Posttraumatic Stress Disorder

By definition, post-traumatic stress disorder (PTSD) occurs in the aftermath of a traumatic event. The characteristic symptoms of the disorder can be divided into intrusive symptoms, avoidance and numbness symptoms, and hyperarousal symptoms. Although initially conceptualized as a normal reaction to an abnormal event, PTSD is increasingly understood as a medical disorder characterized by underlying psychobiological dysfunction [36]. After a traumatic event a range of symptoms is normative; in the majority of cases these gradually diminish, but in PTSD such symptoms persist.

The National Comorbidity Survey in the US found that 60.7% of males and 51.2% of females had experienced a significant traumatic event [37]. The lifetime prevalence of PTSD was 10.4% in females, and 5.0% in males. PTSD is characterized by chronicity of symptoms, significant comorbidity and substantial disability [38]. Early detection and effective treatment is therefore an important goal.

PTSD in combat veterans is well described, and is a routine focus of early detection programmes in the military. It is, however, important to screen for PTSD in populations other than the military. Sexual and physical trauma in children and adolescents is unfortunately a prevalent problem in both the developed and the developing world [39]. Domestic violence is also widespread, and there is a high incidence of PTSD in those exposed to it

[40]. PTSD is associated with high utilization of health care, and screening for exposure to trauma in medical settings is therefore imperative [41]. A range of instruments is available to screen for trauma, interpersonal violence and PTSD [42,43].

There is growing work on risk factors for PTSD [44]. These include demographic factors (e.g. female gender), clinical factors (e.g. dissociation during the trauma, exposure to multiple traumas) and biological variables (e.g. tachycardia, hypocortisolism, decreased dehydroepiandrosterone (DHEA), decreased neuropeptide Y, presence of particular genetic variants) [45]. Symptoms of acute stress disorder after the trauma can be used to determine those at high risk for developing PTSD [46]. Early screening after trauma exposure may also be useful in identifying children at risk for PTSD [47]. There is a need, however, for additional studies to determine how best to screen populations after trauma, in order to optimize the early detection of psychiatric morbidity [48].

Nevertheless, work on psychotherapeutic intervention after exposure to trauma has shown that this is not necessarily helpful. In particular, single-session psychological interventions or ''debriefing'' does not appear to be an effective intervention [49]. The reason for this failure is unclear, but it may reflect the fact that people process trauma in different ways, and that interventions must be more individualized [50]. More intensive cognitive-behavioural programmes may be effective for those with acute stress disorder [51], or with other risk factors for PTSD such as elevated heart rate [52], although, again, further work is still needed in this area.

There is also a growing interest in using pharmacotherapy to prevent post-traumatic symptoms in the aftermath of trauma. The adrenergic system serves as a general alarm system and its activation may play an important role in facilitating the encoding of emotional memories. Pitman et al. [53] have provided evidence that beta-blockers are effective in reducing the psychophysiological reactivity to memory cues of trauma, but had no significant effect on reducing PTSD at 3 months. Subsequent work has, however, provided some indication that PTSD symptoms, as well as PTSD diagnosis, were reduced at 2 months following acute treatment with propranolol [54]. In the immediate aftermath of trauma, severely burned children who received the tricyclic antidepressant imipramine had significantly lower rates of PTSD at 6 months than children who had received chloral hydrate [55]. Benzodiazepines, on the other hand, may exacerbate PTSD symptoms [56]. Additional work with other agents that have different mechanisms of action is needed.

In the future, we can expect approaches to the study of trauma and prevention of its sequelae that integrate biological and psychological approaches. Animal and clinical studies provide an increasingly solid foundation for such work [57]. An interesting recent exemplar of an integrated approach is the work by Fisher et al. [58], in which they reported that, in a small sample of maltreated preschool children, a psychosocial intervention undertaken soon after adoption was able to improve behavioural adjustment and to change hypothalamic-pituitary-adrenal (HPA) axis function (as measured by salivary cortisol). The incorporation of genetic and imaging studies into studies of both preventive pharma-cotherapy and psychotherapy may be useful in delineating moderators and mediators of such interventions.

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