Substance/Medication-Induced Sleep Disorder

Substance/medication-induced sleep disorder is a sleep disorder characterized by a severe change to sleeping patterns enough to warrant independent clinical attention and judged to be primarily caused by the pharmacological effects of a substance (i.e., a drug of abuse, a medication, toxin exposure). Depending on the substance involved, one of four types of sleep disturbances is reported. Insomnia type and day time sleepiness type are most common, while parasomnia-type is seen less often. The mixed type is noted when more than one type of sleep disturbance-related symptom is present and none predominates. As discontinuation/withdrawal states for some substances can be protracted, onset of the sleep disturbance can occur 4 weeks after cessation of substance use, and the disturbance may have features atypical of other sleep disorders (e.g., atypical age at onset or course).

Risk Factors
  • Sleep disturbances with substance intoxication and/or withdrawal: alcohol, caffeine, cannabis, opioids, sedatives (hypnotics or anxiolytics), tobacco, stimulants (such as cocaine), and other substances.
  • Certain medications such as adrenergic agonists/antagonists, dopamine agonists/antagonists, cholinergic agonists/antagonists, serotonergic agonists/antagonists, antihistamines, and corticosteroids can also cause sleep disturbances.
Criterion A

A prominent and severe disturbance in sleep.

Criterion B

There is evidence from time history, physical examination, or laboratory findings of both (1) and (2):

  1. The symptoms in Criterion A developed during or soon after substance intoxication or after withdrawal from or exposure to a medication.
  2. The involved substance/medication is capable of producing the symptoms in Criterion A.
Criterion C

The disturbance is not better explained by a sleep disorder that is not substance/medication-induced. Such evidence of an independent sleep disorder could include the following:

  • The symptoms precede the onset of the substance/medication use
  • The symptoms persist for a substantial period of time (e.g. - about 1 month) after the cessation of acute withdrawal or severe intoxication, or
  • There is other evidence suggesting the existence of an independent non-substance/medication-induced sleep disorder (e.g. - a history of recurrent non-substance/medication-related episodes)
Criterion D

The disturbance does not occur exclusively during the course of a delirium.

Criterion E

The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.


Specify if:

  • Insomnia type: Characterized by difficulty falling asleep or maintaining sleep, frequent nocturnal awakenings, or non-restorative sleep.
  • Daytime sleepiness type: Characterized by predominant complaint of excessive sleepiness/fatigue during waking hours or, less commonly, a long sleep period.
  • Parasomnia type: Characterized by abnormal behavioural events during sleep.
  • Mixed type: Characterized by a substance/medication-induced sleep problem characterized by multiple types of sleep symptoms, but no symptom clearly predominates.

Specify if:

  • With onset during intoxication: This specifier should be used if criteria are met for intoxication with the substance/medication and symptoms developed during the intoxication period.
  • With onset during discontinuation/withdrawal: This specifier should be used if criteria are met for discontinuation/withdrawal from the substance/medication and symptoms developed during, or shortly after, discontinuation of the substance/medication.

Onset Specifier

Specify if: (see Table 1 in the DSM-5 chapter “Substance-Related and Addictive Disorders” for diagnoses associated with substance class):

  • With onset during intoxication: This specifier should be used if criteria are met for intoxication with the substance/medication and symptoms developed during the intoxication period.
  • With onset during discontinuation/withdrawal: This specifier should be used if criteria are met for discontinuation/withdrawal from the substance/medication and symptoms developed during, or shortly after, discontinuation of the substance/medication.

Alcohol-induced sleep disorder typically occurs as insomnia type. During acute intoxication, alcohol produces an immediate sedative effect depending on dose, accompanied by increased stages 3 and 4 non-rapid eye movement (NREM) sleep and reduced rapid eye movement (REM) sleep. Following these initial effects, there may be increased wakefulness, restless sleep, and vivid and anxiety-laden dreams for the remaining 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, followed 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 continue to complain of light, fragmented sleep for weeks to years associated with a persistent deficit in slow-wave sleep.

While there are many functional consequences associated with sleep disorders, the only unique consequence for substance/medication-induced sleep disorder is increased risk for relapse. The degree of sleep disturbance during alcohol withdrawal (e.g., REM sleep rebound predicts risk of relapse of drinking). Monitoring of sleep quality and daytime sleepiness during and after withdrawal may provide clinically meaningful information on whether an individual is at increased risk for relapse.

Caffeine-induced sleep disorder produces insomnia in a dose-dependent manner, with some individuals presenting with daytime sleepiness related to withdrawal.

Acute administration of cannabis may shorten sleep latency, though arousing 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. Polysomnography studies demonstrate reduced slow-wave sleep and increased REM sleep during this phase.

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, tolerance to the sedative effects of opioids develops and there are complaints of insomnia. Consistent with their respiratory depressant effects, opioids exacerbate sleep apnea.

Sedatives, hypnotics, and anxiolytics (e.g., barbiturates, benzodiazepines receptor agonists, meprobamate, glutethimide, methyprylon) 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 non-barbiturate, non-benzodiazepine 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 apnea events.

Parasomnias are associated with use of benzodiazepine receptor agonists, especially when these medications are taken at higher doses and when they are combined with other sedative drugs. Abrupt discontinuation of chronic sedative, hypnotic, or anxiolytic use can lead to withdrawal but more commonly rebound insomnia, a condition of an exacerbation of insomnia upon drug discontinuation for 1-2 days reported to occur even with short-term use.

Sedative, hypnotic, or anxiolytic drugs with short durations of action are most likely to produce complaints of rebound insomnia, whereas those with longer durations of action are more often associated with daytime sleepiness. Any sedative, hypnotic, or anxiolytic drug can potentially cause daytime sedation, withdrawal, or re bound insomnia.

Sleep disorders induced by amphetamine and related substances and other stimulants are characterized by insomnia during intoxication and excessive sleepiness during withdrawal. During acute intoxication, stimulants reduce the total amount of sleep, increase sleep latency and sleep continuity disturbances, and decrease REM sleep. Slow-wave sleep tends to be reduced. During withdrawal from chronic stimulant use, there is both prolonged nocturnal sleep duration and excessive daytime sleepiness. Multiple sleep latency tests may show increased daytime sleepiness during the withdrawal phase. Drugs like 34-methylenedioxyrnethamphetamine (MDMA or "ecstasy") and related substances lead to restless and disturbed sleep within 48 hours of intake; frequent use of these compounds is associated with persisting symptoms of anxiety, depression, and sleep disturbances, even during longer-term abstinence.

Chronic tobacco consumption is associated primarily with symptoms of insomnia, decreased slow-wave sleep with a reduction of sleep efficiency, and increased daytime sleepiness. Withdrawal from tobacco can lead to impaired sleep. Individuals who smoke heavily may experience regular nocturnal awakenings caused by tobacco craving.

Other substances/medications may produce sleep disturbances, particularly medications that affect the central or autonomic nervous systems (e.g., adrenergic agonists and antagonists, dopamine agonists and antagonists, cholinergic agonists and antagonists, serotonergic agonists and antagonists, anti histamines, corticosteroids).

  • Substance intoxication or substance withdrawal
  • Delirium
  • Other sleep disorders
  • Sleep disorder due to another medical condition