Cases reported "Multiple Sclerosis"

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1/32. Lesion development in Marburg's type of acute multiple sclerosis: from inflammation to demyelination.

    We report a patient who suffered from acute inflammatory CNS demyelination and underwent two consecutive diagnostic stereotactic brain biopsies during the early disease course. The first lesion was drawn 33 days after the onset of disseminated neurological symptoms. macrophages and T lymphocytes diffusely infiltrated small vessel walls and the white matter. mRNA for tumor necrosis factor alpha (TNFalpha) and inducible nitric oxide synthase (iNOS) was abundantly expressed. Myelin sheaths were entirely preserved. The second biopsy 76 days later showed confluent demyelinating lesions with a diffuse infiltration of macrophages that were positive for myelin debris, activation markers and TNFalpha and iNOS mRNA. IgG and C9neo deposits were found along myelin sheaths. The patient had received intravenous immunoglobulins (IVIG) prior to biopsy. Findings from this single patient affirm that demyelination follows the migration of inflammatory cells from the circulation into the white matter with subsequent inflammation and demyelination. inflammation alone may be sufficient to cause significant clinical deficits without demyelination. Inflammatory mediators such as TNFalpha and NO are involved at very early stages in the pathogenetic process. IVIG treatment may lead to the deposition of immunoglobulins and to the activation of the complement cascade, but the clinical relevance of this particular finding remains uncertain.
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2/32. tissue plasminogen activator gene expression in multiple sclerosis brain tissue.

    Recent studies have implicated tissue-type plasminogen activator (tPA) in neurodegeneration. We studied multiple sclerosis (MS) brain tissue for tPA gene and protein expression in comparison with reference tissue, by in situ hybridisation and immunohistochemistry. MS is characterised by demyelination in the central nervous system. In this study, neuronal cell bodies in MS brain showed high expression of tPA mRNA and protein, while in reference brains, staining for protein and mRNA expression were very low in neurons and mostly restricted to blood vessel walls. In MS, there was an additional staining of mononuclear cells within perivascular cuffs and foamy macrophages within demyelinating plaques. In view of evidence that the final process of demyelination in MS is thought to be enzyme-mediated, our work suggests the involvement of tPA and by inference plasmin, in the demyelinating process. Blocking tPA or plasmin activity may be a potentially beneficial therapeutic approach in MS.
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3/32. Demyelination in primate autoimmune encephalomyelitis and acute multiple sclerosis lesions: a case for antigen-specific antibody mediation.

    Neuropathological and ultrastructural features of central nervous system demyelination were compared in marmoset experimental autoimmune encephalomyelitis (EAE) induced with myelin/oligodendrocyte glycoprotein (MOG), and in 3 cases of multiple sclerosis (MS) displaying recent lesions. At the edges of EAE and MS lesions, a zone of myelin vacuolation was common, whereas in the lesion proper, myelin sheaths were consistently transformed into vesiculated membranous networks. These networks became dissociated from axons by cell processes from macrophages. Oligodendrocytes were remarkably spared and evidence of myelin repair was present but not prominent. Axonal pathology was more common in the MS material than in marmoset EAE. Immunocytochemistry, using gold-labeled encephalitogenic peptides of MOG and silver enhancement to detect MOG autoantibodies, revealed the presence of MOG-specific autoantibodies over vesiculated myelin networks. gold-labeled antibody to IgG also gave a positive reaction. gold-labeled peptide of myelin basic protein did not react with MOG/EAE tissue, but the same conjugate gave positive staining in MS (and in marmoset EAE induced by whole white matter), perhaps indicating broader spectrum immunoreactivity or sensitization to myelin antigens. Thus, vesicular disruption of myelin was a constant feature in these evolving, highly active lesions in primate EAE and MS and appeared causally related to the deposition of antigen-specific autoantibodies.
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4/32. Spontaneously occurring neutralizing antibodies against granulocyte-macrophage colony-stimulating factor in patients with autoimmune disease.

    There is increasing evidence that spontaneous anticytokine autoantibodies are associated with chronic infections and autoimmune diseases. We report the sporadic occurrence in autoimmune diseases of such autoantibodies to granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine involved in inflammation and the regulation of proliferation, differentiation and function of granulocytic and monocytic cell lineages. In 41 of 425 patients tested, we found low to moderate levels of autoantibodies binding to GM-CSF in serum or plasma. These were most prevalent in patients with myasthenia gravis (MG). However, neutralizing autoantibodies against GM-CSF were very rare, being found in only three patients. Two had autoimmune MG, one with thymoma (Patient A) and the other (Patient B) with 'seronegative' MG, i.e. without the antiacetylcholine receptor autoantibodies characteristic of most MG patients, and a third (Patient D) had multiple sclerosis. Only very limited amounts of Patient A and Patient D serum/plasma were available for analysis and therefore further studies were carried out on the more plentiful samples from Patient B. The anti-GM-CSF autoantibodies of Patient B were predominantly polyclonal immunoglobulin g and strongly neutralized recombinant human (rh) GM-CSF derived from different expression systems. They had similar immunological and immunochemical characteristics to anti-GM-CSF antibodies that developed in immunocompetent colorectal carcinoma patients following (rh)GM-CSF therapy. In serial samples from Patient B, the anti-GM-CSF autoantibodies were undetectable from diagnosis at age 8 years until at least age 13, but then developed spontaneously during (temporary) withdrawal of immunosuppressive treatment. Their neutralizing activity has persisted since their first detection at age 15 years 1 month, and was at its highest level recently at age 17 years 7 months. There was no obvious association with other autoimmune phenomena, nor were any haematological deficiencies overtly manifested, suggesting that any loss of GM-CSF function may have been compensated for by other cytokines.
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keywords = macrophage
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5/32. Clinical, radiological, immunological and pathological findings in inflammatory CNS demyelination--possible markers for an antibody-mediated process.

