A Note on Rem Rebound during Experimental Alcohol Withdrawal in Alcoholics

Abstract

Until recently the effect of alcohol on rapid eye movement sleep (REM) appeared to be a relatively simple and clear aspect of the complicated relationship between alcohol and sleep. In normals, alcohol, even in moderate amounts, reduced REM (Gresham et al., 1963, Yules et al., 1966, Knowles et al., 1968). This was followed by a transient increase in REM, a “REM rebound,” and return to baseline. When increased REM was observed in patients in acute alcohol withdrawal, this was assumed to be a manifestation of the REM rebound following the reduction of REM by the alcohol (Gross et al., 1966, Greenberg and Pearlman, 1967, Gross and Goodenough, 1968, Johnson et al., 1970). Patients in delirium tremens were often observed to have very considerable increases of REM and a level of 100% REM was reported in several instances (Gross et al., 1966, Greenberg and Pearlman, 1967, Johnson et al., 1970). Under experimental conditions, alcoholics appeared to have the REM reduction during alcohol intake and transient REM rebound when alcohol intake was stopped (Greenberg and Pearlman, 1967, Gross et al., 1971, Gross et al., 1973a, Gross et al., 1973b). The high levels of REM observed clinically during alcohol withdrawal in alcoholics were assumed to be quantitative effects of more alcohol intake for longer periods of time than the alcohol administered to normals or experimentally given to alcoholics. There was no evidence that there might be anything more complex in the REM differences between normals and alcoholics than the alcoholics’ ability to tolerate greater alcohol intake, and thereby, produce greater REM reduction and subsequent rebound. The REM reduction and rebound effects appeared to be shared by the other sedative-hypnotics.

Supported by NIAA Grant AA01236