Sleep Deprivation and Pain Modulation

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DESCRIPTION (provided by applicant): Pain is the number one reason why patients visit their physician, costing over $100 billion annually. Insomnia is one of the most disabling correlates of pain, affecting between 50 to 88% of the 50 million adults suffering from chronic pain. In spite of this prevalence, little systematic work has focused on the interrelationships between pain and sleep. Several studies in healthy subjects and some clinical research suggest the possibility that sleep and pain might be reciprocally linked, such that pain disrupts sleep and sleep disruption exacerbates pain. These relationships have yet to be demonstrated in a satisfactory manner in controlled experiments and little or nothing is known about the mechanisms by which sleep might affect the experience of pain. One possibility is that sleep continuity disturbance rod/or sleep deprivation alter central pain modulatory processes, which are implicated in the etiology of chronic pain. This R21 proposal has 3 primary aims: 1) determine the feasibility of a novel sleep deprivation paradigm and refine he model as an analog to the sleep continuity disturbance associated with insomnia; 2) evaluate the effects of partial and total sleep deprivation on pain sensitivity and pain modulation; and 3) evaluate whether partial sleep deprivation achieved by disrupting sleep continuity affects pain sensitivity and modulation to a greater extent than partial sleep deprivation achieved by restricting sleep opportunity. In this 7-day, inpatient experiment, healthy good sleepers will be randomized to one of three sleep conditions after sleeping undisturbed for 2 nights: (1) a control group in which subjects are permitted to sleep undisturbed for the remaining 5 nights; (2) a forced awakening (FA) group in which sleep is interrupted once every hour to permit a maximum of 280 minutes of sleep per night; and (3) a restricted sleep opportunity (RSO) group in which sleep is delayed and total sleep time is yoked to the total sleep time obtained by a matched pair in the FA group. After 3 nights of partial sleep deprivation, both sleep disruption groups will undergo a night of total sleep deprivation, followed by a night of recovery sleep. Sleep will be monitored polysomnographically. Quantitative and sensory tests of pain sensitivity and pain-modulation will be assessed twice a day. It is expected that the experimental procedure will produce a pattern of partial sleep deprivation that includes prolonged awakenings and reduced total sleep time. We hypothesize that this form of sleep deprivation will be associated with enhanced pain sensitivity and impaired pain modulation. Results will yield a novel model to study the effects of insomnia and sleep loss on the central nervous system and ultimately have implications for the prevention and treatment of chronic pain.