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).
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 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 (1988) compared two protocols in which hypnotic drugs were withdrawn from two groups of five chronic users each, one before and one after receiving behavioral therapies. Patients in whom drugs were withdrawn early in treatment achieved a better outcome on sleep-onset latency than those in whom drugs were withdrawn after behavioral therapy.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.
Although behavioral interventions are not always as effective for patients using hypnotic medications as for unmedicated patients (Morin et al. 1994a; Riedel et al. 1998), some studies have reported substantial reductions (45%-80%) in hypnotic use among behaviorally treated insomnia patients (Dashevsky and Kramer 1998; Lichstein and Johnson 1993; Morin et al. 1994b), even though treatment did not specifically focus on reducing hypnotic use.
In a study of benzodiazepine discontinuation in 76 older adults with insomnia (Morin et al. 1998), all three treatment conditions (medication taper alone, cognitive-behavioral therapy alone, and combined taper plus cognitive-behavioral therapy) produced significant reductions (>90%) in both the quantity and the frequency of benzodiazepine use at the end of a 10-week intervention. At posttreatment, 72% of the patients were drug-free, and this proportion was higher in the combined condition (82%) compared with the medication taper alone (71%) or the cognitive-behavioral therapy alone condition (61%). Sleep was slightly improved at posttreatment and more so among patients who received cognitive-behavioral therapy. Treatment benefits were well maintained at 3- and 12-month follow-ups for both the frequency and the quantity of medication used; however, the proportion of patients who were still drug-free decreased to 68% at the 3-month follow-up and 50% at the 12-month follow-up.
As a general rule, the most cost-effective intervention in treating drug-dependent insomnia is to implement a systematic medication-tapering schedule concurrently with cognitive-behavioral therapy (Morin 1993). Cognitive therapy is particularly useful in helping patients reappraise withdrawal symptoms typically associated with discontinuation of short-acting benzodiazepines. Improvements of sleep patterns are usually delayed by a few weeks after the medication is discontinued, and it is particularly important to build in “booster sessions” to prevent relapse after the completion of treatment.
Pharmacological management of substance-induced sleep disorders depends primarily on accurate history taking. This will permit the clinician to identify the sleep-disturbing substance. The diagnosis of substance-induced sleep disorder is confirmed, and treatment best instituted, by withdrawing the offending substance and observing a return to baseline sleep quality.
Several principles can guide the clinician through this process. First, when the individual is using several substances or medications, the clinician should target one substance at a time, leaving the others constant. This is the best way to identify the specific substance that is responsible for the complaints. Second, virtually all medications that affect sleep should be discontinued gradually rather than suddenly. Third, adequate time must be permitted after withdrawal to allow sleep to return to baseline values. For instance, after withdrawing benzodiazepine or antidepressant medications, sleep may not return to baseline for 1-2 weeks. Fourth, the clinician may substitute another, similar medication for the original to determine whether sleep symptoms recur. For instance, a patient having severe nightmares while taking propranolol may not develop symptoms when treated with atenolol, a less lipophilic β-blocker. Finally, the clinician may, in specific circumstances, observe the patient as a single case study, using an on-off-on treatment design. In this way, the specific effect of a substance on sleep can be isolated more definitively.
In some cases, adjusting the timing of medications may be sufficient to alleviate the symptoms of a substance-induced sleep disorder. For instance, a patient who is sensitive to the stimulating effects of theophylline preparations may be able to continue this medication if it is administered earlier in the day. As noted above, it may also be possible to substitute related medications for one that is suspected of causing a sleep disturbance.
Specific medications are usually not indicated for the treatment of substance-induced sleep disorder, but exceptions clearly occur. Most notably, patients who are undergoing withdrawal from barbiturate or alcohol abuse must be treated for their abstinence syndrome, which often includes substance-induced sleep disorder. In these cases, the use of a long-acting benzodiazepine (for alcohol) or a long-acting barbiturate (for barbiturate withdrawal) not only treats symptoms but also can actually prevent life-threatening seizures and other withdrawal symptoms.
Revision date: July 9, 2011
Last revised: by Andrew G. Epstein, M.D.