The contribution of alcohol, thiamine deficiency and cirrhosis of the liver to cerebral cortical damage in alcoholics.
The relative roles of alcohol toxicity, thiamine deficiency and cirrhosis of the liver in the pathogenesis of alcohol-related brain damage are unclear. Brain shrinkage and neuronal loss from four regions of the cortex was determined in 22 alcoholics with the Wernicke-Korsakoff Syndrome (WKS), cirrhosis of the liver or neither of these complications and compared to 22 age-matched non-alcoholic controls. Brain shrinkage was most marked in those alcoholics with WKS. Neuronal loss occurred only from the superior cortex and was of equal magnitude in all alcoholic subgroups. In an animal model of alcohol abuse and thiamine deficiency, neuronal loss from the cerebral cortex occurred in a time-dependent manner. Furthermore, those cells which contained the calcium-binding protein parvalbumin appeared to be preferentially damaged in this model.
Kril
J J
JJ
Department of Anatomical Pathology, Royal Prince Alfred Hospital, Camperdown, Australia.
D000437:Alcoholism / Q000150:complications / Q000473:pathology*; D001925:Brain Damage, Chronic / Q000209:etiology; D001927:Brain Diseases / Q000209:etiology* / Q000473:pathology; D002452:Cell Count; D002540:Cerebral Cortex / Q000473:pathology*; D000431:Ethanol / Q000009:adverse effects; D005625:Frontal Lobe / Q000473:pathology; D006801:Humans; D008104:Liver Cirrhosis, Alcoholic / Q000473:pathology*; D009044:Motor Cortex / Q000473:pathology; D009929:Organ Size; D013832:Thiamine Deficiency / Q000473:pathology*; D014899:Wernicke Encephalopathy / Q000473:pathology
D000431:Ethanol