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)

Within a group of neuro-ophthalmic patients (147 patients with either florid or cured optic neuritis (ON), five (3.4%) were found to be suffering from retinal periphlebitis "Rucker". Of these five patients, three were also suffering from Encephalomyelitis disseminata (E.d.). One patient had ON without E.d.; in another there were sufficient grounds for a tentative diagnosis of ON during the follow-up period. The relatively low percentage of patients with retinal periphlebitis associated with a basic demyelinating condition can be attributed primarily to the fact that the group of patients examined consisted of neuro-ophthalmic patients in most of whom the basic disease manifested itself for the first time. The multi-focal processes involved in demyelinating diseases become apparent through inflammatory focuses with varying degrees of activity, often in the same eye.
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PMID:[Periphlebitis retinae ("Rucker")--a symptom of disseminated encephalomyelitis]. 270 34

Detoxification of hydrogen peroxide by the antioxidant enzyme catalase suppressed the neurologic manifestations of acute experimental allergic encephalomyelitis (EAE) and prevented death of treated adult strain-13 guinea pigs. The oxygen radical scavenger superoxide dismutase (SOD) delayed the onset of paralysis by one day, but did not prevent death from encephalomyelitis common to most of this group and all untreated animals. Histopathologic analysis of the optic nerves confirmed a statistically significant reduction in demyelination with catalase treatment, but not with SOD. Hydrogen peroxide, and/or its conversion products, discharged by phagocytic mononuclear cells, may play a role in the pathogenesis of demyelination in experimental optic neuritis.
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PMID:Antioxidant enzyme suppression of demyelination in experimental optic neuritis. 273 52

We studied the effect of antioxidant enzymes on the loss of integrity of the blood-brain barrier in the optic nerves of strain-13 guinea pigs with chronic experimental allergic encephalomyelitis, a demyelinating disorder with neurologic and histopathologic characteristics similar to multiple sclerosis. Animals with experimental allergic encephalomyelitis received daily intraperitoneal injections of either preservative-free saline (group 1), catalase (group 2), or glutathione peroxidase (group 3) for 2.2 months after the onset of appendicular paralysis. Following intravascular administration, extravascular leakage of horseradish peroxidase was histopathologically graded as mild, moderate, or severe within the optic nerve head and myelinated retrolaminar nerve. Severe extravasation of horseradish peroxidase was exclusive to group 1, in addition to moderate and mild leakage. In groups 2 and 3, leakage of horseradish peroxidase was infrequent, and when detected, it was graded as mild. Detoxification of hydrogen peroxide with catalase and glutathione peroxidase substantially reduced horseradish peroxidase leakage in experimental optic neuritis, suggesting a role for hydrogen peroxide and its reactive by-products in the pathogenesis of increased vascular permeability of the blood-brain barrier in experimental allergic encephalomyelitis.
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PMID:Antioxidant enzymes reduce loss of blood-brain barrier integrity in experimental optic neuritis. 278 67

This study explores the longitudinal assessment of visual evoked potentials (VEPs) in the rabbit as a method for defining factors underlying functional and structural changes associated with optic neuritis and the inflammatory demyelinating diseases. In rabbits with experimental autoimmune encephalomyelitis (EAE) induced by sensitization with guinea pig spinal cord myelin, injection of lymphokines into the posterior chamber of one eye (monocular challenge) produces an early inflammatory response in the retina and optic nerve, and an alteration in the VEP, all limited to the injected eye and its projections. The earliest changes in the timing and distribution of the cortical VEP occur within hours of ocular challenge and precede histopathological evidence of structural demyelination at the light microscope level. Prechallenge assessment allows the induced monocular prechiasmal effects to be distinguished from the more diffuse electrophysiological findings associated with EAE (i.e. those due to sensitization alone). In sensitized/challenged animals there is a clear correspondence between electrophysiological and morphological measures of dysfunction at the time points sampled. These results suggest that this model system afford an excellent opportunity to examine the precise structural correlates of the early functional changes associated with the onset of inflammatory demyelination within the CNS. Furthermore, the stability of the system provides the capacity to monitor alterations over the complete course of inflammation, demyelination and remyelination, induced by experimental manipulations.
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PMID:Electrophysiological analysis of factors involved in the primary demyelinating diseases: the rabbit eye model system. 319 90

A 63-year-old man developed bilateral paresis of horizontal and upward eye movements. He was found to have a small oat cell carcinoma of the lung. Four months later he experienced acute visual blurring on the right side. Examination of the right eye at that time revealed a visual acuity of 3/200 and a central scotoma. There was swelling of the right optic disc. Three weeks after the onset of the visual loss, the acuity of the right eye spontaneously improved to 20/60, the field deficit lessened, and there was a decrease in the swelling of the optic disc. Subsequently, his neuro-ophthalmologic condition remained unchanged but his general health deteriorated, and he died nine months after the onset of the disease. Neuropathologic examination showed mild perivascular lymphocytic infiltration and fibrosis of the meninges throughout the central nervous system, loss of neurons and gliosis in the third and fourth cranial nerve nuclei, perivascular inflammation and gliosis of the optic nerves, and chiasm and central demyelination of the right optic nerve. No tumor cells were seen. These findings were consistent with a diagnosis of paraneoplastic optic neuritis and paraneoplastic encephalomyelitis. The present case confirms the existence of paraneoplastic optic neuritis and illustrates the clinical course of the disease.
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PMID:Paraneoplastic optic neuritis and encephalomyelitis. Report of a case. 334 61

