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Re‐exposure to a Traumatic Event Amplifies the Duration and Severity of Co‐morbid Chronic Pain in an Animal Model of Post‐traumatic Stress Disorder

Post‐traumatic stress disorder (PTSD) is a debilitating condition affecting up to 35% of combat veterans and between 7–8% of the general populace. Heightened anxiety/hyperarousal and chronic pain commonly co‐occur in both civilian and veteran PTSD populations. The shared co‐morbidity of PTSD with chronic pain negatively impacts the treatment of both disorders. Single‐prolonged stress (SPS) is an established animal model of PTSD capable of facilitating development of symptoms similar to those observed in human patients, including decreased pain threshold and amplified anxiety and fear responses. We have reported that SPS produces tactile allodynia that persists for over 5 weeks following the initial stress exposure. Many PTSD patients have experienced multiple traumatic events, and/or re‐experience the stress following exposure to reminders (cues) of that traumatic event. Because the severity of PTSD in humans correlates with the severity of the trauma, we felt it important to explore how re‐exposure to one of the original stressors altered the severity of existing co‐morbid nociceptive hypersensitivity. Therefore we have introduced a latent re‐stress component to the established SPS model in order to better understand how re‐exposure to a traumatic event may alter the duration and intensity of PTSD and co‐morbid symptoms and their molecular underpinnings.