Abstract

The spectrum and time course of different symptoms during alcohol withdrawal may be caused by the involvement of various neurotransmitter systems that are differentially vulnerable to the effects of ethanol. Withdrawal symptomatology results from increased activity of excitatory mechanisms (NMDA-receptor, catecholamines among others) and from reduced functioning of inhibitory receptors (GABAA-, alpha 2-adreno-receptor among others). The neuronal mechanisms are subject to different dynamics of restitution following intoxication. Some of these probably contribute to long-lasting changes in CNS functions by "kindling" processes. Therapeutic guidelines are deduced from results of basic research and clinical trials. It is concluded that clomethiazole and benzodiazepines are superior in treating delirium tremens and certain risk-patients, whereas carbamazepine and clonidine may be helpful in moderate withdrawal syndromes or as adjunctive agents. However, the need for improved methodological standards of method in clinical research is evident.