Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Pain. 2018 Jan;159(1):33-40. doi: 10.1097/j.pain.0000000000001053.
Chronic pain conditions are highly comorbid with insufficient sleep. While the mechanistic relationships between the 2 are not understood, chronic insufficient sleep may be 1 pathway through which central pain-modulatory circuits deteriorate, thereby contributing to chronic pain vulnerability over time. To test this hypothesis, an in-laboratory model of 3 weeks of restricted sleep with limited recovery (5 nights of 4-hour sleep per night followed by 2 nights of 8-hour sleep per night) was compared with 3 weeks of 8-hour sleep per night (control protocol). Seventeen healthy adults participated, with 14 completing both 3-week protocols. Measures of spontaneous pain, heat-pain thresholds, cold-pain tolerance (measuring habituation to cold over several weeks), and temporal summation of pain (examining the slope of pain ratings during cold water immersion) were assessed at multiple points during each protocol. Compared with the control protocol, participants in the sleep-restriction protocol experienced mild increases in spontaneous pain (P < 0.05). Heat-pain thresholds decreased after the first week of sleep restriction (P < 0.05) but normalized with longer exposure to sleep restriction. By contrast, chronic exposure to restricted sleep was associated with decreased habituation to, and increased temporal summation in response to cold pain (both P < 0.05), although only in the past 2 weeks of the sleep-restriction protocol. These changes may reflect abnormalities in central pain-modulatory processes. Limited recovery sleep did not completely resolve these alterations in pain-modulatory processes, indicating that more extensive recovery sleep is required. Results suggest that exposure to chronic insufficient sleep may increase vulnerability to chronic pain by altering processes of pain habituation and sensitization.
慢性疼痛病症与睡眠不足高度共病。虽然这两者之间的机制关系尚未被理解，但慢性睡眠不足可能是中央疼痛调节回路恶化的途径之一，从而随着时间的推移导致慢性疼痛易感性增加。为了验证这一假设，研究人员比较了为期 3 周的限制睡眠和有限恢复的实验室模型（每晚睡眠时间为 4 小时，持续 5 晚，然后每晚睡眠时间为 8 小时，持续 2 晚）与每晚 8 小时的睡眠 3 周（对照方案）。17 名健康成年人参与了研究，其中 14 人完成了两个 3 周的方案。在每个方案的多个时间点评估了自发性疼痛、热痛阈值、冷痛耐受（测量数周内对冷的适应能力）和疼痛的时间总和（检查冷水浸泡过程中疼痛评分的斜率）。与对照方案相比，睡眠限制方案的参与者经历了自发性疼痛的轻度增加（P<0.05）。睡眠限制的第一周后，热痛阈值下降（P<0.05），但随着更长时间的暴露于睡眠限制而恢复正常。相比之下，慢性暴露于限制睡眠与冷痛的适应能力下降和对冷痛的时间总和增加有关（两者均 P<0.05），尽管仅在睡眠限制方案的过去 2 周内。这些变化可能反映了中央疼痛调节过程中的异常。有限的恢复性睡眠并没有完全解决这些疼痛调节过程的改变，表明需要更广泛的恢复性睡眠。结果表明，暴露于慢性睡眠不足可能通过改变疼痛适应和敏感化的过程来增加慢性疼痛的易感性。
