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)

From December, 1997, through November, 2000, 306 deaths were documented among adult and subadult American alligators (Alligator mississippiensis) of Lake Griffin, Florida (USA). Some live alligators were lethargic and unresponsive to approach. To determine the cause, we examined ten alligators captured from Lake Griffin between December 1997 and June 1999. Initially, four alligators, three of which were clinically unresponsive, were sacrificed for routine diagnostic necropsy. The other six Lake Griffin alligators, and five control alligators captured from Lake Woodruff National Wildlife Refuge, Florida, where mortality was negligible, were studied extensively by clinical neurologic examination, electromyography, hematology, serum chemical analyses, and blood culture, then sacrificed and necropsied. Samples of brain, spinal cord, peripheral nerves, skeletal muscle, and major internal organs were examined by light microscopy for abnormalities. Samples of nervous tissue also were examined by electron microscopy, and samples of various tissues were collected for toxicologic analyses. Clinical signs included swimming in circles, inability to submerge, lethargy, weakness, unresponsiveness, slow reflexes, dragging the dorsal surfaces of the hind feet, head tilt, and anisocoria. Lake Griffin alligators had significantly lower distal sciatic nerve conduction velocities than Lake Woodruff alligators, and the most severely affected alligators had the lowest velocities; but morphologic abnormalities in peripheral nerves were not evident in most cases. Three severely affected alligators had acute focal necrosis of the torus semicircularis in the midbrain, two had skeletal myofiber atrophy, another had diffuse nonsuppurative encephalomyelitis, and one mildly affected alligator had skeletal myodegeneration. The cause or causes have not yet been identified.
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PMID:Clinical and necropsy findings associated with increased mortality among American alligators of Lake Griffin, Florida. 1203 32

The multiple sclerosis (MS) lesion is characterized by an inflammatory cell mediated attack on white matter. Oxidative stress appears to play a role in the onset and progression of MS. We reasoned that decreasing oxidative stress might ameliorate MS. One way of decreasing oxidative stress is to induce phase 2 enzymes. The model chosen to test this hypothesis was experimental allergenic encephalomyelitis (EAE) induced in the Lewis rat. The 26 animals were placed into two groups: 1) those on normal rat chow, 2) those on rat chow containing 250 mumoles t-butylhydroxyanisole (BHA)/kg. After 2 weeks, animals were administered 100 micrograms guinea pig myelin basic protein and examined daily in a blinded fashion. Twenty-nine days later, animals were sacrificed, blood collected for glutathione (GSH) measurements and tissues collected for histology. Six of the 13 control chow animals developed hindlimb weakness or paralysis while 5 developed tail weakness only. Only 1 BHA fed animal exhibited symptoms--hindlimb weakness. Clinical symptoms correlated well with the extent of perivascular lymphocyte infiltration. Animals with BHA in the diet had 20% higher red cell GSH indicting induction of phase 2 enzymes. We conclude that dietary phase 2 enzyme inducers should be examined for their ability to ameliorate MS.
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PMID:Amelioration of experimental allergic encephalitis (EAE) through phase 2 enzyme induction. 1208 64

Japanese encephalitis (JE) is an encephalomyelitis involving cortex, subcortex, brainstem and spinal cord. There is paucity of studies on the neurophysiological evaluation in JE. This study aims at comprehensive evaluation of EEG, sensory and motor evoked potentials, nerve conduction and electromyography; and correlate these with clinical findings. Sixty five patients with JE diagnosed on the basis of clinical, radiological and virological criteria were subjected to a detailed clinical evaluation during the acute stage of illness. Cranial CT scan or MRI was carried out in all the patients. All the patients underwent 10 or 18 channel EEG, motor and sensory evoked potentials to both upper and lower limbs bilaterally as well as peroneal and sural nerve conductions and concentric needle EMG. Outcome, was defined at the end of 3 months into poor, partial and complete recovery. The patient's age ranged between 2-65 years. There were 40 males and 25 female patients. Fifteen patients were less than 12 years of age. History of seizure was present in 31 patients. Quadriplegia was seen in 39 and hemiplegia in 8 patients. Muscle wasting was present in 16 patients and tendon reflexes were reduced in 12 and of mixed pattern in 14 patients. Cranial MRI revealed thalamic lesion in 38, basal ganglia in 21, substantia nigra in 30, pons in 5, cerebellum in 3 and cerebral cortex in 7 patients out of 57 patients. EEG revealed nonspecific theta to delta slowing in 45, alpha pattern coma in 5 and epileptiform discharges in 8 patients. EMG revealed fibrillations in 23 patients. Motor evoked potentials were abnormal in 34 out of 46 patients and revealed patchy and focal abnormalities comprising of unrecordable, prolonged and normal pattern. Somatosensory evoked potentials were abnormal in 8 patients only. At 3 month, 26 patients had complete, 13 partial and 15 had poor outcome. Eight patients died in acute stage and 3 were lost to followup. MEP correlated with weakness and 3 month outcome whereas EEG, SEP and EMG did not have any correlation. MEP changes were more frequent in JE and had prognostic significance.
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PMID:Neurophysiological changes in Japanese encephalitis. 1239 49

