Cerebrospinal fluid and plasma beta-endorphin in combat veterans with post-traumatic stress disorder
Cerebrospinal fluid and plasma beta-endorphin in combat veterans with post-traumatic stress disorder
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DOI：
10.1016/s0306-4530(97)00053-x
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发表时间：
1997-10-01
影响因子：
3.7
通讯作者：
Geracioti, TD
中科院分区：
文献类型：
--
作者：
Baker, DG;West, SA;Geracioti, TD
实验动物在创伤应激后会出现阿片类药物介导的镇痛作用，在患有创伤后应激障碍 (PTSD) 的退伍军人中观察到阿片类药物介导的镇痛作用增强。这些观察结果得出这样的假设：创伤后应激障碍 (PTSD) 患者中枢神经系统 (CNS) 阿片能活性增加。然而，缺乏关于 PTSD 患者阿片肽浓度和动态的直接中枢神经系统数据。我们通过一根灵活的留置蛛网膜下导管在 6 小时内抽取脑脊液 (CSF)，并测定 10 名患有 PTSD 的退伍军人和 9 名匹配的正常志愿者每小时 CSF 的免疫反应性 β-内啡肽 (ir beta END) 浓度。同时抽血以获得ir beta END的血浆。通过 CAPS 测量的 PTSD 症状群与神经内分泌数据相关。与正常人相比，PTSD 患者的平均 CSF ir beta END 显着更高，并且 ir beta END 与 PTSD 的侵入性和回避症状之间存在负相关。血浆 ir beta END 之间没有发现组间差异，CSF 和血浆 ir beta END 之间也不存在显着相关性。正如之前报道的那样，免疫反应性 β-促脂素 (ir beta LPH) 和阿片黑皮质素原 (irPOMC) 都是 β END 的前体，它们在人脑脊液中的含量比 β-内啡肽本身要丰富得多。中枢神经系统阿片类药物浓度的增加是否早于创伤应激，从而导致易受解离状态和创伤后应激障碍本身的影响，还是由创伤引起的，仍有待确定。 CSF ir beta END 与回避和侵入症状之间的负相关表明，中枢神经系统阿片类药物的过度分泌可能构成对创伤经历的适应性反应。 CSF 和血浆 ir beta END 之间的相关性较差，限制了使用血浆测量来评估中枢神经系统阿片类药物活性。由爱思唯尔科学有限公司出版
Opioid-mediated analgesia develops in experimental animals following traumatic stress and increased opioid-mediated analgesia has been observed in combat veterans with post-traumatic stress disorder (PTSD). These observations have led to the hypothesis that increased central nervous system (CNS) opioidergic activity exists in patients with PTSD. However, direct CNS data on opioid peptide concentrations and dynamics in patients with PTSD are lacking. We withdrew cerebrospinal fluid (CSF) via a flexible, indwelling subarachnoid catheter over a 6-h period and determined hourly CSF concentrations of immunoreactive beta-endorphin (ir beta END) in 10 well-characterized combat veterans with PTSD and nine matched normal volunteers. Blood was simultaneously withdrawn to obtain plasma for ir beta END. PTSD symptom clusters, as measured by the CAPS, were correlated with neuroendocrine data. Mean CSF ir beta END was significantly greater in patients with PTSD compared with normals and there was a negative correlation between the ir beta END and PTSD intrusive and avoidant symptoms of PTSD. No intergroup difference between plasma ir beta END was found, nor was there a significant correlation between CSF and plasma ir beta END. Immunoreactive beta-lipotropin (ir beta LPH) and pro-opiomelanocortin (irPOMC), both precursors of beta END, were much more plentiful in human CSF than was beta-endorphin itself, as has been previously reported. It remains to be determined whether the increased CNS opioid concentrations predate traumatic stress, thereby conferring a vulnerability to dissociative states and PTSD itself, or result from the trauma. The negative correlation between CSF ir beta END and avoidant and intrusive symptoms suggests that CNS hypersecretion of opioids might constitute an adaptive response to traumatic experience. Poor correlation between CSF and plasma ir beta END limits use of plasma measures to assess CNS opioid activity. Published by Elsevier Science Ltd.