Brain Atrophy in Alcoholics

Abstract

Chronic alcoholics are at risk of developing several neurological alterations, such as the Wernicke–Korsakoff syndrome, the so-called alcoholic dementia, related to brain atrophy, cerebellar atrophy, and less frequently, the Marchiafava–Bignami syndrome, central pontine myelinolysis, and alcohol and tobacco-related amblyopia, in addition to the acute ethanol toxicity, various neurological syndromes related to withdrawal, and a higher incidence of stroke and head trauma. Although pathogenesis is still obscure, cytokine-mediated neuroinflammation and oxidative damage play a role in brain atrophy of uncomplicated alcoholics. In addition, thiamine deficiency, directly involved in the Wernicke–Korsakoff syndrome, and alterations in vitamins A, C, and, especially, vitamin E, related to oxidative damage, may contribute to brain damage. Iron excess, frequently observed in alcoholics, acting as a pro-oxidant, and deficiencies in selenium and zinc, involved in antioxidative capacity, have also been described as pathogenic factors, as is also the case of protein malnutrition, partly a consequence of poor nutrition and the irregular lifestyle of chronic alcoholics. Neuronal death by excitotoxicity, particularly related to binge-drinking episodes, is another mechanism responsible for neurocognitive impairment and brain atrophy in alcoholic patients. Finally, several reports also suggest that patients with chronic liver disease also present neurocognitive impairment independent of alcohol intake. Therefore, pathogenesis of this frequent complication of the alcoholic patient is multifactorial and incompletely understood.