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Statement of the Problem : Pain and posttraumatic stress disorder (PTSD) are highly comorbid conditions. Patients with chronic pain have higher rates of PTSD. Likewise, patients with PTSD are often diagnosed with numerous chronic pain conditions. Despite the high pain-PTSD comorbidity, the pathophysiologic mechanisms underlying this phenomenon are incompletely understood and only recently researchers have started to investigate pain-PTSD overlap using experimental pain models. The aim of the present study was to examine the activation of the pain-processing pathway in a cohort of combat PTSD compared to combat controls in response to a prolonged painful stimulus. Methods : Novel data from the experimental pain model using intramuscular capsaicin comparing a group of 10 Operation Enduring Freedom/Operation Iraqi Freedom (OEF/OIF) veterans with combat-related PTSD and 11 matched OEF/OIF veterans without PTSD will be presented. Intramuscular capsaicin causes a prolonged, deep-aching muscle pain, resembling pain associated with chronic pain states. Following capsaicin injection into the left thigh muscle, subjects underwent functional magnetic resonance imaging scanning while whole brain perfusion was measured with arterial spin labeling (ASL). At every 10 min, samples of cerebrospinal fluid (CSF) were drawn and subjective pain ratings were measured throughout the scanning window (30 min). Following scanning, CSF draws and pain ratings continued and evidence for central sensitization was assessed by temporal summation of repeated pressure pain stimuli. Results : Our results show evidence for an acute form of central sensitization in the PTSD group in comparison to matched combat controls. The maximum pain response and initial pain decrease were not different between the two groups, yet significantly higher pain ratings were observed in the PTSD group 15 min postinjection of capsaicin. ASL showed significant group by time interactions within pain-processing network, whereby PTSD group maintained high levels of brain perfusion in the ventral medial frontal gyurs and other interoceptive and evaluative brain circuits throughout the second half of the scan, similar to subjective pain ratings. Furthermore, significantly higher temporal summation of pain was also noted in the PTSD compared to the control group. Conclusion : We found increased sensitivity to prolonged, deep experimental pain in combat-related PTSD compared to traumatized subjects who never developed PTSD following combat. We posit that this increased pain response on behavioral, spinal, and supraspinal levels is related to a form of acute central sensitization in these individuals in response to a prolonged pain stimulus. Initial neuroimaging findings point to differential activation of frontal systems as potentially underlying pain-PTSD pathways and perhaps provide initial mechanisms for the development of testable models of perturbed pain processing in PTSD.