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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five cases of acute disseminated encephalomyelitis (ADE) with a follow-up longer than 5 years are presented. The clinical picture, CT images, MR and laboratory tests, specially LCR and evoked potentials presented in a variable form. In two cases the symptoms were preceded by viral infection. The course was acute in one case while the other four evolved in a subacute form during weeks. In two patients a pseudotumoral pattern was observed in the CT and MR images leading to difficulties in the diagnosis. Clinical improvement was accompanied by a partial resolution of the lesions. Steroid treatment improved symptomatology in all the cases. Knowledge of this process may avoid the unnecessary practice of other, more aggressive tests.
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PMID:[Disseminated encephalomyelitis. A study of 5 cases]. 835 77

Recovery from viral infection is a result of very complex interactions between specific and nonspecific immune reactions and the infectious agent. A variety of immune mechanisms are undoubtedly important factors in this event and operate together in overcoming the infectious process. However, despite much available information about these viral defense mechanisms, it has proved remarkably difficult to assign a determinative role in vivo to any single antiviral immunological mechanism in recovery from a single viral disease, particularly since the immune response to the virus itself may frequently contribute to the pathology of the disease. Furthermore, if virus-induced immune responses are also directed against normal host components, this may set the stage for an autoimmune disease. In this context acute measles encephalomyelitis is of interest since in this disease autoimmune reactions against brain antigens have been observed and considered of pathogenetic importance. In this short review, virological and immunological findings of measles virus infections in a rat model in relation to autoimmune reactions will be presented and the mechanisms by which measles virus may alter host reactivity against self-antigens discussed.
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PMID:Measles virus-induced autoimmune reactions against brain antigen. 840 53

Theiler's murine encephalomyelitis virus (TMEV) infection and experimental allergic encephalomyelitis (EAE) are considered among the best models of human multiple sclerosis (MS). In both models, clinical disease is characterized by paralysis, while pathological changes consist of inflammatory demyelination. In both models there is a genetic influence on susceptibility/resistance to the development of disease. This has been thoroughly studied in TMEV infection, and it has been found to depend on both major histocompatibility complex (MHC) and non-MHC genes. At least four genes have been so far identified. Because of this genetic influence, some strains of mice are more susceptible to both clinical and pathological changes than others, and susceptibility appears to best correlate with the ability of a certain murine strain to develop a delayed-type hypersensitivity (DTH) response to viral antigens. We have also observed that even among mice which are equally susceptible clinically, striking differences may be seen under pathological examination. These consist of different gradients of severity of inflammation, particularly in regards to the macrophage component. There is an inverse relationship between the number of macrophages, and their length of stay in the CNS, and the ability of mice to remyelinate their lesions. The most severe lesions are in SJL/J mice, and remyelination in this strain is extremely poor. The least severe lesions in terms of macrophage invasion are in strains such as NZW and RIIIS/J, and these are able to remyelinate lesions very successfully. Murine chronic relapsing EAE (CR-EAE) shows pathological changes in many ways similar to those in TMEV-infected SJL/J mice, although less severe in terms of degrees of macrophage infiltration and tissue destruction. Mice with CR-EAE have a correspondingly limited ability to remyelinate their lesions. In both models the pathology appears to be mediated through a DTH response. However, while in EAE the DTH response is clearly against neuroantigens, the response in TMEV infection is against the virus itself. The end result in both models would be that of myelin destruction through a lymphotoxin-cytokine-mediated mechanism. The importance of the DTH response in both models is well illustrated by the effects of tolerance induction in EAE and TMEV infection to neuroantigens and virus, respectively. These are important models of human MS, since the current hypothesis is that a viral infection early in life, on the appropriate genetic background, may trigger a secondary misdirected immune response which could be directed either against myelin antigens and/or possible persistent virus(es).
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PMID:Two models of multiple sclerosis: experimental allergic encephalomyelitis (EAE) and Theiler's murine encephalomyelitis virus (TMEV) infection. A pathological and immunological comparison. 852 56

