• PTSD Symptom Severity (pre, mis, posttreatment, 3 and 6 month follow-up)- PTSD Symptom Scale-Interview (PSS-I; Foa et al., 1993)- Posttraumatic Stress Diagnostic Scale (PDS; self-report; Foa et al., 1997) [ Time Frame: pre, mid, post, 3 and 6 mo FU ] [ Designated as safety issue: No ]
  

• Psychophysiological reactivity will be assessed using a Biopac MP-100 physiology recording system for measurement of heart rate (electrocardiography, ECG), skin conductance, respiration, and end-tidal pCO2 (pre, mid, posttreatment, 3 and 6 mo FU). [ Time Frame: pre, mid, post, 3 and 6 mo FU ] [ Designated as safety issue: No ]
  
• HPA axis reactivity will be assessed with collection of salivary cortisol at each major assessment. Cortisol response to awakening, our measure of general stress reactivity, will be calculated. [ Time Frame: pre, mid, post, 3 and 6 mo FU ] [ Designated as safety issue: No ]
  
• All of below measures are taken at the major assessment points.- Beck Depression Inventory-II- Depression Anxiety Stress Scale- Posttraumatic Cognitions Inventory- Client Satisfaction Questionnaire [ Time Frame: pre, mid, post, 3 and 6 mo FU ] [ Designated as safety issue: No ]
  

Effective treatments for PTSD are available, with exposure therapy (ET) programs, including Prolonged Exposure (PE), having the most empirical evidence for effectiveness (Rothbaum et al., 2000). However, among people receiving treatment for PTSD, many are not receiving psychotherapies with empirically proven efficacy. In one VA VISN, only 10% of PTSD specialist therapists reported using ET routinely (Rosen et al., 2004). They suggested that a lack of training and human resources to provide ET, as well as misconceptions about exposure therapy may drive the deficit. Training efforts would be substantially more cost-effective of the proven treatments could be delivered in group formats. Development and proof of efficacy of a group-based PE would provide far more veterans with access to a treatment that can truly foster recovery from the devastating impact of PTSD. This is a central goal of this proposal.

Little is known about the mechanisms through which PE leads to recovery. Delineation of its mechanisms is a critical step towards the development of treatment refinements to improve effectiveness and efficiency of the treatment. We plan to examine the potential roles of cognitive, psychophysiologic and neuroendocrine factors in symptom improvement. The mechanistic component will provide preliminary data on interactions between cognitive change (increased sense of self-competence and control over negative outcomes), psychophysiological habituation (reduced reactivity to trauma related stimuli), and reduced neuroendocrine sensitivity (reduced hypothalamic-pituitary-adrenal (HPA) axis reactivity). We predict that cognitive change, psychophysiological habituation and reduced HPA reactivity will all be related to symptom improvement with effective treatment.

Thirty-six OEF/OIF veterans with chronic PTSD of at least 3 months duration will be randomly assigned to 15 weeks of twice weekly PE-G or TAU. All veterans will receive psychobiological assessments at pre treatment, mid treatment, post treatment, 3 months and 6 months follow-up. Each of these assessments will include interview and self-report of symptoms (i.e., PTSD, depression, and general anxiety severity), self-report of PTSD-related cognitions, psychophysiological (i.e., heart rate, skin conductance, respiration, and end-tidal CO2) assessment during neutral and trauma scripts, and assessment of salivary cortisol during neutral and trauma scripts. Also, on the morning prior to each laboratory assessment, patients will collect salivary cortisol at the moment of waking and 30 and 45 minutes post-walking. The results from this study will be used as pilot data for VA Merit Award and NIMH R01 applications for larger follow-up studies.