Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

About 30% of weanling rats inoculated with JHM virus developed a subacute demyelinating encephalomyelitis (SDE) 3 weeks after inoculation (a.i.). From the remaining animals, 5% displayed overt neurological signs 3, 6, and 8 months a.i. Animals with and without clinical signs 6-8 months a.i. were morphologically examined. Fresh demyelinating lesions could be demonstrated in paralyzed animals. Viral antigen was demonstrated and infectious JHM virus could be recovered from one animal which developed clinical signs at 3 months a.i. In one animal with clinical onset of 8 months a.i. completely remyelinated areas as well as recent demyelinating lesions were observed, suggesting a recurrence of the disease process. Remyelinated areas were also found in 40% of clinically silent animals. The morphology of the late onset of the demyelination was similar to that occurring in SDE. Remyelination consisted of both CNS and PNS-type. This animal model offers the possibility to investigate the virus-host relationship which is responsible for the induction of a demyelinating process after a long incubation period.
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PMID:Demyelinating encephalomyelitis induced by a long-term corona virus infection in rats. A preliminary report. 22 Aug 34

Purified myelin from the peripheral nervous system of guinea pig, frog (Rana catesbeiana), rat, rabbit, beef, and human in Freund's adjuvant were injected into the Lewis rat. Groups of rats receiving injections of myelin from different species were examined for signs of dysfunction and lesions in the PNS and CNS. Injection of frog PNS myelin into the Lewis rat did not produce any clinical signs or lesions typical of experimental allergic neuritis (EAN) or experimental allergic encephalomyelitis (EAE). Injection of myelin from the PNS of rat, rabbit, beef, and human elicited clinical signs and lesions characteristic of EAN, while guinea pig myelin injection caused superimposed conditions of EAE and EAN. The myelin proteins from the various species were separated by polyacrylamide gel electrophoresis, the gels were scanned and the individual proteins measured. There did not appear to be a correlation between the amount of P2 protein contained in the different myelin species and the severity of the EAN symptoms and lesions produced. Although the Lewis rat is far more susceptible to EAE caused by guinea pig CNS myelin than by any other species, EAN can be easily induced in this animal by injection of PNS myelin from a number of species.
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PMID:Experimental allergic neuritis in the Lewis rat. 31 20

In relapsing experimental allergic encephalomyelitis, recurrent demyelination was found in the anterior roots and dorsal root ganglia with minimal involvement of the posterior roots. To determine whether this is an antigen-related phenomenon, the distribution, type and intensity of the lesions in the proximal PNS of guinea pigs immunized with anterior roots or myelin were compared to those of animals immunized with posterior roots or myelin. Homologous anterior roots were less neuritogenic than posterior roots or posterior root myelin. Thin layer chromatography of myelin samples from anterior and posterior roots, dorsal root ganglia and sciatic nerve revealed the presence of a sulfogalactoglycerolipid, tentatively identified as sulfated galactosylglyceride (SGG) in all but the posterior root myelin samples. Although the PNS lesions of relapsing experimental allergic encephalomyelitis appear to recapitulate the regional distribution of SGG, the reason why its presence in anterior roots myelin renders them less neuritogenic is at present not clear.
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PMID:Neuritogenic and chemical properties of guinea pig anterior and posterior root myelin. 46 42

Lyme disease, like syphilis, a spirochetal infection, can appear with exacerbations and remissions in different stages. The clinical picture is marked by dermatological, neurological, rheumatic and cardiological complications. PNS complications appear in the second and third stage. Tick bite meningoradiculoneuritis neuritis (Garin-Bujadoux-Bannwarth-Syndrome), characterized by painful asymmetrical sensory and motor dysfunctions and inflamed CSF, is a typical manifestation of the second stage. Mononeuritis multiplex appearing in conjunction with acrodermatitis chronica atrophicans is a typical PNS manifestation of the third stage. CNS involvement may also occur in early and late stages of Lyme-Borreliosis, presenting as myelitis or progressive encephalomyelitis. Lyme-Borreliosis is a treatable condition, which should not be missed in the differential diagnosis of PNS and CNS disorders.
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PMID:Neurological complications of Lyme borreliosis. 134 45

