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 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

We report a clinical and neuroradiological description of a severe case of Wernicke's encephalopathy in a surgical patient. After colonic surgery for neoplasm, he was treated for a long time with high glucose concentration total parenteral nutrition. In the early post-operative period, the patient showed severe encephalopathy with ataxia, ophthalmoplegia and consciousness disorders. We used magnetic resonance imaging (MRI) to confirm the clinical suspicion of Wernicke's encephalopathy. The radiological feature showed hyperintense lesions which were symmetrically distributed along the bulbo-pontine tegmentum, the tectum of the mid-brain, the periacqueductal grey substance, the hypothalamus and the medial periventricular parts of the thalamus. This progressed to typical Wernicke-Korsakoff syndrome with ataxia and memory and cognitive defects. Thiamine deficiency is a re-emerging problem in non-alcoholic patients and it may develop in surgical patients with risk factors such as malnutrition, prolonged vomiting and long-term high glucose concentration parenteral nutrition.
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PMID:Wernicke's encephalopathy in a malnourished surgical patient: clinical features and magnetic resonance imaging. 1622 8

Acute Wernicke's encephalopathy (WE) is caused by profound vitamin B1 (thiamine) deficiency and commonly presents with the classic clinical triad of mental confusion, ataxia, and ophthalmoplegia. This characteristic presentation results from the propensity of acute thiamine deficiency to preferentially injure specific brain regions: the dorsomedial thalamus, periaqueductal gray, and mamillary bodies. In these regions, abnormal magnetic resonance signaling on conventional sequences has been well described; however, diffusion restriction has only recently been reported. The authors demonstrate diffusion-weighted imaging (DWI) abnormalities of the splenium of the corpus callosum in a patient with acute WE, which has not been reported previously, and suggest a potential pathological mechanism. With the recent addition of DWI, MRI is becoming more sensitive to the changes in acute WE. Furthermore, the use of apparent diffusion coefficient mapping to evaluate the extent of likely underlying cytotoxic injury may help determine long-term response to vitamin therapy and, thus, disability.
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PMID:Restricted diffusion of the splenium in acute Wernicke's encephalopathy. 1625 4

A 42-year-old woman presented with lowered consciousness, ataxia and ophthalmoplegia; MRI of the brain revealed abnormalities compatible with Wernicke encephalopathy (thiamine deficiency).
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PMID:[Diagnostic image (360). A woman with lowered consciousness]. 1832 12

Wernicke's encephalopathy is caused by thiamine deficiency, and is characterized by acute mental confusion, ataxia, and ophthalmoplegia. It is also a rare neurologic complication of hematopoietic stem cell transplantation (HSCT). However, because of its rare incidence, Wernicke's encephalopathy can easily be overlooked in HSCT patients, and a few misleading steps in the early stage of the disease may result in permanent neurologic disability or even mortality. We recently encountered a case of Wernicke's encephalopathy in a patient who underwent allogeneic HSCT. Based on our own experience and previously published documents, we suggest early radiologic surveillance and treatment for patients with findings compatible with Wernicke's encephalopathy following HSCT.
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PMID:Wernicke's encephalopathy following allogeneic hematopoietic stem cell transplantation. 2125 32

The clinical presentation of beriberi can be quite varied. In the extreme form, profound cardiovascular involvement leads to circulatory collapse and death. This case report is of a 72 year-old male who was admitted to the Neurology inpatient ward with progressive bilateral lower extremity weakness and parasthesia. He subsequently developed pulmonary edema and high output cardiac failure requiring intubation and blood pressure support. With the constellation of peripheral neuropathy, encephalopathy, ophthalmoplegia, unexplained heart failure, and lactic acidosis, thiamine deficiency was suspected. He was empirically initiated on thiamine replacement therapy and his thiamine level pre-therapy was found to be 23 nmol/L (Normal: 80-150 nmol/L), consistent with the diagnosis of beriberi. Cardiovascular magnetic resonance (CMR) showed severe left ventricular systolic dysfunction, markedly increased myocardial T2, and minimal late gadolinium enhancement (LGE). After 5 days of daily 100 mg IV thiamine and supportive care, the hypotension resolved and the patient was extubated and was released from the hospital 3 weeks later. Our case shows via CMR profound myocardial edema associated with wet beriberi.
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PMID:Cardiovascular magnetic resonance in wet beriberi. 2183 1

Wernicke's encephalopathy (WE) is a severe neurological disorder caused by thiamine deficiency. Clinically, it is most frequently observed in people with alcohol abuse. WE, however, can occur in any clinical condition associated with malnutrition or thiamine deficiency. We present the case of a 47-year-old woman with prolonged therapeutic fasting who presented with ophthalmoplegia, ataxia and deep coma. MRI showed unusual symmetric cortical abnormalities in the frontal and parietal lobes, as well as typical lesions surrounding the third ventricle and aqueduct. Although the patient entered a vegetative state, she finally regained consciousness after thiamine supplementation unexpectedly. To the best of our knowledge, it has never been reported to date that the patient with WE in a vegetative state with cortical damage shows a marvelous prognosis, which prompts us to report this case. In the present report, we highlight the role of MRI in the diagnosis of acute WE.
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PMID:Wernicke's encephalopathy in a patient with acute pancreatitis: unusual cortical involvement and marvelous prognosis. 2191 77

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

Morbid obesity is a curable systemic disease that can cause several complications, including hypertension, diabetes mellitus, and osteoarthritis. However, it is not easy to control solely by conservative management. Bariatric surgeries, such as sleeve gastrectomy and gastric banding, are recently developed treatments that are applied to patients with morbid obesity in Korea. However, gastric surgery can cause surgical or metabolic complications, such as thiamine deficiency, which can lead to Wernicke's encephalopathy. This metabolic complication presents with typical symptoms of confusion, ophthalmoplegia, nystagmus, and ataxia. In this case report, we present a case of Wernicke's encephalopathy, which developed slowly following sleeve gastrectomy in a patient with morbid obesity.
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PMID:Wernicke's Encephalopathy after Sleeve Gastrectomy for Morbid Obesity - A Case Report -. 2250 78

The incidence of neurologic complications from bariatric surgery is rising with the prevalence of obesity and the increasing number of bariatric surgeries. We report a 25-year-old woman who developed subacute progressive weakness and areflexia followed by confusion, ophthalmoplegia, and nystagmus following bariatric surgery. While the differential of generalized weakness with altered mental status is broad, vitamin deficiency should be routinely suspected after bariatric surgery to prevent permanent neurological injury. Multifocal neurological dysfunction in our patient represented beriberi and Wernicke's encephalopathy related to vitamin B1 deficiency.
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PMID:Dry Beriberi and Wernicke's encephalopathy following gastric lap band surgery. 2252 60


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