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 and Korsakoff's psychosis represent a continuum of the same pathologic process. The etiology is an absolute deficiency of thiamine rather than a direct toxic effect of alcohol. The triad of Wernicke's encephalopathy--global confusional state, ophthalmoplegia and nystagmus, and ataxia--is occasionally seen in chronic alcoholics and is often attenuated by immediate thiamine treatment. The triad of Korsakoff's psychosis--memory loss, learning deficits and confabulation--may be seen in either the acute or the long-term care setting.
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PMID:The Wernicke-Korsakoff syndrome. 742 67

We report the case of a 34-year old patient who first complained of fever, confusion and transient ophthalmoplegia and then developed akinetic mutism, frontal lobe, pyramidal tract and extrapyramidal signs. Clinical and electrophysiological data support a diagnosis of encephalitis lethargica. Magnetic resonance imaging showed hyperintensive lesions in various brain regions. The patient responded to corticosteroid treatment. Two years after the onset of the first clinical signs he had recovered completely and today, after 5 years, he shows no sign of disease.
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PMID:[Encephalitis lethargica]. 750 Oct 95

A case of subacute progressive painful external ophthalmoplegia of the right eye in a 55-year-old woman is reported. CT scan of the brain, paranasal sinuses and orbits revealed normal findings. Tolosa-Hunt syndrome was diagnosed and high dose prednisolone was given. The patient later developed fever, confusion and stiffneck. Lumbar puncture showed grossly purulent CSF with Gram-positive coccobacilli and rod organism. CSF culture grew Nocardia spp. The patient made a complete recovery with trimethoprim-sulfamethoxazole treatment.
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PMID:Unusual manifestation in a case of nocardial meningitis. 796 40

Wernicke's encephalopathy, neuropathy caused by a deficiency of thiamine is a syndrome characterized by memory troubles, mental confusion, ophthalmoplegia and nystagmus. The authors present a case that came up in a patient who underwent a subtotal gastrectomy because of malignant neoplasm of the stomach. More or less three months after the intervention the patient's general conditions were considerably declined and characterised by alimentary vomit, sensory obnubilation and neuromuscular deficit. After appropriate diagnostic ascertainments a repetition of the neoplastic disease was to be excluded locally and at a distance. So the authors analysed the different etiopathogenic possibilities to get a better clinical view of the syndrome in the surgical patient.
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PMID:Wernicke's encephalopathy post subtotal extended gastrectomy. 854 60

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 a neuropsychiatric disorder caused by thiamine (vitamin B1)-deficiency. WE is most commonly seen among patients with alcohol abuse, and thiamine deficiency is here caused by several factors, among others inadequate diet, insufficient gastrointestinal absorption and enzymatic abnormalities. The syndrome, however, is also seen among non-alcoholic, undernourished patients, e.g. certain patients with cancer or AIDS. The diagnosis WE has traditionally been given when the triad of confusion, ataxia and ophthalmoplegia was present. However, it should be recognised, that these three symptoms are not always present at the same time, partly because the mental symptoms often dominate and cloud, possible ocular abnormalities and ataxia. The syndrome is, according to the author's opinion, still underdiagnosed. The treatment of WE, consisting of large doses of intravenous thiamine, is effective and safe, and therefore it is important to be aware of WE among risk-patients, especially among patients with alcohol abuse, and to institute treatment with intravenous thiamine at the slightest suspicion.
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PMID:[Wernicke's encephalopathy]. 863 25

