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

In brain sections of the Naegleria-caused cases of primary amoebic meningoencephalitis, extensive demyelinization was found in the white matter, besides the severe histopathological changes and large clusters of trophozoites in the grey matter. The myelinoclasis appeared to be a result of a specific phospholipolytic effect, unlike that in post-viral encephalomyelitis, which has been attributed to vascular blockade or hemorrhages. In monkey kidney cell cultures a very early cytopathic effect was observed and traced to the cytolytic property of the seeding culture fluid. Rat brain slices inoculated with Naegleria culture exhibited amoebic growth and demyelinization in 28-52 hours incubation at 35 degrees C. In a chemically defined medium containing sphingomyelin, casein and glucose, the Naegleria produced a limited growth parallelling the clearance of the lipid turbidity during a 72 hour incubation at 35 degrees C. Chromatographic analysis of the turbidity-cleared cultures revealed decomposition of sphingomyeline with liberation of choline, sphingosine and fatty acids. It is, hence, concluded that the pathogenicity of cytopathic effect of pathogenic Naegleria can be attributed to the latter's capacity to liberate a phospholipolytic enzyme or factor during active growth, which "makes holes" in the lipid-rich cytoplasmic membrane of cells as well as demyelinizes nerve tissue.
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PMID:Pathogenesis of pathogenic Naegleria amoeba. 12 Feb 97

Eruptive herpes zoster infection (VZV) and its primary and secondary diseases are reported in 28 patients aged between 25 and 85 years. In 2 cases, malignant primary diseases were found. In 16 patients, a disorder of glucose utilization was diagnosed, 8 of them accompanied by a disorder of fat metabolism and 5 by a hyperuricemia. In one case a severe encephalomyelitis was observed. In 2 patients the activation of the VZV infection was related to the cytostatic or immunosuppressive therapy of a generalized Hodgkin's disease and a multiple sclerosis. Once a liver abscess as a sequel to amebic dysentery was diagnosed and once a megaloplastic anemia with symptoms of a funicular myelopathy following a vitamin B12 deficiency syndrome. In VZV infection the search for basal metabolic disorders is of particular importance.
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PMID:[Significance of diabetes mellitus in the activation of the varicella zoster virus (author's transl)]. 19 45

We reported serial changes of MRIs in a case of acute disseminated encephalomyelitis (ADEM). On November 1, 1990, a previously healthy 73-year-old man had a grand mal seizure following myoclonic jerks of the right arm for six days. On admission, he was drowsy and presented with right facial palsy and incomplete tetraparesis. He became coma on the next day of admission. There was moderate leukocytosis. A spinal tap showed a normal opening pressure, 2 white blood cells/mm3, a total protein of 84 mg/dl, glucose of 89 mg/dl. CSF IgG (6.2 mg/dl) and myelin basic protein (6.7 ng/dl) were slightly increased. Serological examinations for virus titer were all negative. A CT scan on the 2nd day showed no abnormal findings, but MRI revealed small high intensity areas in the left thalamus, left prefrontal gyrus and right corona radiata, internal capsule on both the T2-weighted and proton density sequences. An MRI on the 14th day showed high intensity signals in the white matter of the bilateral frontal lobes, left operculum and right corona radiata. In contrast, the left thalamic lesion became smaller and less conspicuous than on the initial scans, but was enhanced with Gd on the T1-weighted sequences. Our findings indicate that MRIs are valuable in detecting pathophysiological changes of ADEM from the acute to chronic phases.
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PMID:[Serial changes of magnetic resonance imagings in acute disseminated encephalomyelitis]. 161 77

