Brain atrophy and alcoholism.

Alcoholism has no satisfactory definition, yet no more useful term is available to describe chronic and deleterious over-consumption. Alcohol is mostly drunk for its pharmacological effects on the nervous system, so not surprisingly the brain is one of the organs that suffers most-along with the liver, which detoxifies the alcohol. The effects on the nervous system include direct intoxication, the consequences of withdrawal after habituation, cerebral vascular events, cere-bral trauma related to drunkenness, and the results of secondary nutritional deficiency and of liver disease. Atrophy of the brain is also difficult to define with precision, but radiological studies have shown a clear reduction in brain volume in many chronic alcoholics. This is at least partially reversible with abstinence. How far these changes may be correlated with defects of cerebral function remains to be established. Cerebral atrophy may be visualised by air encephalo-graphy' and by computed tomography24; both techniques show enlargement of the ventricles and widening ofthe sulci. These changes slowly resolve with prolonged abstinence." The rate of recovery of the shrinkage of the brain is too gradual for it to be explicable entirely in the terms of a return to normal in its content of water and electrolytes. Other mechanisms that might play a part include the regeneration of glial and neuronal proteins.4 Estimations of changes in cerebral water content by magnetic resonance imaging in alcoholics during alcohol withdrawal have yielded conflicting results. Besson and coworkers reported a decreased free water content during intoxication and an increase during withdrawal of alcohol.7 Smith and colleagues found the reverse-namely, that the brain became excessively hydrated during alcohol consumption and that abstinence led to its dehydration.8 Neuropathological studies in cerebral atrophy have been meagre in the extreme. An attempt to remedy this was recently made by Harper and Kril, who conducted a necropsy study on 26 patients with alcoholism in comparison with 44 controls.9 As an index of brain shrinkage they measured the size of the pericerebral space-that part of the intracranial volume not occupied by the brain. This space was found to be greater in the alcoholics, particularly in those with histological evidence ofWernicke's encephalopathy and in those with alcoholic liver disease. In Wernicke's encephalopathy the lesions have a predominantly periventricular distribution, mainly in the diencephalon and brain stem. These are associated with the classic clinical triad of cognitive dysfunction, ocular abnormalities , and ataxia; associated cerebral atrophy has been reported in …