TY - JOUR
T1 - Alcoholic organic brain disease
T2 - Nosology and pathophysiologic mechanisms
AU - Martin, Peter R.
AU - Adinoff, Bryon
AU - Weingartner, Herbert
AU - Mukherjee, Anil B.
AU - Eckardt, Michael J.
PY - 1986
Y1 - 1986
N2 - 1. 1. Study of alcoholic chronic organic brain syndrome may have applicability to the large population of alcoholics with less severe cerebral dysfunction. 2. 2. Brain Impairment in alcoholics may be conceptualized as two clinically and neuropathologlcally distinguishable organic brain syndromes: alcohol amnestic disorder or Korsakoff's psychosis (KP) and alcoholic dementia. 3. 3. Alcoholic organic brain disease may result from two interacting pathophysiological processes: nutritional (thiamine) deficiency and ethanol neurotoxicity. 4. 4. 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. 5. 5. 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. 6. 6. Studies in animals and humans suggest that a genetic predisposition to thiamine.
AB - 1. 1. Study of alcoholic chronic organic brain syndrome may have applicability to the large population of alcoholics with less severe cerebral dysfunction. 2. 2. Brain Impairment in alcoholics may be conceptualized as two clinically and neuropathologlcally distinguishable organic brain syndromes: alcohol amnestic disorder or Korsakoff's psychosis (KP) and alcoholic dementia. 3. 3. Alcoholic organic brain disease may result from two interacting pathophysiological processes: nutritional (thiamine) deficiency and ethanol neurotoxicity. 4. 4. 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. 5. 5. 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. 6. 6. Studies in animals and humans suggest that a genetic predisposition to thiamine.
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U2 - 10.1016/0278-5846(86)90069-2
DO - 10.1016/0278-5846(86)90069-2
M3 - Article
C2 - 2875490
AN - SCOPUS:0022479512
SN - 0278-5846
VL - 10
SP - 147
EP - 164
JO - Progress in Neuropsychopharmacology and Biological Psychiatry
JF - Progress in Neuropsychopharmacology and Biological Psychiatry
IS - 2
ER -