The effect of gangliosides on the clinical expression of experimental allergic neuritis (EAN), a PNS counterpart of experimental allergic encephalomyelitis (EAE), was tested in Lewis rats sensitized with bovine intradural root myelin in complete Freund's adjuvant (CFA). A mixture of bovine brain gangliosides (GM1, GD1a, GD1b, GT1b) was injected intramuscularly at a daily dose of 20 mg per kg beginning 6 days post inoculation. The results show that GA treatment considerably reduces the incidence of mortality, delays its occurrence, and reduces the severity of clinical scores when either the whole population or survivors only are considered. Benefit from GA treatment appeared roughly proportional to disease severity. The neuronotrophic and anti-inflammatory effects possibly play a role in GA protecting effect.
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PMID:Gangliosides improve the outcome of experimental allergic neuritis (EAN). 213 Jun 64

MS and CIP are inflammatory diseases of the CNS and PNS that are characterized by focal demyelination. Both disorders are thought to involve autoimmune processes. The factors that lead to a chronic inflammatory process have not been completely defined, but the immune system is thought to play a prominent role as has been discussed in this chapter. The role of a persistent or recurrent viral exposure has not been reviewed here but may well be a contributing factor. Since chronic relapsing experimental encephalomyelitis in animal models is a T-cell-mediated disease that pathologically resembles MS, T cells are postulated to be of primary importance in human demyelinating diseases. Oligoclonal T-cell populations can be found in the CSF of MS patients, even though their antigenic specificity is not known. HLA associations (HLA Dw2 and HLA DR2 in MS and HLA Dw3 in chronic inflammatory neuropathy) might relate to the proposed immunopathogenesis, as class II antigens encoded by these loci might serve as restriction elements for T-cell recognition of an autoantigen by encephalitogenic cell populations. Humoral factors are thought to play an important role in the pathogenesis of CIP, as plasma exchange has been shown to be beneficial. Experimental work with an antimyelin glycoprotein monoclonal antibody demonstrates the in vivo demyelinating activity of antibodies as well as the importance of cellular elements in the demyelinating process. Finally, a number of immunoregulatory abnormalities have been demonstrated in MS patients that point to defects in immunoregulation, in particular in the generation of suppression. Decreases in AMLR in active MS might be of importance, as the AMLR is a reaction against self MHC determinants during which suppression is generated. Defects in suppression might allow self-reactive cells to escape regulation and cause inflammatory lesions in the nervous system.
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PMID:Immunologic mechanisms in chronic demyelinating diseases of the central and peripheral nervous system. 215 31

T lymphocytes specific for myelin basic protein (MBP) are responsible for the cellular events leading to autoimmune disease within the central (CNS) and peripheral (PNS) nervous systems. Both in actively induced and T-cell transfer versions of experimental autoimmune encephalomyelitis (EAE) and neuritis (EAN), the autoaggressive T cells are activated outside the nervous system and reach their target tissue via the blood circulation. The target specificity of the autoaggressive T cells is impressive; T-cell lines specific for MBP predominantly home to and affect the white matter of the CNS whereas T cells specific for PNS myelin protein P2 exclusively infiltrate peripheral nerves. Having penetrated the tight blood tissue barriers, the lymphocytes seem to interact with local cells expressing the relevant autoantigen in an immunogenic form. Although the exact mechanism of target finding and destruction is unknown, studies from our laboratory have shown that astrocytes, a main component of the normal CNS glia, can actively present antigen to specific T cells. This observation suggests that astrocytes are involved in natural immune reactivity within the CNS, and that they may be involved in pathological aberrations, such as in the development of autoimmune lesions. Having studied astrocyte/T-cell interactions in more detail, we discovered that encephalitogenic T-cell lines recognizing MBP on astrocytes will subsequently proceed to kill the presenting cells. Here we report that astrocyte killing follows the rules governing 'classical' T-cell-mediated cytolysis; it is antigen-specific, restricted by antigens of the major histocompatibility complex (MHC) and apparently contact-dependent. Our data suggest that the nature of the recognized antigenic epitope determines whether or not antigen recognition is followed by killing; moreover, killing of antigen-presenting astrocytes seems to be correlated with the capacity to transfer encephalomyelitis to normal syngeneic rats.
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PMID:Ia-restricted encephalitogenic T lymphocytes mediating EAE lyse autoantigen-presenting astrocytes. 241 64

