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)

Wernicke's encephalopathy (WE) is a neuropsychiatric condition generally caused by acute thiamine deficiency and classically involves the triad of altered mentation, ataxia and ophthalmoplegia. It is most common among alcoholics, but several other causes have been identified, including total parenteral nutrition (TPN) use. We present eight cases of WE in patients undergoing allogeneic BMT, where thiamine deficiency was caused by a lack of vitamin supplementation during TPN administration. Clinically, WE presented as a severe refractory metabolic acidosis, preceded by 'raspberry tongue', and ophthalmologic and neurologic dysfunction. The sites most affected were the periventricular structures and the thalamus, and no mammilary bodies lesions were found.
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PMID:Iatrogenic Wernicke's encephalopathy in allogeneic bone marrow transplantation: a study of eight cases. 933 55

Wernicke's encephalopathy is an uncommon disorder caused by a thiamine deficiency which is clinically characterized by the triad of ophthalmoplegia, ataxia and disturbances of consciousness, each finding being variably present. The disease is caused by malnutrition or malabsorption, and is often associated with prolonged alcohol intake, neoplasm and extensive inflammatory processes of the digestive tract and parenteral hyperalimentation-induced gastrointestinal mucosal atrophy. Clinical diagnosis can be elusive and MRI may be the only imaging technique able to detect the cerebral lesions, whose type and distribution are characteristic of the Wernicke's encephalopathy, whereas CT is positive only in exceptional cases. We report a case of a 56-year-old woman who developed a Wernicke's encephalopathy 1 month after a colonic resection with signal intensity changes located in the mammillary bodies and in the medial thalamic nuclei.
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PMID:Magnetic resonance imaging in a case of Wernicke's encephalopathy. 968 4

Two rare cases of Wernicke's encephalopathy (WE) in non-alcoholic patients on hemodialysis (HD) are reported. They presented with the clinical triad of WE (ophthalmoplegia, ataxia and disturbance of consciousness) and intravenous administration of thiamine led to complete elimination of these manifestations. Reduced plasma thiamine levels prior to the administration confirmed the diagnosis of WE. Interestingly, a reduction in plasma thiamine levels by about half was seen in one of the patients on HD, suggesting that thiamine, a water-soluble vitamin, can be depleted with HD. In the literature, nine HD-dependent patients have been reported to develop WE, seven of whom were diagnosed postmortem. Their premortem diagnoses included uremic encephalopathy, dysequilibrium syndrome and dialysis dementia, which can often complicate HD and present symptoms similar to those of WE. We therefore emphasize that WE, even though a rare complication, should be suspected in all patients on HD who present with at least one of the clinical triad of WE.
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PMID:Wernicke's encephalopathy associated with hemodialysis: report of two cases and review of the literature. 1046 8

A 34-year-old woman presented with bilateral ophthalmoplegia, ptosis, and mild gait ataxia. Tensilon test, magnetic resonance imaging, and cerebrospinal fluid analysis were normal. She initially denied any alcohol intake but later admitted to significant alcohol and multisubstance abuse. The patient improved dramatically after treatment with thiamine. Wernicke's encephalopathy is discussed, highlighting that it may be present with normal mentation. It should be considered in the differential diagnosis of bilateral ophthalmoplegia even in the absence of altered mental status.
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PMID:Acute bilateral ophthalmoplegia in a young woman. 1090 82

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 is a serious neurologic disorder caused by vitamin-B1 or thiamine deficiency. The classical triad of clinical symptoms described by Wernicke (gait ataxia, ophthalmoplegia, and confusion) are found in only a third of patients upon initial examination. Typical findings upon MR imaging in patients with Wernicke's encephalopathy are well documented, with signal intensities in the medial thalami and periaqueductal regions of the midbrain. We report a case of Wernicke's encephalopathy revealing an unusual contrast enhancement. It is therefore important to note that the acute stage of Wernicke's encephalopathy may be associated with an intense contrast enhancement upon MR-imaging reflecting the disruption of the blood-brain barrier and inflammatory processes caused by thiamine deficiency. As a consequence from the guideline for managing Wernicke's encephalopathy by the Royal College of Physicians early B-vitamin treatment in suspected is recommended cases.
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PMID:Wernicke's encephalopathy: unusual contrast enhancement revealed by magnetic resonance imaging. 1464 3

Postoperative complications and nutritional deficits resulting from bariatric surgery can lead to severe vitamin-deficiency states, such as Wernicke's encephalopathy (WE). Patients with acute WE generally present with the classic clinical triad of inattentiveness, ataxia, and ophthalmoplegia. We describe a patient who presented with acute WE at 2 months after laparoscopic bariatric surgery. Initial MRI of the brain demonstrated the characteristic injuries of WE, and repeat imaging showed resolution after 4 months of thiamine supplementation, at which time the patient had normal gait but persistent memory deficits. Even with early recognition and aggressive therapy, acute WE commonly results in permanent disability due to the irreversible cytotoxic effects on specific regions of the brain. Since the clinical onset of acute WE follows a predictable time-course in post-bariatric surgery patients with malnutrition, we recommend prevention by administration of parenteral thiamine beginning at 6 weeks postoperatively in malnourished patients.
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PMID:Acute Wernicke's encephalopathy following bariatric surgery: clinical course and MRI correlation. 1498 48

Wernicke encephalopathy consists of a triad of ophthalmoplegia, ataxia, and altered mental status. It is caused by thiamine deficiency and although it is commonly seen in alcoholics, patients undergoing gastric bypass surgery for morbid obesity could be a new group of patients to watch for. Florid papilloedema and optic neuropathy are not commonly seen but are still consistent with the diagnosis of Wernicke encephalopathy. The most striking feature remains the dramatic recovery after replacement of thiamine.
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PMID:You are what you eat. 1596 92

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


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