Bruehl Stephen, Chung Ok Yung, Ward Pamela, Johnson Benjamin
Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, TN 37232-1557, USA.
Clin J Pain. 2004 Sep-Oct;20(5):283-92. doi: 10.1097/00002508-200409000-00002.
To test whether endogenous opioid antinociceptive system dysfunction evidenced in response to acute pain stimuli is associated with increased clinical pain intensity in chronic pain sufferers, and to determine whether this association is moderated by disability level.
A double-blind, placebo-controlled, randomized crossover design. Subjects underwent laboratory acute finger pressure pain stimulation and ischemic pain stimulation under placebo and under opioid blockade with naloxone. The primary independent measures, reflecting degree of endogenous opioid antinociception, were opioid Blockade Effects derived to reflect the change elicited by naloxone in pain intensity ratings for the acute pain tasks. High and Low Disability groups were derived based on Pain Disability Index scores to allow examination of the influence of disability level on the relationship between Blockade Effects and chronic pain intensity.
Twenty-eight chronic low back pain sufferers.
Seven-day diary ratings of overall chronic pain intensity based on McGill Pain Questionnaire-Short Form total scores.
Greater daily chronic pain intensity was associated with greater placebo acute pain sensitivity in the laboratory (P < 0.05). Positive Blockade Effects (ie, presence of opioid analgesia) were associated as expected with lower placebo-condition acute pain sensitivity in the laboratory (P < 0.05). In main effects analyses, Blockade Effects were not associated significantly with daily chronic pain intensity. This absence of overall main effects was accounted for by significant opposing interactions between disability level and Blockade Effects (P < 0.05). Negative Blockade Effects (ie, absence of endogenous opioid analgesia to acute pain) in the High Disability group were associated with greater daily chronic pain intensity, consistent with the hypothesized effects of chronic pain-related opioid dysfunction. In contrast, Positive Blockade Effects (ie, effective opioid analgesia to acute pain) were associated with higher daily chronic pain intensity in the Low Disability group.
These results suggest that endogenous opioid antinociceptive system dysfunction may contribute to elevated acute and chronic pain sensitivity among more disabled chronic pain patients. Among less disabled patients, chronic pain may serve as a primer producing up-regulated opioid antinociceptive responses to acute pain
测试在对急性疼痛刺激的反应中所证实的内源性阿片类抗痛觉系统功能障碍是否与慢性疼痛患者临床疼痛强度增加相关，并确定这种关联是否受残疾水平的调节。
双盲、安慰剂对照、随机交叉设计。受试者在安慰剂和纳洛酮阿片类阻断情况下接受实验室急性手指压力疼痛刺激和缺血性疼痛刺激。反映内源性阿片类抗痛觉程度的主要独立测量指标是阿片类阻断效应，其用于反映纳洛酮引起的急性疼痛任务疼痛强度评分的变化。根据疼痛残疾指数得分将受试者分为高残疾组和低残疾组，以检验残疾水平对阻断效应与慢性疼痛强度之间关系的影响。
28名慢性下腰痛患者。
基于麦吉尔疼痛问卷简表总分的7天总体慢性疼痛强度日记评分。
实验室中更高的每日慢性疼痛强度与更大的安慰剂急性疼痛敏感性相关（P<0.05）。如预期的那样，阳性阻断效应（即存在阿片类镇痛作用）与实验室中较低的安慰剂条件下急性疼痛敏感性相关（P<0.05）。在主效应分析中，阻断效应与每日慢性疼痛强度无显著相关性。这种总体主效应的缺失是由残疾水平与阻断效应之间显著的反向相互作用所致（P<0.05）。高残疾组中的阴性阻断效应（即对急性疼痛缺乏内源性阿片类镇痛作用）与更高的每日慢性疼痛强度相关，这与慢性疼痛相关阿片类功能障碍的假设效应一致。相比之下，低残疾组中的阳性阻断效应（即对急性疼痛有效的阿片类镇痛作用）与更高的每日慢性疼痛强度相关。
这些结果表明，内源性阿片类抗痛觉系统功能障碍可能导致残疾程度更高的慢性疼痛患者的急性和慢性疼痛敏感性升高。在残疾程度较低的患者中，慢性疼痛可能起到引发剂的作用，产生对急性疼痛上调的阿片类抗痛觉反应。
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