Models of Risk for PTSD

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DESCRIPTION (provided by applicant): This application seeks to identify cognitive and neurobiological markers of risk for posttraumatic stress disorder (PTSD) and/or major depressive disorder (MDD) in the acute aftermath of trauma. In addition, a plan is outlined for the candidate to acquire the necessary training to develop an independent program of research focused on understanding markers and mechanisms of risk for PTSD and MDD. The candidate's prior training in life stress, mood disorders and PTSD research has allowed him to hone many skills necessary for achieving this goal. However, he requires additional training, mentoring and experience in five key areas: (1) diurnal sympathetic nervous system (SNS) and hypothalamic-pituitary-adrenal (HPA) activity; (2) SNS and HPA reactivity to stress; (3) neurobiological risk markers for PTSD; (4) cognitive risk factors for PTSD and MDD; and (5) longitudinal designs to study coping and neuroendocrine trajectories for the onset and course of PTSD and/or MDD. A comprehensive training plain has been developed that includes hands-on didactic experiences, formal coursework, independent readings, seminars, webinars, mentoring meetings and consultation with experts in these five key areas. The proposed study will investigate longitudinal pathways leading from interpersonal violence (IPV) exposure to PTSD and/or MDD in a sample of 60 women recently exposed to IPV and 40 non-exposed women using four waves of data collection (within 1 month after exposure to IPV, and at 1, 3, and 6 months following the initial assessment). Although women are twice as likely as men to develop PTSD and/or MDD after exposure to trauma, the mechanisms underlying this increased risk remain unclear. Identifying individuals at elevated risk for these disorders is critical for developing effective early intervention programs. The HPA and SNS systems serve as main lines of defense in responding to stress or trauma. Individuals who develop PTSD have reduced activity in the HPA system and increased activity in the SNS following trauma. Cross-sectional studies suggest that a progressive divergence of HPA and SNS activity following trauma may contribute to the maintenance of PTSD, but there is scant longitudinal research to support this hypothesis. Although PTSD and MDD frequently co-occur, the role of MDD symptoms in the patterns of HPA and SNS function following trauma-exposure has not yet been described. The primary aims of the proposed study are to (a) examine whether a progressive divergence in SNS and HPA daily output is associated with higher levels of PTSD symptoms over time, and (b) to determine whether women at greater risk for PTSD fail to habituate in terms of their cortisol responses to a psychosocial stress task. Secondary goals will examine the role of co-occurring MDD symptoms on diurnal secretion and reactivity of HPA/SNS systems. Psychosocial factors such as coping strategies may also determine the risk for PTSD and/or MDD and may influence SNS/HPA function. Results will identify cognitive and neurobiological factors associated with risk for PTSD and/or MDD that could be used to develop more "personalized" early intervention programs.