sleep difficulties and unpleasant dreams have  been reported lasting for several weeks.
Polysomnography studies demonstrate reduced slow-wave sleep and increased REM sleep
during this phase.
Opioids. Opioids may produce an increase in sleepiness and in subjective depth of sleep,
and reduced REM sleep, during acute short-te rm use. With continued administration, tol-
erance to the sedative effects of opioids de velops and there are co mplaints 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 agon ists, meprobamate, glutethimide, methypry-
lon) have similar effects as opioids on sleep. During acute intoxication, sedative-hypnotic
drugs produce the expected incr ease in sleepiness and decrea se in wakefulness. Chronic
use (particularly of barbiturates and the ol der nonbarbiturate, no nbenzodiazepine drugs)
may cause tolerance with subsequent return  of insomnia. Daytime sleepiness may occur.
Sedative-hypnotic drugs can increase the frequency and severity of obstructive sleep ap-
nea events. Parasomnias are associated with us e of benzodiazepine receptor agonists, es-
pecially when these medications are taken at  higher doses and when they are combined
with other sedative drugs. Ab rupt discontinuation of chronic sedative, hypnotic, or anx-
iolytic use can lead to withdrawal but mo re commonly rebound insomnia, a condition of
an exacerbation of insomnia upon drug disc ontinuation for 1–2 days reported to occur