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At least 19 recordsLinked to original sources
PubMed1977

[Gayet-Wernicke encephalopathy].

We have reviewed the aetiology, symptomatology, biology and clinical course of 61 cases of the Gayet-Wernicke encephalopathy. Our results do not differ fundamentally from those of Victor et al. (1971). Nevertheless, our study shows fewer oculomotor palsies in the acute stages, lower mortality and a lower incidence of residual anmesic syndromes. These results demonstrate the importance of early diagnosis and of starting the specific therapy in the initial stage of reversible biochemical lesions.

Adult↗
PubMed1976

Wernicke encephalopathy following prolonged intravenous therapy.

Two nonalcoholic patients who were maintained for extended periods on intravenous fluids manifested the morphologic expressions of Wernicke encephalopathy. A thiamine-deficiency state was not suspected and vitamins were never administered. These cases emphasize the consequences of this disorder and the rapidity with which the state of thiamine depletion can develop.

Aged↗
PubMed1975

Wernicke's encephalopathy: an experimental study in the rhesus monkey.

Experimental Wernicke's encephalopathy, induced in rhesus monkeys with a diet lacking thiamine (vitamin B1), is characterized by cavitary necrosis of the striatum as well as a microvacuolar periventricular lesion of the brain stem such as occurs in man. With high resolution light microscopy and electron microscopy, the primary structural alteration in the brain stem lesion, and probably also in the striatum, appears to be that of widespread "blister" formation due to splitting of myelin at the intraperiod line. Microvascular alterations were minimal, even in the most severely affected regions. It is the myelin blisters which give rise to the spongy texture of the neuropil. A similar splitting of myelin has been described in several other experimental encephalopathies, and it is probable that it also occurs in Wernicke's encephalopathy in man.

Animals↗
PubMed1978

Thermolability in Wernicke's encephalopathy.

A patient with signs of Wernicke's disease had low body temperature and showed thermolability when challenged with cold and heat. This man expressed no feelings of thermal discomfort about his persistently low core temperature or about induced changes in his core temperature. He also showed abnormalities in his febrile response to pyrogen and in his circadian temperature rhythm. Treatment with thiamine hydrochloride resulted in substantial improvement in these thermoregulatory deficits.

Alcoholism↗
PubMed1992

Coma and death in unrecognized Wernicke's encephalopathy. An autopsy study.

Eleven out of 36 autopsied cases of Wernicke's encephalopathy had developed coma. None of these patients had the diagnosis during life. There were six men and five women with ages ranging from 26 to 50 years (mean 36.6). Seven of these patients were heavy drinkers, three exhibited signs of severe malnutrition, whereas one was being evaluated for a disseminated gastric cancer and one was in treatment of hyperemesis gravidarum. Two patients were brought to the hospital after found unconscious at home. Neuropathological examination disclosed gross changes in the mammillary bodies in eight cases and microscopic changes in all cases. In one case there was atrophy of the anterior superior part of the vermis. Petechial hemorrhages were observed particularly in the walls of the third ventricle. Microscopically there were in addition to hemorrhages, glial proliferation, endothelial hypertrophy and necrosis of nerve cells and myelin. Central pontine myelinolysis was observed in one case. Wernicke's encephalopathy is a clinically underdiagnosed condition. Coma may mask its classical clinical picture or even be the sole manifestation. Although coma points to a poor outlook it may be reversed by thiamine administration. Any patient with coma of unknown etiology should be given parenteral thiamine.

Adult↗
PubMed1979

Wernicke's encephalopathy: a more common disease than realised. A neuropathological study of 51 cases.

During a four year peirod, 51 cases of Wernicke's encephalopathy were diagnosed at necropsy, an incidence of 1.7% of all necropsies performed at the Royal Perth Hospital and by the Perth City coroner. Only seven had been diagnosed during life. Many of the patients died suddenly and unexpectedly, apparently as a result of haemorrhagic brainstem lesions, typical of acute Wernicke's encephalopathy, since no other cause of death was found. There was a high incidence of epilepsy and four patients were hypothermic. The diagnosis of Wernicke's encephalopathy may be missed at necropsy unless the brain is examined histologically. Cerebral atrophy and ventricular dilatation were common findings. This is a more common disease than is generally recognised, one which can be readily treated and, more importantly, prevented by adequate nutrition.

Adult↗
PubMed1977

[Excessive hyperplasia of the exocrine pancreatic tissue and Wernicke's encephalopathy (author's transl)].

A 52 year old woman with a history of mild pancreatitis had a palpable mass in the upper abdomen. She died in an unexplained coma. The autopsy revealed an excessive hyperplasia of the exocrine pancreatic tissue resulting in the largest pancreas ever reported (254 gramm). This hyperplasia was accompanied by a chronic pancreatitis. In the central nervous system a Wernick's encephalopathy had developed; severe loss of neurons was stated in the thalamus; extensive degeneration was found in the upper vermis of the cerebellum. The discussion of this case includes the relationship between the diseases of the pancreas and neuropsychiatric and neuropathologic findings. It is assumed that the hyperplasia of the exocrine pancreatic tissue could only be an additional factor in the occurence of post alcoholic complications. This hyperplasia of the exocrine pancreatic tissue is considered to be a hamartom-like formation and it should therefore be distinguished from other pancreatic hyperplasia.

Diagnosis, Differential↗