Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 28-year-old woman with inoperable gastric carcinoma was given continuous infusion of 5-fluorouracil (5-FU) and low-dose cisplatin (CDDP) for 4 weeks while receiving intravenous hyperalimentation (IVH). Eleven days after her last treatment, she developed acute diplopia, deafness and gait ataxia, followed by severe confusion. She became markedly acidotic and hypotensive with a systolic blood pressure of 60 mmHg, necessitating intubation, dopamine treatment and hemodialysis for 7 h. She was also given thiamine. Thereafter, her blood pressure stabilized, the acidosis improved, and her deafness, diplopia, and confusion were resolved. This case suggests that FP (5-FU/CDDP) therapy toxicity, manifested as acute metabolic acidosis and Wernicke's encephalopathy, may be associated with IVH and thiamine deficiency.
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PMID:Severe acute metabolic acidosis and Wernicke's encephalopathy following chemotherapy with 5-fluorouracil and cisplatin: case report and review of the literature. 876 81

A 28-year-old man presented with a bilateral visual loss of acute onset, and was diagnosed as having optic neuropathy by an ophthalmologist. It disappeared spontaneously within 2 months. A visual loss at the left side relapsed ten months later, followed by a dysarthria, horizontal defective saccade, ataxia, and mild weakness of four extremities, which also subsided within one month only by multi-vitamin therapy. These signs recurred episodically with characteristic clinical features of dysarthria, horizontal ophthalmoplegia, defective saccade, ataxia, and weakness, during the next year. Clinical features mimicked those of various neurological disorders, especially multiple sclerosis, Wernicke encephalopathy, brainstem encephalitis, Fisher syndrome, disorders of amino acid metabolism and episodic ataxia. Tablets of bromvalerylurea were incidentally found at the bedside and bromides were detected in his sera. Drugs containing bromides are now easily available without prescription, so we should keep the intoxications of those drugs in mind in facing undiagnosed patients with various episodic neurological symptoms.
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PMID:[A case of chronic bromvalerylurea intoxication with episodic neurological manifestations such as optic neuropathy ophthalmoplegia and ataxia]. 893 4

A 24-year-old pregnant woman started to have hyperemesis gravidarum 6 weeks before admission. Four weeks later she had vertigo, diplopia, staggering gait, mild dyspnea, dysphagia, and incontinence of urine. On admission she presented with ophthalmoplegia, ptosis, ataxia, decreased tendon reflex, and memory disturbance. Brain magnetic resonance imaging revealed abnormal intensities in medial thalamic-hypothalamic regions and the periaqueductal area, and she was diagnosed with Wernicke's encephalopathy. Urodynamic studies revealed decreased bladder volume and detrusor hyperreflexia. Six weeks after the administration of 100 mg/day of thiamine, urge incontinence gradually recovered, together with neurological signs. Lesions of the medial thalamic-hypothalamic area and the periaqueductal gray matter seemed to be mainly responsible for micturitional disturbance in our patient with Wernicke's encephalopathy.
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PMID:Micturitional disturbance in Wernicke's encephalopathy. 904 73

We report a 29-year-old HIV-positive patient admitted with dysarthria, ataxia and somnolence. Imaging findings were typical of Wernicke's encephalopathy, but autopsy revealed cytomegalovirus encephalitis and primary cerebral lymphoma.
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PMID:Cytomegalovirus encephalitis and primary cerebral lymphoma mimicking Wernicke's encephalopathy. 912 41

A 53-year-old man presented with progressive ataxia two and a half years prior to admission. Initially he was treated in a local hospital for 4 months with a diagnosis of spinocerebellar degeneration. Subsequently he developed psychomotor excitement with hallucination and was admitted to a mental hospital for 7 months with a diagnosis of Wernicke's encephalopathy. After a year of partial remission, he presented with increasing difficulty in thinking and walking. On admission he developed mental agitation and excitement, ocular flutter and opsoclonus, and prominent cerebellar ataxia. A lymphocytic pleocytosis in the CSF and a high-intensity lesion in the superior cerebellar peduncle of the upper brainstem revealed on a T2-weighted MRI led to a diagnosis of brainstem encephalitis. Treatment with steroid (two series of 3 days of 1,000mg methylprednisolone DIV, followed by 60mg oral prednisolone) brought about a dramatic improvement in mental and ocular symptoms corresponding with the CSF findings. He was left with mild cerebellar ataxia and returned to work on a small dose of steroids. Differential diagnoses including Bickerstaff's encephalitis and pathomechanism were discussed.
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PMID:[Steroid responsive chronic brainstem encephalitis featuring mental symptoms, abnormal eye movement and cerebellar ataxia]. 923 54

