Substance/Medication-Induced Sleep Disorder 417
Alcohol. Alcohol-induced sleep disorder typica lly occurs as insomnia type. During
acute intoxication, alcohol produces an immedi ate sedative effect depending on dose, ac-
companied by increased stages 3 and 4 non– rapid eye movement (NREM) sleep and re-
duced rapid eye movement (REM) sleep. Following these initial e ffects, 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 br eathing-related sleep disorder. With habitual
use, alcohol continues to show a short-lived sedati ve 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 drea ming, which in extreme form, constitutes part
of alcohol withdrawal delirium. After acut e 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 latenc y 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–enha ncing effects develops. Upon withdrawal,
sleep difficulties and unpleasant dreams have  been reported lasting for several weeks.