Sanne J H van Rooij1, Jennifer S Stevens2, Timothy D Ely2, Rebecca Hinrichs2, Vasiliki Michopoulos2, Sterling J Winters2, Yvonne E Ogbonmwan2, Jaemin Shin3, Nicole R Nugent4, Lauren A Hudak5, Barbara O Rothbaum2, Kerry J Ressler6, Tanja Jovanovic2. 1. Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia. Electronic address: sanne.van.rooij@emory.edu. 2. Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia. 3. Center for Advanced Brain Imaging, Georgia Institute of Technology, Atlanta, Georgia. 4. Division of Behavioral Genetics, Department of Psychiatry, Rhode Island Hospital, Providence, Rhode Island; Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, Providence, Rhode Island. 5. Department of Emergency Medicine, Emory University School of Medicine, Atlanta, Georgia. 6. Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia; McLean Hospital, Department of Psychiatry, Harvard Medical School, Belmont, Massachusetts.
Abstract
BACKGROUND: Understanding the neurobiological mechanisms that predict posttraumatic stress disorder (PTSD) in recent trauma survivors is important for early interventions. Impaired inhibition of fear or behavioral responses is thought to be central to PTSD symptomatology, but its role in predicting PTSD is unknown. Here we examine whether brain function during response inhibition early after a civilian trauma can predict future PTSD symptoms. METHODS: Participants (original sample, n = 27; replication sample, n = 31) were recruited in the emergency department within 24 hours of trauma exposure. PTSD symptoms were assessed in the emergency department and 1, 3, and 6 months posttrauma. A Go/NoGo procedure in a 3T magnetic resonance imaging scanner was used to measure neural correlates of response inhibition 1 to 2 months posttrauma. Elastic net regression was used to define the most optimal model to predict PTSD symptoms at 3 and 6 months among demographic, clinical, and imaging measures. RESULTS: Less hippocampal activation was a significant predictor in the model predicting PTSD symptoms at 3 months (F11,22 = 4.33, p = .01) and 6 months (F9,19 = 4.96, p = .01). Other significant predictors in the model were race and pain level in the emergency department (3 months), and race and baseline depression symptoms (6 months). Using these predictors in a linear regression in the replication sample again resulted in significant models (3 months [F3,23 = 3.03, p = .05], 6 months [F3,20 = 5.74, p = .007]) with hippocampal activation predicting PTSD symptoms at 3 and 6 months. CONCLUSIONS: Decreased inhibition-related hippocampal activation soon after trauma predicted future PTSD symptom severity. This finding may contribute to early identification of at-risk individuals and reveals potential targets for intervention or symptom prevention in the aftermath of trauma.
BACKGROUND: Understanding the neurobiological mechanisms that predict posttraumatic stress disorder (PTSD) in recent trauma survivors is important for early interventions. Impaired inhibition of fear or behavioral responses is thought to be central to PTSD symptomatology, but its role in predicting PTSD is unknown. Here we examine whether brain function during response inhibition early after a civilian trauma can predict future PTSD symptoms. METHODS:Participants (original sample, n = 27; replication sample, n = 31) were recruited in the emergency department within 24 hours of trauma exposure. PTSD symptoms were assessed in the emergency department and 1, 3, and 6 months posttrauma. A Go/NoGo procedure in a 3T magnetic resonance imaging scanner was used to measure neural correlates of response inhibition 1 to 2 months posttrauma. Elastic net regression was used to define the most optimal model to predict PTSD symptoms at 3 and 6 months among demographic, clinical, and imaging measures. RESULTS: Less hippocampal activation was a significant predictor in the model predicting PTSD symptoms at 3 months (F11,22 = 4.33, p = .01) and 6 months (F9,19 = 4.96, p = .01). Other significant predictors in the model were race and pain level in the emergency department (3 months), and race and baseline depression symptoms (6 months). Using these predictors in a linear regression in the replication sample again resulted in significant models (3 months [F3,23 = 3.03, p = .05], 6 months [F3,20 = 5.74, p = .007]) with hippocampal activation predicting PTSD symptoms at 3 and 6 months. CONCLUSIONS: Decreased inhibition-related hippocampal activation soon after trauma predicted future PTSD symptom severity. This finding may contribute to early identification of at-risk individuals and reveals potential targets for intervention or symptom prevention in the aftermath of trauma.
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