Acute encephalomyelitis in children refers to an insult of cortical white matter leading to acute disseminated encephalomyelitis, insult of the spinal cord leading to multifocal myelopathy, or a combined form of encephalomyelitis. We report here the clinical presentations and outcome of 16 children with severe acute encephalomyelitis analyzing the effect of high-dose methylprednisolone or intravenous immunoglobulins, administered separately or in combination. Five children developed acute disseminated encephalomyelitis alone, eight developed severe multifocal myelopathy accompanied in two of them by radiculoneuropathy, and three developed the most severe form of combined encephalomyeloradiculoneuropathy. The indications for treatment with either high-dose methylprednisolone, intravenous immunoglobulin, or a combination of the two were severe acute disseminated encephalomyelitis, visual loss, or severe flaccid weakness accompanied by bladder and bowel incontinence. Overall, 10 children had remarkably responded to high-dose methylprednisolone alone and recovered within 10 days. One patient with severe myelopath, developing paraplegia, who failed oral corticosteroids completely recovered following intravenous immunoglobulin. Of the isolated acute disseminated encephalomyelitis group, all patients were initially treated with high-dose intravenous methylprednisolone and recovered within 10 days, including visual remission in the child with severe optic neuritis. All six children with solitary severe multifocal myelopathy were treated with high-dose methylprednisolone alone and recovered within the first week. Two patients had severe myeloradiculoneuropathy and were therefore treated with combined high-dose methylprednisolone and intravenous immunoglobulin: one remains paraplegic, whereas the second was ventilated for 3 weeks and recovered after 2 months. The three children with the most severe form of encephalomyeloradiculoneuropathy were treated with combined high-dose methylprednisolone and intravenous immununoglobulin; two remain severely handicapped, of whom one is paraplegic, and the third unexpectedly recovered within 3 months. Therefore, our experience indicates that either high-dose methylprednisolone or intravenous immunoglobulin, given separately or combined, may be efficacious in severe debilitating pediatric-onset acute encephalomyelitis. In children with the most severe form of encephalomyeloradiculoneuropathy, we suggest initially administering high-dose methylprednisolone and intravenous immunoglobulin combined, given the poorer outcome of our patients with combined severe central and peripheral demyelination.
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PMID:Outcome of severe encephalomyelitis in children: effect of high-dose methylprednisolone and immunoglobulins. 1258 19

A 17-year-old male presented with chronic diplopia and generalized motor weakness. He was previously diagnosed with chronic inflammatory demyelinating polyradiculoneuropathy and acute disseminated encephalomyelitis in childhood. Cranial magnetic resonance imaging (MRI) revealed a rarely reported finding of thickening and enhancement of multiple cranial nerves. Nerve conduction studies and electromyography showed peripheral nerve demyelination with axonal involvement. There was improvement in the clinical examination, MRI, and electrophysiologic studies after combined corticosteroid and plasma exchange therapy. We review the clinical presentation, course, and response to therapy among children with chronic inflammatory demyelinating polyradiculoneuropathy, with specific emphasis on the frequency and pattern of cranial nerve involvement.
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PMID:Childhood-onset chronic inflammatory demyelinating polyradiculoneuropathy with cranial nerve involvement. 1258 21

The severity of the experimental autoimmune encephalomyelitis (EAE) induced by peptide myelin oligodendrocyte glycoprotein(35-55)(pMOG(35-55)) is thought to be predominantly influenced by the major histocompatibility complex (MHC), so that C57BL6/J mice, on H2(b) strain, were only mildly sick. However, it remains unclear as to how non-MHC gene regions affect EAE. To determine whether the immunization protocol could have an influence on clinical signs, C57BL6/J mice were immunized with a multiple antigen peptide (MAP) containing eight pMOG(35-55)branches synthesized directly onto a lysine core, myelin oligodendrocyte glycoprotein (35-55)-multiple antigen peptide (MOG(35-55)-MAP), in complete Freund's adjuvant (CFA). In most of the mice, clinical onset (marked weakness) occurred approximately at day 15. All mice injected with MOG(35-55)-MAP had more severe symptoms than those injected with pMOG(35-55), which developed no leg paralysis. All MOG(35-55)-MAP-immunized mice developed EAE symptoms, but 50% had primary-progressive EAE, while the other 50% had relapsing-remitting disease. Leukocyte infiltrations, associated with increased glial fibrillary acidic protein (GFAP) expression by reactive astrocytes, were observed around the lateral ventricles and blood vessels in the brain. Significant positive correlations were established between anti-MOG(35-55)antibody levels and clinical scores or GFAP positivity in the spinal cord. The heterogeneity of EAE progression, observed in these genetically identical individuals, suggests that the environment rather than the genetics plays a role. This observation is highly pertinent as it corresponds to what is seen in clinical MS.
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PMID:Optimization of an animal model of experimental autoimmune encephalomyelitis achieved with a multiple MOG(35-55)peptide in C57BL6/J strain of mice. 1260 12

