Changes in the Concept of PTSD and Trauma

by Rachel Yehuda, Ph.D. *
Psychiatric Times April 2003 Vol. XX Issue 4

Posttraumatic stress disorder develops in response to experiencing, witnessing or even learning about a terrifying event. The event--or trauma--is usually life-threatening, or at least capable of producing bodily harm, and it typically involves either interpersonal violence or massive disaster (e.g., rape, assault, torture, terrorism, car or plane crashes, earthquake, tornado, or flood). Traumatic events have in common the ability to elicit intense and immediate fear, helplessness, horror and distress. These subjective responses lead to a cascade of adverse psychological reactions that can result in the symptoms of PTSD and the resultant disability that is associated with this condition.

The diagnosis of PTSD did not appear in the DSM until 1980. This reflected the reluctance of the mental health field to recognize that the psychological effects of traumatic experiences could be long lasting. Prior to 1980, stress-related symptoms were generally viewed as transient and not requiring intensive treatment. This was in keeping with the pervasive feeling that, with time, people ought to be able to "get over" the effects of a traumatic experience and "move on" without noticeable impairment. According to the DSM and DSM-II, people who developed long-term symptoms following trauma were perceived as constitutionally vulnerable (Yehuda and McFarlane, 1995). The diagnosis of PTSD was meant to pave the way for an improved understanding of the long-term, and possibly even permanent, impact of trauma exposure. Ultimately, systematic testing of hypotheses about the relationship between trauma exposure and long-term symptoms has led to a better understanding of the causes of PTSD and its longitudinal course and biologic basis.

Clinical Features of PTSD

Posttraumatic stress disorder defines a rather specific syndrome in which trauma survivors are unable to get the traumatic event out of their minds. Three symptom clusters are associated with PTSD: 1) reexperiencing symptoms refers to distressing images, unwanted memories, nightmares or flashbacks of the event that cause distress and attendant physical symptoms such as palpitations, shortness of breath and other panic symptoms; 2) the avoidance of reminders of the event, including people, places or things associated with the trauma and becoming emotionally numb, constricted or generally unresponsive to the environment; and 3) hyperarousal, which is reflected in physiological symptoms such as insomnia, irritability, impaired concentration, hypervigilance and increased startle responses. To meet DSM criteria for PTSD, symptoms in each of the three domains must not only be present, but also must be severe enough to cause substantial impairment in social, occupational or interpersonal domains. Furthermore, symptoms must be present for at least one month.

Trauma Exposure

Posttraumatic stress disorder is the fourth most common DSM-III-R disorder, afflicting 7% to 14% of the population at some time in their lives (Yehuda, 2002). Although exposure to trauma is thought to be the major cause of PTSD, there is a marked discrepancy between the number of people exposed to trauma and the number of people who develop PTSD. If one considers the prevalence of PTSD solely among individuals who have been exposed to a potentially traumatic event as defined by the DSM-IV, it would become clear that only about 9% of men and 20% of women who are so exposed develop this disorder (Kessler et al., 1995).

The nature of the trauma experienced seems to be a highly significant factor in determining whether PTSD will develop. Events involving interpersonal violence, such as torture, rape, assaultive violence and combat, are more potent elicitors of PTSD than experiences such as motor vehicle accidents and natural disasters. The former events produce PTSD in as many as 50% to 75% of trauma survivors, whereas the latter types of events often result in PTSD <10% of the time (Kessler et al., 1995). A general point that can be made, however, is that for any given trauma, only a subset of people exposed will subsequently develop PTSD. These statistics suggest that viewing trauma survivors as a homogenous group and trying to base conclusions that might apply generally to such people may result in imprecise conclusions.

Neural/Hormonal Correlates

Exposure to traumatic stress results in a fear response that involves the initiation of concurrent and instantaneous biological responses that help assess the level of danger and then organize an appropriate behavioral response. The amygdala begins the process of activating the neurochemical and neuroanatomical circuitry of fear by activating the startle response, the parasympathetic and sympathetic nervous systems, and the hypothalamic-pituitary-adrenal responses to stress. The hippocampus is involved in helping to terminate these responses. Indeed, this coordinated response to stress is ultimately contained by the release of cortisol from the adrenal gland. The important question in PTSD has been whether and to what extent the normal processes involved in the mounting and containment of stress responses are relevant.

Recent data from prospective studies suggest that, in individuals who develop PTSD, there is an attenuated rise in cortisol in the immediate aftermath of the trauma, and there is evidence of greater sympathetic nervous system arousal (i.e., increased heart rate), suggesting that the fear response is not effectively contained (Yehuda et al., 1998). Relatively lower cortisol levels following trauma may constitute a biologic risk factor for PTSD. Indeed, relatively lower cortisol levels have been noted in adults with chronic PTSD (Yehuda, 2002).

Thus, one model explaining the development of PTSD following trauma proposes that the increased sympathetic nervous system activity leads to an exaggerated sympathetic nervous system response to the trauma, manifested by an increased concentration of adrenaline. This in turn initiates a process in which traumatic memories become over-consolidated or inappropriately remembered due to an exaggerated level of distress. The primary mechanism through which adrenaline facilitates memory formation is by maintaining organisms at a high level of arousal. If cortisol fails to adequately shut down adrenaline, this arousal might be prolonged and the consolidation of the memory facilitated. The increased distress every time there are traumatic reminders would further activate stress-responsive systems, resulting in secondary biological alterations associated with anxiety and hyperarousal (Yehuda, 2002).

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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