Nonobese diabetic (NOD) mice spontaneously develop an autoimmune form of diabetes associated with insulitis. A number of immunomodulatory therapies have been investigated as a treatment for the disease process. Oral administration of the autoantigens myelin basic protein and collagen type II suppresses experimental models of encephalomyelitis and arthritis. We have now found that oral administration of insulin delays the onset and reduces the incidence of diabetes in NOD mice over a 1-year period in animals administered 1 mg of porcine insulin orally twice a week for 5 weeks and then weekly until 1 year of age. As expected, orally administered insulin had no metabolic effect on blood glucose levels. The severity of lymphocytic infiltration of pancreatic islets was also reduced by oral administration of insulin. Furthermore, splenic T cells from animals orally treated with insulin adoptively transfer protection against diabetes, demonstrating that oral insulin administration generates active cellular mechanisms that suppress disease. These results show that oral insulin affects diabetes and the pancreatic cellular inflammatory process in the NOD mouse and raise the possibility that oral administration of insulin or other pancreatic autoantigens may provide a new approach for the treatment of autoimmune diabetes.
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PMID:Suppression of diabetes in nonobese diabetic mice by oral administration of porcine insulin. 194 45

Traditionally, research in experimental allergic encephalomyelitis (EAE) has focussed on immunological and histopathological aspects. The present review introduces a physiological approach to EAE. As EAE is characterized by many small, focal lesions in the central nervous system (CNS), methods with a high spatial resolution should be used to conduct studies on regional pathophysiology in the condition. Quantitative autoradiography seems an ideal method as it offers, 1) high regional resolution (approximately 50 um), 2) precise quantitation and, 3) a direct correlation between regional histopathology and pathophysiology. By the use of this method, the author has performed studies on 1) regional blood-brain barrier (BBB) permeability, and 2) regional metabolism of energy substrate and related subjects, (i.e. regional cerebral blood flow, regional cerebral glucose metabolic rate and regional pH). Corresponding to the EAE lesions (lymphocytic accumulations), there is a considerable increase in BBB permeability. Metabolism of energy substrate at the lesion sites is severely deranged, which is expressed in a CBF/CMR ratio of 3 ml/mumol compared to the normal 1.5 ml/mumol. No changes in regional pH are seen in the lesions. Unrelated to the lesion sites there is a 50% decrease in blood flow in cerebral cortex. This observation probably reflects a functional decrease in cortical flow due to sensory motor impairment.
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PMID:Pathophysiological aspects of acute experimental allergic encephalomyelitis. 306 29

We report two patients with chronic encephalomyelitis due to Borrelia burgdorferi in whom the definite diagnosis was delayed because of atypical clinical features. The first patient presented with chronic spastic paraparesis, slight ataxia and nystagmus of several years' duration. A tentative diagnosis of multiple sclerosis was made in spite of important abnormalities of the CSF biological characteristics. The second patient presented with an acute aphasia and a bilateral Babinski's sign. He was thought to suffer from benign herpetic meningoencephalitis. Several months later, as the patient experienced relapses with cerebellar and spinal cord involvement, falsely positive tests for syphilis were found and an antibiotic treatment was given. High protein content, low glucose levels, pleocytosis and oligoclonal bands were observed in all CSF samples, but the definite diagnosis was based on the detection of serum and CSF antibodies against B. burgdorferi.
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PMID:[Borrelia burgdorferi encephalomyelitis]. 318 97

Regional cerebral blood flow (rCBF), regional cerebral glucose metabolic rate (rCMR), and regional pH (r-pH) were measured simultaneously in fulminant acute experimental allergic encephalomyelitis (EAE) by the use of triple-label autoradiography. No changes were found in the absence of lesions (lymphocytic accumulations). In the lesions, rCBF was 79% increased and rCRM was 13% increased, whereas r-pH was unaltered compared to normal values. The reported changes result in a CBF/CMR ratio of almost 3 in the lesions compared to the normal value of 1.5. The changes may be interpreted as primary disturbances in glucose metabolism, resulting in a secondary increase in CBF. This theory is supported by quoted observations on abnormal morphology and abnormal enzyme content in brain mitochondria in EAE.
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PMID:Simultaneous determination of regional cerebral blood flow, glucose metabolism, and pH in acute experimental allergic encephalomyelitis. 365 98

