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)

Cortical somatosensory evoked potentials (c-SEP) and flash visual evoked potentials (f-VEP) were serially recorded in acute monophasic and chronic relapsing experimental allergic encephalomyelitis (EAE) in the Lewis rat. In acute EAE, a significantly delayed latency and broadened peak of the c-SEP were observed corresponding to the clinical onset, and then returned to normal with the disappearance of clinical signs. In chronic EAE, the c-SEP showed the same changes as in acute EAE, also reflecting the first attack, remission and relapsing phase. However, chronic EAE, when paralysis had recovered in the relapsing phase, showed c-SEP abnormalities suggestive of subclinical active lesions. In contrast, the f-VEP showed no obvious abnormalities in acute or chronic EAE. These findings suggest that the c-SEP is an objective and sensitive index for detecting clinical and pathological changes in acute and chronic EAE in the Lewis rat.
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PMID:Electrophysiological follow-up of acute and chronic experimental allergic encephalomyelitis in the Lewis rat. 139 Sep 49

Experimental allergic encephalomyelitis (EAE) is a T cell-mediated autoimmune disease. It is widely used as an animal model of multiple sclerosis (MS). We studied the prophylactic effects of FK 506 electrophysiologically and immunohistochemically in acute EAE. Female Lewis rats were sensitized with guinea pig spinal cord in complete Freund's adjuvant. FK 506 suspended in distilled water was orally administered at 1.0, 3.2, 5.0 or 10.0 mg/kg per day for 12 successive days starting from the day of sensitization. A placebo was used as the control. Administration of FK 506 at doses of 3.2 mg/kg per day and over significantly delayed the onset of clinical signs. However, the FK 506 group showed a relapse or a chronic state following the onset of EAE. We made a time course recording of cortical somatosensory evoked potential (cortical SEP: P 15). P 15 latency in the placebo group was significantly delayed in accordance with the clinical signs and showed immediate improvement upon recovery. Prolongation of P 15 latency in the FK 506 group also occurred concomitantly with the clinical signs, but the delay continued after the loss of symptoms as well. After the onset of EAE, the infiltrating lymphocyte subset was examined by the avidin-biotin peroxidase complex (ABC) method in the lumbar spinal cord. In the placebo group, the number of OX3+ (Ia) cells and the W 3 25+: OX8+ (helper/inducer T: suppressor/cytotoxic T) ratio clearly reflected the development and remission of EAE. In the FK 506 group, however, increases in OX8+ lymphocytes were observed irrespective of clinical sign fluctuation, and there were corresponding decreases in the W 3/25+: OX8+ ratio.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of novel immunosuppressant FK 506 in acute experimental allergic encephalomyelitis]. 169 82

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

A patient with exanthem and fever showed progressive disturbance of consciousness and flaccid quadriplegia predominantly in the lower extremities. Antibiotics, aciclovir, high-dose methylprednisolone (1 g/day for 3 consecutive days) and IVIG (400 mg/kg/day for 5 consecutive days) were not effective. Nerve conduction study and SEP in the lower extremities showed peripheral and central conduction block. EEG showed irregular sharp and slow waves predominantly in the left hemisphere. ABR and SEP in the upper extremities were normal. Consecutive studies of cranial and spinal MRIs showed no abnormalities. A diagnosis of acute disseminated encephalomyelitis (ADEM) was made. We started administration of ultra-high-dose methylprednisolone (5.4 mg/kg/h for 47 hours), the dose for acute spinal cord injury based on the randomized controlled trial of The Third National Acute Spinal Cord Injury Study in the USA. After this, she regained consciousness and the quadriplegia improved. The abnormalities in the electrophysiological studies also normalized. It is thought that the neuroprotective mechanism of ultra-high-dose methylprednisolone could be attributed to its inhibition of lipid peroxidation, secondary, ischemia, energy failure and so on. If the usual treatment is not effective for severe encephalomyelitis cases, we can consider the administration of ultra-high-dose methylprednisolone as one of the new treatment options.
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PMID:[A patient of ADEM with central and peripheral conduction block improved with ultra-high-dose methylprednisolone]. 1247 95

Generalized 1Hz, burst-and-slow-wave complexes were observed in a comatosed patient with acute disseminated encephalomyelitis (ADEM) when she showed extremely intractable, generalized convulsions and fragmented myoclonus in the whole body. Two types of short-latency SEPs were obtained separately during the burst and slow phase of the EEG (SEP-burst and SEP-slow, respectively), which showed a two fold greater amplitude of N20 in the former than in the latter. This suggests enhanced responsiveness to the peripheral stimuli during the burst phase as compared with the slow phase. CSF and serum were positive for autoantibodies to NMDA receptors. The "burst and slow complexes" reported here are considered to be an atypical EEG pattern of a generalized epileptic phenomenon.
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PMID:"Burst and slow complexes" in nonconvulsive epileptic status. 1656 28

FTY720 (fingolimod) is an oral sphingosine 1-phosphate (S1P) receptor modulator under development for the treatment of multiple sclerosis (MS). To elucidate its effects in the central nervous system (CNS), we compared functional parameters of nerve conductance in the DA rat model of myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) after preventive and therapeutic treatment. We demonstrate that prophylactic therapy protected against the emergence of EAE symptoms, neuropathology, and disturbances to visual and somatosensory evoked potentials (VEP, SEP). Moreover, therapeutic treatment from day 25 to 45 markedly reversed paralysis in established EAE and normalized the electrophysiological responses, correlating with decreased demyelination in the brain and spinal cord. The effectiveness of FTY720 in this model is likely due to several contributing factors. Evidence thus far supports its role in the reduction of inflammation and preservation of blood-brain-barrier integrity. FTY720 may also act via S1P receptors in glial cells to promote endogenous repair mechanisms that complement its immunomodulatory action.
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PMID:FTY720 sustains and restores neuronal function in the DA rat model of MOG-induced experimental autoimmune encephalomyelitis. 1784 5