BACKGROUND: Uncontrollable stress is frequently accompanied by a primarily opioid-mediated stress analgesia. In posttraumatic stress disorder (PTSD) exaggerated stress-induced analgesia to trauma reminders was proposed. The present study investigated whether enhanced analgesia occurs in response to a trauma-unrelated cognitive stressor in PTSD. METHODS: Functional magnetic resonance imaging data were obtained from fourteen outpatients with PTSD and 14 trauma-exposed subjects without PTSD (NPTSD) during mechanical painful stimulation before and after stress. Blood oxygenation level-dependent (BOLD) responses were assessed during painful stimulation. Pain ratings, pain thresholds and pain tolerance were assessed pre- and post-stress. Heart rate and blood pressure were recorded before, during and after stress. RESULTS: In comparison to NPTSD, PTSD-patients showed significantly more analgesia in terms of an increase of pain threshold and tolerance and a decrease in pain ratings after the stressor. Post-stress, PTSD-patients compared to NPTSD displayed more activation of the rostral anterior cingulate cortex and decreased neural activity in brain areas associated with pain perception. However heart rate increase during stress and blood pressure decrease post-stress was lower in PTSD pointing to a dysregulation of the cardiovascular system in response to stress. LIMITATIONS: The small sample size represents a limiting factor in interpreting the results and might have led to low levels of significance for the group differences in BOLD response changes. CONCLUSIONS: These findings show enhanced stress reactivity and accompanying reduced pain perception in PTSD-patients in contrast to traumatized participants without PTSD. The results suggest that the previously reported enhanced analgesic response after trauma-related stress in PTSD transfers to trauma-unrelated stressors.
BACKGROUND: Uncontrollable stress is frequently accompanied by a primarily opioid-mediated stress analgesia. In posttraumatic stress disorder (PTSD) exaggerated stress-induced analgesia to trauma reminders was proposed. The present study investigated whether enhanced analgesia occurs in response to a trauma-unrelated cognitive stressor in PTSD. METHODS: Functional magnetic resonance imaging data were obtained from fourteen outpatients with PTSD and 14 trauma-exposed subjects without PTSD (NPTSD) during mechanical painful stimulation before and after stress. Blood oxygenation level-dependent (BOLD) responses were assessed during painful stimulation. Pain ratings, pain thresholds and pain tolerance were assessed pre- and post-stress. Heart rate and blood pressure were recorded before, during and after stress. RESULTS: In comparison to NPTSD, PTSD-patients showed significantly more analgesia in terms of an increase of pain threshold and tolerance and a decrease in pain ratings after the stressor. Post-stress, PTSD-patients compared to NPTSD displayed more activation of the rostral anterior cingulate cortex and decreased neural activity in brain areas associated with pain perception. However heart rate increase during stress and blood pressure decrease post-stress was lower in PTSD pointing to a dysregulation of the cardiovascular system in response to stress. LIMITATIONS: The small sample size represents a limiting factor in interpreting the results and might have led to low levels of significance for the group differences in BOLD response changes. CONCLUSIONS: These findings show enhanced stress reactivity and accompanying reduced pain perception in PTSD-patients in contrast to traumatized participants without PTSD. The results suggest that the previously reported enhanced analgesic response after trauma-related stress in PTSD transfers to trauma-unrelated stressors.