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

We present here 2 cases of Wernicke's encephalopathy developed several years after total gastrectomy. Case 1. A 48-year-old male developed impaired recent memory and unsteady gait. He had undergone total gastrectomy for advanced gastric cancer 5 years previously; he had been on tegafur regimen for 4 and a half years. He had had 630 ml of beer every day for 6 months until admission. On admission, there were bilateral abducens palsy, horizontal nystagmus, gait ataxia, and areflexia. Cranial MR imaging was unremarkable. After intravenous infusion of vitamin B1, the patient improved. Case 2. A 56-year-old male developed exertional dyspnea, memory loss, and unsteady gait. He had undergone total gastrectomy for a large submucosal tumor 4 years previously; he had had 300-500 ml of sake almost every day thereafter. Examination revealed bilateral abducens palsy, severe gait ataxia, and areflexia. Chest CT scans demonstrated moderate amount of pericardial effusion. Blood vitamin B1 level was abnormally low. After administration of vitamin B1, he improved. Both patients had had alcoholic drinks; laboratory findings demonstrated no liver dysfunction. Drinking alcohol, even in relatively small quantities, could precipitate the development of Wernicke's encephalopathy in gastrectomized individuals. Our 2 cases stress the importance of supplementary vitamin B1 administration after total gastrectomy.
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PMID:[Wernicke's encephalopathy developed several years after total gastrectomy. Report of 2 cases]. 950 77

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

A report is presented on a patient with Wernicke's encephalopathy secondary to hyperemesis gravidarum. The 25-year-old female presented 11 weeks into pregnancy with prolonged vomiting. Neurological examination 8 weeks later demonstrated obtunded sensations, nystagmus and ataxia of gait. MR imaging revealed bilateral lesions in the mediodorsal nuclei of thalami, in the hypothalamus and in the periaqueductal gray matter (1). The neurological signs and the MRI findings pointed to a diagnosis of Wernicke's encephalopathy. The patient was treated with intramuscular vitamin B1 followed by oral thiamine until the end of pregnancy. The subsequent course of the pregnancy was uncomplicated, and resulted in the delivery of a healthy 2970 g male infant. A review of the literature published during the last 30 years revealed an additional 20 cases of Wernicke's encephalopathy induced by hyperemesis gravidarum. Only half of these pregnancies resulted in the birth of a normal infant.
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PMID:Wernicke's encephalopathy induced by hyperemesis gravidarum. 1010 Sep 65

Wernicke's encephalopathy may be fatal if untreated. Because Wernicke's encephalopathy is suspected to be underdiagnosed in children, the authors wished to assess the frequency of overlooked diagnosis and to establish pertinent findings that could lead to early identification of pediatric Wernicke's encephalopathy. The authors performed multiple literature searches seeking pediatric patients with Wernicke's encephalopathy (age = 20 years or younger). A total of 30 patients was found, and the authors added a new patient. Each case report had its clinical, radiologic, and laboratory data, diagnostic method, and outcome analyzed. Of 31 patients, 16 were female and 15 male; the median age +/- S.D. was 11 +/- 6.5 years. The most frequent underlying disorder was malignancy in 11. Thirteen patients died undiagnosed, 16 recovered with thiamine therapy (eight with sequelae), and two died of infection soon after thiamine replacement was initiated. Only six presented with the Wernicke's encephalopathy clinical triad (mental status changes, ocular signs, and ataxia) at neurologic onset; nine eventually demonstrated this triad. The high rate of patients diagnosed only at postmortem examination (41.9%) confirms that Wernicke's encephalopathy is underdiagnosed in children. Thiamine therapy is warranted if any component of the Wernicke's encephalopathy triad is present in an appropriate clinical setting.
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PMID:Early diagnosis of pediatric Wernicke's encephalopathy. 1032 78


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