This work was supported by Center Grant 5 P50 AA07378 from the National Institute on Alcohol Abuse and Alcoholism. This study was presented in part at the annual meetings of the Research Society on Alcoholism in Washington, D.C., in June 1996 and in San Francisco, CA, in July 1997.
Polysomnographic and Subjective Sleep Predictors of Alcoholic Relapse
Article first published online: 30 MAY 2006
Alcoholism: Clinical and Experimental Research
Volume 22, Issue 8, pages 1864–1871, November 1998
How to Cite
Brower, K. J., Aldrich, M. S. and Hall, J. M. (1998), Polysomnographic and Subjective Sleep Predictors of Alcoholic Relapse. Alcoholism: Clinical and Experimental Research, 22: 1864–1871. doi: 10.1111/j.1530-0277.1998.tb03995.x
- Issue published online: 30 MAY 2006
- Article first published online: 30 MAY 2006
- Received for publication April I, 1998; accepted August 3, 1998
- Alcohol Dependence;
Previous studies indicate that subjectively reported and objectively measured sleep abnormalities at baseline can increase the risk of relapse in treated alcoholics. However, previous studies did not include both subjective and objective sleep measures in the same group of patients. We utilized polysomnography and the Sleep Disorders Questionnaire to determine if baseline polysomnography increased the ability to predict relapse beyond the prediction with subjective measures alone, after controlling for nonsleep variables that were associated with relapse. We followed 74 patients with a DSM-III-R diagnosis of alcohol dependence, of whom 36 relapsed to at least some drinking during an average follow-up interval of 5 months. Univariate analyses revealed that relapsed patients did not differ from abstinent patients at baseline in demographics or psychiatric co-morbidity, but they had more prior treatment episodes for alcoholism, more difficulty falling asleep, more complaints of abnormal sleep, and, on polysomnography, longer sleep latencies, shorter rapid eye movement sleep latencies, and less stage 4 sleep percentage than abstinent patients. With a series of logistic regression analyses, which controlled for age and gender, we demonstrated that sleep measures improved the prediction model compared with non-sleep variables alone, and that polysomnography-measured sleep latency was the most significant predictor variable. We conclude that subjective and objective measures of baseline sleep are predictors of relapse in treated alcoholic patients. These data also suggest that neurophysiological dysfunction contributes strongly to the etiology of relapse. Finally, sleep disturbance warrants clinical attention as a target of alcoholism treatment.