Bruehl Stephen, Chung Ok Yung, Burns John W, Biridepalli Sujatha
Department of Anesthesiology, Vanderbilt University Medical Center, Vanderbilt University School of Medicine, 504 Oxford House, 1313 Twenty-First Avenue South, Nashville, TN 37232-1557, USA Department of Psychology, The Chicago Medical School, North Chicago, IL, USA.
Pain. 2003 Dec;106(3):317-324. doi: 10.1016/S0304-3959(03)00319-1.
Recent work suggests that an expressive anger management style (anger-out) is associated with elevated acute pain sensitivity due to endogenous opioid antinociceptive dysfunction. We tested the hypothesis that this opioid dysfunction mediates the previously reported positive association between anger-out and chronic pain intensity. To assess endogenous opioid antinociception in the laboratory, 71 subjects with chronic low back pain received opioid blockade (8 mg naloxone i.v.) or placebo in counterbalanced order in separate sessions. During each, subjects participated in a 1-min finger pressure pain task followed by an ischemic forearm pain task, providing acute pain ratings on the McGill Pain Questionnaire-Short Form (MPQ) immediately following each task. Subjects also completed a 7-day chronic pain diary based on the MPQ between laboratory sessions. To index opioid antinociceptive function, blockade effects were derived, subtracting placebo from blockade condition pain ratings. Greater anger-out was associated with both smaller blockade effects (suggesting impaired opioid antinociception) and greater chronic pain intensity, and blockade effects were inversely associated with chronic pain intensity. Sequential hierarchical regressions suggested that opioid dysfunction partially mediates the positive association between anger-out and total MPQ chronic pain intensity. Inclusion of blockade effects in the first step of the regression resulted in a decrease from 7 to 3% in chronic pain variance accounted for by anger-out. Opioid dysfunction did not mediate the positive association between anger-in and chronic pain. These results provide preliminary support for the hypothesis that the positive association between anger expression and chronic pain intensity is mediated by opioid antinociceptive system dysfunction.
近期研究表明,一种表达性的愤怒管理方式(愤怒外显)与因内源性阿片类抗痛觉功能障碍导致的急性疼痛敏感性升高有关。我们检验了这样一个假设,即这种阿片类功能障碍介导了先前报道的愤怒外显与慢性疼痛强度之间的正相关。为了在实验室中评估内源性阿片类抗痛觉作用,71名慢性下腰痛患者在不同的 sessions 中以平衡顺序接受阿片类阻滞剂(静脉注射8毫克纳洛酮)或安慰剂。在每次 session 期间,受试者先参与1分钟的手指压痛疼痛任务,随后进行缺血性前臂疼痛任务,并在每项任务后立即根据麦吉尔疼痛问卷简表(MPQ)提供急性疼痛评分。受试者还在实验室 sessions 之间完成了基于MPQ的7天慢性疼痛日记。为了衡量阿片类抗痛觉功能,通过将安慰剂条件下的疼痛评分从阻滞剂条件下的疼痛评分中减去来得出阻滞剂效应。更高的愤怒外显与更小的阻滞剂效应(表明阿片类抗痛觉功能受损)以及更高的慢性疼痛强度均相关,且阻滞剂效应与慢性疼痛强度呈负相关。逐步分层回归表明,阿片类功能障碍部分介导了愤怒外显与MPQ慢性疼痛总强度之间的正相关。在回归的第一步纳入阻滞剂效应后,愤怒外显所解释的慢性疼痛方差从7%降至3%。阿片类功能障碍并未介导愤怒内隐与慢性疼痛之间的正相关。这些结果为以下假设提供了初步支持,即愤怒表达与慢性疼痛强度之间的正相关是由阿片类抗痛觉系统功能障碍介导的。
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