Journal of Neurology, Neurosurgery, and Psychiatry 1983;46:593-598 The incidence of Wernicke's encephalopathy in Australia-a neuropathological study of 131 cases

SUMMARY In a nine year necropsy study in Western Australia, the incidence of Wernicke's encephalopathy was 2-8%. The incidence appears to be increasing. Although Wernicke's encephalopathy is a nutritional disorder, the majority of cases occur in the alcoholic population. Only 20 % of the 131 cases studied had been diagnosed clinically as Wernicke's encephalopathy. This large discrepancy between numbers of cases diagnosed clinically and pathologically suggests that chronic Wernicke's encephalopathy, which comprised 83 % of the cases, may be the end result of repeated subclinical episodes of Wernicke's encephalopathy. Thus, Wernicke's encephalopathy could be considered a "progressive " disorder and as patients respond well to thiamine replacement therapy, early diagnosis is important. Alternatively, prevention by vitamin enrichment of alcoholic beverages may have to be considered in an attempt to minimise the social and economic impact of Wernicke's encephalopathy on Western society. Clinical and pathological studies throughout Australia indicate a high, and probably rising, inci-dence of a potentially preventable disease caused by thiamine (vitamin B1) deficiency-Wemicke's encephalopathy or the Wemicke-Korsakoff syn-drome.'-5 A similar trend is apparent in other West-ern civilisations67 and probably exists even in Third World countries8 though largely overlooked because of lack of formal epidemiological studies. Although Wemicke's encephalopathy is caused by a nutri-tional deficiency of thiamine, it is seen today almost exclusively in the alcoholic population.'9 From a clinical point of view, the traditional triad of confu-sion, ataxia and ophthalmoplegia will only be evi-dent in a small percentage of cases and the diagnosis has been unsuspected prior to death in a significant proportion of cases.'01 ' In the acute stage of Wer-nicke's encephalopathy, there is a dramatic response to parenteral thiamine. Thus, this disease is poten-tially preventable and the group at risk an obvious one, although not readily accessible