Cases reported "Multiple Sclerosis"

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1/11. Expression of jc virus T-antigen in a patient with MS and glioblastoma multiforme.

    OBJECTIVE: To investigate the presence of human polyomavirus jc virus genome and the expression of the viral oncoprotein T-antigen in neoplastic cells of a patient with MS and a glioblastoma multiforme. BACKGROUND: The postmortem examination of an immunocompetent patient with a neurologic disorder revealed the concurrence of MS plaques in the white matter of the brain and a glioblastoma multiforme in the region of the thalamus. methods AND RESULTS: PCR analysis of DNA from demyelinated plaques and the tumor area using primers derived from specific regions of the jc virus genome revealed the presence of viral DNA corresponding to the viral early and late genes. Further examination of the samples for the jc virus regulatory region identified the presence of sequences identical to jc virus Mad-4 and jc virus W1 viral isolates in the tumor and the demyelinated regions. Results from immunohistochemistry showed the detection of the viral early protein, T-antigen, and the cellular tumor suppressor protein, p53, in the nuclei of neoplastic cells. Interestingly, expression of T-antigen, but not p53, was observed in neurofilament-positive cells with neuronal morphology and in glial fibrillary acidic protein-positive astrocytes in the cortex juxtaposed to the MS plaques. Examination of viral late gene expression by immunohistochemistry showed no evidence for viral capsid proteins, thus ruling out productive replication of jc virus in the tumor and MS demyelinated plaques. CONCLUSIONS: These observations provide molecular and clinical evidence of the association of jc virus in the brain of a patient with concurrent glioblastoma multiforme and MS.
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2/11. Human herpesvirus 6 genome and antigen in acute multiple sclerosis lesions.

    Evidence for a candidate multiple sclerosis (MS) virus, human herpesvirus 6 (HHV-6), was sought in biopsy specimens of acute lesions that presented clinically as cerebral tumors obtained from 5 patients. Histopathology, magnetic resonance imaging, and clinical course confirmed the diagnosis of MS in each case. A sensitive in situ polymerase chain reaction (ISPCR) method was used to detect HHV-6 genome, in conjunction with immunocytochemical staining (ICC) to detect viral and cellular antigens. ISPCR revealed numerous oligodendrocytes, lymphocytes, and microglia containing HHV-6 genome within all lesions, whereas ICC showed only the HHV-6 glycoprotein 116 antigen in some reactive astrocytes and microglia. High frequencies of neuroglial and inflammatory cells containing HHV-6 genome were present in acute-phase lesion tissue from patients who were free of the effects of chronic MS and had not been received immunomodulatory therapy for MS. The prevalence of HHV-6 genome-containing cells, including oligodendrocytes, in each lesion suggests that HHV-6 plays a role in the demyelinative pathogenesis of MS; the significance of the discrepant expression of viral antigens remains uncertain.
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3/11. A role for hypertrophic astrocytes and astrocyte precursors in a case of rapidly progressive multiple sclerosis.

    The purpose of this study was to examine the roles played by astrocytes in a case of rapidly progressive multiple sclerosis (MS). Within early-active and active lesions, hypertrophic astrocytes played an important role in lesion pathology through the phagocytosis of myelin and axonal debris and through the internalization of other glial cells, including astrocytes. In addition to this critical role, hypertrophic astrocytes, in areas that lack significant inflammation (within the adjacent normal appearing white matter and within late remyelinating lesions) were found to be active in myelin and axonal debris phagocytosis with no evidence of cellular internalization. Hypertrophic astrocytes therefore not only play an important role in the pathogenesis of MS lesions but also exert a continued deleterious effect upon tissue in the absence of significant inflammation. In addition, we found evidence for a significant population of vimentin-positive, glial fibrillary acidic protein (GFAP)-negative, bipolar, astrocyte precursors within the late remyelinating lesions. Their significance is not known but a possible role may include their participation in the successful remyelination of the lesion.
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4/11. diagnosis and treatment of multiple sclerosis and amyotrophic lateral sclerosis: neuropathies from bordetella pertussis.

