The
Canadian Journal of Psychiatry
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| Volume
47 |
Ottawa,
Canada, December 2002 décembre
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Number
10
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Guest Editorial
Taking Aim at Posttraumatic Stress Disorder: Understanding Its Nature and Shooting Down Myths
Murray B Stein, MD, FRCPC1
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In this issue, we are privileged to have 2 state-of-the-art reviews on
the topic of posttraumatic stress disorder (PTSD), written by preeminent
authorities in the field. Dr Naomi Breslau provides a critical overview
of the epidemiology of PTSD, highlighting sex differences and comorbidity.
Dr Gordon Asmundson and colleagues’ insightful synthesis of the literature
linking PTSD to chronic pain emphasizes clinical and research implications.
Both papers contain succinct summaries that will inform readers of cutting-edge
thinking in these areas.
Growing up and doing much of my residency training in Canada, I had little
exposure to or teaching about PTSD. Many American physicians, on the other
hand, have done at least some of their training in Veterans Affairs hospitals
and have tended to become more familiar with PTSD through their encounters
with the Vietnam Veterans who carry this label. This is a mixed blessing:
chronic PTSD in Vietnam Veterans who are still symptomatic decades later
tends to be a very difficult-to-treat entity. This may have made some psychiatry
trainees in the US skeptical about the nature of PTSD and its treatment.
Conversely, Canadian physicians’ initial experiences with PTSD patients
tend to come from outside the military setting, although it is now becoming
clear that Canadian soldiers are by no means immune to PTSD (1). I recall
the first individual with a diagnosis of PTSD I ever treated—although I
almost certainly missed prior cases that were misdiagnosed (as panic disorder
or major depression, for example). The patient was a young woman who had
been the driver in a motor vehicle collision in which her passenger was
killed. As Dr Breslau points out in her article, nonmilitary trauma is
by far the most common source of PTSD, even in the US. It is ironic that
PTSD, thought not so long ago to be synonymous with an adverse effect of
combat exposure in men, turns out to be a disorder that predominantly strikes
civilian women. Accordingly, although combat-related PTSD continues to
be the focus of considerable research effort—and deservedly so, given that
war shows no signs of going away in our lifetime—researchers have increasingly
focused on trying to understand the nature of PTSD in other settings.
One of these settings is exposure to terrorism. After the attacks of September
11, 2001, several epidemiologic surveys were designed to help us understand
both the extent of the psychiatric adversity associated with terrorist
attacks and the risk and resiliency factors that may be involved. From
studies reviewed by Dr Breslau, and from additional recent surveys (for
example, 2), we have come to appreciate that most individuals are remarkably
resilient, even in the face of the most horrific stressors. This has led
to scrutiny of the individual differences that may influence susceptibility
to PTSD. Several recent studies that have emerged may shed additional light
on this topic. In my work with colleagues at the University of British
Columbia, we are finding a genetic basis for PTSD symptoms that explains
about one-third of the variance in symptom expression (3). Of interest,
this genetic vulnerability seems to include a propensity for being exposed
to assaultive traumatic events (such as, serious fights, muggings, and
sexual trauma). This finding raises the possibility that exposure to trauma
and susceptibility to psychiatric symptoms in the aftermath of trauma may
be intertwined in a way we did not altogether expect. Certainly, though,
there are many forms of exposure to serious trauma (for example, exposure
to terrorist attacks) that can hardly be attributed to individual behaviour.
What characteristics might explain the resistance of some individuals and
the vulnerability of others to adverse psychological effects associated
with these exposures?
An intriguing finding in the PTSD literature is that many (but not all)
studies detect reduced volume of the hippocampus in persons with PTSD.
It has been speculated that this might be a direct effect of exposure to
stress, resulting in hippocampal neurotoxicity (for example, 4). However,
this hypothesis has been challenged on several fronts. It is clear that
reduced hippocampal volume is not specific to PTSD; it has been posited
as a vulnerability factor for other disorders, such as schizophrenia (5).
