic research
Conceptualization of the liability for schizophrenia:
clinical implications
Ming T. Tsuang, William S. Stone, Stephen V. Faraone ____ 153
Pharmacological aspects
Psychostimulants in the treatment of treatment-resistant
depression: review of the literature and findings from
a retrospective study in 65 depressed patients
Gabriele Stotz, Brigitte Woggon, Jules Angst ____________ 165
The therapeutic transnosological use of
psychotropic drugs
Manfred Ackenheil, Lazara Karelia Montané Jaime ______ 175
Instructions for authors at the back of each issue
For information on this journal contact: Dr Marc-Antoine CROCQ
FORENAP - Institute for Research in Neuroscience and Neuropsychiatry - BP29 - 68250 Rouffach - France
Tel: +33 3 89 78 71 20 / 70 18 - Fax: +33 3 89 78 51 24 - E-mail: macrocq@forenap.asso.fr
This publication is supported by an educational grant from Servier
Editor in Chief: Jean-Paul MACHER
Posters & images in neuroscience
Magnetoencephalography of cognitive responses.
A sensitive method for the detection
of age-related changes
Peter H. Boeijinga ____________________________________ 182
Clinical research
Validity of nosological classification
Petr Smolik __________________________________________ 185
Diagnostic classification of psychiatric disorders
and familial-genetic research
Wolfgang Maier ______________________________________ 191
Letters to the editor ____________________________ 197
2000 · Volume 2 · No. 1
Posttraumatic Stress Disorder
Editorial
Jean-Paul Macher, Marc-Antoine Crocq __________________ 01
In this issue
Marc-Antoine Crocq __________________________________ 05
State of the art
Posttraumatic stress disorder and the nature of trauma
Bessel van der Kolk ____________________________________ 07
Basic research
Neurobiological findings in posttraumatic stress disorder: a review
Kumar Vedantham, Alain Brunet, Thomas C. Neylan,
Daniel S. Weiss, Charles R. Marmar ______________________ 23
Ethical aspects of research on psychological trauma
Dan J. Stein, Allen Herman, Debra Kaminer, Solomon
Rataemane, Soraya Seedat, Ronald C. Kessler,
David Williams ________________________________________ 31
Pharmacological aspects
Update on the epidemiology, diagnosis, and treatment of
posttraumatic stress disorder
Joseph Zohar, Daniella Amital, Heidi D. Cropp, Gadi
Cohen-Rappaport, Yaffa Zinger, Yehuda Sasson __________ 37
Posters & images in neuroscience
An overview of the Peritraumatic Distress Scale
Alain Brunet __________________________________________ 44
Clinical research
From shell shock and war neurosis to posttraumatic
stress disorder: a history of psychotraumatology
Marc-Antoine Crocq, Louis Crocq ______________________ 47
Lifelong posttraumatic stress disorder: evidence from
aging Holocaust survivors
Yoram Barak, Henry Szor ______________________________ 57
After the MV Estonia ferry disasters A Swedish
nationwide survey of the relatives of
the MV Estonia victims
Kristina Brandänge, J. Petter Gustavsson ________________ 63
A social interaction model for war traumatization
Self-processes and postwar recovery in Bosnia in subjects
with PTSD and other psychological disorders
Willi Heinz Butollo ____________________________________ 71
00 ST 375 BA