Glutamatergic function, particularly that mediated by the N-methyl-D-aspartate (NMDA) receptor, has been implicated in the pathophysiology of alcohol dependence. Preclinical and human laboratory studies of memantine, an NMDA-receptor channel blocker, suggest that it may reduce alcohol consumption.
We conducted an 8-week, open-label study of memantine to examine its potential utility in promoting reduced drinking or abstinence in 20 alcohol-dependent individuals (mean age=50.1 y, 12 women). Memantine was administered orally, initially at a dosage of 5 mg/d, with weekly increases of 5 mg/d to a target dosage of 20 mg/d. Subjects also received 7 coping skills therapy sessions.
Most subjects (n=16 or 80%) achieved the maximal dosage and completed treatment (n=17 or 85%). Memantine was generally well tolerated, with no serious adverse events. During the course of the study, subjects reported significantly reduced drinking days, heavy drinking days, and mean drinks/wk, and also reduced urge to drink and alcohol-related consequences (all P's<0.02).
Memantine at a dosage of 20 mg/d is well tolerated in alcohol-dependent individuals. Because it is not possible from this study to draw a firm conclusion regarding the efficacy of memantine to reduce drinking, further evaluation of the medication as a treatment for alcohol dependence is warranted.
*Alcohol Research Center, Department of Psychiatry, University of Connecticut School of Medicine
‡Department of Psychiatry, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-2103
†Department of Psychiatry, Yale University, West Haven, CT 06516
Supported by NIH grants P50 AA03510, M01 RR06192, and K24 AA13736 (to HRK).
Reprints: Henry R. Kranzler, MD, Department of Psychiatry, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-2103 (e-mail: firstname.lastname@example.org).