Ziv Ben-Zion1, Moran Artzi2, Dana Niry3, Nimrod Jackob Keynan4, Yoav Zeevi5, Roee Admon6, Haggai Sharon7, Pinchas Halpern8, Israel Liberzon9, Arieh Y Shalev10, Talma Hendler11. 1. Sagol Brain Institute Tel Aviv, Wohl Institute for Advanced Imaging, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. 2. Sagol Brain Institute Tel Aviv, Wohl Institute for Advanced Imaging, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. 3. Department of Radiology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. 4. Sagol Brain Institute Tel Aviv, Wohl Institute for Advanced Imaging, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; School of Psychological Sciences, Faculty of Social Sciences, Tel Aviv University, Tel Aviv, Israel. 5. Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel; Department of Statistics and Operations Research, Tel Aviv University, Tel Aviv, Israel. 6. Department of Psychology, University of Haifa, Haifa, Israel. 7. Sagol Brain Institute Tel Aviv, Wohl Institute for Advanced Imaging, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Institute of Pain Medicine, Department of Anesthesiology and Critical Care Medicine, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; Pain Management and Neuromodulation Centre, Guy's and St Thomas' National Health Service Foundation Trust, London, United Kingdom. 8. Department of Emergency Medicine, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. 9. Department of Psychiatry, Texas A&M Health Science Center, Bryan, Texas. 10. Department of Psychiatry, New York University Langone Medical Center, New York, New York. 11. Sagol Brain Institute Tel Aviv, Wohl Institute for Advanced Imaging, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; School of Psychological Sciences, Faculty of Social Sciences, Tel Aviv University, Tel Aviv, Israel. Electronic address: hendlert@gmail.com.
Abstract
BACKGROUND: Low hippocampal volume could serve as an early risk factor for posttraumatic stress disorder (PTSD) in interaction with other brain anomalies of developmental origin. One such anomaly may well be the presence of a large cavum septum pellucidum (CSP), which has been loosely associated with PTSD. We performed a longitudinal prospective study of recent trauma survivors. We hypothesized that at 1 month after trauma exposure the relation between hippocampal volume and PTSD symptom severity will be moderated by CSP volume, and that this early interaction will account for persistent PTSD symptoms at subsequent time points. METHODS: One hundred seventy-one adults (87 women, average age 34.22 years [range, 18-65 years of age]) who were admitted to a general hospital's emergency department after a traumatic event underwent clinical assessment and structural magnetic resonance imaging within 1 month after trauma. Follow-up clinical evaluations were conducted at 6 (n = 97) and 14 (n = 78) months after trauma. Hippocampal and CSP volumes were measured automatically by FreeSurfer software and verified manually by a neuroradiologist (D.N.). RESULTS: At 1 month after trauma, CSP volume significantly moderated the relation between hippocampal volume and PTSD severity (p = .026), and this interaction further predicted symptom severity at 14 months posttrauma (p = .018). Specifically, individuals with a smaller hippocampus and larger CSP at 1 month posttrauma showed more severe symptoms at 1 and 14 months after trauma exposure. CONCLUSIONS: Our study provides evidence for an early neuroanatomical risk factors for PTSD, which could also predict the progression of the disorder in the year after trauma exposure. Such a simple-to-acquire neuroanatomical signature for PTSD could guide early management as well as long-term monitoring.
BACKGROUND: Low hippocampal volume could serve as an early risk factor for posttraumatic stress disorder (PTSD) in interaction with other brain anomalies of developmental origin. One such anomaly may well be the presence of a large cavum septum pellucidum (CSP), which has been loosely associated with PTSD. We performed a longitudinal prospective study of recent trauma survivors. We hypothesized that at 1 month after trauma exposure the relation between hippocampal volume and PTSD symptom severity will be moderated by CSP volume, and that this early interaction will account for persistent PTSD symptoms at subsequent time points. METHODS: One hundred seventy-one adults (87 women, average age 34.22 years [range, 18-65 years of age]) who were admitted to a general hospital's emergency department after a traumatic event underwent clinical assessment and structural magnetic resonance imaging within 1 month after trauma. Follow-up clinical evaluations were conducted at 6 (n = 97) and 14 (n = 78) months after trauma. Hippocampal and CSP volumes were measured automatically by FreeSurfer software and verified manually by a neuroradiologist (D.N.). RESULTS: At 1 month after trauma, CSP volume significantly moderated the relation between hippocampal volume and PTSD severity (p = .026), and this interaction further predicted symptom severity at 14 months posttrauma (p = .018). Specifically, individuals with a smaller hippocampus and larger CSP at 1 month posttrauma showed more severe symptoms at 1 and 14 months after trauma exposure. CONCLUSIONS: Our study provides evidence for an early neuroanatomical risk factors for PTSD, which could also predict the progression of the disorder in the year after trauma exposure. Such a simple-to-acquire neuroanatomical signature for PTSD could guide early management as well as long-term monitoring.
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