Bruehl Stephen, Chung Ok Yung
Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, TN, USA.
Pain. 2006 Oct;124(3):287-294. doi: 10.1016/j.pain.2006.04.018. Epub 2006 May 24.
A family history of chronic pain has previously been linked to increased incidence of spontaneous acute pain and risk for chronic pain. Mechanisms underlying these associations are unknown, although similar effects on both acute and chronic pain suggest that central endogenous analgesic system differences may be relevant. This study tested whether a positive parental chronic pain history (PH+) was associated with impaired endogenous opioid analgesic responses to acute pain. Seventy-three chronic low back pain patients (LBP) and 46 pain-free controls received opioid blockade (8mg naloxone i.v.) and placebo blockade (saline) in randomized, 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 pain intensity ratings during and immediately following each task. To assess opioid analgesic function, blockade effects were derived by subtracting placebo from blockade condition pain responses. Placebo condition analyses indicated that both PH+ subjects and LBP subjects reported greater acute pain sensitivity than respective comparison groups (p's<.05). Multivariate analyses indicated that, beyond any influence of current chronic pain status, PH+ subjects failed to exhibit any endogenous opioid analgesia to acute ischemic pain, whereas PH- subjects elicited effective opioid analgesia (p<.05). A significant multivariate PHxSubject Type interaction (p<.05) indicated that opioid analgesic impairments were most prominent in PH+ LBP subjects. Similar analyses for finger pressure pain blockade effects were nonsignificant (p>.10). The possible heritability of endogenous opioid analgesic dysfunction observed in individuals with a positive parental chronic pain history remains to be investigated.
慢性疼痛的家族史此前已被证明与自发性急性疼痛的发病率增加以及慢性疼痛的风险相关。尽管对急性和慢性疼痛的类似影响表明中枢内源性镇痛系统差异可能与之相关,但这些关联背后的机制尚不清楚。本研究测试了父母有慢性疼痛史(PH+)是否与内源性阿片类药物对急性疼痛的镇痛反应受损有关。73名慢性下腰痛患者(LBP)和46名无疼痛对照者在不同的 sessions 中以随机、平衡的顺序接受阿片类药物阻断(静脉注射8mg纳洛酮)和安慰剂阻断(生理盐水)。在每次实验中,受试者参与1分钟的手指按压疼痛任务,随后进行缺血性前臂疼痛任务,并在每个任务期间及之后立即提供疼痛强度评分。为了评估阿片类药物的镇痛功能,通过从阻断条件下的疼痛反应中减去安慰剂来得出阻断效应。安慰剂条件分析表明,PH+受试者和LBP受试者均报告比各自的对照组具有更高的急性疼痛敏感性(p值<.05)。多变量分析表明,除了当前慢性疼痛状态的任何影响外,PH+受试者对急性缺血性疼痛未能表现出任何内源性阿片类药物镇痛作用,而PH-受试者则引发了有效的阿片类药物镇痛作用(p<.05)。显著的多变量PHx受试者类型交互作用(p<.05)表明,阿片类药物镇痛障碍在PH+ LBP受试者中最为突出。对手指按压疼痛阻断效应的类似分析无统计学意义(p>.10)。在父母有慢性疼痛史阳性的个体中观察到的内源性阿片类药物镇痛功能障碍的可能遗传因素仍有待研究。