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Psychiatric Times. Vol. 20 No. 4
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Changes in the Concept of PTSD and Trauma

By Rachel Yehuda, Ph.D.
| April 1, 2003
Dr. Yehuda is professor of psychiatry at the Mount Sinai School of Medicine and founder and director of the Traumatic Stress Studies Program at the Mount Sinai School of Medicine and Bronx Veterans Affairs Hospital.

Risk and Resilience

The observation that the development of PTSD is the exception rather than the rule in the aftermath of trauma has led to the search for risk factors that contribute to the development of chronic PTSD following exposure to trauma (Yehuda, 1999). In addition to the nature and severity of the traumatic event, previous exposure to trauma, particularly in childhood; a history of psychological and behavioral problems; and familial factors such as parental PTSD and family history of anxiety and depression have been noted as risk factors for PTSD. Gender also appears to be a potent risk factor for the development of this disorder, and studies consistently demonstrate a twofold increase in the prevalence of PTSD in women (Breslau et al., 1991). This issue can only be resolved by studying the prevalence of PTSD in men and women who have been exposed to similar events.

Epidemiological studies that have attempted to examine risk factors have identified clusters of factors that are clearly interrelated. For example, lower levels of education and income, differences in ethnicity, poverty, and lower intellectual functioning have been identified as risk factors for the development of PTSD. These variables are also associated with a greater exposure to traumatic events (Breslau et al., 1991).

A history of family instability is associated with increased incidence of PTSD, and numerous studies have indicated that familial psychiatric history may place an individual at higher risk of PTSD (Davidson et al., 1998). In particular, parental PTSD appears to be a very specific risk factor for the development of PTSD in offspring (Yehuda et al., 2001). It is not clear whether the tendency to develop PTSD is genetic. An intriguing finding examining PTSD in twins has demonstrated that as much as 30% of some PTSD symptoms may have a genetic basis (True et al., 1993).

The development of PTSD may also be associated with the interpretations of the traumatic event and with pre-existing ideas about personal safety. Individuals who believe that the trauma has wide-ranging negative implications for the safety of the world, for the trust they can place in others and for their own ability to cope are more likely to develop chronic PTSD following a trauma. In addition, interpreting initial symptoms as signs of falling apart or being permanently altered for the worse may serve to maintain them. Since such coping styles appear to be shaped by prior experience, they may, in part, explain why earlier trauma can place an individual at risk. Unfortunately, at this time, little is known about resiliency factors that prevent the development of PTSD or increase recovery once this condition develops.

One of the major difficulties in understanding issues related to risk and resiliency in PTSD is that PTSD is not a dichotomous variable. Although it is not technically possible to diagnose PTSD in the immediate aftermath of a trauma because of the diagnostic stipulation that symptoms occur for at least one month, it is true that nearly all (94%) trauma survivors exhibit some degree of acute symptoms (Rothbaum and Foa, 1993). So, initially, most trauma survivors seem to have some type of PTSD response that gradually recedes in most people over time (Kessler et al., 1995). Thus, PTSD may represent the failure to recover from a universal set of reactions (Yehuda, 2002).

If PTSD does represent a failure to recover, it could be assumed that during a specific time period immediately following the traumatic event, the manifestation of symptoms is normal. This raises questions about whether, or more precisely, when, to provide mental health treatment in the aftermath of trauma. The most obvious answer to this, of course, is when the survivor requests treatment, but many trauma experts advocate for treating survivors in the immediate aftermath of trauma, even before they have a chance to fully process what has happened to them. The justification for this approach is that it might help symptoms remit faster and forestall the development of PTSD.

One of the difficulties is that it is unclear at the time of a traumatic event who is experiencing the beginning of a psychiatric disorder and who is manifesting normal symptoms that will abate with time. There is a concern that certain interventions can interfere with the process of normal recovery (Mayou et al., 2000), so this issue is by no means trivial.

PTSD and the Future

The next great challenge in the study of PTSD is to tackle the questions of when and how to define a pathologic state and in whom the risk factors are greatest. The issue of whether PTSD should be defined as the presence of symptoms after an arbitrary cutoff point should be re-examined. Indeed, there is emerging evidence for an alternative approach: to consider those who develop PTSD as those who are most likely to develop the disorder as a result of prior risk factors. In this case, the development of PTSD would represent an alternative trajectory to the normative response. It may very well be that the failure to contain or control the initial biologic response to stress leads to a cascade of events resulting in symptoms of hyperarousal, recollection of intrusive events and avoidance of reminders. In this case, the challenge in the aftermath of a trauma would be to determine who is at risk for failing to recover.

As we contemplate the 23-year history of the diagnosis of PTSD, it seems that the pendulum has swung from failing to acknowledge the effects of trauma to an almost zealous embracing of trauma as a necessary etiologic agent. Although current events provide us with a natural laboratory of recently traumatized people to study and follow, it is essential that the phenomenology and neurobiology of the chronic course serve to ground the perspectives from studies of those acutely distressed.

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References
1. Breslau N, Davis GC, Andreski P, Peterson E (1991), Traumatic events and posttraumatic stress disorder in an urban population of young adults. Arch Gen Psychiatry 48(3):216-222.
2. Davidson JR, Tupler LA, Wilson WH, Connor KM (1998), A family study of chronic post-traumatic stress disorder following rape trauma. J Psychiatr Res 32(5):301-309.
3. Kessler RC, Sonnega A, Bromet E et al. (1995), Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 52(12):1048-1060.
4. Mayou RA, Ehlers A, Hobbs M (2000), Psychological debriefing for road traffic accident victims: three-year follow up of a randomised controlled trial. Br J Psychiatry 176:589-593 [see comments].
5. Rothbaum BO, Foa FB (1993), Subtypes of posttraumatic stress disorder and duration of symptoms. In: Posttraumatic Stress Disorder: DSM-IV and Beyond, Davidson JRT, Foa EB, eds. Washington, D.C.: American Psychiatric Press, pp23-35.
6. True WR, Rise J, Eisen S et al. (1993), A twin study of genetic and environmental contributions to liability for posttraumatic stress disorder. Arch Gen Psychiatry 50(4):257-264 [see comment].
7. Yehuda R (1999), Risk Factors For Posttraumatic Stress Disorder. Washington, D.C.: American Psychiatric Press.
8. Yehuda R (2002), Post-traumatic stress disorder. N Engl J Med 346(2):108-114.
9. Yehuda R, Halligan SL, Bierer LM (2001), Relationship of parental trauma exposure and PTSD to PTSD, depressive and anxiety disorders in offspring. J Psychiatr Res 35(5):261-270.
10. Yehuda R, McFarlane AC (1995), Conflict between current knowledge about posttraumatic stress disorder and its original conceptual basis. Am J Psychiatry 152(12):1705-1713 [see comments].
11. Yehuda R, McFarlane AC, Shalev AY (1998), Predicting the development of posttraumatic stress disorder from the acute response to a traumatic event. Biol Psychiatry 44(12):1305-1313.


 
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