The present study examined the structural validity of the 25-item Connor-Davidson Resilience Scale (CD-RISC) in a large sample of U.S. veterans with military service since 9/11/2001. Participants (n=1981) completed the 25-item CD-RISC, a structured clinical interview and a self-report questionnaire assessing psychiatric symptoms. The study sample was randomly divided into two sub-samples, an initial sample [Sample 1: n = 990] and a replication sample [Sample 2: n = 991]. Findings derived from exploratory factor analysis (EFA) did not support the five-factor analytic structure as initially suggested in Connor and Davidson’s (2003) instrument validation study. Although Parallel Analyses (PA) indicated a two-factor structural model, we tested one to six factor solutions for best model fit using confirmatory factor analysis (CFA). Results supported a two-factor model of resilience, comprised of adaptability (8-item) and self-efficacy (6-item) themed items however, only the adaptability themed factor was found to be consistent with our view of resilience —a factor of protection against the development of psychopathology following trauma exposure. The adaptability themed factor may be a useful measure of resilience for post 9/11 U.S. military veterans.

The present study used archival clinical data to analyze the delivery and effectiveness of prolonged exposure (PE) and ancillary services for posttraumatic stress disorder (PTSD) among Operation Enduring Freedom, Operation Iraqi Freedom, and Operation New Dawn veterans (N = 69) with histories of mild to severe traumatic brain injury (TBI). Data from standard clinical assessments of veterans and active duty personnel treated in both inpatient and outpatient programs at 2 Department of Veteran Affairs medical centers were examined. Symptoms were assessed with self-report measures of PTSD (PTSD Checklist) and depression (Beck Depression Inventory-II) before and throughout therapy. Mixed linear models were utilized to determine the slope of reported symptoms throughout treatment, and the effects associated with fixed factors such as site, treatment setting (residential vs. outpatient), and TBI severity were examined. Results demonstrated significant decreases in PTSD, B = -3.00, 95% CI [-3.22, -2.78]; t(210) = -13.5; p < .001, and in depressive symptoms, B = -1.46, 95% CI [-1.64, -1.28]; t(192) = -8.32; p < .001. The effects of PE treatment did not differ by clinical setting and participants with moderate to severe injuries reported more rapid gains than those with a history of mild TBI. The results provide evidence that PE may well be effective for veterans with PTSD and TBI.

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Socioeconomic disadvantage is associated with increased exposure to victimization and traumatic stress. The present study evaluates longitudinal pathways linking victimization and trauma to depressive symptoms in a socioeconomically disadvantaged sample of African-American adolescent girls seeking mental health services (N = 177, 12-16 years old at baseline). Girls completed four assessments over the course of three years (T1-T4). Depressive symptoms were assessed at T1-T3 using clinical interviews and questionnaires. At T4, lifetime history of victimization and traumatic stressors was evaluated with in-person interviews. Separate structural equation models tested longitudinal pathways from stressor frequency, severity, and duration to depressive symptoms. In all three models, higher levels of victimization and traumatic stressors were associated with significantly higher levels of depressive symptoms. More frequent stressors prior to T1 directly predicted depressive symptoms at T1 and indirectly predicted depressive symptoms at T2, which, in turn, predicted depressive symptoms at T3. A similar pattern emerged in the stressor severity and duration models. Findings support the idea that victimization and traumatic stressors are associated with higher levels of depressive symptoms and that, among treatment-seeking low-income adolescent girls, these effects occur through both direct and indirect paths. Implications of these findings are discussed in the context of the stress-generation and stress proliferation models of psychopathology.