No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Multiple Sclerosis: Experimental and Clinical Aspects
... Los TPx de la E.M pueden presentarse como forma de inicio o en el transcurso clínico de la enfermedad en un 10 a 20% de los enfermos [2][3] . ...
The presence of paroxystical symptoms(PS) in Multiple Sclerosis is well known. We found PS (44 episodes) in 30 of 155 patients (19.34%), whose mean age is 35 years (17- 63 years).12 patients presented more than one PS (40%), 12 PS were considered relapses (27.3%), 10 PS (22.7%) happened as form of presentation, 22 (50%) in the period RR, 9 (20.4%) in the stage of secondary progression and 3 (6.8%) in progressive primary form. They were more common at the beginning, in the form RR and during the first five years of the disease. It was considered besides that 4 patients of the total (2.6%) that started with relapses as PS, constituted a clinically isolated syndrome, that later were converted in MS. The PS are a manifestation of the disease, that according to the moment they happen are relevant for the early diagnosis of MS and when they seem relapses during the disease they must be considered for the control of the current treatments.
... Los TPx de la E.M pueden presentarse como forma de inicio o en el transcurso clínico de la enfermedad en un 10 a 20% de los enfermos [2][3] . ...
symptoms(PS) in Multiple Sclerosis is well known. We found PS (44 episodes) in 30 of 155 patients (19.34%), whose mean age is 35 years (17- 63 years).12 patients presented more than one PS (40%), 12 PS were con- sidered relapses (27.3%), 10 PS (22.7%) happened as form of presentation, 22 (50%) in the period RR, 9 (20.4%) in the stage of secondary progression and 3 (6.8%) in progressive primary form. They were more common at the beginning, in the form RR and during the first five years of the disease. It was considered besides that 4 patients of the total (2.6%) that started with relapses as PS, constituted a clinically isolated syndrome, that later were converted in MS. The PS are a manifestation of the disease, that according to the moment they happen are relevant for the early diagnosis of MS and when they seem relapses during the disease they must be con- sidered for the control of the current treatments.
Thoracic flexion, a rapid forward flexion at the waist, can elicit a circumferential electrical sensation in some patients with multiple sclerosis. The clinical and radiographic features of this phenomenon are described here. This symptom is typically a sensory band around the T6-T7 dermatomes and is usually associated with recent thoracic cord lesions. It is clinically independent of cervical pathology and Lhermitte’s sign. Similar to the vertical radiation of symptoms upon neck flexion due to cervical cord lesions, this sign may help localize MS plaques to the thoracic cord, even when thoracic MRI is negative.
Neurocisticercose (NC) continua a destacar-se em países em desenvolvi-mento e, também, naqueles considerados do primeiro mundo como a principal afecção do sistema nervoso central (SNC) causada por parasitas animais 15,58,63. A gravidade das lesões que pode provocar e a complexidade da sintomatologia, apesar dos avanços nas últimas décadas quanto a aspectos diagnósticos e tera-pêuticos, levam a considerar a profilaxia a melhor arma contra a afecção. Na atualidade, pelo menos três critérios devem ser considerados conjuntamente para o estudo da NC: o clínico, o tomográfico (TC) e o do líquido cefalorraqueano (LCR). Os três trazem informação de ordem diversa quanto ao diagnóstico, tratamento e controle da evolução. Um complementa o outro, porém, um não substitui o outro 10,35,45,51,54. o LCR é a parte do compartimento aquoso do SNC mais acessível em seres humanos ao estudo de fenômenos neuroimuno¬ lógicos. Na afecção continua válido, portanto, afirmar ser básico o estudo do LCR para o diagnóstico, acompanhamento evolutivo e controle de terapêu-ticas 20,29,50. No final da década de 1970, foi introduzido no tratamento medicamentoso da NC derivado pirazinoisoquinoleínico denominado praziquantel, o qual tem-se mostrado satisfatório em certas formas da doença. No entanto, até o presente, não existe estudo sistematizado seqüencial, durante longo período de evolução, dos fenômenos neuroimunológicos por ele induzidos e observados no LCR 16,38,42,55,56 Dentre os estudos neuroimunológicos de interesse à NC destacam-se aque-les relativos à imunidade humoral, que levam em conta anticorpos anti-Cysticercus cellulosae detectados no LCR e soro e a ocorrência de imunoprodução local, excluída a eventual interferência de danos provocados pela doença na barreira hêmato-encefálica (BHE). Relações e índices, bem como a verificação de bandas oligoclonais de globulinas gama apenas no LCR, permitem avaliar o compor-tamento da imunidade humoral em processos patológicos do SNC que desen-cadeiem reação inflamatória local, como a NC 22-25,31,60.
