Alcoholic organic brain disease: nosology and pathophysiologic mechanisms.
Study of alcoholic chronic organic brain syndrome may have applicability to the large population of alcoholics with less severe cerebral dysfunction. Brain impairment in alcoholics may be conceptualized as two clinically and neuropathologically distinguishable organic brain syndromes: alcohol amnestic disorder or Korsakoff's psychosis (KP) and alcoholic dementia. Alcoholic organic brain disease may result from two interacting pathophysiological processes: nutritional (thiamine) deficiency and ethanol neurotoxicity. Subcortical periventricular lesions associated with KP result primarily from thiamine deficiency, whereas ethanol neurotoxicity and various secondary effects of alcoholism may contribute to the cortical neuropathological changes associated with alcoholic dementia. These two patterns of brain damage may be differentiable in individual alcoholics using cognitive tests and other measures of CNS function and, therefore, allow selection of a treatment strategy based on pathophysiological considerations. Studies in animals and humans suggest that a genetic predisposition to thiamine deficiency may contribute to alcoholism-associated dysfunction of brain and other organ systems and possibly have a causative role in the development of alcoholism.
D000425:Alcohol Amnestic Disorder / Q000209:etiology / Q000378:metabolism; D000437:Alcoholism / Q000145:classification / Q000150:complications* / Q000503:physiopathology; D001921:Brain / Q000503:physiopathology; D003704:Dementia / Q000209:etiology; D005947:Glucose / Q000378:metabolism; D006801:Humans; D018377:Neurotransmitter Agents / Q000378:metabolism; D009748:Nutrition Disorders / Q000150:complications; D019966:Substance-Related Disorders / Q000145:classification / Q000209:etiology* / Q000503:physiopathology; D014055:Tomography, Emission-Computed
D018377:Neurotransmitter Agents; D005947:Glucose