Cases reported "Meningoencephalitis"

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1/10. Vascular changes in tuberculous meningoencephalitis.

    Our report refers two cases of tuberculous encephalomeningitis which differ in the course and pathological changes. In case 1 blood vessels showed features of peri, endo-, or panvasculites. In some vessels endothelium proliferation leading to the stenosis or obliteration of the vascular lumen was observed. necrosis was an effect of vessels occlusion. In case 2 many fewer vessel were involved in onflammation process. Vascular changes were also less extensive and were observed more rarely. Tuberculous infection often caused less tissue lesions than vascular changes. Different pathological changes probably depend on the type and virulence of Myobacterium tuberculosis and on the host immune response to the infection.
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2/10. Nonvasculitic autoimmune inflammatory meningoencephalitis (NAIM): a reversible form of encephalopathy.

    Five patients, age 54 to 80 years, presented between 3 weeks and 18 months after symptomatic onset of progressive cognitive decline, psychosis, and unsteady gait that proved to be due to a steroid-responsive nonvasculitic autoimmune inflammatory meningoencephalitic syndrome. CSF examination showed elevated immunoglobulin (Ig)G index and IgG synthesis rate in all three patients in whom it was checked, and brain biopsy revealed perivascular lymphocytic infiltrates without vessel wall invasion.
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3/10. Meningoencephalomyelitis with vasculitis due to varicella zoster virus: a case report and review of the literature.

    Varicella zoster virus (VZV) encephalitis is associated with large or small vessel vasculopathy. We report the case of a 67-year-old woman with a history of non-Hodgkin's lymphoma and cancers of the breast and colon, who presented with a zosteriform rash and brown-sequard syndrome. Despite 10 days therapy with intravenous acyclovir, meningoencephalitis developed and the patient died 15 days after onset of neurological symptoms. autopsy showed meningoencephalomyelitis with necrotising vasculitis of leptomeningeal vessels, which is a rare complication of VZV, and we review the literature of the nine similar published cases. polymerase chain reaction of cerebrospinal fluid for VZV was negative 6 days after onset of neurological symptoms, but became positive by day 10. Only one multinucleated giant cell with intranuclear Cowdry type A inclusions was seen within an endothelial cell in a leptomeningeal vessel involved by vasculitis.
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4/10. Nonvasculitic autoimmune inflammatory meningoencephalitis.

    Caselli and colleagues described five cases with encephalopathy, progressive cognitive decline, ataxia, abnormal CSF studies and steroid responsiveness, and proposed the term non-vasculitic autoimmune inflammatory meningoencephalitis (NAIM). Many of these cases had brain biopsy showing mild leptomeningeal perivascular lymphocytic inflammation, however, none of the cases had a post-mortem. Nonvasculitic autoimmune mediated meningoencephalitis has been described in patients with sjogren's syndrome, systemic lupus erythematosus and, more recently, with Hashimoto's disease. The present study is the first post-mortem report of a case with a clinical diagnosis of NAIM. Neuropathological examination revealed a panencephalitis with intact vessel walls. T and B immunostaining showed a mixture of T and B cells. The findings were not consistent with other reported findings in collagen vascular diseases including sjogren's syndrome, CNS vasculitis or Hashimoto's encephalopathy. There was no evidence of neoplasia, bacteria, acid-fast bacilli, fungi or atypical infectious agents. This is the first post-mortem report of a case with a clinical diagnosis of NAIM and demonstrates a panencephalitis without evidence of a vasculitis. The pathology seems unique, however, Sjogren and Hashimoto's encephalopathy might be variants of NAIM.
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5/10. amyloid-beta peptide remnants in AN-1792-immunized Alzheimer's disease patients: a biochemical analysis.

    Experiments with amyloid-beta (Abeta)-42-immunized transgenic mouse models of Alzheimer's disease have revealed amyloid plaque disruption and apparent cognitive function recovery. Neuropathological examination of patients vaccinated against purified Abeta-42 (AN-1792) has demonstrated that senile plaque disruption occurred in immunized humans as well. Here, we examined tissue histology and quantified and biochemically characterized the remnant amyloid peptides in the gray and white matter and leptomeningeal/cortical vessels of two AN-1792-vaccinated patients, one of whom developed meningoencephalitis. Compact core and diffuse amyloid deposits in both vaccinated individuals were focally absent in some regions. Although parenchymal amyloid was focally disaggregated, vascular deposits were relatively preserved or even increased. immunoassay revealed that total soluble amyloid levels were sharply elevated in vaccinated patient gray and white matter compared with Alzheimer's disease cases. Our experiments suggest that although immunization disrupted amyloid deposits, vascular capture prevented large-scale egress of Abeta peptides. Trapped, solubilized amyloid peptides may ultimately have cascading toxic effects on cerebrovascular, gray and white matter tissues. Anti-amyloid immunization may be most effective not as therapeutic or mitigating measures but as a prophylactic measure when Abeta deposition is still minimal. This may allow Abeta mobilization under conditions in which drainage and degradation of these toxic peptides is efficient.
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6/10. The treatable dementia of sjogren's syndrome.