We describe a novel, biotin-responsive basal ganglia disease in 10 patients. At onset, it appears as a subacute encephalopathy, with confusion, dysarthria and dysphagia with occasional supranuclear facial nerve palsy or external ophthalmoplegia, and progresses to severe cogwheel rigidity, dystonia and quadriparesis. These symptoms disappear within a few days if biotin (5-10 mg/kg/day) is administered, and there are no neurological sequelae. They reappear within 1 month if biotin is discontinued. Patients diagnosed late, or who have had repeated episodes, suffer from residual symptoms such as paraparesis, mild mental retardation or dystonia. The numerous biochemical studies of intermediary metabolism, like the autoimmune and toxicological studies, enzyme assays including biotinidase, carboxylase and lysosomal activities, and bacterial and viral studies were all normal. The aetiology may be related to a defect in the transporter of biotin across the blood-brain barrier. The only consistent radiological abnormality was central necrosis of the head of the caudate bilaterally and complete, or partial, involvement of the putamen on brain MRI. This was present during the initial acute encephalopathy and remained unchanged during follow-up of 3-10 years. Although its aetiology is unknown, it is important to recognize this disease, since its symptoms may be reversed and the progression of its clinical course prevented simply by providing biotin.
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PMID:Biotin-responsive basal ganglia disease: a novel entity. 967 79

Hemodialysis(HD) patients are at risk for thiamine deficiency because of low intake and accelerated loss of thiamine during HD. We report here an HD patient, an 82-year-old woman, who developed acute encephalopathy due to thiamine deficiency with hyperammonemia. She was admitted to Nishikawa Town Hospital due to pneumonia and was treated with ABPC/SBT for one week. While she was cured of pneumonia, she had a persistently poor appetite. On the twenty-fourth day after admission, HD with intradialytic parenteral nutrition(IDPN), which consisted of 10% glucose 500 ml, in order to correct her malnutrition, was started. She suddenly presented confusion, speech disturbance and ophthalmoplegia. HD with IDPN was stopped after two hours because of her symptoms. Laboratory studies disclosed plasma glucose of 186 mg/dl and serum ammonium of 155 micrograms/dl. Arterial blood gas analysis(inhaling 3 l/min O2) showed severe metabolic acidosis and respiratory acidosis (pH 7.138, pCO2 44.8 mmHg, pO2 108.9 mmHg, HCO3- 15.1 mmol/l). Her malnutrition, unexplained metabolic acidosis and neurological presentation raised the suspicion of acute encephalopathy due to thiamine deficiency. Fursultiamine 100 mg was administered intravenously. After two hours, metabolic acidosis disappeared (pH 7.437, pCO2 33.9 mmHg, pO2 161.0 mmHg, HCO3- 22.9 mmol/l), and she regained her clear consciousness and serum ammonium decreased at 16 micrograms/dl on the next morning. Serum lactate and thiamine level were shown later to be 57.5 mg/dl and 27 nmol/l, respectively. Her clinical course suggests that the glucose load including IDPN may have caused deterioration of the neurological disorder under the condition of thiamine deficiency. Furthermore, it is possible that a relationship exists between thiamine deficiency and hyperammonemia.
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PMID:[Acute encephalopathy due to thiamine deficiency with hyperammonemia in a chronic hemodialysis patient: a case report]. 1280 78

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

Pituitary apoplexy is an uncommon syndrome characterised by sudden onset of headache, meningeal signs, visual disturbances, ophthalmoplegia and confusion. Documented recurrent apoplexy or treated apoplexy is even rarer with only few reports in the literature. Between 1994 and 2001, 18 patients were treated for pituitary apoplexy at Bayindir Medical Centre through transsphenoidal route. In all, topical bromocriptine was applied after tumour resection as described by Ozgen. We hereby present the cases of two patients with recurrent apoplexy 3 and 7 years after the initial surgical treatment for pituitary adenoma with apoplexy. The patients were treated non-surgically with success. Additional treatment in the form of radiosurgery was found necessary for the first patient. Surgical excision of the pituitary tumours with apoplexy reduces the risk of recurrent bleedings but eradication is not a rule. These patients need to be followed closely in the postoperative period for possible recurrence of bleeding.
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PMID:Late recurrent bleeding after surgical treatment for pituitary apoplexy. 1517 12


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