Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of spinal cord infarction in the anterior spinal artery territory with selective involvement of the anterior horns. A 35-year-old Mauritanian woman was hospitalized because of an acute and severe flaccid paraplegia without any sphincter dysfunction or sensory disturbance. MRI abnormalities (hypersignal on T2-weighted sequences) were restricted to the anterior horns of the lower thoracic spinal cord and conus medullaris. Adamkiewicz's artery appeared abnormally thin at arteriography. The infarction was probably related to vasculitis of schistosomal origin.
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PMID:[Spinal infarction in the anterior spinal territory with possible relation with bilharziasis]. 196 71

In most cases the only manifestation of nervous system pathology associated with HTLV-1 infection is spastic paraplegia. The virus is transmitted by breast-feeding from mother to child, by transfusion of contaminated blood (or by syringes of intravenous drug addicts) or sexually from husband to wife. Paraplegia usually begins progressively after the age of 30 years by motor and sphincteral disorders, followed by a phase of stabilization. Other clinical entities, such as pseudo-LAS syndromes, polymyositis, lymphocytic alveolitis, vasculitis or meningitis, may coexist or show varying degrees of expression. There is no treatment capable of modifying the course of the disease, but corticosteroids are worth trying, notably in the initial stages of paraplegia and in polymyositis.
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PMID:[Neurologic pathology and HTLV-I virus]. 223 16

A 68-year-old man with suspected allergic granulomatosis and angiitis is reported. He had received 10 mg of prednisolone daily since July 1988 for asthma. He abruptly developed muscle weakness of the lower extremities, followed two days later by paraplegia. Six days after the onset of the muscle weakness, he was hospitalized. He showed disturbance of recent memory, disorientation, neck rigidity, paraplegia, mild muscle fasciculation and hypesthesia. He also showed paralytic ileus. Laboratory findings showed leukocytosis (24580/mm3), eosinophilia (56% of the peripheral white blood cells and 19% of the cells in the cerebrospinal fluid), on erythrocyte sedimentation rate of 31 mm/h, and the IgE level of 1200 IU/ml. The ECG showed loss of the r-wave in V1 and V2. A granulomatous lesion anterior to the spinal cord was found on myelography and MRI. Prednisolone was given at a dose of 60 mg daily resulting in improvement of the clinical symptoms and eosinophilia. There was disappearance of the granuloma on MRI performed after prednisolone therapy. Despite the severe manifestation of allergic granulomatosis and angiitis, prednisolone therapy had a marked effect in this patient. The granulomatous lesion anterior to the spinal cord shown by MRI suggested an eosinophilic granuloma, and may have been the etiology of some of the neurological symptoms.
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PMID:[A case of suspected allergic granulomatosis and angiitis with a rapid clinical course of paraplegia]. 224 87

To define the pathophysiology of spinal cord dysfunction associated with spinal epidural abscess formation, we developed an experimental model. Spinal epidural abscesses were produced in rabbits by injecting Staphylococcus aureus into the posterior thoracolumbar epidural space under direct vision. Progressive neurological deficits were detected in 18 of 20 animals; severe paraparesis or paraplegia occurred in 75%, and sphincter dysfunction occurred in 55%. Clinical data, including the results of plain spine roentgenography, myelography, and biochemical and bacteriological examination of the cerebrospinal fluid, were recorded. Epidural abscesses with varying degrees of spinal cord compression were confirmed pathologically in 95% of the experimental group. Spinal cord white matter changes included vacuolization, loss of myelin, and axonal swelling. The gray matter of the spinal cords was relatively preserved. There was no microscopic evidence of thrombosis or vasculitis in the major blood vessels supplying the spinal cords. Histopathological changes detected in the spinal cords were more consistent with direct compression of neural tissue than with infarction. The progressive clinical course and the histopathological changes in the spinal cord after compression by abscess closely resembled those of experimental compression of the spinal cord by epidural neoplasm.
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PMID:Experimental spinal epidural abscess: a pathophysiological model in the rabbit. 361 65

A 51-year-old man received cyclophosphamide, vincristine, procarbazine and prednisone in the treatment of a small-cell undifferentiated lymphoma. Two years later, he developed a rapidly progressive neurological syndrome characterized by a decline in alertness, deafness, blindness and paraplegia. Examination of his eyes revealed severe hemorrhagic chorioretinitis. Leg weakness was thought to be due to transverse myelopathy at a thoracic level. He had a grand mal convulsion and died from terminal bronchopneumonia. Autopsy examination of the eyes revealed sweeping destruction of the retina due to inclusion body chorioretinitis. The brain and spinal cord showed multiple small infarcts accounting for the deafness and paraplegia. The lesions were due to occlusive arteritis in gray and white matter. Veins were also involved. Tissue surrounding the foci of necrosis contained cells with intranuclear an intracytoplasmic inclusion bodies. Some of the Cowdry type A inclusion bodies were large, measuring 30 micrometer in diameter and were located in enlarged cells. Electron microscopy of retina and brain tissue disclosed virus particles compatible with cytomegalovirus. The subject of cerebral and ocular angiitis due to herpes virus infections is reviewed.
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PMID:Central nervous system vasculitis in cytomegalovirus infection. 626 57