The distribution of the class II major histocompatibility (Ia) antigens has been studied in the normal nervous system and in acute lesions of experimental allergic encephalomyelitis (EAE). EAE was induced in Lewis rats with guinea pig spinal cord in Freund's complete adjuvant. Frozen sections from cord, including the roots and ganglia, were stained for Ia antigens, and some sections were also stained for the hydrolytic enzyme acid phosphatase. In the normal CNS and PNS, there were a few vessel-associated cells or small leukocyte-like cells which expressed Ia antigens. No cells were found which expressed both Ia and acid phosphatase [the phenotype used to describe the activated macrophage group of antigen presenting cells (APCs)]. In EAE, Ia positive cells increased in number prior to the detection of clinical signs. Some of these Ia-positive cells were thought to be astrocytes rather than inflammatory cells. At the height of the disease process large numbers of cells in the EAE lesions were Ia-positive. Among these infiltrating cells were some large acid phosphatase-positive cells which also expressed Ia antigens. These double-positive cells appeared to be APCs in the form of activated macrophages, cells known to be involved in the demyelinating processes of EAE. Our results show that some vascular and vessel-associated cells in the normal nervous system express Ia antigens. We suggest that these and other Ia-positive cells in acute EAE lesions may have a role in antigen presentation.
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PMID:Ia antigens in the normal rat nervous system and in lesions of experimental allergic encephalomyelitis. 387 81

A 42-year-old woman demonstrated recurrent, progressive neurological symptoms of peripheral and central nervous system damage of undefined infectious origin. Laboratory investigations showed abnormalities in the CSF and serum, suggesting subacute viral infection. Neuropathological examination revealed complete, widespread necrosis in the cervical and thoracic segments of the spinal cord with mononuclear and microglial infiltrations. There was pronounced thickening and fibrinoid necrosis of the vessel walls with mononuclear cuffs along the spinal cord. Dispersed, similar but less intensive inflammatory changes were present in the medulla oblongata, midbrain and basal ganglia. Surprisingly, there was diffuse demyelination with only slight glial and inflammatory reactions throughout the white matter of both hemispheres. The finding of coarse- and fine-grained deposits of IgG and C3 component of complement in the vessel walls of the spinal cord and vasa nervorum of cervical roots and peripheral spinal nerves, together with positive heterologous complement binding and the results of glycine-HC1 buffer elution, suggested immune-complex-mediated disseminated vasculomyelinopathy of the CNS and PNS. Consequent local ischemic changes and hypersensitivity phenomena led to frank necrosis of the cervical spinal cord and to extreme white matter demyelination in the brain. The case was diagnosed as allergic encephalomyelitis in which diffuse demyelination occurred coincidentally with spinal cord necrosis.
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PMID:Necrotic changes of the spinal cord with immune-complex-mediated disseminated vasculitis in a case of atypical allergic encephalomyelitis. 390 21

Paraneoplastic neurological syndromes have attracted attention in recent years. Detection of auto-antibodies directed against CNS and PNS structures have suggested an autoimmune etiology. This review is based on reports from the past 10 years and summarizes the therapeutic results in 258 patients suffering from paraneoplastic neurological disease including paraneoplastic encephalomyelitis, sensory neuronopathy, cerebellar degeneration, motor neurone disease and stiff man syndrome. The results show that in some entities such as Lambert-Eaton syndrome successful treatment can be expected. In other syndromes such as subacute sensory neuronopathy or paraneoplastic cerebellar degeneration therapeutic success varies from 5 to 10%.
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PMID:Anti-tumour therapy in paraneoplastic neurological disease. 778 65


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