Effects of alcohol withdrawal on sleep
Chronic alcohol users have significant problems with their sleep during detoxification; the withdrawal syndrome manifests as hyperactivity, a lowered seizure threshold, and worsening sleep disruption, usually starting within 2 days after the last drink. During this subacute withdrawal period, some alcoholics have marked difficulty with sleep-onset insomnia, a subsequent decrease in total sleep time, and a higher REM density during the first REM period compared with healthy control subjects, at the expense of decreased slow wave sleep (Gillin et al. Biol Psych. 1990;27[5]:477). The prevalence of insomnia can be as high as 58% in chronic alcoholics during the first week of acute alcohol withdrawal. Untreated alcoholics can progress from withdrawal into delirium tremens, characterized by increased adrenergic activity, delirium, agitation, and hallucinations. The sleep of these patients is very disturbed with polysomnographic features of wakefulness alternating with REM sleep without atonia mixed into light sleep (which has been called stage 1-REM); slow wave sleep tends to be absent during this period (Lugaresi et al. Sleep Med. 2011;12[suppl 2]: S3). The hallucinations that are commonly reported during alcohol withdrawal and delirium tremens may represent an intrusion of REM sleep into wakefulness, similar to what is seen in narcoleptics.
Sleep in alcoholics during protracted abstinence from alcohol
After 1-2 months of sobriety, the sleep of alcoholics is characterized by an increased sleep latency and increases in stage 1, 2, and REM sleep with continued impairment in slow wave sleep, although the intrusion of REM features into wakefulness usually resolves. Sleep continuity continues to be affected with significant increases in the number of nocturnal awakenings and decreased sleep efficiency. Although these polysomnographic abnormalities can attenuate over time, a persistence of fragmented sleep with decreased deep sleep and increased REM sleep has been reported even years after abstinence (Drummond et al. Alcohol Clin Exp Res. 1998;22[8]:1796). Such persistent disturbances may predict the risk of relapse to alcoholism by impeding normalization of quality of life among quitters; patients with subjective sleep complaints have been shown to resume drinking at significantly higher rates. Optimization of sleep latency and sleep quality using pharmacologic agents may forestall relapse; gabapentin is one promising therapeutic agent to treat insomnia in these patients since it inhibits the release of excitatory neurotransmitters and can promote sleep. Furthermore, gabapentin is not metabolized by the liver and has no known abuse potential, in contrast to benzodiazepines and other drugs used as hypnotics; patients treated with gabapentin have shown subjective improvement in their sleep quality and may be more likely to remain abstinent (Mason et al. Addict Biol. 2009;14:73), though more studies are needed to evaluate the benefits of this drug in preventing relapse. Cognitive-behavioral therapy for insomnia in abstinent alcohol-dependent patients has shown subjective improvement in sleep efficiency compared with placebo (Arnedt et al. Behav Res Ther. 2011;49[4]:227). Despite the improvements in the sleep quality of these patients, cognitive-behavioral therapy had no significant impact on the rate of relapse to alcohol.
Summary
Alcohol has a deleterious effect on sleep, which can be long lasting, even after protracted periods of sobriety. Continued abstinence from alcohol can improve but may not normalize sleep. Early diagnosis and treatment of sleep disorders, especially insomnia, should be prioritized, as it may prevent the development of alcoholism in healthy subjects and prevent relapse among previously alcohol-dependent patients.
Francoise Roux, MD, PhD, FCCP
Yale University
Pulmonary, Critical Care and Sleep Section
Department of Internal Medicine
Yale University School of Medicine
New Haven, Connecticut
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