By Robert S.; Thimann, Kenneth V.; Marrian, G. F. Harris
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No satisfactory conclusion is reached. There is some evidence to suggest that the condition may be benefited by large doses of niacinamide intravenously. The syndrome appears when the niacin and riboflavin intake in a community is low. Deficiency of these substances may, therefore, play a major part in the production of the syndrome. There is recent evidence which has yet to be confirmed, that deficiency of pantothenic acid is responsible for the syndrome. IV. WERNICKE’SENCEPHALOPATHY I . ” In Wernicke’s original description the presenting features were ocular paralysis, a reeling gait, and disturbances of consciousness.
They claimed to have cured other patients with large doses of the B complex but did not give details. b. Experimental Evidence. On the experimental side, evidence was also being brought forward in favor of thiamine deficiency as the etiological factor. Pappenheimer and Goettsch (1931) produced foci of edema, necrosis, and petechial hemorrhage, limited to the cerebellum, in chicks fed on a diet deficient in thiamine. The intake of “vitamin B2” was adequate. Prickett (1934), and later Church (1935) made similar observations in rats fed on a thiamine-free diet.
At the same time the electrolyte and fluid balance must be adjusted by appropriate measures and thereafter a properly balanced high calorie, high vitamin diet given when possible. When treatment is initiated early, recovery should be complete, but if delayed, there may be disappearance of the vomiting and ocular manifestations, with persistence of the mental changes. 5. Summary There is good evidence that Wernicke’s encephalopathy results from acute thiamine deficiency. The dominant pathological lesions are focal hemorrhages in the brain stem most marked in the corpora mamillaria and frequently involving the peri-aqueductal gray matter including the oculomotor nuclei.
Advances in Research and Applications by Robert S.; Thimann, Kenneth V.; Marrian, G. F. Harris