Smith Michael T, Edwards Robert R, Stonerock Gregory L, McCann Una D
Johns Hopkins University School of Medicine, Behavioral Medicine Research Laboratory and Clinic, 600 North Wolfe Street, Meyer 1-108, Baltimore, MD 21287, USA.
Sleep. 2005 Jul;28(7):809-12. doi: 10.1093/sleep/28.7.809.
Sleep-deprivation experiments suggest that sleep loss increases pain sensitivity. It is unclear from preliminary studies, however, whether sleep-related processes are directly associated with pain perception or whether hyperalgesia is due to the secondary effects of sleep deprivation and/or demand characteristics. Consequently, we sought to evaluate relationships between sleep architecture and laboratory measures of pain processing in healthy women, sleeping under normal conditions.
Correlational, 2-night polysomnographic study with laboratory pain testing conducted on subsequent days.
General clinical research center inpatient unit with private room.
Sixteen healthy, female, pain-free good sleepers, free from centrally acting agents (mean age = 24 +/- 4.5 years).
Standard polysomnographic sleep-continuity and architecture variables and subject responses to standard noxious thermal stimuli delivered to the ventral and dorsal surfaces of the forearm via thermal sensory analyzer. Ratings of thermal pain threshold as well as suprathreshold indices of central pain processing (mean/peak ratings and intensity of painful aftersensations) were obtained. Averaging across nights/days, we found significant negative relationships between rapid eye movement sleep latency and suprathreshold pain ratings, ie, measures of heightened central pain processing (r = -.64 to -.73, P < .01). Significant positive relationships were also found between percentage of rapid eye movement sleep and suprathreshold ratings(r = .56 to .66, P < .050).
These data are the first to demonstrate a relationship between individual variation in rapid eye movement sleep and pain-modulatory processes. The results have implications for the etiology of pain disorders and suggest that neurobiologic substrates regulating sleep may also play a role in central pain processing.
睡眠剥夺实验表明，睡眠不足会增加疼痛敏感性。然而，从初步研究中尚不清楚与睡眠相关的过程是否与疼痛感知直接相关，或者痛觉过敏是否是由于睡眠剥夺和/或需求特征的继发效应所致。因此，我们试图评估健康女性在正常睡眠条件下睡眠结构与疼痛处理实验室测量之间的关系。
相关性研究，为期两晚的多导睡眠图研究，并在随后几天进行实验室疼痛测试。
设有私人病房的综合临床研究中心住院部。
16名健康、无疼痛、睡眠良好的女性，未服用中枢作用药物（平均年龄 = 24 ± 4.5岁）。
标准多导睡眠图的睡眠连续性和结构变量，以及受试者对通过热感觉分析仪施加在前臂腹侧和背侧表面的标准有害热刺激的反应。获得热痛阈值评分以及中枢疼痛处理的阈上指标（平均/峰值评分和疼痛后感觉强度）。跨夜/日平均计算，我们发现快速眼动睡眠潜伏期与阈上疼痛评分之间存在显著负相关，即中枢疼痛处理增强的指标（r = -0.64至-0.73，P < 0.01）。快速眼动睡眠百分比与阈上评分之间也发现显著正相关（r = 0.56至0.66，P < 0.05）。
这些数据首次证明了快速眼动睡眠的个体差异与疼痛调节过程之间的关系。研究结果对疼痛障碍的病因学具有启示意义，并表明调节睡眠的神经生物学底物可能也在中枢疼痛处理中发挥作用。
