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

In order to determine if axonal transport changes in chronic experimental allergic encephalomyelitis (EAE) were due to blockade or increased discharge of fast transported proteins from the inner retina, we examined the presence of pulse labeled proteins in autoradiograms of the optic nerve head, retinal ganglion cell and nerve fiber layers of juvenile strain-13 guinea pigs with chronic EAE and normal controls. Quantitative analysis of silver grains, performed six and twenty-four hours following the intravitreal injection of tritiated leucine, showed a decrease in inner retinal radioactivity in those with EAE, whereas no difference was detected between the two groups after three days. Grain counts within the optic nerve heads of guinea pigs with EAE were reduced at all time intervals studied. These results are consistent with an increase in discharge of fast transported proteins from retinal ganglion cells into optic nerve axons and support our previous observations of increased radioactivity at the foci of optic nerve demyelination.
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PMID:Quantitative analysis of labelled inner retinal proteins in experimental optic neuritis. 270 41

In order to determine if changes in axonal transport were different in adult animals with acute experimental allergic encephalomyelitis (EAE), in comparison to juvenile animals with chronic EAE, the effects of this acute demyelinating disorder on axonal transport were examined in the optic nerves of adult strain-13 guinea pigs. Utilizing autoradiographic analysis of silver grain counts, both the fast and slow components of orthograde transport were studied at intervals of thirty minutes, three hours, one day and three days after tritiated leucine injection into the vitreous cavity. In order to determine the contribution of fiber loss in acute EAE, optic nerve fiber density was analyzed from electron micrographs of normal and demyelinated nerves. Animals with acute EAE had a decrease in radioactivity at the lamina retinalis and lamina choroidalis after thirty minutes and three hours, and at the lamina scleralis and foci of demyelination after one and three days. A 16% loss of fibers did not account for as much as a 74% reduction in radioactivity with acute EAE. The global reductions in axonal transport observed in acute EAE animals may contribute to their progressive deterioration and eventual demise by lack of delivery of tubulo-vesicular materials for synaptic transmission, axolemmal proteins for electrogenesis and neurofilamentary components of the cytoskeleton. Moreover, they are unlike the increase of fast axonal transport associated with recovery of physiologic function characteristic of animals with the chronic form of the disease.
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PMID:Axonal transport reductions in acute experimental allergic encephalomyelitis: qualitative analysis of the optic nerve. 270 42

Central nervous system lesions in guinea pigs sensitized for chronic relapsing experimental allergic encephalomyelitis for between 18 and 36 months have been found to possess a small but probably significant degree of axonal involvement. Axonal identity was established by light and electron microscopy and immunocytochemistry. The axonal changes were restricted to white matter and consisted of massive (up to 95 microns) scattered axonal spheroids which displayed lateral branches and vacuoles; small groups of spheroids filled with a wide assortment of axoplasmic organelles; and deeper, more extensive collections of affected demyelinated axons and spheroids which frequently displayed abortive axonal regeneration into the Virchow-Robin space. Although accumulations of most axoplasmic organelles occurred in the spheroids and reactive axons, microtubules were relatively rare. These formations were never seen in adjacent unaffected white matter and spinal cord tissue from normal aged animals contained only the occasional spheroid. It is hypothesized that the disease process in experimental allergic encephalomyelitis may be more dynamic than previously described and that prolonged interruption in normal axon-glial relationships in chronically demyelinated (sometimes remyelinated) gliotic lesions might lead to a block in axoplasmic transport and a disruption of the axonal cytoskeleton. Although most affected axons appeared intact, some of the spheroids probably represented proximal stumps from which sprouting occurred, leading to neuroma-like formations. The implications of the findings are discussed in reference to long-term demyelination and multiple sclerosis where almost identical profiles have been documented.
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PMID:Axonal dystrophy as a consequence of long-term demyelination. 271 84

