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 a lesion of the central nervous system in Wegener's granulomatosis with neuritis of craniocerebral nerves, granulomas, vasculitis and foci of ishemic necrosis and hemorrhages in the brain tissue is reported. Diagnosis of Wegener's granulomatosis in a female aged 48 years was confirmed morphologically and by detection of specific antibodies. In spite of prednisolone (20 mg/day) and cyclophosphamide treatment (200 mg per week), hemiplegia, aphasia appeared which progressed and resulted in a death of the patient. Histologically lesions in many organs were found: middle ear, lungs, kidneys, brain, destructive vasculitis, necrotic foci and polymorphic lung granulomas, fibrosing alveolitis, polymorphocellular granulomas, multiple infarctions in the kidneys, endothrombovasculitis, necrotic foci and granulomas with glial reaction in the brain tissue.
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PMID:[Affection of the central nervous system in Wegener's granulomatosis]. 1544 87

Enterovirus infection has been rarely reported to cause cerebral infarction in infants. We describe a 2-month-old boy with right focal seizure and right hemiparesis associated with enterovirus infection during an epidemic of enterovirus 71 infection in Taiwan in 1998. Magnetic resonance imaging and angiography showed vasculitis in the left anterior cerebral artery with cerebral infarction. In the unclarified pathogenesis of cerebral disease in enterovirus infection, this case suggests focal vasculitis with subsequent cerebral infarction. Enterovirus-related vasculitis of the central nervous system is thus another consideration when facing a child with focal seizure, acute hemiplegia and cerebral infarction.
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PMID:Cerebral infarction associated with possible enteroviral infection in an infant. 1586 15

Pediatric human immunodeficiency virus type 1 (HIV-1) infection is endemic throughout southern Africa. Neurologic complications are described in 20% to 60% of published series, mostly related to HIV-1 encephalopathy. With increasing HIV prevalence, more atypical cases are presenting. We present, as illustrative cases, seven children (three girls) with unusual neurologic sequelae as a consequence of HIV-1 infection. The median age at presentation was 33 months (range 7 months-6 years). Five of the seven children were developmentally normal before presentation. They presented with progressive multifocal leukoencephalopathy, myelopathy, intractable seizures, acute vasculitis and blindness, hemiplegia, peripheral neuropathy, and paraspinal lymphoma. Neuroimaging of the brain was performed in five patients, of whom one had basal ganglia calcification. All children had poor outcome with incomplete recovery or continued deterioration. In conclusion, children with HIV-1 infection who survive beyond the first year of life can present with a wide variety of neurologic complications. A similar spectrum of neurologic manifestations is likely to occur in other sub-Saharan African countries, characterized by high HIV prevalence. The case histories demonstrate that the neurologic features of pediatric HIV infection do not easily fit into a simplified classification system.
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PMID:Specific neurologic complications of human immunodeficiency virus type 1 (HIV-1) infection in children. 1697 Aug 87

Primary angiitis of the central nervous system (PACNS) is a rare, idiopathic vasculitis diagnosed most frequently in adults. We describe 2 children presenting with hemiplegia from PACNS treated with cyclophosphamide. Diagnosis in one child was based on abnormal angiography. Oral, but not intravenous (IV), cyclophosphamide was effective in preventing progressive weakness. The second child had unremarkable angiography, but brain biopsy revealed vasculitis; IV cyclophosphamide prevented further weakness. Both cases highlight the importance of early diagnosis and treatment.
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PMID:Cyclophosphamide treatment of primary angiitis of the central nervous system in children: report of 2 cases. 1701 23

We describe the case of a 69-year-old man with systemic granulomatosis who presented with left-sided hemiplegia. Initial diagnosis concerning the neurological troubles was cerebral vasculitis. Corticosteroids associated with antituberculosis therapy showed a rapid but transient amelioration followed by neurological aggravation. Two weeks later, JC virus was detected in cerebrospinal fluid by PCR and the diagnosis of progressive multifocal leukoencephalopathy (PML) was made. Treatment with cytarabine and cidofovir was initiated but the patient died three months after the first neurological signs. In the presence of central neurological symptoms occurring during systemic granulomatosis before specific therapy, PML should be evoked.
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PMID:Progressive multifocal leukoencephalopathy mimicking cerebral vasculitis in systemic granulomatosis. 1705 59

