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

A previously unrecorded nervous disease in pigeons was investigated. The disease, characterized by paresis, paralysis of the extremities, head-shaking, and torticollis, is contagious and spreads slowly. The mortality rate of affected pigeons was very high. The disease appeared to spread among pigeon flocks in spring and summer. The predominant gross change in most cases examined was congestion of the visceral organs. Some cases had grayish spots on the pancreas and kidneys. The histologic changes are characterized by neuronal and myelin degeneration with mononuclear cell infiltration and perivascular cuffing. Degeneration of the parenchyma and marked congestion are prominent in the visceral organs. The causal agent, found to be a virus, produced pock lesions on chorioallantoic membranes of developing chick embryos and failed to aagglutinate chicken RBCs. Antisera against Newcastle disease virus and avian encephalomyelitis virus did not neutralize the isolated virus. The virus produced typical signs in experimentally inoculated pigeons.
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PMID:Viral encephalomyelitis of pigeons: pathology and virus isolation. 54 2

Twenty-two fetal lambs were inoculated in utero with tissue suspension prepared from lambs born with weakness, incoordination and clonic tremor. Clinically, affected newborn lambs had clonic tremor, were generally weak and had abnormally pigmented hairy fleece. The inoculation resulted in a disseminated encephalomyelitis with secondary teratologic changes in a significant number of fetuses. The mononuclear inflammatory changes were most obvious 14 days after inoculation, after which there was rapid resolution. Changes seen at birth were chronic astrocytosis with neuron loss in the spinal cord and cerebellar dysplasia. Single radioimmunodiffusion studies showed consistently low IgG in infected fetuses and high IgG in lambs at birth.
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PMID:Transmissible congenital demyelinating encephalopathy of lambs. 62 70

Eastern equine encephalomyelitis (EEE) was the cause of heavy mortality in coturnix quail (Coturnix coturnix) reared commercially in South Carolina. The birds showed depression, tremor, and partial paralysis that advanced into complete paralysis, torticollis, and death within a few hours. The only consistent lesion on necropsy was a catarrhal enteritis in the duodenal area. The disease spread rapidly to all pens throughout the two houses on the farm in all birds over 2 weeks old, and mortality ranged from 40 to 90% in the various pens within the house. Total mortality exceeded 90,000 birds. Age groups on the farm ranged from 1 day to 8 weeks, at which time the birds went for slaughter. It appears that the initial infection was spread by cannibalism. EEE was diagnosed by isolating the virus in fertile eggs and suckling mice, with subsequent identification by complement-fixation. This is the first documented case of EEE in coturnix quail.
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PMID:Eastern equine encephalomyelitis outbreak in coturnix quail. 69 63

Severe hypothermia and an ascending impairment of shivering are previously undescribed clinical signs in hyperacute experimental allergic encephalomyelitis (EAE) in the Lewis rat. These occurred in hyperacute EAE induced by inoculation with guinea pig spinal cord homogenate and heat-killed Bordetella pertussis. Hypothermia was first detected on day 6-7 post-inoculation, within 12-24 h of the onset of neurological signs, and became more severe as the disease progressed. Rectal temperatures less than or equal to 30 degrees C were common at ambient temperatures of 19-22 degrees C. Shivering was assessed by palpation and by cold tremor electromyography. Shivering was absent in the tail by day 6-7 post-inoculation. The impairment then progressed to affect the hindlimbs, thorax and occasionally the forelimbs. Shivering was absent in hindlimbs with only mild or moderate weakness. Histological studies revealed perivascular inflammation with polymorphonuclear and mononuclear cells, oedema, fibrin deposition, haemorrhage, primary demyelination and axonal degeneration in the spinal cord, dorsal root ganglia and spinal roots. The brainstem was also involved but the cerebral hemispheres, including the hypothalamus, were spared. The close relationship between the severity of hypothermia and the extent of shivering impairment indicates that reduced shivering is an important cause of hypothermia in hyperacute EAE. It is concluded that this impairment of shivering is due not to hypothalamic damage but to lesions elsewhere in the central and peripheral nervous systems.
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PMID:Hypothermia due to an ascending impairment of shivering in hyperacute experimental allergic encephalomyelitis in the Lewis rat. 261 69

A 54-year-old housewife became ill with transient diplopia followed by facial paralysis, tremor of the right hand and a progressively worsening disturbance in gait. Four years after the first appearance of the disease bilateral hypacusia, paralysis of the right hypoglossal nerve, dysarthria, severe spastic tetraparesis with ataxia, urinary retention and an organically induced character change were present. Lumbar puncture fluid contained 51/mm3 lymphocytes and 1164 mg/dl protein. Immunoglobulin A, G and M, synthesised locally, could be detected in cisternal fluid. The serum had a high antibody titre against Ixodes ricinus-Borrelia antigen and the same antibodies, formed locally, were present in the lumbar fluid. The neurological deficiencies improved markedly under parenteral penicillin treatment and the antibody titre decreased. The detection of Borrelian antibodies, especially those synthesised locally in the CSF, enabled an aetiological diagnosis to be made in seven other patients aged 18-47 years in whom the disease had been present for 1 to 8 years. These patients likewise presented symptoms characteristic of a disseminated disease of the CNS, with spastic pareses and evidence in the spinal fluid of chronic inflammation and disruption of CSF barriers in particular. This progressive encephalomyelitis differs from the common and spontaneously healing meningo-polyneuritis (Garin-Bujadoux-Bannworth), the usual manifestation of erythema chronicum migrans of the nervous system, in its progressive nature, its invasion of the CNS and the possible long lasting severe damage when not specifically treated.
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PMID:[Progressive Borrelia encephalomyelitis. Chronic manifestation of erythema chronicum migrans disease of the nervous system]. 400 60

