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)

mAb reactive with T suppressor factors (TsF) were used to alter the course of myelin basic protein-induced experimental allergic encephalomyelitis in (SJL/J x PL/J)F1 mice. In vivo administration of mAb 14-12, reactive with effector TsF, exacerbated the clinical expression of encephalomyelitis as evidenced by prolonged periods of total limb paralysis in affected animals. This aggravation of disease signs is probably related to the inhibition of effector Ts function by mAb 14-12 thus allowing T cell autoreactivity to proceed unchecked. Disease course was influenced more favorably by i.v. administration of mAb 14-30 reactive with a subset of inducer TsF. Ten days of treatment with this mAb resulted in a reduction in the incidence and severity of disease, noted as the development of minimal limb weakness but no paralysis in the majority of affected animals. Adoptive transfer experiments revealed the presence of Ag-specific Ts in mAb 14-30-treated mice that inhibited recipient Lyt-1+ responses to myelin basic protein, the immunizing autoantigen. Suppression by transferred Ts was revealed only by treatment of the donor population with anti-Lyt-1.2 plus C, however, indicating a role for contrasuppressor activity in the regulation of autoimmune T cell function. Results are considered relevant to the potential for immunotherapeutic management of multiple sclerosis in man.
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PMID:Modulation of experimental allergic encephalomyelitis with anti-T suppressor factor antibodies. 290 41

Kunjin virus encephalomyelitis is described in a 49-year-old man who presented with an episode of acute encephalitis. He developed profound bulbar, truncal and proximal muscle weakness suggestive of damage to cranial motor nuclei and anterior horn cells. This resolved very slowly. A marked rise in antibody titres to Kunjin virus was shown by haemagglutination inhibition tests. Specific IgM antibodies were detected only against Kunjin virus.
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PMID:Kunjin virus encephalomyelitis. 300 85

Catecholamine concentrations of the spleen were studied with neurochemical techniques in rats injected with myelin basic protein to produce an experimental allergic encephalomyelitis (EAE). Thirteen to 14 days postinoculation the affected rats showed peak clinical signs of weakness, especially in the lower extremities. Resolution of the disease then progressed rapidly with full clinical recovery at day 21. Splenic concentrations of norepinephrine (NE), 3,4-dihydroxyphenylalanine (DOPA), epinephrine (EPI) and 3,4-dihyxroxyphenylethylamine (DA) were determined by HPLC with electrochemical detection. DOPA concentrations were significantly increased (+62%) while DA concentrations were decreased (-29%) in the EAE rats on day 14 postinoculation. NE and EPI concentrations tended to be elevated in the EAE group, but this was not statistically significant. No differences in splenic catecholamines were detected on day 7 and 52 postinoculation between EAE and control animals. These results indicate that changes in the metabolic pathways of splenic catecholamines occur at the peak of the clinical symptoms of EAE; the increase in DOPA and the decrease in DA concentrations suggest that the activity of DOPA-decarboxylase or its co-factor is altered.
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PMID:Altered splenic catecholamine concentrations during experimental allergic encephalomyelitis. 311 Jul 96

Histological and electrophysiological studies were performed on Lewis rats with acute experimental allergic encephalomyelitis (EAE) induced by inoculation with guinea-pig spinal cord and Freund's adjuvants, in order to determine the cause of the neurological signs. These studies demonstrated demyelination-induced nerve conduction block in the large and also the smaller diameter fibres at the ventral root exit zone (VREZ) of the lumbar spinal cord. The demyelination at the VREZ affected both centrally and peripherally myelinated internodes, but predominantly the former. Studies on the H reflex recorded from a hindfoot muscle indicated normal peripheral nerve motor conduction but interruption of the monosynaptic reflex arc, as would be anticipated from this efferent conduction block and previously reported afferent conduction abnormalities. It is concluded that conduction block in alpha, beta and gamma motor fibres at the VREZ is an important cause of hindlimb weakness in whole spinal cord-induced acute EAE.
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PMID:The pathophysiology of acute experimental allergic encephalomyelitis induced by whole spinal cord in the Lewis rat. 325 77

Histological and electrophysiological studies were performed in Lewis rats with experimental allergic encephalomyelitis (EAE) to determine the cause of the neurological signs. The ventral root exit zone of the spinal cord was shown to be a major site of demyelination and conduction block. It is concluded that demyelination-induced conduction block in this region is an important cause of hindlimb weakness and paralysis in Lewis rats with EAE.
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PMID:Conduction block due to demyelination at the ventral root exit zone in experimental allergic encephalomyelitis. 348 24