The authors report on a case of a metastatic choriocarcinoma that mimicked systemic necrotizing vasculitis on a cerebral angiogram. A 35-year-old woman presented with right hemiplegia and a drowsy mental state. A computed tomography (CT) scan revealed an intracerebral hemorrhage in the left frontal region. A cerebral angiogram showed multiple microaneurysms arising from the bilateral anterior cerebral arteries and middle cerebral arteries, and the renal angiogram showed multiple microaneurysms arising from the left distal renal artery. A chest CT scan revealed multiple metastatic lesions in the left lower lung field. The hematoma and microaneurysms were surgically removed. Choriocarcinoma was diagnosed after histological examination. Despite receiving postoperative chemotherapy, the patient died 1 month after the operation.
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PMID:Metastatic choriocarcinoma with multiple neoplastic intracranial microaneurysms: case report. 1844 21

Ischemic stroke following snake bite is rare. We report an 18-year male who developed right hemiplegia with expressive aphasia following a Russell's viper bite. T2-weighted magnetic resonance imaging revealed infarct in the left middle cerebral artery territory. The possible mechanisms for cerebral infarction in this scenario include disseminated intravascular coagulation, toxin induced vasculitis and endothelial damage.
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PMID:Acute ischemic infarct in the middle cerebral artery territory following a Russell's viper bite. 1977 May 52

Sarcoidosis is a chronic disease of unknown aetiology. Neurosarcoidosis is registered in 5% of patients with sarcoidosis. Clinical manifestations of sarcoidosis are numerous and diverse. Manifestation of Neurosarcoidosis includes partial- and grand-mal seizures, low-grade fever, headache, increased intracranial pressure, visual disturbances, diabetes insipidus, amenorrhea- galacterorrhea syndrome and pituitary failure, hypogonadotropic hypogonadism, hyperprolactinemia, unilateral and bilateral facial palsy, infiltration of meninges (aseptic meningitis) and nerve roots, leptominingitis, pachymeningitis with cranial neuropathies, pseudotumor, mild cognitive disorder, psychosis, delirium, dementia, disorientation, amnesia, progressive visual deterioration and proptosis, axonal polyneuropathies, mononeuropathies, chronic polyradiculoneuritis, peripheral neuropathy, cranial nerve abnormalities, radiculopathies, peripheral neuropathy, mononeuritis multiplex, progressive numbness and deep sensation disturbance in bilateral lower extremities, hemiplegia, hyperreflexia with pathological reflexes and hypesthesia, upward gaze palsy, spinal cord compression, dysarthria, dysphagia, weakness, episodes of blurred vision, diplopia, intracerebral hemorrhage, neuro-ophthalmic manifestations, intranuclear ophthalmoplegia, dysorientation, vasculitis presenting with strokes, intracranial hypothalamic lesion, paresthesis, hemiparesis, myelopathy in the cervico-thoracic region, lumbar pain, sensory level and inability of lateral gaze (Tab. 2, Ref. 60).
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PMID:Clinical manifestations of neurosarcoidosis. 1982 43

Clinical reports of cerebrovascular system involvement in sarcoidosis are extremely rare though pathological studies frequently describe granulomatous cerebral arterial and venous lesions. We report the case of a 47-year-old man with a history of pulmonary sarcoidosis at age 32 and abducens palsy at age 40, who presented cerebral pseudotumoral histologically proven sarcoidosis. He was admitted for acute left hemiplegia. Brain CT scan and MRI demonstrated a right posterior parietal haematoma associated with a superior sagittal sinus occlusion. He received intravenous corticosteroids and anticoagulant therapy. Six months later, he presented a right motor status epilepticus. MRI revealed new parenchymal haematomas. Cerebral angiography demonstrated cerebral vasculitis.
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PMID:Cerebrovascular symptomatic involvement in sarcoidosis. 2130 68

Although peripheral neuropathy is a common complication of microscopic angiitis, manifestations involving the muscle and the central nervous system have been rarely reported. We describe a 48-year-old man who rapidly developed a clinical picture of mononeuritis multiplex. A month after the appearance of the primary symptoms, he became comatose and had left hemiplegia in relation with a massive cerebral haematoma. Laboratory data revealed signs of inflammation, glomerular dysfunction with microhaematuria, and positive myeloperoxidase-antineutrophil cytoplasmic antibodies. The neuromuscular biopsy disclosed a small-vessel vasculitis, consisting with microscopic angiitis, associated with myositis and extensive axonal loss. The patient had surgical evacuation of the haematoma and received immunosuppressive therapy with good outcome. Thus, microscopic angiitis should be considered as a differential diagnosis in cases of myositis and intracerebral haemorrhage.
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PMID:Microscopic polyangiitis presenting with peripheral and central neurological manifestations. 2168 67


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