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)

The significance of the effect of histamine (Hi) in CNS has been demonstrated. By way of the inhibition of imidazol-N-methyltranspherase the amount of Hi in the brain can be increased, whereas by means of decaborane or thiazolil-metoxamine it can be lowered. It has been shown that Hi sensitizes the effect of acetylcholine (ACh) in CNS and, consequently, intensifies or weakens certain pharmacological reactions associated with ACh. It has been noted, as the most important result of the decreased Hi in CNS, that certain symptoms of motion sickness (such as vomiting, nistagmus etc.) disappear. Similarly, the increase of Hi in CNS prevents the development of the allergic encephalomyelitis in rats.
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PMID:Central effects of certain drugs and allergic encephalomyelitis in the circumstances of increased or decreased histamine in CNS. 116 23

The pathogenicity of hemagglutinating encephalomyelitis virus isolated from the brain of each of 5 pigs with clinical signs and microscopic lesions of encephalomyelitis (1 pig from each of 5 naturally infected herbs) was tested under experimental conditions. Each isolant was administered intranasally to 5 neonatal pigs. Clinically affected pigs developed either an acute or chronic form of illness, commencing 4 to 8 days after exposure. Listless, inappetence, and vomiting were clinical signs common to both forms. Additional signs of the acute form were paddling, muscle tremors, and hyperesthesia. Additional signs of the chronic form were loss of condition and either loss of weight or failure to gain weight at a rate similar to nonaffected littermates.
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PMID:Pathogenicity of field isolants of hemagglutinating encephalomyelitis virus for neonatal pigs. 124 57

Hemagglutinating encephalomyelitis virus (HEV; also designated vomiting and wasting disease virus) was inoculated oronasally in 26 colostrum-deprived pigs. Anorexia and vomition were seen after an incubation period of 4 to 6 days. In pigs killed during the incubation period or within 2 days after the onset of the clinical signs, HEV could be isolated regularly from the tonsils and the respiratory tract, irregularly from the digestive tract, rarely from the blood, and never from lymph nodes and spleen. The brainstem almost always contained virus after clinical signs appeared, but was only one positive during the incubation period. Olfactory bulb, cerebrum, cerebellum, and vagal nerve were also frequently virus positive in pigs which were ill when killed. The results of the examination by immunofluorescent antibody technique indicated that HEV multiplies in the epithelium lining the respiratory tract and the tonsillar crypts, in neuroepithelium of the nasal mucosa, and in neurons of the digestive tract. The neuronotropism of HEV was also shown by the presence of fluorescence in the perikaryon of neurons in the brainstem and in the trigeminal ganglion without the involvement of other cell types. The presence of viral antigens in the perikaryon of trigeminal sensory ganglion cells in pigs killed during the incubation period was considered as positive evidence for viral spread via nerves.
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PMID:Virus isolated and immunofluorescence in different organs of pigs infected with hemagglutinating encephalomyelitis virus. 624 2

Cesarean-derived colostrum-deprived and conventionally reared pigs were orally inoculated with the coronavirus-like agent, CV 777, isolate from an outbreak of epizootic diarrhea in swine of all ages. Viral particles detected by electron microscopy in the feces and intestinal contents of inoculated pigs had the typical coronavirus morphology. The present studies provided further evidence that this coronavirus-like agent is different from the two known porcine coronaviruses, transmissible gastroenteritis virus and hemagglutinating encephalomyelitis virus. The experimental infection of pigs with this new agent resulted in vomiting, diarrhea, and dehydration. This coronavirus-like agent was shown to replicate in the epithelial cells covering the small intestinal villi but, unlike transmissible gastroenteritis virus, it also replicated in the epithelial cells covering the large intestinal villi.
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PMID:Experimental infection of pigs with a new porcine enteric coronavirus, CV 777. 624 3

Hemagglutinating encephalomyelitis virus (HEV; also designated vomiting and wasting disease virus) was inoculated oronasally in 14 colostrum-deprived pigs at the day of birth. Anorexia and vomition were seen after 4 days. Pigs were killed at different times after inoculation, and the results of the examination by immunofluorescent antibody technique revealed that the epithelial cells of nasal mucosa, tonsils, lungs, and small intestine served as sites of primary viral replication. After the local replication near the sites of entry, the virus spread via peripheral nervous system to the CNS. During the incubation period, viral antigens were detected in the trigeminal ganglion,the inferior vagal ganglion, the superior cervical ganglion, the intestinal nervous plexuses, the solar ganglion, and the dorsal root ganglia of the lower thoracic region. In the brain stem, the infection started in the trigeminal and vagal sensory nuclei and spread to other nuclei and to the rostral part of the brain stem. In later stages of the infection, viral spread into the cerebrum, cerebellum, and spinal cord was sometimes also observed. Viral replication in nervous plexuses of the stomach was not present during the incubation period, but was detected in all except 1 of the pigs that were ill when killed. The question whether the vomition is induced centrally by viral replication in the brain stem or is due to viral replication in peripheral nervous tissues remains unanswered.
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PMID:Immunofluorescence studies on the pathogenesis of hemagglutinating encephalomyelitis virus infection in pigs after oronasal inoculation. 625 37