Mice with targeted disruption of the A beta gene of major histocompatibility complex class II molecules (Abo) were used to investigate the role of class II gene products in resistance or susceptibility to virus-induced chronic demyelination in the central nervous system (CNS). Class-II-deficient mice from the resistant H-2b [H-2b(Abo)] and nonmutant H-2b backgrounds were infected with Theiler's murine encephalomyelitis virus intracerebrally and examined for CNS virus persistence, demyelination, and neurologic clinical signs. Virus titers measured by plaque assays showed that 8 of 10 normally resistant nonmutant H-2b mice had cleared the virus within 21 days, whereas the other 2 mice had low titers. In contrast, all class II-deficient Abo mice had high virus titers for up to 90 days after infection (4.30 log10 PFU per g of CNS tissue). Virus antigens and RNA were localized to the brains (cortex, hippocampus, thalamus, and brain stem) and spinal cords of Abo mice. Colocalization identified persistent Theiler's murine encephalomyelitis virus in oligodendrocytes and astrocytes but not in macrophages. There was demyelination in 11 of 23 and 6 of 9 Abo mice 45 and 90 days after virus infection, respectively, whereas no demyelination was observed in infected nonmutant H-2b mice. Demyelinating lesions in Abo mice showed virus-specific CD8+ T cells and macrophages but no CD4+ T cells. Spasticity and paralysis were observed in chronically infected Abo mice but not in the nonmutant H-2b mice. These findings demonstrate that class II gene products are required for virus clearance from the CNS but not for demyelination and neurologic disease.
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PMID:Theiler's virus persistence and demyelination in major histocompatibility complex class II-deficient mice. 862 94

The association of viral infections with autoimmune central nervous system (CNS) diseases such as post-infectious encephalomyelitis and possibly multiple sclerosis (MS) prompted the investigation to understand how virus infection could modulate autoimmune responses. Recombinant vaccinia viruses encoding an encephalitogenic portion of myelin basic protein (MBP) were evaluated in an animal model for human demyelinating disease, experimental allergic encephalomyelitis (EAE). We have determined that mice vaccinated with recombinant viruses encoding an encephalitogenic region of MBP were protected from EAE. In vivo depletion of CD8+ T cells did not abrogate this protection, suggesting lack of regulation by this cell type. These studies demonstrate that virus infection may be a means to modulated immune responsiveness to CNS disease.
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PMID:Virus encoding an encephalitogenic peptide protects mice from experimental allergic encephalomyelitis. 863 58

Neuropsychiatric complications in the course of plasmodium falciparum infection are usually summarized as cerebral malaria. Heterogeneous clinical symptoms, different courses and inconstant parasitemia, however, suggest different pathogenic mechanisms. We report a case of an acute symptomatic psychosis occurring two weeks after successful therapy of a primary manifestation of plasmodium falciparum infection. The diagnosis of meningoencephalitis was based on lymphocytic pleocytosis of cerebrospinal fluid and hyperintense lesions in cranial magnetic resonance imaging. Due to the lack of plasmodium falciparum parasitemia and of serological evidence of viral infection a final diagnosis was not possible. Considering the pertinent literature, an immune-mediated complication of plasmodium falciparum infection (acute disseminated encephalomyelitis, ADEM) appears to be more probable than a direct viral or plasmodium CNS infection. We propose to reverse the term cerebral malaria for the cases with direct pathogenic influence of plasmodium falciparum, and to distinguish it from cases with possible immune-mediated pathogenesis.
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PMID:[Acute organic psychosis after malaria tropica]. 867 92