A 67-year-old woman had fever, myalgias, progressive weakness, and respiratory insufficiency. In 9 days, flaccid areflexic quadriparesis and bulbar palsy developed. She died 26 days after the onset of her illness. Serum and cerebrospinal fluid serology were positive for West Nile virus. Neuropathological study showed changes consistent with a viral encephalomyelitis, similar to poliomyelitis. The brainstem showed neuronal loss and multiple foci of necrosis. The spinal cord showed severe loss of anterior and posterior horn neurons. Immunohistochemistry identified West Nile virus antigens in the brainstem and spinal cord. Paralysis, in West Nile virus encephalitis, is caused by destruction of motor neurons.
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PMID:Neuropathological findings in West Nile virus encephalitis: a case report. 1452 Jun 73

Experimental allergic encephalomyelitis (EAE) serves as an animal model for certain neuroinflammatory diseases of the central nervous system, in particular multiple sclerosis (MS). EAE is accompanied by transient weakness or paralysis of hind limbs. We have investigated the effect of partial and transient conduction failure in the central nervous system on skeletal muscle function. At approximately 2.5 days after development of maximal clinical signs, body and medial gastrocnemius muscle mass were lower (by approximately 21 and 33%, respectively; P < 0.05) in EAE rats compared with controls. Fiber cross-sectional area was lower by 40-50% in all fiber types. Maximal force and power were substantially lower (by 58% and 73%) in EAE rats, as was the force normalized for muscle mass (35%). However, no such weakness was found when lower stimulation frequencies were used. Generation of similar submaximal forces was attributable to a slower relaxation in EAE muscles. This advantage for the EAE muscles was lost during repeated exercise. While fatigability was similar, the difference in relaxation rate between EAE and control disappeared in fatigue. Our data suggest that, as a result of central neuroinflammatory diseases, maximal performance of skeletal muscle is impaired but submaximal performance is relatively well maintained.
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PMID:Changes in characteristics of rat skeletal muscle after experimental allergic encephalomyelitis. 1498 35

MS is a chronic, immune-mediated inflammatory and neurodegenerative disease of the central nervous system (CNS), with an etiology that is not yet fully understood. The prevalence of MS is highest where environmental supplies of vitamin D are lowest. It is well recognized that the active hormonal form of vitamin D, 1,25-dihydroxyvitamin D (1,25-(OH)(2)D), is a natural immunoregulator with anti-inflammatory action. The mechanism by which vitamin D nutrition is thought to influence MS involves paracrine or autocrine metabolism of 25OHD by cells expressing the enzyme 1 alpha-OHase in peripheral tissues involved in immune and neural function. Administration of the active metabolite 1,25-(OH)(2)D in mice and rats with experimental allergic encephalomyelitis (EAE, an animal model of MS) not only prevented, but also reduced disease activity. 1,25-(OH)(2)D alters dendritic cell and T-cell function and regulates macrophages in EAE. Interestingly, 1,25-(OH)(2)D is thought to be operating on CNS constituent cells as well. Vitamin D deficiency is caused by insufficient sunlight exposure or low dietary vitamin D(3) intake. Subtle defects in vitamin D metabolism, including genetic polymorphisms related to vitamin D, might possibly be involved as well. Optimal 25OHD serum concentrations, throughout the year, may be beneficial for patients with MS, both to obtain immune-mediated suppression of disease activity, and also to decrease disease-related complications, including increased bone resorption, fractures, and muscle weakness.
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PMID:Multiple sclerosis and vitamin D: an update. 1505 36

We describe the case of a 30-month-old boy who developed acute disseminated encephalomyelitis (ADEM) after hepatitis A virus (HAV) infection and ultimately died. As far as we know, this is only the second case of HAV-associated ADEM to be reported in the literature. The child was brought to hospital with fever, lethargy and weakness of 2 days duration. He had developed jaundice, abdominal pain and malaise 2 weeks beforehand and these problems had resolved within 2 days. Neurological examination revealed lethargy, generalised weakness and positive Babinski's signs bilaterally. Cerebrospinal fluid examination showed mild lymphocytic pleocytosis, increased protein and elevated anti-HAV IgM and IgG titres. Serum HAV IgM and IgG titres were also elevated. Despite aggressive treatment with ceftriaxone, acyclovir and anti-oedema measures, he developed papilloedema and coma within 24 hours of admission. Magnetic resonance imaging of the brain revealed diffuse cerebral oedema and multifocal hyperintensities on T2-weighted images, with most lesions in the white matter of both cerebral hemispheres. The diagnosis of ADEM was established and high-dose steroids and intravenous immunoglobulin were added to the treatment regimen. However, his clinical condition continued to deteriorate and he died on the 20th day in hospital. This case shows that HAV infection can be linked with ADEM. Patients with HAV infection should be examined carefully for central nervous system symptoms during follow-up. Likewise, the possibility of HAV infection should be investigated in cases of ADEM.
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PMID:Acute disseminated encephalomyelitis associated with hepatitis A virus infection. 1518 42


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