Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:Transmissible congenital demyelinating encephalopathy of lambs. 62 70

Donkeys experimentally infected with Trypanosoma brucei showed dullness, weakness, fever, inappetence, conjunctivitis, tachycardia and polydyspnoea soon after detectable parasitaemia. The parasitaemia was generally low with transient high peaks except in the terminal stage when there was sustained high parasitaemia. A moderate anaemia was present as from the second week of infection but it was not progressive. There was a marked leucopoenia within 24 h of patent parasitaemia. Death occurred 2 to 2 1/2 months after infection and at necropsy there was severe emaciation as well as mild serous effusion. Histologically, there was a nonsuppurative encephalomyelitis, cranial neuritis, extensive haemosiderosis, hyperplasia of follicles in lymph nodes and spleen and giant cell reaction in lymph nodes. Trypanosomes were present in the cerebrospinal fluid, the eye and serous effusions. These observations are similar to those previously reported in other animals infected with T. brucei.
 ...
PMID:Clinical, haematological and pathological studies in donkeys experimentally infected with Trypanosoma brucei. 90 95

Guinea pigs with paralysis or other severe neurological signs of experimental allergic encephalomyelitis (EAE) always exhibited typical histological inflammatory lesions. A few animals inoculated with either the encephalitogenic emulsion or only the control adjuvant emulsion had mild weakness or slowness but no histologic lesion. In some instances, these signs were explained by coincidental non-neural disease or trauma. Therefore, such mild clinical signs cannot be considered pathognominic of EAE. Reports from the literature suggesting that animals have developed clinical signs without histological lesions in EAE are considered invalid because of the nonspecificity of clinical signs, the occurrence of intercurrent diseases, the inadequacy or incorrect timing of histologic evaluations, and the lack of controls for specificity of the signs. There is no basis for the supposition that autoimmunity can cause major neurological signs in the absence of inflammatory lesions in the nervous system.
 ...
PMID:Do neurological signs occur in experimental allergic encephalomyelitis in the absence of inflammatory lesions of the central nervous system?. 118 42

Six epizootics of encephalomyeltis in suckling pigs in Minnesota were attributed to infection with hemagglutinating encephalomyelitis virus. The disease occurred in 74 litters of pigs and was characterized by sudden onset of tremors, inappetence, weakness, atazia, and hyperesthesia, with high morbidity and case fatality rate. Pathologic changes consisted of marked nonsuppurative, nondemyelinating encephalomyelitis characterized by perivascular mononuclear cuffing, gliosis, neuronal death, and satellitosis. Clinical disease was limited principally to suckling pigs during a single farrowing period and did not recur in the herds involved during the ensuing 18 months.
 ...
PMID:Porcine encephalomyelitis caused by hemagglutinating encephalomyelitis virus. 124 58

We studied 71 patients with "paraneoplastic" encephalomyelitis, sensory neuronopathy, or both associated with the presence of the anti-Hu antibody in their serum. Most (78%) had small-cell lung cancer. In 9 patients no tumor was detected. Fifty-two patients (73%) had signs and symptoms of multifocal involvement of the nervous system; in 28 (39%), 2 areas, and in 24 (34%), 3 or more areas were clinically affected. Sensory neuronopathy was present in 52 patients (74%), but in only 44 (62%) did it dominate the course of the disease. Other predominant findings were: motor neuron dysfunction (14 patients, 20%), limbic encephalopathy (14, 20%), cerebellar symptoms (11, 15%), brainstem encephalopathy (10, 14%), and autonomic nervous system dysfunction (7, 10%). The presence of the anti-Hu antibody prompted a search for the tumor in 60% of the patients; the tumor when found was usually small and remained localized until death, or was demonstrated only at autopsy. Treatment using steroids and plasmapheresis, immunosuppressants, or both, did not improve the paraneoplastic symptoms. Autonomic and respiratory failure, either of central origin or secondary to neuromuscular weakness, were the principal causes of death. Patients with rapidly developing sensory neuropathy or symptoms of encephalomyelitis should be studied for the presence of the anti-Hu antibody; if the antibody is found, the possibility of small-cell lung cancer should be investigated. If a tumor is not found in the initial search, one may become evident in several months.
 ...
PMID:Anti-Hu--associated paraneoplastic encephalomyelitis/sensory neuronopathy. A clinical study of 71 patients. 131 11