    Having found positive the research for anti-Bordetella antibodies in the 95.47% of 92 patients affected by defined multiple sclerosis and in the 100% of 55 patients affected by non-patched neuropathies (amyotrophic lateral sclerosis and correlated neuropathies), I reassessed the pathogenesis of the neuropathies from bordetella pertussis. In the two categories of neuropathies (with and without patches), the beginning pathogenetic mechanisms are the same: 1) pertussis re-infection in patients with mucociliary barrier defect; 2) pertussis toxins passage in the blood; and 3) formation of circulating immune complexes. In multiple sclerosis, astrocytes produce class II human leukocyte antigens, the endothelia of the small brain vessels show the "adhesion molecules," and the immune complexes fall in the central nervous system (patches are formed). In amyotrophic lateral sclerosis and in the other non-patched neuropathies, the astrocytes do not produce the class II human leukocyte antigens, the endothelia do not show adhesion molecules, and immune complexes do not fall in the central nervous system; but they increase in blood until they inhibit the ulterior antibodies production. For relative antibodies lack, pertussis toxins fix directly on neuro-epithelia; their pathogenic power and physiopathologic astrocytes role in the central nervous system produce the damage. With a blood sample, we can assess Bordetella etiology. In all these neuropathies, an extended antibiotic therapy to clear mucosae and to prevent reinfections is necessary.
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5/11. Multinucleated astrocytes in old demyelinated plaques in a patient with multiple sclerosis.

    A 51-year-old woman with MS of 26 years duration is reported. The patient's MS history began at the age of 25 years with an initial relapsing-remitting course, followed by slow progression without distinct relapses. She became bed-ridden at the age of 40 years. A post-mortem examination revealed numerous demyelinated plaques that exhibited fibrillary gliosis with Rosenthal fibers, but without lymphocytic cuffing or foamy macrophages. Activated microglia were found mainly in the marginal portion of the plaques. These plaques were consistent with so-called 'slowly expanding plaques'. Interestingly, multinucleated astrocytes were observed within the plaques, being more numerous in the area where microglial infiltration had occurred. These findings suggest that mild persistent inflammatory processes are present even in old plaques and that certain inflammatory stimuli cause multinucleation of astrocytes. This might explain the gradual deterioration without definite relapses observed in the late stage of MS.
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6/11. multiple sclerosis: a role for astroglia in active demyelination suggested by class II MHC expression and ultrastructural study.

    central nervous system (CNS) tissue was studied by immunocytochemistry and electron microscopy from three cases of multiple sclerosis (MS) in which evidence of ongoing myelin breakdown could be documented. The study focussed upon the role of glial cells in the pathogenesis of demyelination. In acute MS, demyelination involved the vesicular dissolution of myelin from intact axons and a paucity of fibrillary astrogliosis. Foamy macrophages, many of them probably derived from transformed and recently proliferated microglia, contained recognizable myelin debris and lipid droplets and were abundant throughout the lesions. These cells formed the major phagocytic population and stained positively for class II major histocompatibility complex antigens (HLA-DR; Ia). In acute MS lesions, rounded astrocytes were encountered which possessed membrane-bound compartments enclosing phagocytosed fragments of myelin basic protein-positive debris. Despite the superficial resemblance of these cells to foamy macrophages, the presence of intermediate filaments, glycogen granules and diffuse glial fibrillary acidic protein positivity supported an astroglial identity. Astrocyte processes were involved in myelin removal and invested recently demyelinated axons. Hypertrophic fibrous astrocytes were common in chronic active lesions, were capable of myelin degradation and on occasion, contained myelin debris attached to clathrin-coated pits. These astrocytes were sometimes Ia . Oligodendrocytes were depleted from the center of active lesions but were numerous at the lesion margin, suggesting survival and proliferation. They stained positively for myelin-associated glycoprotein, a marker for immature oligodendrocytes. However, they were invariably Ia-. The findings confirm and further support a role for the astrocyte as both an antigen presenting cell and a phagocyte in the CNS during MS.
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7/11. multiple sclerosis: oligodendrocytes in active lesions do not express class II major histocompatibility complex molecules.

