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| Subscribe to Clinical Compass™ | VOLUME 2, ISSUE 10 - MAY 8, 2007 | ||||||||||||||||||||||||||||||||||||||||||||||||
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FROM THE CLINICAL KNOWLEDGE CENTER Sleep: What You Don't Get, Can Hurt You by Michelle Ostrander, PhD May 2007 is designated Better Sleep Month by the Better Sleep Council (BSC). Within the United States, a "24/7" mentality which demands an ever-ready willingness to work and socialize, has led to an epidemic of sleep deprivation. Sacrificing sleep time to meet work, family, and social obligations is glorified whereas societal views of the natural physiologic need for sleep range from "laziness" to a "lack of moral fiber," thus resulting in an erosion of the importance that Americans place upon sleep in their daily lives. Chronic lack of sleep can negatively impact many aspects of our lives, including school and work performance. Consider the following statistics from the BSC's 2007 Better Sleep Month Survey:
Determining the etiology of impaired sleep and wakefulness is frequently complex as these deficits may result from any of the following:
Researchers are only recently beginning to understand the health consequences of chronic sleep restriction. Sleep deprivation has been linked with metabolic dysfunction and insulin resistance, as well as an increased incidence of bodily pain. Many chronic pain disorders are characterized by sleep/wake disturbances such as insomnia and sleep loss. Polysomnographic studies indicate that chronic pain conditions are linked with poor sleep continuity, decreased total sleep time, and alterations in sleep architecture. Preliminary experimental studies and longitudinal research suggest that one consequence of chronic pain is disturbed sleep, and that sleep disruption itself may directly contribute to enhanced pain sensitivity. A study published in the April 2007 issue of Sleep sought to fill the gap in the literature linking sleep deprivation and hyperalgesia by determining whether sleep loss and disruptions in sleep continuity impair endogenous pain inhibition. The study also evaluated the impact of partial sleep deprivation on reports of spontaneous clinical pain. Thirty-two healthy, adult females underwent polysomnography for 7 consecutive nights. Subjects were randomized to Control (n = 12), Forced Awakening (FA, n = 10), or Restricted Sleep Opportunity (RSO, n = 10). Control subjects were permitted to sleep undisturbed for the duration of the study. The FA group was exposed to 8 forced awakenings (one per hour) on Nights 3-5, for a total possible sleep time of 280 minutes per night. The RSO subjects underwent partial sleep deprivation as their total sleep time was matched to that of the FA group through a delay in bedtime. Both the FA and RSO groups were exposed to 36 hours of total sleep deprivation on Night 6, followed by 11 hours of recovery sleep on Night 7. Endogenous pain inhibition was assessed through the Diffuse Noxious Inhibitory Control (DNIC) test that involves the simultaneous administration of 2 types of noxious stimuli to distant anatomic regions. Decreases in DNIC scores are interpreted as loss of pain inhibition. The Pennebaker Inventory of Limbic Languidness (PILL) is a 54-item questionnaire that instructs subjects to assess on a 5-point Likert scale the degree to which nonpainful and painful somatic symptoms are experienced. The FA group had significantly lower normalized DNIC scores than the Control and RSO groups on each of the days following a night of partial sleep deprivation (p's < .05), indicative of decreased pain inhibition. In contrast, there were no differences in DNIC scores between any groups after either total sleep deprivation or a night of recovery sleep. On measures of spontaneous somatic pain measured by the PILL, the FA group reported higher symptom levels after the second and third night of partial sleep deprivation (Days 5 and 6) than the other two groups (p < .05). In addition, both the FA and RSO groups exhibited higher levels of spontaneous somatic pain symptoms after a night of total sleep deprivation (p < .05), which normalized after a night of recovery sleep. For spontaneous nonpainful somatic symptoms, the FA group displayed higher scores than the Control and RSO groups (p < .05), but only after the second night of partial sleep deprivation (Day 5). Both the FA and the RSO groups exhibited higher nonpainful somatic symptoms after the third night of partial sleep deprivation and after total sleep deprivation (Days 6 and 7). These findings of an association between disrupted sleep continuity, decreased pain inhibition, and enhanced spontaneous pain have important clinical implications. They provide the first mechanistic support for prior longitudinal findings of sleep disruption as a risk factor for chronic pain and suggest that aggressive attempts to treat insomnia in the early stages of chronic pain conditions may provide at least partial amelioration of pain. Educating patients about the importance of quality sleep and appropriate wakefulness should therefore be a goal for all practitioners, regardless of their discipline. Simple steps, such as instituting good sleep/wake hygiene habits, can dramatically enhance the quality of sleep and improve wakefulness. Good sleep/wake hygiene includes the following:
For more information on sleep and sleep disorders: National Sleep Foundation National Heart Lung and Blood Institute Do you have feedback for the author? Click here to send us an email. References
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