Michael T Smith1, Robert R Edwards, Gregory L Stonerock, Una D McCann. 1. Johns Hopkins University School of Medicine, Behavioral Medicine Research Laboratory and Clinic, 600 North Wolfe Street, Meyer 1-108, Baltimore, MD 21287, USA. msmith62@jhmi.edu
Abstract
STUDY OBJECTIVES: 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. DESIGN: Correlational, 2-night polysomnographic study with laboratory pain testing conducted on subsequent days. SETTING: General clinical research center inpatient unit with private room. PARTICIPANTS: Sixteen healthy, female, pain-free good sleepers, free from centrally acting agents (mean age = 24 +/- 4.5 years). MEASUREMENT AND RESULTS: 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). CONCLUSIONS: 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.
STUDY OBJECTIVES: 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. DESIGN: Correlational, 2-night polysomnographic study with laboratory pain testing conducted on subsequent days. SETTING: General clinical research center inpatient unit with private room. PARTICIPANTS: Sixteen healthy, female, pain-free good sleepers, free from centrally acting agents (mean age = 24 +/- 4.5 years). MEASUREMENT AND RESULTS: 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). CONCLUSIONS: 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.
Authors: Jeremy A Weingarten; Boris Dubrovsky; Robert C Basner; Susan Redline; Liziamma George; David J Lederer Journal: Sleep Date: 2016-08-01 Impact factor: 5.849
Authors: Caroline E Wright; Dana H Bovbjerg; Guy H Montgomery; Christina Weltz; Alisan Goldfarb; Benjamin Pace; Jeffrey H Silverstein Journal: J Pain Symptom Manage Date: 2008-08-23 Impact factor: 3.612