The effect of unilateral peripheral nerve lesions on the inflammatory response of experimental allergic encephalomyelitis (EAE) in rat central nervous system (CNS) was studied. Immunostaining for major histocompatibility complex (MHC) antigens and T-cell subsets demonstrated that MHC class I expression was markedly enhanced in as well as around axotomized motor neurons and that MHC class II expression was induced on several cells, probably microglial cells, in close proximity to the axotomized motor neurons. There was also a pronounced increase in interleukin 2 receptor-positive lymphocytes as well as T-cells and the T-cell subsets on the injured as compared to the non-injured contralateral side. These effects were present particularly in the initial phase of EAE and persisted for several weeks. The results suggest that neurons may communicate immunoregulatory signals to their microenvironment and that retrograde axonal signals from the distant periphery may alter the immune response locally within the CNS.
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PMID:Local enhancement of major histocompatibility complex (MHC) class I and II expression and cell infiltration in experimental allergic encephalomyelitis around axotomized motor neurons. 278 5

Infection of athymic (nu/nu) mice with Theiler's murine encephalomyelitis virus results in an acute encephalitis which resembles poliomyelitis. Immunohistochemistry and in situ hybridization were used to delineate the presence of viral proteins and RNA in the nervous systems of nude mice infected with the Daniels strain of Theiler's virus. This system permits the analysis of a viral infection in the absence of an effective immune response. By immunohistochemistry, viral antigen was found in the processes and cell bodies of neurons and glial cells. Besides the presence of viral antigen in these cell types, by in situ hybridization, Theiler's virus RNA was also found in cells associated with vascular endothelium in the brains and spinal cords of these infected mice. Theiler's virus RNA-positive endothelial cells were observed not only near the primary lesions but also away from demonstrable lesions in normal-appearing regions in the central nervous system. Earlier work had suggested an intra-axonal dissemination for this virus (M. C. Dal Canto and H. L. Lipton, Am. J. Pathol. 106:20-29, 1982). Our findings are consistent with this model but also suggest an additional mechanism for virus spread within the central nervous system, i.e., by infecting vascular cells and crossing the blood-brain barrier. Lastly, after Theiler's murine encephalomyelitis virus infection, not only glial cells but also endothelial cells express major histocompatibility complex class II (la) antigen on their surface (M. Rodriguez, M. L. Pierce, and E. A. Howie, J. Immunol. 138:3438-3442, 1987). Our demonstration of Theiler's virus-infected endotheliumlike cells may explain interactions of virus products in stimulating antigen presentation.
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PMID:Theiler's virus infection in nude mice: viral RNA in vascular endothelial cells. 284 61

A morphological study of selected white matter lesions was carried out in three dogs with canine distemper encephalomyelitis. Two dogs had experimental infections while the third was a spontaneous case. Two stages were identified in the process of demyelination. The earliest evidence of myelin injury was a ballooning change in myelin sheaths involving single or multiple axons. This was followed by a progressive stripping of compact sheaths by the cytoplasmic fingers of phagocytic cells which infiltrated and removed myelin lamellae. Some axonal necrosis also accompanied these changes. Where demyelination occurred, canine distemper viral nucleocapsids were found in astrocytes, macrophages, ependymal cells and infiltrating lymphocytes. In contrast, oligodendrocytes were conspicuous by their apparent lack of infection. Thus it seems that myelin loss cannot be ascribed to oligodendrocyte infection. Perturbed astrocyte function following canine distemper viral infection may cause oedema of myelin sheaths, leading to ballooning and primary demyelination. Cells which phagocytosed myelin were mainly identified as microglial cells with lesser involvement by astrocytes. Rarely, oligodendrocytes also acted as macrophages. Myelin debris was engulfed in bulk or as small droplets into coated pits. Remyelination was present in established plaques although not in great abundance, perhaps due to the diminished oligodendrocyte numbers and a relative increase in immature forms of these cells. These observations are compared to similar changes observed in other demyelinating diseases of animals and man.
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PMID:Demyelination in canine distemper encephalomyelitis: an ultrastructural analysis. 345 Jul 94

