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The reciprocal interaction between sleep and pain has been reported by numerous studies. Patients with acute or chronic pain often complain of difficulty falling asleep, frequent awakenings, shorter sleep duration, unrefreshing sleep, and poor sleep quality in general. According to the majority of the experimental human studies, sleep deprivation may produce hyperalgesic changes. The selective disruption of slow wave sleep has shown this effect more consistently, while results after selective REM sleep deprivation remain unclear. Patients with chronic pain have a marked alteration of sleep structure and continuity, such as frequent sleep-stage shifts, increased nocturnal awakenings, decreased slow wave sleep (SWS), decreased rapid eye movement (REM) sleep, and alpha-delta sleep. Many analgesic medications can alter sleep architecture in a manner similar to the effects of acute and chronic pain, suppressing SWS and REM sleep. [ABSTRACT FROM AUTHOR]