Multiple sclerosis and acute disseminated encephalomyelitis are demyelinating disorders of the central nervous system that can present initially as an acute focal demyelinating syndrome. We report an 11-year-old girl who initially presented with intractable vomiting and hypertension and later developed a subacute onset of focal neurologic (brainstem) signs. Magnetic resonance imaging (MRI) demonstrated a large solitary demyelinating lesion of the brain stem consistent with acute disseminated encephalomyelitis. Because of the morbidity associated with biopsy and its questionable value in the course of management of this patient, she was treated empirically with aggressive supportive measures and high-dose corticosteriod therapy. She had near full recovery, with only minimal neurologic sequelae. Six months later, she presented with similar focal neurologic signs, and a new lesion was found on MRI. Because of the separation of her two episodes in time and central nervous system location, a diagnosis of multiple sclerosis was made. Herein, we used this patient to illustrate the difficulty in distinguishing acute disseminated encephalomyelitis from multiple sclerosis in patients who present initially with an acute focal demyelinating syndrome.
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PMID:Brainstem multiple sclerosis in an 11-year-old child presenting as acute disseminated encephalomyelitis. 857 60

Nine patients below 20 years of age (4 males and 5 females), who were diagnosed to have acute disseminated encephalomyelitis (ADEM) by clinical findings and magnetic resonance imaging (MRI), were reviewed retrospectively. They ranged from 4 months to 20 years of age with an average of 8.6 years. Seven patients (78%) received neurophysiological studies, which included electroencephalography, multimodality evoked potentials (EPs), nerve conduction velocity and/or F-wave measurement. The presentation symptoms were mainly headache, vomiting, consciousness change and motor deficits. Seven (78%) of nine patients had symptoms preceded by fever or upper respiratory tract infections; one (11%) was preceded by trivalent mumps, measles, rubella vaccination and no definite predisposing factor was found in another. Computed tomography (CT) scans were abnormal in five (71 %) of seven children, while MRI showed multiple lesions in seven (78%) of nine children. The lesions in MRI were mainly in the brainstem (n = 6), basal ganglion (n = 5), thalamus (n = 4), periventricular white matter (n = 4) and cerebellum (n = 4). EPs disclosed spinal cord involvement in all patients who received the examination. Peripheral neuropathy was disclosed in one patient. It was concluded that associated radiculoneuropathy is possible in patients with ADEM. Both MRI and neurophysiologic studies are complementary for diagnosis of ADEM.
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PMID:Acute disseminated encephalomyelitis in children: clinical, neuroimaging and neurophysiologic studies. 875 75

We report a case of multiphasic disseminated encephalomyelitis (MDEM) following viral illness presenting as multiple sclerosis (MS) in a 7-year-old boy. The patients had two episodes of alternating hemiparesis and other neurologic symptoms following viral infection, which were separated by 3 years. Neuroimaging studies demonstrated multiple, discrete, small nodules and large globular lesions in the cerebral white matter, basal ganglia, brainstem and cerebellar areas. Based on typical appearance of magnetic resonance imaging (MRI) and clinical manifestations including systemic symptoms such as fever, nausea, vomiting, headache and seizures followed by consciousness disturbance and other multifocal neurologic signs, the diagnosis of MDEM rather than that of MS was made. Because it is difficult to differentiate between MDEM and MS on the basis of the clinical history, the cerebrospinal fluid examination and evoked potential studies, this report emphasizes that the MRI study of the brain may provide an important clue for the diagnosis.
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PMID:Multiphasic disseminated encephalomyelitis mimicking multiple sclerosis. 889 Dec 39

The patient is a 10-year-old male who experienced somnolence and incomplete quadriplegia after headache and vomiting, without exanthema, for 3 days. The clinical course and magnetic resonance imaging findings of the brain and spinal cord were compatible with acute disseminated encephalomyelitis. The serologic examination revealed that the patient had rubeola because titers of IgM and IgG antibody to measles virus measured by enzyme immunoassay were 0.91 and 40 (cutoff = 0.80 and 2), respectively, at 5 weeks after the onset, the IgM titer had become negative (0.56), and the IgG titer had decreased to 17.7 at 13 weeks after the onset. Because the patient had received a measles-mumps-rubella vaccine at 12 months of age, the acute disseminated encephalomyelitis was thought to be attributed to the modified measles resulting from measles vaccine failure.
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PMID:Acute disseminated encephalomyelitis with probable measles vaccine failure. 1037 90

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


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