CD40 is a protein on microglia that is up-regulated with interferon (IFN)-γ and is engaged by CD40L, found on CD4+ T cells, B cells, and monocytes. These interactions may be important in central nervous system inflammatory diseases. Microglia have been shown to be a source of chemokines, whose expression plays a key role in central nervous system pathologies. We examined the expression of CD40 on microglia in human immunodeficiency virus (HIV) encephalitic brain, and the effects of CD40-CD40L interactions on the expression of chemokines by cultured microglia. We found significantly increased numbers of CD40-positive microglia in HIV-infected brain tissue. Treatment of cultured microglia with IFN-γ and CD40L increased expression of several chemokines. IFN-γ- and CD40L-induced MCP-1 protein was mediated by activation of the ERK1/2 MAPK pathway, and Western blot analysis demonstrated phosphorylation of ERK1/2 upon stimulation of microglia. In contrast, IFN-γ- and CD40L-induced IP-10 protein production was mediated by the p38 MAPK pathway. Our data suggest a mechanism whereby CD40L+ cells can induce microglia to secrete chemokines, amplifying inflammatory processes seen in HIV encephalitis and multiple sclerosis, and implicate CD40-CD40L interactions as a target for interventional strategies.
Interferons (IFN) are biological molecules with anti-viral, anti-proliferative and immunomodulatory actions. There is evidence that IFN-γ increases the frequency of exacerbations of multiple sclerosis (MS) whereas IFN-β may reduce their frequency. Here we present evidence that IFN-β significantly decreases concanavalin A (Con A)-induced proliferation of peripheral blood mononuclear cells (PBMC) of MS patients and healthy individuals. Similar results were obtained when PBMS were activated through the T cell receptor (TcR) by anti-CD3 monoclonal antibody or independently of it by phorbol ester and Ca2+ ionophore. These effects of IFN-β were also noted when IFN-γ and IFN-β were added together. Furthermore, IFN-β decreased proliferation when added to cells that were already pre-activated. Activated CD4+ and CD8+ T cells were downregulated to approximately the same extent. Analysis of cytokine production showed that IFN-γ production by Con A activated PBMC was increased in MS when compared to controls. IFN-β significantly decreased IFN-γ production in MS patients and control individuals. Con A activated cultures treated with IFN-β showed decreased IL2R expression and accumulation of IL2. These results show that IFN-β decreases T cell activation and IFN-γ production in vitro, effects that may be beneficial in MS.
Multiple sclerosis (MS) is one of the most common demyelinating diseases of the central nervous system affecting adults between the ages of 20 and 40 years. Clinically, it is characterized by episodes of exacerbations and remissions. Although the cause of MS is unknown, it is generally believed that one or more infectious agents triggers an autoimmune response that causes myelin destruction. There is no known cure for this disease; however, early diagnosis is helpful in the management of patients with MS. The diagnosis of MS is commonly made on the basis of established clinical criteria. No specific laboratory diagnostic test exists, but detection of abnormalities in cerebrospinal fluid (CSF) is a useful aid to support the clinical diagnosis of MS. This review describes the most common CSF abnormalities. These include (a) elevation of immunoglobulin G (IgG), IgG index and IgG synthesis rate; and (b) detection of oligoclonal IgG bands in the CSF by electrophoresis and isoelectric-focusing procedures.
To analyze immunopathologic events within the central nervous system (CNS) during various stages of actively induced chronic relapsing EAE in SJL/J mice, animals were sampled at various timepoints post inoculation (PI) and T cells, T-cell subsets, Ia+ cells and Ig+ cells, albumin, and Ig deposits were localized in frozen sections by immunocytochemical techniques. Furthermore, sections were stained for the demonstration of Ia antigen, myelin basic protein (MBP), and galactocerebroside (GC) on endothelial cells and astrocytes. During the acute phase of the disease, large numbers of all types of inflammatory cells studied (Lyt-1.2+, L3T4+, Lyt-2+, Ia+, Ig+) were randomly distributed throughout lesions, a finding similar to that described previously for acute EAE. A more distinct distribution pattern of infiltrating T cells was found during active chronic disease in that L3T4+ cells predominated within the CNS parenchyma, while Lyt-2+ cells were more numerous in meningeal and perivascular areas. During all chronic stages, a low-grade diffuse infiltration of the neuraxis by hematogenous cells was present. Ia and myelin antigens were detectable on some endothelial cells and astrocytes. Damage to the blood-brain barrier, as indicated by albumin and Ig deposits, was more extensive during the acute than during chronic stages of the disease. Taken in concert, the results further support the possibility of local antigen presentation on endothelial and astroglial cells and an essential involvement of helper (L3T4+) T cells in CNS lesion formation. These findings correlate well with events reported previously in acute and chronic multiple sclerosis lesions.
Natural killer (NK) cells are evolutionarily early lymphocytes that lack antigen-specific receptors and, hence, are considered to be part of the innate immune system. The majority of research on NK cells has focused on their ability to lyse "target cells", generally identified by low or absent MHC Class I expression, such as tumor cells and virus infected cells. However, an alternative role of these leukocytes as regulators of adaptive (and potentially destructive) immune responses, in particular organ-specific autoimmune diseases, has been increasingly recognized. Here we discuss the growing body of evidence that NK cells limit damage in autoimmune demyelinating disease by inhibiting autoreactive T cell responses without harming resident neurons or glia.
ResearchGate has not been able to resolve any references for this publication.