    The expression of major histocompatibility complex (MHC) molecules by oligodendrocytes has been proposed as evidence for their involvement in the multiple sclerosis (MS) lesion although the literature on the subject is controversial and based largely upon observations in vitro. With a modified immunocytochemical procedure on 1 micron epoxy sections, the present study has examined the expression of class II MHC molecules (Ia) on cells within actively demyelinating lesions in a central nervous system biopsy from a case of acute MS. White Ia was readily demonstrable on microglial cells and astrocytes, it was never detected on adjacent surviving oligodendrocytes. Unexpectedly, in parallel sections, the oligodendrocytes stained positively for myelin-associated glycoprotein, a marker for immature oligodendrocytes. The unequivocal lack of Ia expression by oligodendrocytes in MS makes it unlikely that they serve as immunomodulators in lesion pathogenesis.
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keywords = astrocyte
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8/11. Late-onset malignant astrocytoma in a case of multiple sclerosis. Clinical, neuropathological, virological, and tissue culture studies.

    An unusual case of concurrent MS and anaplastic astrocytoma is presented. MS was diagnosed in a female patient at the age of 22 years. A left side thalamotomy was performed for relief of severe intention tremor at age 28 and at age 32 she received immunosuppressive therapy for 1 year. At the age of 36 after a severe exacerbation of her symptoms a left side fronto-temporal tumor was diagnosed and a subtotal neurosurgical extirpation was performed. Histopathologically, the tumor was an anaplastic astrocytoma, which was further substantiated by electron microscopy and establishment of a permanent cell line in vitro. The cultured tumor cells were negative for measles virus by immunofluorescence. The relationship between the reactive astrocytes in MS plaques and astrocytic neoplasia is discussed.
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9/11. multiple sclerosis. Oligodendrocyte survival and proliferation in an active established lesion.

    Oligodendrocytes have been studied ultrastructurally in relationship to areas of active demyelination in multiple sclerosis. The tissue came from a central nervous system plaque sampled at biopsy during a neurosurgical procedure to correct severe intention tremor in a case of chronic progressive multiple sclerosis. cells interpreted as oligodendrocytes were abundant within the demyelinated zone, were easily identifiable, and sometimes occurred as nests of cells suggestive of proliferation. Oligodendrocytes were also common within areas of active demyelination where numerous macrophages displayed active phagocytosis of myelin. These oligodendrocytes were paler and perhaps represented residual, surviving cells. In the relatively normal white matter adjacent to the plaque, increased numbers of oligodendrocytes occurred in association with remyelination. In the demyelinated zone, the astrocyte:macrophage:oligodendrocyte ratio was 1:2.25:4.5; within the region of ongoing demyelination, 1:4:4; and in the adjacent white matter, 1:0.1:2.1. On the basis of an apparent proliferation and survival of oligodendrocytes, the findings support the notions that there is no selective depletion of oligodendrocytes either during or shortly following central nervous system demyelination in multiple sclerosis, and that the myelin sheath is the primary target.
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10/11. Case report: dna fragmentation in glial cells in a cerebral biopsy from a multiple sclerosis patient.

    multiple sclerosis is characterized by myelin destruction and oligodendrocyte loss. The neuropathological hallmark of the disease is the presence of demyelinated plaques in the central nervous system. We have recently found a gliotoxic factor in MS cerebrospinal fluid which induces programmed cell death in vitro, in glial cells. Here we show dna fragmentation and glial cell death in biopsy samples, obtained from a patient who underwent surgery with suspicion of tumor, and whose disease record, including brain autopsy, demonstrated an active multiple sclerosis. We used the in situ TUNEL technique, a method which sensitively detects the dna fragmentation accompanying programmed cell death in tissue sections, and compatible with classical fixation techniques. We found intense dna fragmentation in nuclei of glial cells at-or very near-to the site of demyelination. A double labeling technique showed that glial fibrillary associated protein positive astrocytes may undergo programmed cell death in multiple sclerosis.
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