Trauma and Stressor Related Disorders and Disasters
Mattea Pezza, B.S.
Graduate Student
University of Nevada, Las Vegas
Las Vegas, Nevada, United States
Rachel Weese, B.S.
Clinical Research Coordinator
University of Nevada, Las Vegas
Henderson, Nevada, United States
Regine Deguzman-Lucero, B.S.
Graduate Student
University of Nevada, Las Vegas
Las Vegas, Nevada, United States
Jenny Black, Other
Director of Forensic Nursing
SAFE Austin
Austin, Texas, United States
Karen Serrano, M.D.
Medical Director, Forensic Nursing Program
UNC School of Medine
Chapel Hill, North Carolina, United States
Samuel McLean, M.P.H., M.D.
Director
University of North Carolina at Chapel Hill
Chapel Hill, North Carolina, United States
Kara Petitt, None
Student
University of North Carolina at Chapel Hill
Chapel Hill, North Carolina, United States
Nicole A. Short, Ph.D.
Assistant Professor
University of Nevada, Las Vegas
LAS VEGAS, Nevada, United States
Background: Adverse Childhood Experiences (ACEs) have deleterious physical and mental health effects, and over half of adults have experienced at least one ACE. While the experience of childhood adversities is associated with an increased risk of developing posttraumatic stress disorder (PTSD) after an adult trauma, the effect of this relationship has rarely been explored over time. The current study examined the effects of ACEs on the PTSD symptoms at three time points following a new sexual assault. We hypothesized that ACEs would significantly predict PTSD symptoms at the time of emergency care, one week, and seven weeks post-assault. We also hypothesized that ACEs would significantly predict pre-assault PTSD symptoms, which would mediate the association between ACEs and current PTSD symptoms.
Methods: Fifty-seven female participants (Mage=25.98, SD=6.33; White [61.4%], Latina/Hispanic [31.6%], Black/African American [15.8%], Asian [1.8%], Multiple/Other [10.6%]) completed a series of self-report surveys after presenting to one of two emergency care sites in the Better Tomorrow Network after experiencing a sexual assault. Surveys were completed at the time of emergency care, one week, and seven weeks post-assault. Childhood trauma exposure was measured using the 10-item ACE scale, and PTSD symptoms were measured using the PTSD Checklist for DSM-5 (PCL-5). Participants were randomized to treatment conditions post-assault, so treatment condition was included as a covariate.
Results: Five hierarchical linear regressions were conducted with treatment condition as a covariate. First, ACEs were included as a predictor, with PCL score at each time point as dependent variables. Increased ACEs were significantly associated with elevated PTSD symptoms immediately after the assault (β=.47, t=3.44, p=.001, sr2=.22), one week post-assault (β=.36, t=2.41, p=.021, sr2=.13), and at seven weeks post-assault (β=.35, t=2.45, p=.019, sr2=.12). To test our second hypothesis, ACEs were included as a predictor of pre-assault PCL score, then pre-assault PCL score was entered as a predictor of post-assault PCL score. ACEs were not significantly associated with pre-assault PTSD symptoms (β=.10, t=.64, p=.525, sr2=.01), and pre-assault PTSD symptoms were not significantly associated with post-assault PTSD symptoms (β=.06, t=.42, p=.675, sr2< .01). Since the a and b paths were not significant, we did not analyze the indirect effect to demonstrate mediation.
Conclusion: Greater childhood trauma exposure was associated with elevated PTSD symptoms after an adult sexual assault. Our results do not suggest pre-assault PTSD symptoms as a mediator of this relationship. These findings are in line with the stress sensitization hypothesis, such that increased exposure to ACEs predicts later development of PTSD after a new adult trauma. Findings also suggest this relationship is not simply the outcome of higher pre-assault levels of PTSD. These results contribute to the research demonstrating childhood trauma exposure as a serious risk factor for development of PTSD as an adult. Future research should explore mediators of this relationship and preventative mechanisms for populations with greater ACE exposure.