Which clinical history findings are characteristic of substance-induced sleep disorders?

Updated: Oct 09, 2018
  • Author: Sufen Chiu, MD, PhD; Chief Editor: Caroly Pataki, MD  more...
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Substance-induced sleep disorder most commonly occurs during intoxication with substances such as alcohol, amphetamine and related substances, caffeine, cocaine, opioids and sedatives, hypnotics, or anxiolytics. Substance-induced sleep disorder can also occur in association with withdrawal from these same classes of substances. Patients may report that the substance is used to trreat a primary sleep disorder.

Diagnostic criteria for substance-induced sleep disorder include the following:

  • Prominent disturbance in sleep that is sufficiently severe to warrant independent clinical attention

  • Evidence from the history, physical examination, or laboratory findings of both (1) symptoms that developed during or soon after substance intoxication or withdrawal and (2) medication use that is etiologically related to the sleep disturbance

  • Disturbance that is not better accounted for by a sleep disorder that is not substance induced or occurs exclusively during the course of delirium.

Evidence that the symptoms are better accounted for by a sleep disorder that is not substance induced might include the following:

  • Symptoms preceding the onset of the substance use (or medication use).

  • Symptoms persisting for a substantial period (eg, about 1 month) after the cessation of acute withdrawal or severe intoxication

  • Symptoms that are substantially in excess of what would be expected from the type or amount of the substance used or the duration of use, or the presence of other evidence suggesting an independent non–substance-induced sleep disorder

Alcohol-induced sleep disorder typically occurs as the insomnia type. Alcohol, which often facilitates sleep onset, can lead to decreased REM sleep and sleep disruption. Acute intoxication initially results in increased sleepiness and reduced wakefulness for 3–4 hours.

An increase in stages 3 and 4 of NREM sleep is a typical feature of this initial stage. After these initial effects, the individual experiences increased wakefulness, restless sleep, and, often, vivid and anxiety-laden dreams during the second half of the night. In addition, alcohol can increase the number of obstructive sleep apnea events and result in fragmented sleep. With continued habitual use, alcohol continues to show a short-lived sedative effect for several hours, followed by sleep continuity disruption for several hours.

During alcohol withdrawal, sleep architecture is grossly disturbed. Sleep tends to be fragmented and accompanied by an increase in the amount and intensity of REM sleep. Vivid dreams often accompany this stage of sleep.

During the period of acute intoxication, amphetamines produce sleep disruption associated with increased sleep latency, reduced total sleep time, fragmented sleep, an increase in body movements, and a decrease in REM sleep. Slow-wave sleep tends to be reduced. During withdrawal from long-term amphetamine use, hypersomnia with prolonged nocturnal sleep duration and excessive daytime sleepiness tends to be the rule.

Caffeine-induced sleep disorder is characterized by insomnia during intoxication and by hypersomnia and excessive daytime sleepiness during withdrawal. Caffeine is known to result in increased wakefulness and sleep fragmentation, which may be documented on PSG as prolonged sleep latency, multiple arousals, and a decrease in slow-wave sleep. Lack of awareness of the long half-life of caffeine and its metabolities, up to 15 hours, contribute to this disorder. As discussed earlier, caffeine-related products contribute to esophageal reflux, which can disrupt sleep.

Short-term use of opioids produces increased sleepiness and reduced REM sleep. Insomnia and frequent arousals become common with prolonged use. Opioid withdrawal generally produces symptoms and signs of CNS hyperactivity, though some patients may report hypersomnia.

Use of sedative-hypnotic medications produces an increase in sleepiness and PSG findings of decreased REM sleep and an increase in sleep-spindle activity. On the other hand, long-term use of sedatives may be accompanied by symptoms of insomnia and tolerance to these medications. Patients may be reluctant to discontinue use of these medications even though insomnia has relapsed due to perceived benefit for anxiety.

Withdrawal from sedative-hypnotics and anxiolytics is associated with anxiety and insomnia. The manifestation of withdrawal symptoms depends on the half-life of the drug used. Withdrawal from drugs with short half-lives typically produces insomnia. Medications with long half-lives are associated with symptoms of excessive sedation during their use.

Heavy adult users of cannabis have reduced REM and slow wave sleep (SWS), increased sleep latency, and increased vulnerability to sleep deprivation effects. During abstinence, there are PSG changes. [16] Cannabis use in adolescents is on the decline but may increase with states legalizing it for medicinal and recreational purposes. Adolescents who use cannabis show functional decline in sleep quality, with similar changes in sleep as those seen in adult users. [17] Adult users of cannabis often have early-morning sleepiness, which would exacerbate the common problem of adolescent daytime sleepiness during the first 2 periods of school.

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