Prominent and severe sleep disturbances can occur in association with intoxication with the following classes of substances: alcohol; caffeine; cannabis; opioids; sedatives, hypnotics, 0r anxiolytics; stimulants (including cocaine); and other (or unknown) sub- stances. Prominent and severe sleep disturbances can occur in association with withdrawal from the following classes of substances: alcohol; caffeine; cannabis; opioids; sedatives, hypnotics, or anxiolytics; stimulant (including cocaine); tobacco; and other (or unknown) substances. Some medications that invoke sleep disturbances include adrenergic agonists and antagonists, dopamine agonists and antagonists, cholinergic agonists and antagonists, serotonergic agonists and antagonists, antihistamines, and corticosteroids.
Alcohol. Alcohol-induced sleep disorder typically occurs as insomnia type. During acute intoxication, alcohol produces an immediate sedative effect depending on close, ac- duced rapid eye movement (REM) sleep. Following these initial effects, there may be increased wakefulness, restless sleep, and vivid and anxiety-laden dreams for the remain- ing sleep period. In parallel, stages 3 and 4 sleep are reduced, and wakefulness and REM sleep are increased. Alcohol can aggravate breathing-related sleep disorder. With habitual use, alcohol continues to show a short—lived sedative effect in the first half of the night, fol- lowed by sleep continuity disruption in the second half. During alcohol withdrawal, there is extremely disrupted sleep continuity, and an increased amount and intensity of REM sleep, associated frequently with vivid dreaming, which in extreme form, constitutes part of alcohol withdrawal delirium. After acute withdrawal, chronic alcohol users may con- tinue to complain of light, fragmented sleep for weeks to years associated with a persistent deficit in slow-wave sleep.
Caffeine. Caffeine-induced sleep disorder produces insomnia in a dose-dependent man- ner, with some individuals presenting with daytime sleepiness related to withdrawal.
Cannabis. Acute administration of cannabis may shorten sleep latency, though arous- ing effects with increments in sleep latency also occur. Cannabis enhances slow-wave sleep and suppresses REM sleep after acute administration. In chronic users, tolerance to the sleep-inducing and slow-wave sleep—enhancing effects develops. Upon withdrawal, sleep difficulties and unpleasant dreams have been reported lasting for several weeks.
during this phase.
Opioids. Opioids may produce an increase in sleepiness and in subjective depth of sleep, and reduced REM sleep, during acute short-term use. With continued administration, tol- erance to the sedative effects of opioids develops and there are complaints of insomnia.
Consistent with their respiratory depressant effects, opioids exacerbate sleep apnea.
Sedative, hypnotic, or anxiolytic substances. Sedatives, hypnotics, and anxiolytics (e.g., barbiturates, benzodiazepines receptor agonists, meprobamate, glutethimide, methypry-
Ion) have similar effects as opioids on sleep. During acute intoxication, sedative-hypnotic drugs produce the expected increase in sleepiness and decrease in wakefulness. Chronic use (particularly of barbiturates and the older nonbarbiturate, nonbenzodiazepine drugs) may cause tolerance with subsequent return of insomnia. Daytime sleepiness may occur.