We have produced hybridoma antibodies directed against immunoglobulins present in the cerebrospinal fluid of a patient with multiple sclerosis (MS). One hybridoma antibody recognized an idiotypic determinant of an immunoglobulin population [an idiotype (Id)] which constituted approximately 1% of the immunoglobulin present in the cerebrospinal fluid. The Id focused in the pH range 8.0-8.4. It was present at roughly 10- to 15-fold higher relative (compared to total immunoglobulin) concentration in cerebrospinal fluid than in serum of the homologous MS patient. The Id could not be detected in three cerebrospinal fluid samples and 28 serum samples of heterologous MS patients or in the serum of 43 optic neuritis patients. The Id persisted in the homologous MS patient at increased concentration over the entire (6 years) observation period. The Id could be shown to react with a Theiler murine encephalomyelitis virus strain WW which was isolated from mice after inoculation with periplaque white matter from brain in a histologically confirmed case of MS.
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PMID:Analysis of a predominant immunoglobulin population in the cerebrospinal fluid of a multiple sclerosis patient by means of an anti-idiotypic hybridoma antibody. 694 28

A case of a 4-year-old white girl affected with unilateral optic neuritis and acute cerebellar ataxia is presented. Visual evoked potentials (VEP) demonstrated prolonged latency of the right optic nerve as well as the left retrochiasmal pathways. This child had complete resolution of the cerebellar ataxia and the optic neuritis with return to normal of her VEP. This case is an example of a disease characterized by a single episode of multifocal involvement of the CNS differing from diffuse encephalomyelitis and multiple sclerosis.
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PMID:Acute cerebellar ataxia of childhood and optic neuritis with retrochiasmal involvement. 712 63

Optic nerve tissue from strain 13 guinea pigs sensitized for chronic (relapsing) experimental allergic encephalomyelitis has been examined up to 3 years postinoculation. The changes were compared with the clinical history in each case, with lesions occurring elsewhere in the central nervous system and with optic nerve tissue from a single case of chronic multiple sclerosis. In chronic experimental allergic encephalomyelitis was found that optic neuritis was a consistent finding. Active lesions in the optic nerve were a feature of animals sampled up to 4 months postinoculation. Unlike lesions in the spinal cord, changes occurring in long term animals did not parallel clinical signs. The absence of active lesions in long term animals was apparently not due to a resistance to recurrent disease on the part of the tissue since a second challenge with central nervour system tissue was capable of producing active inflammation in the optic nerve. It appears, therefore, that in its unmanipulated state, chronic experimental allergic encephalomyelitis is more a disease of the spinal cord. Optic nerve changes in the case of multiple sclerosis did not compare well with the guinea pit lesions--discrepancies which we speculate as being related to differences in anatomy, age, species, and longevity of the disease process (among others), rather than a difference in pathogenesis.
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PMID:Optic neuritis and chronic relapsing experimental allergic encephalomyelitis: relationship to clinical course and comparison with multiple sclerosis. 718 1

Experimental allergic encephalomyelitis (EAE) was produced in 6 adult rhesus monkeys. All the animals developed acute EAE. Optic neuritis developed in all eyes. A vasculo-occlusive retinopathy was seen in five of the 12 eyes. Conjunctivitis and iridocyclitis were seen in some eyes. The available evidence indicates that the retinopathy is secondary to the optic nerve changes and represents central retinal vein occlusion by intraneural compression. Histopathologic studies revealed no evidence of inflammatory infiltration in the retina or around the retinal vessels.
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PMID:Experimental allergic encephalomyelitis. II. Retinal and other ocular manifestations. 719 94

Experimental allergic encephalomyelitis (EAE) was produced in six adult rhesus monkeys. The animals were evaluated serially by ocular, ophthalmoscopic, fluorescein fundus angiographic, pupillary, visual evoked potential, neurologic, cerebrospinal fluid (CSF), and hematologic examinations and by postmortem detailed histopathologic examination. All the animals developed acute EAE. Four of the monkeys, surviving longer than 1 month, developed chronic relapsing EAE and were sacrificed 3 to 14 months after sensitization. All 12 eyes developed acute optic neuritis (with variable degrees of optic disc edema and visual loss). Later on, all the eyes of animals with chronic EAE developed optic atrophy with total or almost total blindness. Histopathologic examination of the optic nerve and central nervous system revealed inflammatory infiltrates, extensive demyelination, and axonal degeneration, without inflammation in the retina or optic nerve head (i.e., nonmyelinated neural tissue). Relapsing EAE was reflected in episodic increases of CSF proteins and pleocytosis. The various findings are correlated.
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PMID:Experimental allergic encephalomyelitis. I. Optic nerve and central nervous system manifestations. 725 9


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