Substance-Induced Sleep Disorder

Substance-induced sleep disorder includes a prominent disturbance in sleep for which there is evidence from the history, physical examination, or laboratory findings of substance use, intoxication, or withdrawal. The diagnosis rests on temporal coincidence of substance use or withdrawal and the development of sleep symptoms. The sleep disturbance must cause significant distress or impairment and be severe enough to warrant independent clinical attention. The clinician should specify whether onset occurred during use of or withdrawal from a substance. Further, the clinician should specify the prominent type of symptom, whether insomnia, hypersomnia, parasomnia, or mixed type.

Many different drugs and medications can cause prominent sleep-related symptoms (Buysse 1991).

A list of the major substances causing sleep disorders is shown in Table 89-5. The occurrence of sleep disturbances related to these substances may vary among individuals. A dose or duration of drug use that causes symptoms in one individual may not cause similar symptoms in another. Such differences may ultimately relate to individual physiological differences. For instance, Merlotti et al. (1991) showed that the severity of "rebound insomnia" after short-term treatment with benzodiazepines varies as a function of baseline sleep efficiency. In the specific case of benzodiazepine withdrawal, dose may also play a role in the development of withdrawal insomnia; higher doses of short-acting agents lead to more substantial rebound (Roehrs et al. 1986b). Finally, factors related to the mode of administration or withdrawal may affect symptoms associated with substance-induced insomnia. For instance, Greenblatt et al. (1987) noted that even with short-acting benzodiazepines, gradual tapering of the dose leads to fewer withdrawal symptoms.

Behavioral/Psychotherapeutic Treatment

Behavioral interventions for substance-induced sleep disorder have focused exclusively on hypnotic-dependent insomnia. Espie et al. (1988) compared two protocols in which hypnotic drugs were withdrawn from two groups of five chronic users each, one before and one after receiving behavioral therapies. Patients in whom drugs were withdrawn early in treatment achieved a better outcome on sleep-onset latency than those in whom drugs were withdrawn after behavioral therapy. Four of the 10 patients (1 in early withdrawal and 3 in late withdrawal), however, had resumed use of hypnotic medications at 1-year follow-up evaluation. These results suggest that substitution of behavioral therapy for drug treatment may be effective in the short term, but that follow-up sessions are critical in preventing relapse.

In another study, conducted with 12 hypnotic-dependent women (Kirmil-Gray et al. 1985), stress management and a brief consultation were both effective in eliminating medication use in an average of 8 weeks. Although sleep improvements were modest at posttreatment, possibly because of persisting rebound effects, subjects receiving stress management showed greater improvements in sleep and mood than those receiving a brief consultation that focused exclusively on medication withdrawal.