Key points are not available for this paper at this time.
The salient clinical features of Wernicke's syndrome (1) are partial to complete paralysis of extra-ocular muscles (most commonly the external recti), nystagmus, ataxia and mental disturbances. Postmortem examination reveals changes in the nervous structures adjacent to the third and fourth ventricles and the aqueduct. The lesions are characterized by varying degrees of necrosis of both nerve cells and nerve fibers with appropriate reactions of microglia and astrocytes, alteration of the small blood vessels, and in some cases, petechial hemorrhages (2-5). The syndrome is usually associated with chronic alcoholism and for that reason has sometimes been attributed to a neurotoxic effect of the alcohol; but the occurrence of the same clinical sequence in non-alcoholic patients with malnutrition (1, 2, 4-8) has directed attention to nutritional deficiency as the etiological basis. Moreover, similar pathological lesions have been produced in the rat (9, 10), fox (11, 12), and pigeon (3, 9, 13, 14), by maintaining these animals on thiamine-deficient diets.
Phillips et al. (Wed,) studied this question.