Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Author has noticed bilateral ophthalmoplegia in consequence of B1 avitaminosis due to alcoholism. Recognition of the cerebral beriberi with ophthalmoplegia as a leading symptom (Wernicke's encephalopathy) is easy. The importance of the diagnosis is that this life threatening condition can be abolished promptly by the administration of Vitamin B1. On the basis of the frequent occurrence of alcoholism it seems likely, that several similar beriberi cases could be found nowadays.
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PMID:[Cerebral beriberi with ophthalmoplegia as the leading symptom in an alcoholic patient]. 195 87

Wernicke's encephalopathy has been associated rarely with fasting. We describe a middle-aged patient who presented in a subacute fashion with features of thiamin deficiency after marked weight reduction. Associated features were chest pain, possibly related to cardiac involvement, and a proximal myopathy. The Wernicke-Korsakoff syndrome has been described in the literature for around 100 years. However, the classic triad of ataxia, ophthalmoplegia and impaired conscious state that occurs in a person with chronic alcoholism is by no means its exclusive presentation.
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PMID:Wernicke's encephalopathy after prolonged fasting. 373 79

Thirty-two cases of Wernicke's encephalopathy were admitted to hospital for treatment in a period of 33 months; this represented a relatively low incidence in total hospital admissions. Thiamin status was deficient, borderline and normal in 21 (66%), five (16%) and six (19%) patients, respectively, and responded immediately to treatment in those who had abnormal thiamin status. Ophthalmoplegia responded rapidly to treatment. Nystagmus, ataxia, disturbance of mental function and peripheral neuropathy responded incompletely to treatment in both the short-and the long-term. The overall setting for the development of Wernicke's encephalopathy appears to be chronic alcohol abuse, accompanied by cerebral "atrophy" and liver disease, but often without gross evidence of malnutrition.
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PMID:Wernicke's encephalopathy in a metropolitan hospital. A prospective study of incidence, characteristics and outcome. 394 14

Thiamine deficiency is known to lead to certain neurological sequelae including Wernicke- Korsakoff encephalopathy. Signs attributable to this condition include ataxia, ophthalmoplegia, nystagmus, and mental confusion. Recognised predisposing conditions include alcoholism gastric carcinoma, pyloric obstruction, hyperemesis gravidarum, and prolonged intravenous feeding. We have recently encountered two cases of Wernicke's encephalopathy after vertical banded gastroplasty for morbid obesity . Other neurological sequelae are recognised after vertical banded gastroplasty, including Guillain-Barre syndrome, psychosis, and pseudoathetosis, but the causes are multifactorial.
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PMID:Wernicke's encephalopathy after vertical banded gastroplasty for morbid obesity. 863 78

Wernicke's encephalopathy (WE) is most commonly associated with alcoholism, although other causes have also been implicated. In the years 1994-1997, 9 patients with no history of alcohol abuse presented with acute signs of ophthalmoplegia or nystagmus and ataxia which resolved within 48 h after intravenous thiamine. There were 7 women and 2 men aged 17-57 (7 below the age of 30). Precipitating events included vomiting 2, drastic weight-reducing diet 2, renal colic in a postpartum woman 1, colonic surgery 2 and chronic hemodialysis 1. In 2 patients there was no obvious precipitating event but their history was suggestive of a genetic predisposition. Mental changes were slight or absent in all patients and all of them made good functional recovery. These cases suggest that the diagnosis of WE should be considered more often in nonalcoholics in various clinical settings.
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PMID:Thiamine-responsive acute neurological disorders in nonalcoholic patients. 1115 Aug 38

A 55-years-old man with a history of alcoholism, hypertension and obesity was diagnosed of epidermoid carcinoma of the middle third portion of the esophagus. He was treated with two cycles of cytostatics with cisplatin and 5-fluorouracil. Due to his poor general health an inability to swallow solids and liquids, he received parenteral nutrition for 20 days using a commercial formula lacking in vitamins and minerals. During distal esophagectomy we observed a tendency to hypotension and severe metabolic acidosis that was unexplained by the hemodynamic profile and that persisted throughout the first 24 hours after surgery. Once these complications were corrected, he was weaned from mechanical ventilation and the following neurological signs were observed: temporal and spacial disorientation, aphasia, ophthalmoplegia with divergent strabismus and later conduction aphasia, amnesia and confabulation. Circulation was hyperdynamic, requiring inotropics and vasoconstrictors. Korsakoff syndrome secondary to Wernicke's encephalopathy was diagnosed, and the response to thiamine treatment was favorable. Beriberi can be found in hospitalized patients and the anesthesiologist may be involved in their perioperative care. Symptoms resolve easily with vitamin B1 treatment, which is ideally provided along with other hydrosoluble vitamins. Treatment should be prompt because delay leads to greater morbiomortality.
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PMID:[Beriberi after esophagectomy]. 1267 75