Expression of class II major histocompatibility complex (MHC) molecules by non-immune cells (e.g., parenchymal cells) leads to the presentation of self-antigens, and may have a role in the pathogenesis of many diseases mediated by autoimmunity. Such diseases, characterized by demyelination of the central nervous system and expression of class II MHC molecules on neural cells, include multiple sclerosis, experimental allergic encephalitis and Theiler's murine encephalomyelitis virus infection. Canine distemper encephalitis probably does not have an autoimmune character, but it shares many similarities with the aforementioned diseases. For this reason, the expression of class II MHC molecules in the brains of dogs with canine distemper encephalitis was investigated immunohistochemically. The results presented here demonstrate that canine microglia and astrocytes "upregulate" class II MHC expression in cases of encephalitis associated with chronic canine distemper.
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PMID:Neural cells from dogs with spontaneous distemper encephalitis express class II major histocompatibility complex molecules. 872 79

We report a case of multiphasic disseminated encephalomyelitis (MDEM) following viral illness presenting as multiple sclerosis (MS) in a 7-year-old boy. The patients had two episodes of alternating hemiparesis and other neurologic symptoms following viral infection, which were separated by 3 years. Neuroimaging studies demonstrated multiple, discrete, small nodules and large globular lesions in the cerebral white matter, basal ganglia, brainstem and cerebellar areas. Based on typical appearance of magnetic resonance imaging (MRI) and clinical manifestations including systemic symptoms such as fever, nausea, vomiting, headache and seizures followed by consciousness disturbance and other multifocal neurologic signs, the diagnosis of MDEM rather than that of MS was made. Because it is difficult to differentiate between MDEM and MS on the basis of the clinical history, the cerebrospinal fluid examination and evoked potential studies, this report emphasizes that the MRI study of the brain may provide an important clue for the diagnosis.
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PMID:Multiphasic disseminated encephalomyelitis mimicking multiple sclerosis. 889 Dec 39

Intracerebral infection of susceptible mouse strains with Theiler's murine encephalomyelitis virus (TMEV) results in an immune-mediated demyelinating disease (TMEV-IDD) similar to human multiple sclerosis (MS). Although the etiology of MS remains unknown, a role of an infectious agent has been implicated in its onset. Previously we have shown the ability of bacterial lipopolysaccharide (LPS) to alter susceptibility to TMEV-IDD in genetically resistant C57BL/6 mice. In this study, the potential of LPS to alter pathogenicity of a low/non-pathogenic variant of TMEV was investigated. After intraperitoneal treatment of genetically susceptible SJL/J mice with LPS before and during viral infection, 80-100% of the mice developed clinical symptoms, while without LPS treatment none of the mice were affected. However, clinical severity in these LPS-treated mice was much milder than the level induced by the wild type pathogenic virus. Increased susceptibility to the disease after LPS treatment did not correlate with splenic T cell proliferative responses against viral antigens. However, by reverse transcriptase polymerase chain reaction (RT-PCR) analyses, an early increase in the production of Th1-type proinflammatory cytokine messages (e.g., interferon-gamma [IFN-gamma] and enhancement of viral persistence was observed in the CNS of LPS-treated, virus-infected animals as compared to mice infected with the variant virus alone. These results indicate that environmental factors such as a bacterial infection (e.g., LPS) promoting proinflammatory cytokine production can significantly enhance the pathogenicity of demyelination induced by a normally non-pathogenic virus.
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PMID:Treatment with lipopolysaccharide enhances the pathogenicity of a low-pathogenic variant of Theiler's murine encephalomyelitis virus. 889 89

We present the unusual case of 16-year-old girl who developed intractable convulsions five days after the onset of a cold. Meningeal signs, lymphopenia, proteinuria, and lupus anticoagulant were also present. Treatment with anticonvulsants, antituberculous agents, and adenine arabinoside were ineffective. The initiation of methylprednisolone pulse therapy immediately resolved convulsions and fever. The diagnosis, suggested by the clinical course and the marked improvement of the meningoencephalitis by pulse therapy, was an encephalitic form of acute disseminated encephalomyelitis. Clinical and laboratory findings indicated that an immune disorder may have triggered an abnormal response to a viral infection leading to this patient's neurologic disorder.
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PMID:Patient with both lupus anticoagulant and acute disseminated encephalomyelitis. 889 67


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