Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of cerebral venous thrombosis with familial antithrombin III (AT III) deficiency was reported and we discussed the anticoagulant therapy of cerebral venous thrombosis from the viewpoint of AT III. The patient, a 17-year-old boy, was admitted to our clinic with severe bifrontal headache, generalized convulsions and progressive disturbance of consciousness. He developed deep vein thrombosis in his right leg and pulmonary emboli two years earlier when he was placed on heparin and so forth, followed by warfarin sodium. Warfarin was terminated 9 months prior to his recent illness. On neurological examination on admission, he was semicomatous with blurred disc margins, roving eye movements with right abducens nerve palsy, nuchal stiffness and right flaccid hemiplegia. Left carotid angiogram and CT scan revealed extensive superior sagittal sinus thrombosis, complicated with hemorrhagic infarcts in bilateral frontal lobes. When examined for coagulation studies, the patient and his father had decrease in AT III activity and antigen levels. He was treated successfully with antiedematous agents and anticonvulsants during acute phase of illness. He was thereafter placed on warfarin 5-6 mg/day with no further clinical thromboembolic event for 2 years 9 months. There was no neurological abnormality when he was last examined, although he was treated with valproic acid 1,200 mg/day and phenytoin 250 mg/day to control occasional adversive seizures. A coagulation study following infusion of 5,000 units of AT III was carried out. Warfarin was discontinued the day before the study. 0.64 U/kg of AT III administration resulted in a 1% increase in AT III level after the infusion. The biological half life of AT III was 14.4 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral venous thrombosis with familial antithrombin III deficiency]. 404 Dec 90

A 31-year-old veterinarian developed seizures, left hemiparesis, loss of memory, and behavioral disorders 5 months after intensive antirabies vaccination, the longest incubation period yet recorded. Computed tomographic scan revealed a right frontal contrastenhanced mass that extended to the left frontal lobe through the corpus callosum. Brain biopsy showed foci of primary demyelination largely confined to the white matter. The lesions were characteristic of the demyelinating encephalomyelitis that follows treatment with certain vaccines against rabies. The hemiplegia improved, but seizures, memory impairment, and abnormal behavior persisted.
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PMID:Delayed onset of post-rabies vaccination encephalitis. 613 53

A patient with subdural hygroma in the perinatal period developed into a right hand sided spastic hemiplegia with epileptic seizures and intellectual deficit. On the age of 17 years a linear dermatosis that proved to be a naevus unislateris was remarked. The combination of linear nevi and neurological deficit is known as the epidermal nevus syndrome.
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PMID:Linear cutaneous lesions and neurological deficit. A case report. 632 76

The clinical courses of 31 episodes of brain abscess and one episode of meningitis occurring in patients with hereditary hemorrhagic telangiectasia are reviewed. Pulmonary arteriovenous malformations were demonstrable in all but two patients and presumably permitted septic microemboli to evade the normal pulmonary capillary filter and lodge in the brain. Obtundation, headache, visual disturbances, hemiplegia, and seizures were the most common presenting features. Cyanosis, clubbing, polycythemia, and hypoxemia were routinely encountered, but leukocytosis and fever were present in a minority of cases, and all blood cultures were sterile. Anaerobic and microaerophilic streptococci were the commonest pathogens found in the brain abscesses. Thirteen patients died, and patients without abscess drainage or with delayed diagnosis had a higher mortality rate. A brain abscess may develop in approximately 1 percent of patients with hereditary hemorrhagic telangiectasia, and awareness of this risk should lead to early investigation of any patient with hereditary hemorrhagic telangiectasia who has neurologic symptoms.
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PMID:Central nervous system infections associated with hereditary hemorrhagic telangiectasia. 637 93

A new essential hypereosinophilic syndrome has been reported in a 53 years old man who presented an important blood and bone marrow hypereosinophilia of unknown etiology since 5 years. The evolution of the clinical course included neurological accidents (hemiplegia, spasmodic quadriplegia, seizures) congestive heart failure, hepatomegaly, transient renal involvement, pulmonary infiltrates with pleural hemorrhage, episodes of diarrhea and fever with weight loss. The cytological study of the eosinophiles showed the existence of abnormal inclusions which were confirmed by the electron microscope. These and cytoenzymological abnormalities led to discussion of the relationship between the essential hypereosinophilic syndrome and eosinophilic leukemia.
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PMID:[An essential hypereosinophilic syndrome. Cytological, cyto-enzymological and ultrastructural studies (author's transl)]. 645 47