In two men presenting with muscle weakness and disturbances of equilibrium neurophysiological examination by repeated stimulations revealed responses suggestive of Lambert-Eaton syndrome. In the first month of the disease very high levels of anti-Hu antibody were found in the serum and CSF, betraying a malignant lesion. This was confirmed by autopsy 4 months later in one patient and by bronchial biopsy 16 months later in the other patient. Both had small-cell lung carcinoma associated with paraneoplastic encephalomyelitis.
 ...
PMID:[Paraneoplastic encephalomyelitis and Lambert-Eaton syndrome]. 133 34

Selective depletion of central nervous system norepinephrine (NE) by the neurotoxin 6-hydroxydopamine (6-OHDA) in rats subsequently inoculated with myelin basic protein (MBP) and complete Freund's adjuvant (CFA) produced experimental autoimmune encephalomyelitis (EAE) without the usual expected degree of weakness. The preservation of strength occurred in spite of continued weight loss. Post-decapitation myoclonic convulsive kick latency and kick number, which are known to depend on spinal cord NE, agreed well with the degree of weakness through the clinical disease course. The only difference between EAE groups was that the stronger 6-OHDA pretreated EAE animals did not have an elevated pons-medulla NE compared to saline intracisternal-ventricular (i.c.v.) pretreated controls. We conclude that 6-OHDA can influence the clinical course of weakness by interfering with central noradrenergic activity independent of other features associated with disease in EAE. This effect of 6-OHDA may be exerted through alteration of the blood-spinal cord barrier function and/or central nervous system blood flow.
 ...
PMID:Suppression of clinical weakness in experimental autoimmune encephalomyelitis associated with weight changes, and post-decapitation convulsions after intracisternal-ventricular administration of 6-hydroxydopamine. 168 41

Guinea pigs immunized with bovine spinal cord ventral horn homogenate develop muscle weakness with electromyographic and morphologic evidence of denervation. Pathological examination demonstrates a loss of motoneurons and scattered inflammatory foci primarily localized to the spinal cord. Immunohistochemical techniques document the presence of immunoglobulin G at the motor end plate and around the external membrane and within the cytoplasm of motoneurons. This syndrome of experimental autoimmune gray matter disease (EAGMD) differs from experimental autoimmune motor neuron disease induced by inoculation with purified motoneurons and also differs from experimental autoimmune encephalomyelitis. The existence of two different forms of immune-mediated motoneuron destruction suggests that a number of cytoplasmic and membrane antigens may give rise to an immunologically based attack on the motor system.
 ...
PMID:Motor neuron destruction in guinea pigs immunized with bovine spinal cord ventral horn homogenate: experimental autoimmune gray matter disease. 169 Jul 52

Experimental allergic neuritis (EAN) was studied in the SJL/J mouse and compared to EAN in the Lewis rat. The Lewis rat developed hind limb weakness and weight loss while the SJL/J mouse had no discernible clinical abnormalities. The SJL/J mouse, however, suffered subclinical damage to peripheral nerve (PN) myelin. Both species reproducibly developed electrophysiologic dysfunction of PN and histopathology confined to the peripheral nervous system (PNS). Understanding of autoimmune demyelination in the central nervous system was greatly enhanced by the development of experimental allergic encephalomyelitis in the SJL/J mouse. We believe that EAN in the SJL/J mouse could lead to a similar increase in our understanding of autoimmune demyelination in the PNS.
 ...
PMID:Experimental allergic neuritis in the SJL/J mouse: dysfunction of peripheral nerve without clinical signs. 195 68

After intranasal inoculation, mouse hepatitis virus (MHV) gains entry into the central nervous system (CNS) via the olfactory and trigeminal nerves. Under the appropriate conditions, some mice develop clinically apparent demyelinating encephalomyelitis several weeks later, with virus always present in the spinal cord. To determine the pathway by which virus reaches the cord, brains and spinal cords of infected, asymptomatic mice were analyzed by in situ hybridization. Viral RNA was always detected in the anterior part of the upper spinal cord. A similar analysis of mice with the recent onset of hindlimb weakness showed that viral RNA was detected in the same location. The results suggest that MHV is transported to the spinal cord via well-defined neuroanatomic pathways and that viral amplification with resultant clinical disease occurs from this site of persistence in the anterior spinal cord. This process of viral amplification may involve the generation of viral variants as has been described for MHV-infected rats. No major changes in viral RNA or protein could be detected when MHV isolated from mice with hindlimb paralysis was analyzed. The data suggest that the generation of viral variants is not important in the pathogenesis of the late onset of neurological disease induced by MHV in mice.
 ...
PMID:Identification of the spinal cord as a major site of persistence during chronic infection with a murine coronavirus. 215 80


1 2 3 4 5 6 7 8 9 10 Next >>