Elsevier

Sleep Medicine Reviews

Volume 10, Issue 5, October 2006, Pages 357-369
Sleep Medicine Reviews

CLINICAL REVIEW
Sleep deprivation and pain perception

https://doi.org/10.1016/j.smrv.2005.08.001Get rights and content

Summary

Chronically painful conditions are frequently associated with sleep disturbances, i.e. changes in sleep continuity and sleep architecture as well as increased sleepiness during daytime. A new hypothesis, which has attracted more and more attention, is that disturbances of sleep cause or modulate acute and chronic pain. Since it is well-known that pain disturbs sleep the relationship between the two has since recently been seen as reciprocal. To fathom the causal direction from sleep to pain we have reviewed experimental human and animal studies on the effects of sleep deprivation on pain processing. According to the majority of the studies, sleep deprivation produces hyperalgesic changes. Furthermore, sleep deprivation can interfere with analgesic treatments involving opioidergic and serotoninergic mechanisms of action. The still existing inconsistency of the human data and the exclusive focus on REM sleep deprivation in animals so far do not allow us to draw firm conclusions as to whether the hyperalgesic effects are due to the deprivation of specific sleep stages or whether they result from a generalized disruption of sleep continuity.

Introduction

Patients with chronic pain syndromes often suffer from insomnia.1, 2 However, it is a chicken and egg problem to determine the direction of causation between pain and sleep disturbance. The usual perspective favors an arousal enhancing function of pain, which prevents the initiation or the continuation of sleep and leads in addition to sleepiness and napping during daytime.3 Alternatively, it is believed that the modulation of pain and sleep-wake regulation share common neurobiological systems, in particular the central serotoninergic neurotransmission.4 Consequently, pain and disturbed sleep might be secondary phenomena due to a common neurobiological dysfunction. Finally, a rather recent perspective is that poor sleep can interfere with pain processing. We adopted this latter perspective when reviewing the literature with a clear focus on experimental studies (for an earlier review see5).

The majority of studies on the relationship between sleep and pain was not based on an experimental design, but relied on correlational data. In the first section, we give a brief summary of these clinical studies, which are nevertheless descriptively helpful although being limited in determining causal relations. In the second section we provide a comprehensive review of animal and human experiments, in which sleep deprivation was used as independent variable and pain processing as dependent one. In the third section we are concerned with the potential algesic mechanisms of sleep deprivation. Various neurochemical changes during and after sleep deprivation have been observed, which are likely involved in processing of pain. As an example, sleep deprivation affects 5-hydroxytryptamine (5-HT) turnover,6 the firing rate of serotoninergic neurons in the dorsal nucleus raphé7 and 5-HT receptor functions.8 There is a well-known central pain inhibitory effect of serotonin, which allows putting forward the hypothesis of a serotoninergic mechanism bridging hyperalgesia and sleeping deprivation.

Section snippets

Correlational analysis of the relationship between sleep and pain

The overnight increase in muscular pain of fibromyalgia patients led to the assumption of a pathogenic role of disturbed sleep in this pain condition. As a consequence, Moldofsky et al.9 investigated in parallel sleep physiology and pain in fibromyalgia patients. They observed an increased ratio of alpha waves during non-rapid eye movement (NREM) sleep, the so-called ‘alpha-delta sleep’, which is indicative for an increased arousal during slow wave sleep. This change was assumed to interfere

Experimental analysis of the effect of sleep deprivation on pain perception

This review of the literature is based on a medline research for the years 1962 to February 2005 using the keywords ‘sleep’, ‘sleep deprivation’, ‘sleep interruption’ combined with ‘pain’ for human and animal studies. An article was included if sleep deprivation in its total, selective or partial form was used as an independent variable, and any subjective or behavioral measure of pain as dependent variable. Furthermore, only studies that meet minimal methodological demands, regarding sample

Future research

Besides more descriptive studies on the active part of sleep deprivation (which type and stages of sleep have to be deprived in which form?) when it affects pain perception studies focusing on the mechanisms of action are badly needed in the future. To achieve the latter, experiments, which are designed to examine specific mediating factors (such as opioidergic and serotoninergic neurotransmission) and which are capable of delineating the affected part of the pain system, are necessary. A

Conclusion

In this review evidence was examined for the hypothesis that the deprivation or the disturbance of sleep enhances pain sensitivity and causes pain. Pain disturbs sleep by inducing arousal and triggering all other neurobiological sequels of stress, which are incompatible with an undisturbed sleep. Hence, an ongoing cycle might arise starting either with disturbed sleep or with pain, in which the two components maintain or even augment each other. Accordingly, sufficient management of disturbed

Acknowledgements

This project is supported by the German Ministry for Education and Research within the promotional emphasis “German Research Network on Depression”.

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