The clinical signs, enteritis, weight depression, and hypoglycemia of spiking mortality syndrome were experimentally reproduced in broiler breeders and broiler chicks. Inocula included 1) virus-like particles from intestines of chicks with spiking mortality syndrome that had been banded in a discontinuous Renograffin gradient, 2) homogenized darkling beetles collected from litter of farms where spiking mortality syndrome had occurred repeatedly, and 3) homogenized embryos which had been inoculated with the Renograffin-banded material. Arkansas variant infectious bronchitis virus and arenavirus-like particles were identified in the inocula. Serology on samples from surviving chicks suggested the presence of an avian encephalomyelitis virus in one of the inocula. One-day-old (n = 172) and 2.5-day-old (n = 30) chicks were inoculated orally, and some were also injected intraperitoneally or subcutaneously, with 0.5 ml of the inocula. Twelve to fourteen days postinoculation, chicks were fasted for 4-6 hours, then briefly stressed with a cool water spray. Within 1.5 hours, inoculated chicks began dying with severe hypoglycemia and clinical signs of spiking mortality syndrome. Body weights were significantly depressed. Uninoculated controls (n = 130) from the same hatches, also fasted and stressed, were unaffected clinically and were not hypoglycemic. One group (n = 52) of inoculated chicks exposed to a controlled lighting program was unaffected clinically, had significantly higher mean plasma glucose levels, and had significantly less body weight depression than chicks exposed to continuous lighting. We concluded that exposure to controlled amounts of light/darkness can ameliorate much of the hypoglycemia, mortality, and runting-stunting associated with spiking mortality syndrome of chickens. The significance of the viruses and virus-like particles detected in the inocula is currently under investigation.
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PMID:Experimental reproduction of severe hypoglycemia and spiking mortality syndrome using field-derived and embryo-passaged preparations. 871 30

We report a 30-year-old man with acute disseminated encephalomyelitis (ADEM) accompanying Mycoplasma pneumoniae (M. pneumoniae) infection. He was admitted to our hospital because of headache, disturbed behavior, and unconsciousness following an upper respiratory tract infection on December 19, 1996. On admission, he was febrile (37.3 degrees C) and showed hypersomnia and neck stiffness. There were scattered rhonchi in both lungs. Cerebrospinal fluid (CSF) contained 19 white cells; the protein was 20 mg/dl and glucose 71 mg/dl (blood glucose 170 mg/dl); no organisms were seen or cultured. Cranial MRI showed multiple T 2-weighted hyperintense in the periventricular region of the cerebral white matter. M. pneumoniae antibody titer in serum was remarkably elevated. ADEM related to M. pneumoniae was suspected. Although intravenous methylprednisolone, piperacillin and clindamycin were administered, there was no subsequent improvement in the symptoms. Further MRI scan revealed extension of the inflammatory lesion. He had both pneumonia and he required mechanical ventilation. Since the end of the critical period, he has been in an akinetic mutism. We conclude that M. pneumoniae has to be considered as a possible cause of ADEM with severe respiratory symptoms.
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PMID:[A case of acute disseminated encephalomyelitis accompanying Mycoplasma pneumoniae infection]. 1051 58

Peroxisome proliferator-activated receptor-gamma (PPAR-gamma), a member of the nuclear hormone receptor superfamily, plays a critical role in adipocyte differentiation and glucose homeostasis. It has been implicated that PPAR-gamma functions as a regulator of cellular proliferation and inflammatory responses. In the present study, we examined whether troglitazone, a selective PPAR-gamma agonists, ameliorated experimental autoimmune encephalomyelitis (EAE) induced by administration of myelin oligodendrocyte glycoprotein (MOG) peptide 35-55 in C57BL/6 mice. We found that troglitazone attenuated the inflammation and decreased the clinical symptoms. It was suggested that the amelioration was attributed to the attenuation of pro-inflammatory cytokine gene expressions.
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PMID:Amelioration of experimental autoimmune encephalomyelitis in C57BL/6 mice by an agonist of peroxisome proliferator-activated receptor-gamma. 1131 28


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