Most recently, Gilbertson and colleagues’ elegant twin study provides evidence
to suggest that reduced hippocampal volume (antecedent to traumatic stress
exposure) is a risk factor for vulnerability to stress-related psychological
trauma, rather than an outcome (6). Although controversial, as thoughtfully
outlined in a review that accompanies the article (7), these data force
us to rethink some of our popularly held notions about the etiology of
PTSD. Future research efforts will surely be directed toward uncovering
a common genetic basis for susceptibility to traumatic stress and hippocampal
morphology. In my opinion, delineating the neurobiological basis of PTSD
is one of the most exciting areas in psychiatric neuroscience. Stay tuned
for future developments—they are sure to surprise.
On the clinical front, those of us who treat people with PTSD know that
medical comorbidity is frequently intertwined with psychological symptoms.
Patients with PTSD are among the highest users of medical services in primary
care settings (8). In their review, Asmundson and colleagues note that
complaints of pain may drive much of this utilization. Ongoing chronic
pain may serve as a constant reminder of the trauma that perpetuates its
remembrance (that is, the “mutual maintenance” theory). Alternatively,
the development of chronic pain and PTSD in the aftermath of traumatic
stress may represent a shared vulnerability to both of these outcomes.
Asmundson and colleagues offer us a scholarly review of these theories
and present a research agenda that holds the promise of significantly illuminating
our knowledge in this area. Having recently reviewed the literature on
treatment of PTSD as part of a clinical case review (9), I have come to
appreciate how little we know about factors that influence treatment outcomes.
Chronic pain is a factor that deserves further evaluation in this regard.
The article by Asmundson and colleagues raises awareness of the tremendous
comorbidity of chronic pain and PTSD. It will interest clinicians and researchers
alike.
I have learned a lot reading these 2 articles on PTSD. I hope that you
will, too, and that you will be spurred to follow this fascinating literature
as it unfolds in the years to come.
Funding and Support
Writing of this editorial was supported in part by grants to Dr Stein from
the National Institute of Mental Health (MH64122-01 and MH62037-01) and
by Veterans Affairs Merit funding.
References
1. Asmundson GJG, Stein MB, McCreary DR. PTSD symptoms influence health
status of deployed peacekeepers and non-deployed military personnel. J
Nerv Ment Dis. Forthcoming.
2. Schlenger WE, Caddell JM, Ebert L, Jordan BK, Rourke KM, Wilson D, and
others. Psychological reactions to terrorist attacks: findings from the
National Study of Americans’ Reactions to September 11. JAMA 2002;288:581–8.
3. Stein MB, Jang KL, Taylor S, Vernon PA, Livesley WJ. Genetic and environmental
influences on trauma exposure and posttraumatic stress disorder symptoms:
a twin study. Am J Psychiatry 2002;159:1675–81.
4. Bremner JD. Does stress damage the brain? Biol Psychiatry 1999;45:797–805.
5. Seidman LJ, Faraone SV, Goldstein JM, Kremen WS, Horton NJ, Makris N,
and others. Left hippocampal volume as a vulnerability indicator for schizophrenia:
a magnetic resonance imaging morphometric study on nonpsychotic first-degree
relatives. Arch Gen Psychiatry 2002;59:839–49.
6. Gilbertson MW, Shenton ME, Ciszewski A, Kasai K, Lasko NB, Orr SP, and
others. Smaller hippocampal volume predicts pathologic vulnerability to
psychological trauma. Nature Neuroscience 2002;11:1242–7.
7. Sapolsky RM. Chickens, eggs and hippocampal atrophy. Nature Neuroscience
2002;11:1111–3.
8. Stein MB, McQuaid JR, Pedrelli P, Lenox R, McCahill ME. Posttraumatic
stress disorder in the primary care medical setting. Gen Hosp Psychiatry
2000;22:261–9.
9. Stein MB. A 46-year-old man with anxiety and nightmares after a motor
vehicle collision. JAMA 2002;288:1513–22.
Author(s)
1. Professor of Psychiatry in Residence, University of California San Diego,
La Jolla, California; Director, Anxiety and Posttraumatic Stress Disorder
Clinics, Veterans Affairs San Diego Healthcare System, San Diego, California.
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