Department of Cognitive and Clinical Neuroscience, Central Institute of Mental Health, University of Heidelberg, Mannheim, Germany.
J Affect Disord. 2012 Feb;136(3):1247-51. doi: 10.1016/j.jad.2011.06.013. Epub 2011 Jul 6.
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.
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.
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.
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.
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.
无法控制的压力通常伴随着主要由阿片类介导的应激镇痛。在创伤后应激障碍（PTSD）中，提出了创伤记忆引起的应激性镇痛过度。本研究旨在探讨 PTSD 患者是否会对创伤无关的认知应激源产生增强的镇痛反应。
在机械性疼痛刺激前后，对 14 名 PTSD 门诊患者和 14 名无 PTSD 的创伤暴露受试者（NPTSD）进行功能磁共振成像（fMRI）数据采集。在疼痛刺激期间评估血氧水平依赖性（BOLD）反应。在应激前后评估疼痛评分、疼痛阈值和疼痛耐受力。在应激前、中、后记录心率和血压。
与 NPTSD 相比，PTSD 患者在应激后表现出更明显的镇痛作用，表现在疼痛阈值和耐受力增加，疼痛评分降低。与 NPTSD 相比，PTSD 患者在应激后显示出前扣带回皮质前部更活跃，与疼痛感知相关的脑区神经活动减少。然而，PTSD 患者在应激期间的心率增加和应激后血压下降较低，表明心血管系统对压力的反应失调。
样本量小是解释结果的一个限制因素，可能导致 BOLD 反应变化的组间差异的显著性水平较低。
这些发现表明，与未经历过创伤的 NPTSD 参与者相比，PTSD 患者的应激反应增强，同时伴随疼痛感知降低。结果表明，先前报道的 PTSD 患者在创伤相关应激后增强的镇痛反应转移到创伤无关的应激源。