The authors report a case of Parry-Romberg disease with predominantly facial left atrophy, seizures, amnesic aphasia, mental retardation, right hemiplegia and hemianesthesia, and cerebellar syndrome. The rarity of cerebellar atrophy (only one case thus far reported in the literature surveyed) is emphasized, as well as the correlation between the clinical abnormalities and the computerized axial tomography of the skull.
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PMID:[Progressive facial hemiatrophy: report of a case]. 646 49

In 19 children with acute infantile hemiplegia an ischemic cerebral infarct was found clinically and by serial computertomography. In 11 patients an angiography has been performed in addition. 9 of the children had chronic diseases which are known as predisposing factors for cerebrovascular disease (congenital heart disease in 7 and chronic renal failure with hypertension in 2). One child had a severe hypernatremic dehydration due to infantile diarrhea and in 1 child thrombosis of the internal carotid artery occurred 3 days after a perforating trauma of the soft palate. No obvious reason for the ischemic stroke could be evaluated in 8 children. The onset of symptoms was either acute or slowly progressive. An altered state of consciousness was present in 11 children. Hemiparesis was found in 18 patients (13 right, 5 left) accompanied by facial palsy in 12 and aphasia in 6. Seizures occurred in 6 patients. One patient with incomplete occlusion of a vertebral artery showed acute cerebellar ataxia. In children without predisposing factors the prevalence of girls was higher (2 : 6) and there was a history of a preceding acute febrile illness in 5 of 8 patients. Laboratory investigations showed polycythemia in 4 children with cyanotic heart disease and additional hypochromia in two. Blood sedimentation rate was increased in 6 out of 8 patients without a known predisposing factor. Cerebrospinal fluid (CSF) showed a slight increase of erythrocytes (36-88/cmm) in 4 children, in two others purulent CSF was obtained after the infarct had developed into a brain abscess. The etiology of ischemic stroke in childhood and the possibility of an inflammatory vascular disease are discussed.
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PMID:Acute infantile hemiplegia caused by cerebral ischemic infarction. Etiology, clinical features and investigations. 647 69

The cerebral arterial occlusion was observed from nine patients aged from 2,5 to 12 years old, between 37 children with acute acquired hemiplegia. The thrombosis had an embolic origin in three cases of cardiopathy. Six patients had primary arterial occlusion, but all these patients were febrile and the onset of hemiplegia was accompanied by seizures in five cases. The site of arterial was demonstrated by the angiography in eight cases: cervical internal carotide in one case of cardiomyopathy, intracranial portion of the internal carotide in four cases, middle and anterior cerebral artery in three cases. The regression of hemiplegia was observed in all but one case of atrial myxoma. The autopsy of this patient revealed renal and hemispheric cerebral arterial thrombosis with myxoma embolus.
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PMID:[Acute hemiplegia due to cerebral artery occlusion in children. Apropos of 9 cases]. 662 43

Two cases of acute hemiplegia with the occlusion of the posterior cerebral artery were reported in children. Both patients were low-birth-weight infants with a history of febrile convulsions. Cerebral edema due to prolonged seizures was considered to be an etiologic factor of the occlusion of posterior cerebral artery. When the seizure is focal or the patient has perinatal difficulty, febrile convulsions should be treated carefully, as the possibility of epilepsy exists.
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PMID:Acute hemiplegia in childhood with the occlusion of the posterior cerebral artery. 668 46

The records of 68 patients with hemoglobin SC disease and 68 age- and sex-matched control patients were reviewed for neurological problems. A significant increase in retinopathy, stupor/coma, and seizures was noted in the hemoglobin SC group. Hemiplegia, noted in two young patients, was probably also secondary to hemoglobin SC disease. Hemoglobin SC disease may often go unrecognized as a cause of stupor and coma in older patients without other obvious manifestations of a sickling hemoglobinopathy. Factors known to precipitate sickling crisis and the associated neurological complications should be avoided, especially in patients undergoing surgery or parturition.
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PMID:Neurological complications of hemoglobin SC disease. 669 47


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