Serotonin mediated bulbospinal motor activities were examined in rats with experimental allergic encephalomyelitis (EAE)-induced-paraplegia. Treatment with monoamine oxidase inhibitors and L-tryptophan failed to elicit the components of the serotonin syndrome which involved levels of the neuraxis manifesting flaccid paralysis. Straub tail, hindlimb abduction and hindlimb rigidity did not occur. The motor responses represented at spinal segments just above the level of paraplegia, lateral head weaving and forepaw treading, were present but altered in the diseased rats. No impairment was evident in the production of head tremor or hyper-reactivity to accoustic and tactile stimuli. Similarly, in urethane-anesthetized EAE rats, serotonergically-evoked automatic swallowing activity was unchanged as judged by the effects of serotonin receptor agonists, and a serotonin precursor, a reuptake blocker and an antagonist. Our data support the conclusion that EAE-induced impairment of serotonergic neurotransmission is correlated with motor deficits manfested during the acute paralytic stage of the disease.
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PMID:Central serotonin receptor sensitivity in rats with experimental allergic encephalomyelitis. 696 16

We present a female patient with typical third stage neuroborreliosis with progressive chronic encephalomyelitis. One month after a tick bite, in the first stage of Lyme disease, she had myalgias during ten days and after one year polyarthralgias and polyarthritis. Neurological problems occurred 15 years after the tick bite with headache, nystagmus, intentional tremor and spastic paraparesis with sphincter disturbances. Etiological diagnosis was established after three years. Cytobiochemical findings in cerebrospinal liquor were normal but oligoclonal IgG bands were found. Fluorescent antibody test was positive in serum (1:75) as well as ELISA (1:447). The patient reacted favourably to intravenous crystal penicillin 20 x 10(6) units daily during 18 days. Till now, she is in remission and has only mild paresis of the left leg.
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PMID:[Chronic encephalomyelitis caused by Borrelia burgdorferi. Case report]. 826 11

Myelin/oligodendrocyte glycoprotein (MOG) is a minor myelin protein that belongs to the immunoglobulin gene superfamily and evokes demyelination based on immunological response. Localized preferentially at the external surfaces of myelin sheaths, it is one of the primarily target autoantigens in experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. Elevated MOG content has been found in the myelin fraction of the rabbits affected by the mild form of paralytic tremor (pt) disease, evoked by natural, point mutation in exon 2 of plp gene. A single T-->A transversion results in substitution of histidine36 by glutamine in PLP and it's splicing variant DM-20 molecules. The affected animals, although strictly controlled for pt trait, differ significantly in their phenotypes, distinguished by the severity of neurological symptoms. It was shown that the degree of CNS hypomyelination and deficiency of PLP/DM-20 correlates well with the severity of neurological symptoms and is highest in the most strongly affected animals. Variety of phenotypes generated from pt genotype together with previously observed MOG hyperexpression suggested possible contribution of immunological component to the pt disease. Present studies indicate that MOG expression depends both on the phenotype and the age of affected rabbits and most probably mirrors retardation in myelinogenesis process caused by pt mutation.
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PMID:pt point mutation in plp gene results in hyperexpression of MOG in hypomyelinated rabbit. 878 15

Three children ranging in age from 2 to 5 years with acute disseminated encephalomyelitis (ADEM) were successfully treated with high-dose intravenous immunoglobulin (IVIG). Their symptoms were somnolence, fever, headache, vomiting, and resting tremor. In all of these patients, it was difficult to distinguish the condition from viral encephalitis before analyzing the myelin basic protein. ADEM was diagnosed because of increased levels of myelin basic protein in their cerebrospinal fluid and abnormal high-signal intensity on T2-weighted magnetic resonance imaging. All patients were given IVIG at a dose of 400 mg/kg/day for 5 consecutive days. The patients rapidly regained consciousness in 14 hours, 2 days, and 4 days and demonstrated a complete clinical improvement within 18 days, 10 days, and 7 days of the initiation of the treatment, respectively. IVIG may prove useful as an alternative treatment to corticosteroids for ADEM.
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PMID:Intravenous immunoglobulin therapy in acute disseminated encephalomyelitis. 1046 50

Chronic relapsing experimental allergic encephalomyelitis (CREAE) is an autoimmune model of multiple sclerosis. Although both these diseases are typified by relapsing-remitting paralytic episodes, after CREAE induction by sensitization to myelin antigens Biozzi ABH mice also develop spasticity and tremor. These symptoms also occur during multiple sclerosis and are difficult to control. This has prompted some patients to find alternative medicines, and to perceive benefit from cannabis use. Although this benefit has been backed up by small clinical studies, mainly with non-quantifiable outcomes, the value of cannabis use in multiple sclerosis remains anecdotal. Here we show that cannabinoid (CB) receptor agonism using R(+)-WIN 55,212, delta9-tetrahydrocannabinol, methanandamide and JWH-133 (ref. 8) quantitatively ameliorated both tremor and spasticity in diseased mice. The exacerbation of these signs after antagonism of the CB1 and CB2 receptors, notably the CB1 receptor, using SR141716A and SR144528 (ref. 8) indicate that the endogenous cannabinoid system may be tonically active in the control of tremor and spasticity. This provides a rationale for patients' indications of the therapeutic potential of cannabis in the control of the symptoms of multiple sclerosis, and provides a means of evaluating more selective cannabinoids in the future.
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PMID:Cannabinoids control spasticity and tremor in a multiple sclerosis model. 1071 47


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