An ascending impairment of tail nociception is a previously undescribed clinical sign of acute experimental allergic encephalomyelitis (EAE) in the rat. It occurs in EAE induced by inoculation with purified central nervous system (CNS) myelin basic protein (MBP) as well as with whole spinal cord. It is invariably present and consists of an absence of the vocalization response to noxious mechanical stimulation of the tail. This impairment of nociception evolves over 1-3 days, simultaneously with the development of tail weakness, and resolves more rapidly than the tail weakness. Light-microscopic, electron-microscopic and electrophysiological studies indicate that it is due to demyelination-induced conduction block in the small diameter myelinated afferent (A delta) fibres in the sacral and coccygeal dorsal root ganglia, dorsal roots and dorsal root entry zones. Unmyelinated fibres appear to be largely spared.
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PMID:Ascending impairment of nociception in rats with experimental allergic encephalomyelitis. 349 May 42

Experimental allergic encephalomyelitis (EAE) was induced in guinea pigs with bovine myelin basic protein (BP) with adjuvant of either synthetic muramyl dipeptide (Mdp) or Mycobacterium tuberculosis (Tbc). The following results were obtained: (1) The body temperature of the animals was studied serially after sensitization and its elevation was shown to be an early sign of EAE. (2) Several animals developed the clinical and histological signs of hyperacute EAE. (3) An optimal combined dosage of BP and adjuvant was found for induction of clinical EAE and for the the production of complement fixing (CF) antibodies. (4) Little passive hemagglutinating (PH) antibody was produced by single immunization. These results displayed no essential difference in EAE induced by either adjuvant. (5) Detectable PH antibodies developed later in addition to CF antibodies in a few animals immunized with Tbc adjuvant. These animals were skin-tested to BP, and had recovered from body weight loss or limb weakness. The results suggest that humoral antibodies play a role in modifying the disease process, even if they are not essential in production of EAE.
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PMID:Experimental allergic encephalomyelitis induced by basic protein with synthetic adjuvant in comparison with Freund's complete adjuvant. Role of antibodies in correlation with the clinicopathological features. 617 Jul 38

12 Lewis rats were inoculated with a guinea pig spinal cord tissue preparation. They developed experimental allergic encephalomyelitis (EAE) after 12-14 days manifested by weight loss, tail flaccidity, ataxia, hind limb paresis or paralysis and urinary incontinence. Concomitantly with EAE, all animals developed vestibular hyperreactivity (VH) of canal and otolith reflexes. Other signs of brain-stem dysfunction were also observed: abducens paralysis, facial weakness, tachypnoe and mydriasis with defective pupillary light reflex. The vestibular and other abnormalities subsided with some delay after recovery from clinical EAE, whilst histological abnormalities were still present in the CNS.
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PMID:Physiological abnormalities in experimental allergic encephalomyelitis (EAE): II. Correlation between clinical signs and vestibular hyperreactivity and other signs of brain-stem dysfunction in rats with EAE. 633 24

A case of brachial plexus neuropathy (BPN) associated with infectious mononucleosis (IM) in a 13 year old boy is presented. The essential clinical picture of BPN is discussed and the main points are: acute pain at onset across the top of the shoulder-blade followed by weakness and atrophy on muscles supplied in most cases by superior brachial plexus. The prognosis is good and most patients began to note improvement within months. The main neurological complications of IM are lymphocytic meningitis, peripheral neuropathy and encephalomyelitis and they can occur without any classical findings as pharyngitis, adenopathy or splenomegaly. The association of BPN and IM was described previously in only 7 cases and as the present case all of them had a complete recovery.
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PMID:[Brachial plexus neuropathy (amyotrophic neuralgia) and infectious mononucleosis: report of a case]. 649 19

Proteolipid protein (PLP) is the major protein of central nervous system (CNS) myelin. In some species, intradermal inoculation with PLP and adjuvants causes experimental autoimmune encephalomyelitis (PLP-EAE) characterized by neurological signs of tail and limb weakness and by inflammation and demyelination in the CNS. A previous study found that inoculation of Lewis rats with 100 micrograms of PLP causes PLP-EAE with a low incidence of neurological signs and a highly variable clinical course. In the present study we assessed PLP-EAE produced by inoculation with 1000 micrograms of PLP per rat. Fifty-one of 59 (86%) Lewis rats developed neurological signs 8 to 20 days (mean = 12.0 +/- 2.0) after inoculation with 1000 micrograms of PLP. In such rats, mononuclear cell infiltrates were present in the brain and spinal cord while primary demyelination occurred mainly in the subpial regions of the spinal cord, especially in the dorsal root entry and ventral root exit zones. The histological findings were compared with those in acute EAE induced in the Lewis rat by inoculation with whole CNS tissue or with myelin basic protein: in PLP-EAE, in contrast to these other models, the disease was essentially restricted to the CNS. This form of EAE should be useful in future studies of the consequences of autoimmunity to PLP.
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PMID:Clinical and histological findings in proteolipid protein-induced experimental autoimmune encephalomyelitis (EAE) in the Lewis rat. Distribution of demyelination differs from that in EAE induced by other antigens. 752 Apr 80


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