The Forssman carotid syndrome was induced in guinea pigs to study the mechanism of demyelination-like lesions in this animal model and to compare it with experimental allergic encephalomyelitis days after intracarotid injection of rabbit anti-Forssman antibody and chronic lesions at 7-21 days post injection, using routine histological, immunofluorescent, and electron-microscopic techniques. The results were compared to those in a group of guinea pigs with acute or chronic lesions of EAE. The picture was remarkably similar in the two conditions, in regard to localization in the central nervous system (CNS), composition of cellular infiltrates, diameter of lesions produced, myelin loss and axonal degeneration, together with gamma globulin deposition in small vessels in affected areas. The differences were that in the Forssman carotid syndrome, in contrast to EAE, there were no mononuclear cell infiltrates in the acute phase, and no evidence of macrophages invading myelin sheaths was detected. Perivascular lesions consisted of demyelination within infiltrates of mono-nuclear cell in chronic relapsing EAE, but not in the Forssman carotid syndrome. It is suggested that investigation of the CNS may be of benefit in the pathogenetic study of demyelinating disease.
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PMID:Similarities between the Forssman carotid syndrome and experimental allergic encephalomyelitis. 351 33

The fine structure is described of a new model of chronic relapsing experimental allergic encephalomyelitis in the SJL/J mouse induced by the single adoptive transfer of myelin basic protein-sensitized lymph node cells. The neuropathology of the condition compared favorably with that seen in other species, and unlike a similar disease in the same strain of mouse induced by active sensitization with a central nervous system emulsion, there was little axonal pathology. Typical of mouse experimental allergic encephalomyelitis was the consistent involvement of polymorphonuclear leukocytes and extravasated material in central nervous system lesions. Remissions showed remyelination to be the major feature in the central nervous system, and clinical relapses were matched pathologically by fresh waves of inflammation and demyelination. Unusually large, apparently organized, sinusoidal collections of lymphoid cells (some of them displaying evidence of proliferation) were seen in the periventricular areas of the brain. The ability to induce chronic relapsing demyelination by passive means indicates that an antigen depot is not necessary for the perpetuation of the disease which is possibly transferred by memory cells in the inoculum. This model has virtue in its applicability to the pathogenesis and therapy of multiple sclerosis.
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PMID:Adoptively transferred chronic relapsing experimental autoimmune encephalomyelitis in the mouse. Neuropathologic analysis. 620 9

The clinical and pathologic manifestation of Theiler's murine encephalomyelitis are age related. Animals infected during the first week of life die of a fulminant encephalitis analogous to human poliomyelitis. By contrast, animals infected within 2 and 4 weeks of age survive but develop chronic relapsing demyelination and persistent infection of the central nervous system. The neonatal infection results in widespread necrosis beginning with neuronal vacuolar degeneration followed by inflammatory infiltrates. Electron microscopy reveals paracrystalline arrays of 27-nm viral particles characteristic of picornaviruses within neurons and macrophages. In addition, oligodendrocytes show reactive changes and intracytoplasmic vacuoles. Immunoperoxidase studies show viral antigen primarily localized within neurons of the cerebral cortex, basal ganglia, hippocampus, and anterior horn cells. Viral antigen is found within the apical dendrites and axonal projections of hippocampal pyramidal cells suggesting that Theiler's murine encephalomyelitis may travel intraaxonally.
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PMID:Neonatal infection with the Daniels strain of Theiler's murine encephalomyelitis virus. 636 74

The cytology of cerebrospinal fluid samples from horses is described. The samples were obtained from 24 normal horses, 35 horses with axonal degeneration and/or spinal cord compression, 29 horses with encephalomyelitis, 14 horses with other lesions of the nervous system, and eight horses with signs of neurologic dysfunction of undetermined origin. (Three of the latter were suspected botulinum intoxications.) Fluid was aspirated from the atlanto-occipital space following general anesthesia or immediately after a lethal dose of barbiturate. In two horses, fluid also was aspirated from the lumbosacral space. Small mononuclear cells were predominant in normal horses, and in most horses with axonal degeneration and encephalomyelitis. Several horses with encephalomyelitis also had neutrophils, eosinophils, and some mitotic figures. Although the cytologic findings were abnormal in many of the horses with disease of the central nervous system, in most horses the cytologic findings were normal.
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PMID:Cytology of equine cerebrospinal fluid. 663 63


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