    The present report describes immunopathological, radiologcal and serological characteristics of antibody-mediated demyelination in a multiple sclerosis (MS) case with the main findings: (1) immunoglobulin and complement deposits in areas of active demyelination accompanied by massive macrophage activation; (2) ring-enhancing lesions in T1-weighted MRI after gadolinium application; (3) high titers of serum anti-myelin antibodies; and (4) signs of macrophage activation in the serum. plasmapheresis may be a successful treatment for the type of inflammatory demyelination shown in the present case.
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6/32. Synchronous multifocal osteosarcoma with lymphatic spread in the lung: an autopsy case report.

    Synchronous multifocal/multicentric osteosarcoma (MOS) is a rare variant of osteosarcoma. We report here an autopsy case of a 15-year-old boy with MOS. Radiological examinations showed multiple sclerotic lesions in the left distal femur and in the ipsilateral proximal tibia without pulmonary metastasis at the first examination. Histological examination showed osteoblastic-type osteosarcoma. Despite high-dose chemotherapy the patient died of multiple bone and lung involvements 6 months after the initial diagnosis. autopsy examination revealed prominent invasion of the tumor cells into lymphatic vessels and pleural dissemination without the formation of bulky, nodular metastasis in the lungs. Metastases in pulmonary hilar lymph nodes were noted without metastasis in other organs. immunohistochemistry revealed that p53 protein was positive in most of the tumor cells. In summary, the present case was characterized by multiple bone involvement and prominent lymphatic spread of sarcoma cells in the lungs.
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keywords = bone
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7/32. Retinal periphlebitis and retinal pigment epithelium changes associated with multiple sclerosis: a report of two cases.

    Two patients with definite MS and no significant visual loss are presented, because of the marked bilateral sheathing of retinal veins, and diffuse pigmentary changes in the first patient, and the previously unreported paravenous pigmentation with bone corpuscular configuration in the second patient. The lesions in the second patient are similar to paravenous retinitis pigmentosa. We assume that the RPE lesions may be secondary to perivasculitis, which is not uncommonly seen in MS patients.
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ranking = 0.00016203512448134
keywords = bone
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8/32. MR imaging in acute multiple sclerosis: ringlike appearance in plaques suggesting the presence of paramagnetic free radicals.

    MR studies in three patients with multiple sclerosis have shown clearly defined rings within plaques of demyelination, having signal characteristics consistent with the presence of paramagnetic material. It is suggested that these appearances represent the presence of free radicals in the macrophage layer forming the margin of an acute plaque.
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9/32. Waldenstrom's macroglobulinemia developing in a patient with multiple sclerosis: coincidence or association?

    multiple sclerosis (MS) has been reported in association with haematological abnormalities, including monoclonal gammopathies. We present a 54-year-old male patient with a 30-year history of MS who was admitted to our hospital for investigation of anaemia and increased erythrocyte sedimentation rate. A monoclonal IgM protein was detected by serum protein immunofixation, while bone marrow biopsy indicated a 70% infiltration by small lymphoplasmacytoid cells, in the context of a lymphoplasmacytoid immunocytoma, findings compatible to the diagnosis of Waldenstrom's macroglobulinemia (WM). To our knowledge, this is the first report of WM in a patient with MS. Further to the coexistence of the two diseases observed in the case presented here, there is additional evidence suggesting that the association of MS with plasma cell dyscrasias may not be coincidental.
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ranking = 0.00016203512448134
keywords = bone
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10/32. Neuropathology of white matter disease in Leber's hereditary optic neuropathy.

    Leber's hereditary optic neuropathy (LHON) is associated with point mutations in the mitochondrial dna (mtDNA), coding for a mitochondrial respiratory chain complex I subunit. It is characterized by bilateral, usually sequential, optic neuropathy and may co-occur with multiple sclerosis-like white matter lesions. Despite repeated clinical reports including MRI and histopathological examination of the visual system, neuropathological descriptions of LHON associated with multiple sclerosis-like syndrome are lacking. We present here the case of a female patient with a point mutation at nucleotide position T14484C, who suffered from relapsing episodes of visual loss of both eyes and consecutively developed Hashimoto thyroiditis as well as widespread demyelinating CNS lesions outside the visual system. She died of bronchopneumonia at the age of 44 years, after a disease duration of 19 years, with progressive deterioration, epileptic seizures and immobility. Immunohistochemical analysis on formalin-fixed and paraffin-embedded tissue reveals a spectrum of neuropathological changes, including actively and inactively demyelinating plaques in the white matter and optic nerve, vacuolation and cystic necrosis with CD8-positive T cells in the frontal lobe, axonal damage, and vacuolation of white matter. Tissue destruction is associated with upregulation of mitochondrial manganese superoxide dismutase within the lesions and an increase in the expression of inducible nitric oxide synthase within macrophages and microglia. This variable phenotype of extraoptic LHON disease suggests that mtDNA mutations may affect the nervous system on a common metabolic basis and occasionally may aggravate or initiate autoimmune pathology.
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