Exposure to traumatic stress can result in post-traumatic stress disorder (PTSD) which combines the symptoms re-experiencing (criterion B), avoidance (C), and arousal (D) (DSM-IV-TR; American Psychiatric Association, 2000). Occurrence of these and dissociative symptoms during the initial month after the traumatic experience is termed acute stress disorder (ASD). Whereas, the majority of victims of civil trauma such as road traffic accidents or assault show improvement over time (Scholes, Turpin, & Mason, 2007), those suffering from ASD have been reported to carry a high risk of also developing PTSD (Harvey & Bryant, 1998). This stress disorder can, in turn, promote the development of a number of other disorders. Creamer, Burgess, and McFarlane, (2001) found sequelae in over 80% of PTSD patients. Most frequently reported was depression in 58%, substance-related disorder in 43% and phobias and generalized anxiety in a third of the patients. Given the disabling nature of PTSD and its potential to trigger further psychological disorders, it seems of paramount importance to provide early intervention to individuals who are likely to develop PTSD.
Cognitive behavior therapy (CBT) for ASD is usually employed 2–5 weeks following the trauma and combines approaches such as prolonged exposure with cognitive restructuring and anxiety management techniques. This treatment was found to be effective compared to a wait-list control condition (Bisson et al., 2004 and Foa et al., 1995), a self-help booklet (Ehlers et al., 2003), supportive counseling (Bryant et al., 1998b, Bryant et al., 2005, Bryant et al., 2003 and Bryant et al., 1999) and cognitive restructuring (Bryant et al., 2008) although there are also discrepant reports showing no significant differences between treatment conditions (Echeburúa et al., 1996 and van Emmerik et al., 2008). Additional anxiety management training (Bryant et al., 1999) or hypnotherapy (Bryant et al., 2005) failed to be more efficacious than CBT on its own. Long-term follow-ups tended to confirm the short-term results (Bryant et al., 2006) although there are also reports of a long-term convergence of groups (Foa, Zoellner, & Feeny, 2006) suggesting that treatment merely accelerates recovery. In the majority of these studies, the control group received psychoeducation and general problem-solving training which does not permit conclusions as to the differential efficacy of the various CBT components. In order to evaluate the unique contribution of trauma-related exposure, relaxation was included in both treatment conditions. It was expected to address arousal symptoms but not specifically trauma-related stress symptoms.
Throughout the previous studies, outcome measures were those of self-report, be it in the form of standardized interviews or of questionnaires, the tacit assumption being that all other components of the stress response show similar recovery. There is ample evidence that PTSD is associated with physiological reactivity, in particular, heart rate (HR) acceleration on exposure to trauma-related stimuli (for a review see Orr, Metzger, & Pitman, 2002) and PTSD patients without physiological reactions were reported to be less severely affected by re-experiencing symptoms and depression (Keane et al., 1998). Trauma victims with ASD were also found to exhibit HR-acceleration to pictures, which they judged to be trauma-relevant, compared to trauma victims without ASD and control subjects not exposed to a traumatic event (Elsesser et al., 2008, Elsesser et al., 2004 and Rabe et al., 2006). Compared to neutral pictures, generally aversive ones elicited brief cardiac deceleration in all groups. This attentional, so-called “orienting” response is usually found in response to interesting stimuli (Jennings, 1986) and is considered to lower the perceptual threshold thereby enhancing stimulus input and processing (Graham, 1979). Amplitude of the accelerative cardiac response to trauma-relevant pictures was positively correlated with the number of re-experiencing symptoms and both were predictive of the development of PTSD symptoms after 3 months (Elsesser, Sartory, & Tackenberg, 2005). It is well established in other anxiety disorders that the HR response to fear-relevant contents subsides with successful treatment, in particular, with exposure methods (e.g., Sartory, Eves, & Foa, 1987). PTSD patients also evidenced attenuation of the HR response to trauma-related stimuli after CBT (Blanchard et al., 2002 and Rabe et al., 2006). So far it has not been investigated whether the HR response is attenuated together with the symptomatic relief in the treatment of ASD nor, indeed, whether the initial HR response is predictive of treatment outcome.
In the present study, trauma victims with ASD were treated either with prolonged exposure or supportive counseling in addition to psychoeducation and progressive relaxation which was given to both groups. Assessments took place before and after treatment and after another 3 months and included the measurement of the HR response to trauma-related pictures. Additionally, patients were contacted by telephone approximately four and a half years later and asked whether they had received further treatment. We expected prolonged exposure to be more effective than supportive counseling in terms of long-lasting symptomatic relief and to have a more attenuating effect on the accelerative HR response. The latter was also thought to be predictive of treatment outcome in the prolonged exposure group.
