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)

We reported an autopsy case of thrombotic occlusion of the superior cerebral vein with hemorrhagic laminar necrosis of the right parietal cortex. A 68-year-old woman was admitted to our hospital because of a severe headache and left hemiplegia of acute onset. There was a past history of hypertension, fever of unknown origin, leukocytopenia and nasal dermatitis. Magnetic resonance images (MRI) disclosed thrombosis of the superior sagittal sinus and of the right parietal cortical vein as well as right parieto-occipital cerebral infarction. Although she improved with mild sequelae, the subsequent MRI showed a recurrent thrombosis of the superior sagittal sinus. Ten months after the onset she died suddenly, presumably due to acute myocardial infarction. Pathologically, thrombotic occlusion of the right parietal cortical vein, recurrent thrombosis of the superior sagittal sinus and old hemorrhagic cortical laminar necrosis of the right parietal region were revealed. Moreover, intracranial arteritis and phlebitis were observed, as well as arteriolitis in the peripheral nerves. In our case, MRI was useful for the diagnosis and following the course of cerebral venous thrombosis. Cerebral noninfective vasculitis may well have caused the venous thrombosis.
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PMID:[Thrombosis of the superior cerebral vein with hemorrhagic cerebral infarction--serial MRI and pathological study of a case]. 225 22

The authors report a new case of necrosing angeitis similar to those individualised by Churg and Strauss in 1951. After a persistent rhinitis, the patient developed serious asthma, left hemiplegia 8 months later (secondary to an intracerebral hemorrhage) polyneuritis and extensive necrosis of the small intestine. There was no renal or cardiac involvement. Anatomopathological examination of the small intestine revealed an arteriolitis with periarterial granuloma and severe inflammation. Complementary investigations revealed a hypereosinophilia, an inflammatory syndrome, a reduction in the hemolytic 50 complement and of the C4 fraction. Corticosteroid therapy associated with cyclophosphamide formed the basis of treatment. Plasmapheresis have been a useful aid. The follow-up is too short to assess the long term prognosis. A familial immune deficiency, disseminated lupus erythematosis in a sister, and rheumatoid purpura in one of the patient's children are interesting features of this text.
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PMID:[Severe visceral necrotizing angiitis with hereditary immune disorders: a case]. 613 87