Smith Michael T, Edwards Robert R, McCann Una D, Haythornthwaite Jennifer A
Behavioral Sleep Medicine Program, Johns Hopkins Bayview, Johns Hopkins University School of Medicine, Baltimore MD 21287, USA.
Sleep. 2007 Apr;30(4):494-505. doi: 10.1093/sleep/30.4.494.
Impaired central pain modulation is implicated in the pathophysiology of chronic pain. In this controlled experiment, we evaluated whether partial sleep loss altered endogenous pain inhibition and reports of spontaneous pain. Thirty-two healthy females were studied polysomnographically for 7 nights. On Nights 1-2 (Baseline), subjects slept undisturbed for 8 hours. After Night 2, subjects were randomized to Control (N = 12), Forced Awakening (FA, N = 10), or Restricted Sleep Opportunity (RSO, N = 10) conditions. Controls continued to sleep undisturbed. FA underwent 8 forced awakenings (one per hour) on Nights 3-5. RSO subjects were yoked to FA on total sleep time (TST), receiving partial sleep deprivation by delayed bedtime. On Night 6, both FA & RSO underwent 36 hours total sleep deprivation (TSD), followed by 11-hour recovery sleep (Night 7). Subjects completed twice-daily psychophysical assessments of mechanical pain thresholds and pain inhibition (Diffuse Noxious Inhibitory Controls), via use of a conditioning stimulus (i.e., cold pressor) paradigm. FA and RSO demonstrated 50% reductions in total sleep time and increases in nonpainful somatic symptoms during partial sleep deprivation. While sleep deprivation had no effect on pain thresholds, during partial sleep deprivation the FA group demonstrated a significant loss of pain inhibition and an increase in spontaneous pain; neither of the other 2 groups showed changes in pain inhibition or spontaneous pain during partial sleep deprivation. These data suggest that sleep continuity disturbance, but not simple sleep restriction, impairs endogenous pain-inhibitory function and increases spontaneous pain, supporting a possible pathophysiologic role of sleep disturbance in chronic pain.
中枢性疼痛调制受损与慢性疼痛的病理生理学有关。在这项对照实验中,我们评估了部分睡眠剥夺是否会改变内源性疼痛抑制以及自发性疼痛报告。对32名健康女性进行了7晚的多导睡眠图研究。在第1 - 2晚(基线期),受试者不受干扰地睡8小时。第2晚后,受试者被随机分为对照组(N = 12)、强制觉醒组(FA,N = 10)或睡眠机会受限组(RSO,N = 10)。对照组继续不受干扰地睡眠。FA组在第3 - 5晚经历8次强制觉醒(每小时1次)。RSO组受试者在总睡眠时间(TST)上与FA组匹配,通过延迟就寝时间接受部分睡眠剥夺。在第6晚,FA组和RSO组都经历了36小时的完全睡眠剥夺(TSD),随后是11小时的恢复睡眠(第7晚)。受试者通过使用条件刺激(即冷加压)范式,每天进行两次机械性疼痛阈值和疼痛抑制(弥漫性伤害性抑制控制)的心理物理学评估。FA组和RSO组在部分睡眠剥夺期间总睡眠时间减少了50%,非疼痛性躯体症状增加。虽然睡眠剥夺对疼痛阈值没有影响,但在部分睡眠剥夺期间,FA组表现出疼痛抑制的显著丧失和自发性疼痛的增加;其他两组在部分睡眠剥夺期间疼痛抑制或自发性疼痛均未出现变化。这些数据表明,睡眠连续性干扰而非单纯的睡眠限制会损害内源性疼痛抑制功能并增加自发性疼痛,支持了睡眠干扰在慢性疼痛中可能的病理生理作用。