Wernicke's encephalopathy (WE) is an acute neuropsychiatric condition due to thiamine deficiency (vitamin B1) most commonly associated with chronic alcohol abuse. WE is difficult to diagnose because the classical triad of signs (confusion, ataxia and ophthalmoplegia) occurs in only 10% of cases. The presentation is often one of a non-specific confusional state which may easily be attributed to intoxication, alcohol withdrawal or to a concurrent morbidity such as head injury. To improve the outcome, it is important to make a presumptive diagnosis of WE and treat the patients as soon as possible with high-dose parenteral thiamine. Patients with an alcohol problem associated with malnutrition should all be offered a preventive treatment with parenteral thiamine in view of the impaired oral thiamine absorption.
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PMID:[Prevalence, prophylaxis and treatment of Wernicke encephalopathy. Thiamine, how much and how do we give it?]. 1611 48

Wernicke described the clinical features of three patients, including two alcoholics, suffering from confusion, ataxia and ophthalmoplegia in whom pathologically he found 'polioencephalitis haemorrhagica superioris'. Korsakoff's doctoral thesis related similar findings but expanded the confabulation and amnesic elements, relating them to alcoholism. This paper, which summarises the salient aspects of the syndrome, discusses their work and shows important earlier descriptions by James Jackson, (1822) Samuel Wilks (1868) and Charles Gayet (1875).
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PMID:Wernicke-Korsakoff encephalopathy. 1793 84

While Wernicke's encephalopathy (WE) is a well-characterized syndrome in alcoholism and malnutrition, little is written of its prevalence or presentation in patients with psychiatric illness. We present a case of a 37-year-old Nigerian male with schizophrenia and malnutrition who presented with delirium and ophthalmoplegia. The clinical diagnosis was supported by dramatic reversal of the symptoms and signs following the administration of intravenous thiamine. Owing to the high rate of mortality and morbidity, WE should be considered in the evaluation of any patient with unexplained nystagmus, gaze palsies, gait ataxia, or confusion, especially if a condition associated with malnutrition is present. This is particularly important in psychiatric patients where the clinical history and syndrome may be obscured and treatment delayed.
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PMID:Wernicke's encephalopathy in a Nigerian with schizophrenia. 1835 48

Wernicke's encephalopathy is a syndrome characterized by ataxia, ophthalmoplegia, and confusion with thiamine deficiency. We reported on two Japanese brothers with a newly discovered recessively inherited syndrome similar to Wernicke's encephalopathy that developed in the second decade of life; this syndrome was manifested clinically as thiamine-responsive diplopia, ataxia and confusion without serum thiamine deficiency. The patients had complex partial seizure. The administration of high-dose thiamine improved these symptoms. MRI of the brain showed high-intensity signals in the bilateral medial thalamus and periaqueductal region on fluid-attenuated inversion recovery images; these signals were characteristic of findings in Wernicke's encephalopathy. There was no history of chronic alcoholism. The clinical and images features resembling Wernicke's encephalopathy in these patients suggested that the syndrome was caused by a genetic disorder of thiamine metabolism. Genomic analysis of SLC10A3 encoding human thiamine transporter 2 revealed that the patients were compound heterozygotes for the K44E and E320Q mutations. Gene-expression analyses of mammalian culture cells showed that intracellular thiamine uptake activities were decreased significantly. High expression of SLC19A3 RNA in the thalamus may explain the selective thalamic lesions on MRI. The identification of this syndrome proves insight into the thiamine metabolism associated with Wernicke's encephalopathy in humans.
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PMID:[Familial Wernicke's-like encephalopathy]. 2192 71


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