The clinical presentation of brain damaged alcoholics is heterogenous and includes minimal cognitive impairment, amnesia and dementia. Whichever neurobiological technique is used, eg neuropathology, structural and functional neuroimaging, the clinico-pathological evidence suggests that thiamine malnutrition, affecting the diencephalon, can account for all clinical forms. Alcohol neurotoxicity can cause neuronal damage in cerebral cortex and can contribute to cognitive impairment but there is little direct evidence to support the need for a distinct clinical category of alcoholic dementia. Most organic brain syndromes in alcoholics therefore can be considered as variants of the Wernicke-Korsakoff syndrome and rigorous attention should be paid to the nutritional status of all alcoholics.
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Eileen M. Joyce (1994) studied this question.