A spontaneous acute spinal epidural haematoma during the course of an immune vasculitis is reported. Decompression by laminectomy after acute onset of paraplegia was followed by complete neurological recovery.
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PMID:[Acute spinal epidural haematoma in the course of immune vasculitis]. 715 55

To date, 271 cases of HTLV1-associated paraplegia have been observed in Martinique (French West Indies). The clinical picture consisted mostly in a spastic paraparesis or paraplegia with sphincter disturbances (80%) and lower limbs pains (60%). The severity of the disease appeared variable: after a mean disease duration of 6.5 years, 40% of the patients could walk without help, 35% used a single crutch, and 25% used a couple of crutches or were confined to a wheelchair. A variable neuromuscular component was observed in 70 cases (25.4%). In 38 cases, the peripheral signs (SIGNS) or the myositis were only mild. In contrast, 25 patients presented with severe amyotrophy evoking amyotrophic lateral sclerosis, and 7 other had features of dermatopolymyositis. Lastly, an extra-neural spreading of the disease was extremely frequent, including lymphocytic alveolitis (76%), sicca syndrome (69%) and more rarely uveitis, arthritis or vasculitis.
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PMID:[Paraplegia associated with HTLV 1 in Martinique. Study of 271 cases including 70 with neuromuscular involvement]. 781 96

A 50-year-old man with long standing ankylosing spondylitis developed cauda equina syndrome, which was found to be coexistent with a spinal arterio-venous malformation. Paraplegia ensured following an acute exacerbation of back pain along with an attack of uveitis. Vasculitis changes were found on resected abnormal vessels.
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PMID:Coexistence of spinal arteriovenous malformation and ankylosing spondylitis--are they related? 783 25

A 30-year-old AIDS patient with no history of cutaneous eruption, presented with rapidly progressive flaccid paraplegia, hypoesthesia, urinary retention, moderate psychomotor slowing and fever (39.8 degrees C), leading to death within 1 week. CD4 count was 290/mm3. Cerebrospinal fluid contained 210 white blood cells and 238 mg/100 ml protein. Neuropathology revealed HIV encephalitis and diffuse ventriculitis with Cowdry type A inclusions in the ependymal cells. Extensive necrotic and hemorrhagic changes with marked recrotizing vasculitis involved the entire spinal cord and spinal roots. Immunocytochemistry revealed numerous inclusion bodies positive for varicella-zoster virus (VZV) and negative for cytomegalovirus (CMV) and herpes simplex virus type 1 and 2, in ependymal cells, subpial glial cells, endothelial cells and Schwann cells. Electron microscopy confirmed herpes virus-like particles. In situ hybridization confirmed VZV genome in leptomeninges, brain, spinal cord and spinal roots. Comparable neuropathological findings and numerous VZV inclusion bodies were also found in the brain, spinal cord, and spinal roots of a 40-year-old AIDS patient who died from a fulminant ascending myeloradiculopathy previously reported as "necrotizing vasculitis of the nervous system". Direct infection of the brain by VZV, in AIDS patients, has been shown to cause leukoencephalitis and cerebral non-inflammatory vasculopathies. Our observations demonstrate that, in AIDS patients, VZV infection of the central nervous system may also be responsible for meningo-myelo-radiculitis possibly secondary to ventriculitis as in CMV infection. The role of VZV in the pathogenesis of some AIDS-related vasculitides seems also very likely.
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PMID:Acute varicella-zoster virus ventriculitis and meningo-myelo-radiculitis in acquired immunodeficiency syndrome. 831 Aug 22

Mediterranean spotted fever is an infectious disease due to Rickettsia conorii usually considered as benign; however, 10% of cases may have severe complications. We report a patient with celiac disease who developed encephalomeningomyelitis secondary to Mediterranean spotted fever. Meningoencephalitic involvement occurred during the acute phase, with myelitis appearing early during convalescence, as acute onset paraplegia involving the lumbosacral spinal cord. A magnetic resonance study showed multifocal white matter disturbances, with no lesions in the spinal cord. One month following onset, R. conorii antibodies serum level was 1/640. A cutaneous biopsy performed during the acute phase revealed endothelial hyperplasia, intraluminal thrombosis and lymphocytic perivascular infiltrate. Several immunological disturbances were found (circulating immune complexes, antinuclear antibodies, IgG paraproteinemia). The development of a systemic vasculitis is the major pathogenetic factor in the origin of systemic complications of Mediterranean spotted fever. We review the neurological syndromes reported in association with R. conorii infection. Our case is the second described as acute myelopathy complicating Mediterranean spotted fever.
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PMID:[Neurological complications of Mediterranean boutonneuse fever. Presentation of a case of acute encephalomeningomyelitis and review of the literature]. 1007 92


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