Changes in the Concept of PTSD and Trauma
Changes in the Concept of PTSD and Trauma
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.
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
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).