Abstract
Our increasing understanding of the neurobiology of the alcohol withdrawal syndrome has been accompanied by its safe and efficacious treatment. In this review, the biologic alterations that are associated with the signs and symptoms of withdrawal, and their relationship to current pharmacologic treatments, will be discussed. Potential long-term neurotoxic effects of alcohol withdrawal will also be reviewed. The role of the GABAK-benzodiazepine receptor complex, the N-methyl-D-aspartate (NMDA) receptor, the sympathetic nervous system, the hypotha-lamic-pituitary-adrenal axis, and limbic neuronal sensitization in the acute changes and persistent consequences of alcohol withdrawal will be the focus of this discussion. Potential treatment strategies based on these neurobiologic changes will be proposed.