    Progressive dementia developed during a 15-month period in a 56-year-old woman with serologically and clinically documented primary sjogren's syndrome. Findings from magnetic resonance imaging and angiography were normal, but a brain biopsy disclosed perivascular lymphocytic inflammation in leptomeningeal and parenchymal vessels. Treatment with high-dose corticosteroids produced rapid and nearly complete resolution of the dementia.
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7/10. Cerebral hemiatrophy in systemic lupus erythematosus: report of a case.

    An 18-year-old woman with systemic lupus erythematosus developed neuropsychiatric disorders, including aseptic meningoencephalitis, organic brain syndrome and seizure. A series of computed axial tomography scans revealed the progression of marked atrophy of the right cerebral hemisphere for a period of 3 years without occlusion or stenosis of large vessels on cerebral angiography. I-123 IMP single photon emission computed tomography disclosed a markedly decreased uptake of I-123 IMP in the right cerebral hemisphere, and also in the left cerebellar hemisphere (crossed cerebellar diaschisis), which disappeared within 2 years.
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8/10. Correlation of the distribution of rickettsia conorii, microscopic lesions, and clinical features in South African tick bite fever.

    Three South African patients with severe rickettsia conorii infection had complicated courses of illness with 2 fatal cases and 1 with gangrene of multiple digits. Immunofluorescent organisms of R. conorii were demonstrated in vascular endothelium of brain, leptomeninges, renal glomerular arterioles and capillaries, renal arteries and veins, myocardial capillaries and arteries, pulmonary alveolar capillaries, pancreatic septa, splenic arterioles, and dermis. Rickettsiae were also observed in hepatic sinusoidal lining cells, splenic and lymph node macrophages, and the blood vessels of the partially viable zone of the amputated digits. Pathologic lesions included cerebral and cerebellar perivascular mononuclear leukocytes, mild mononuclear leptomeningitis, glomerular arteriolitis, vascular and perivascular mononuclear cell-rich inflammatory foci in the kidney, pancreas, skin, and myocardium, hepatocellular necrosis, and pulmonary edema. The sites of lesions and rickettsiae showed strong topographical correlation. Thrombi and hemorrhage occurred in a minority of the sites of vascular injury. Rickettsiae were the apparent direct cause of meningoencephalitis, peripheral gangrene, and other foci of vascular injury. Fatal R. conorii infection with disseminated organ involvement emphasizes the pathogenic potential of this disease.
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9/10. Disseminated cutaneous and meningeal sporotrichosis in an AIDS patient.

    We report the first proven case of sporothrix meningoencephalitis in an AIDS patient. The patient had dramatic, wide-spread ulcerative and infiltrative disease with progressive meningoencephalitis in spite of amphotericin and itraconazole therapy. sporothrix was cultured from premortem cerebrospinal fluid and seen in the meninges and in brain vessels at autopsy.
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10/10. Neuro-Behcet's disease.

    We are reporting a case of Bechcet's disease without vasculitis but with acute neutrophilic inflammation which involved the brain and other organs. The patient exhibited waxing and waning neurological deficits which were unresponsive to treatment. The neuroradiologic findings simulated those of multiple sclerosis. The neuropathological examination revealed an acute, focal, though disseminated encephalitis involving the frontal lobe, internal capsule, basal ganglia, cerebellum, and brainstem. The acute inflammation consisted of a neutrophilic and eosinophilic infiltration of the perivascular spaces and parenchyma without evidence of vasculitis, fibrinoid necrosis, or thrombosis. Cultures and special stains for microbial organisms were negative. Ultrastructural examination revealed no viral structures or other microorganisms. in situ hybridization for Epstein-Barr virus (EBV), herpes simplex virus type I (HSV-I), and cytomegalovirus (CMV) was negative. In this case, the lack of inflammation in the vessel walls points out that the necrotizing lesions in neuro-Bechcet's disease need not be the result of vasculitis and superimposed thrombosis, but may occur as a result of primary, acute neutrophilic inflammation.
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