An autopsy case of acute and nonalcoholic thiamine-deficient encephalopathy.

unwitnessed interval by family was approximately 1 day, and the patient did not have a habit of drinking alcohol. A medicolegal autopsy revealed severe pyloric stenosis with dilatation of the stomach ( fig. 1 a, b). Histologic examination showed proliferation and invasion of atypical cells with glandular formation, suggestive of moderately differentiated adenocarcinoma ( fig. 1 c). Metastasis of tumor cells was seen in many of the circumferential lymph nodes, but not in other organs. Because of the amount of gastric contents filling the upper airway, the direct cause of death was considered to be asphyxia due to aspiration. There was also a small abscess in the right upper lung lobe. The brain weighed 1,350 g and, macroscopically, no significant atrophy was seen in the cerebrum, cerebellum, or brain stem. On coronal sections of the cerebrum, bilateral mammillary bodies showed petechial and local hemorrhage without obvious brown discoloration and atrophy ( fig. 2 a). The third ventricle was mildly dilated, and the folia of the superior vermis and dorsomedial portion of the cerebellar hemispheres were not atrophic ( fig. 2 b). On light microscopy, fresh petechial hemorrhages were prominent with some foci of proliferation of immature small Dear Sir, Thiamine deficiency can cause a severe neurological disorder known as Wernicke’s encephalopathy (WE). While this encephalopathy is considered common in alcoholics [1] , only a small number of nonalcoholic cases have been reported [2–5] . The important pathological and radiological features of thiamine-deficient encephalopathy are the selective vulnerability of specific brain regions to pathologic changes [6] . We report a case of autopsy-proven acute nonalcoholic thiamine-deficient encephalopathy without medical treatment antemortem.