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The present findings suggest that sleep deprivation produces hyperalgesic changes that cannot be explained by nonspecific alterations in somatosensory functions.

P atients with chronic pain syndromes often suffer from sleep disturbances (1). However, it is difficult to determine the direction of cause between pain and sleep disturbance. The usual perspective favours an arousal-augmenting function of pain, which prevents the initiation or the continuation of sleep. Alternatively, it is believed that the modulation of pain and sleep-wake regulation share common neurobiological systems, in particular the central serotoninergic one (2). Consequently, the association of pain and disturbed sleep might be a secondary phenomenon due to a common neurobiological dysfunction. Finally, a rather unusual perspective is that poor sleep can interfere with pain processing. With this latter direction of relation in mind, we have addressed the following issues by reviewing the literature with a clear focus on experimental studies. The following perspectives may help to integrate the reviewed findings. The relationship between sleep disturbances and pain assuggested by correlational data. The majority of studies on the relationship between sleep and pain were not based on an experimental design, but relied on correlations only. In this section, a brief summary of the clinical investigations is given, including their first clues concerning the influence of disturbed sleep on pain, and their limitation in deriving causal relations.2. Sleep deprivation as a methodological approach to mimic disturbed sleep and derive experimental evidence for algesic effects. A comprehensive review of animal and human studies, which used sleep deprivation as an independent variable and examined its influence on pain processing, is provided.3. Assumptions on the algesic mechanisms of sleep deprivation.Results from animals studies suggest various neurochemical changes during and after sleep deprivation, which seemed to be involved in the modulation of pain. With a focus on the serotoninergic system, sleep deprivation affects 5-hydroxytryptamine (5-HT) turnover (3), the firing rate of serotoninergic neurons in the dorsal nucleus raphé (4) and 5-HT receptor functions (5). Given the well-known pain inhibitory effects of 5-HT, these changes may be tentatively integrated into a serotoninergic model of hyperalgesic action of sleep deprivation. Chronic pain syndromes are associated with alterations in sleep continuity and sleep architecture. One perspective of this relationship, which has not received much attention to date, is that disturbances of sleep affect pain. To fathom this direction of cause, experimental human and animal studies on the effects of sleep deprivation on pain processing were reviewed. According to the majority of the studies, sleep deprivation produces hyperalgesic changes. Furthermore, sleep deprivation can counteract analgesic effects of pharmacological treatments involving opioidergic and serotoninergic mechanisms of action.The heterogeneity of the human data and the exclusive interest in rapid eye movement sleep deprivation in animals so far do not allow us to draw firm conclusions as to wheth...

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