Clonidine attenuates opiate withdrawal syndrome, via reduction in catecholamine activity in the brain, most probably at the locus ceruleus. Clonidine and locus ceruleus lesions, in animals with alcohol dependency as with the opiates, modify alcohol withdrawal. Both alcohol loading and withdrawal from steady alcohol use alter catecholamines in man and animals. Clonidine's potential to treat alcoholics in withdrawal is reviewed. Several double blind studies showed clonidine, or similar analogues, to be somewhat superior to placebo in acute alcohol withdrawal. Major improvements were in pulse, blood pressure and composite alcohol withdrawal scores. Side effects were minor and mainly included mild sedation, or postural hypotension. In the only available published study clonidine compared reasonably well to a standard sedative in alcohol withdrawal, and greatly influential in plasma catecholamine levels. Other components of alcohol withdrawal, as seizures and hallucinations-delirium tremens have not been documented to change with clonidine. The alpha-2-adrenergic agonists in alcohol treatment seemed modestly effective for treatment of some parts of alcohol withdrawal. They represent a promising, novel, but still investigational approach. Additional data, particularly comparing them to the benzodiazepines, are needed before their potential in therapeutics can be assessed.