By Robert S.; Thimann, Kenneth V.; Marrian, G. F. Harris
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Since there was no history of alcoholism, he suggested endogenous toxins elaborated in an abnormally functioning gut with liver damage preventing adequate detoxication, as the cause. In the discussion he considered nutritional deficiency as a possible cause, but discarded the idea in favor of the toxin theory. By 1939, however, the view that thiamine deficiency was an important factor in the production of Wernicke’s encephalopathy was gaining ground and was supported by Ecker and Woltman (1939), who reported one case where there were associated signs of nutritional defi- 30 ERIC K.
The gait in severe cases is slow and hobbling on account of the pain, but there is no mode of progression that can be regarded as typical of the condition. d. Cardiovascular System. Tachycardia at rest may occur but the heart rate is usually within normal limits. An interesting feature of the syndrome in some reported series (Cruickshank, 1946; Harrison, 1946; and Smitskamp, 1947) is hypertension of a moderate degree appearing during the course of the syndrome. It may be present in from 10 to 20 % of cases and is usually found in severe long-standing sufferers.
The histological findings in the brain of these animals were small, symmetrical, punctate hemorrhages in the floor of the fourth ventricle, in the corpora quadrigemina, in certain nuclei ventral and lateral to the aqueduct of Sylvius, in the thalamus, and in certain parts of the cerebral cortex; and, therefore, very similar t o the changes in the rats observed by Prickett (1934) and Church (1935). Alexander and his colleagues (1938,1940), by feeding pigeons a diet deficient in thiamine but otherwise adequate, produced pinpoint hemorrhages within areas of subacute necrosis in the paraventricular and paramedian nuclei of the thalamus and in the nuclei of the eye muscles, with significant regularity.