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 differential diagnosis of acute loss of vision in children includes acute loss of vision due to retinal or optic nerve disease, and cortical blindness. The retinal disorders which may be mis diagnosed as optic neuritis include Leber neuroretinitis, Leber hereditary optic neuropathy, and Stargardt macular dystrophy. Retinal changes which evolve in neuroretinitis, and the pseudopapilledema in Leber heredity optic neuropathy are helpful in differentiating these disorders from optic neuritis. Stargardt macular dystrophy, a disorder associated with a variety of mutations, may be mis diagnosed as psychogenic visual loss due to the early normal appearance of the retina, and the loss of vision over a period of weeks. The differentiation of optic neuritis from anterior ischemic optic neuropathy (AION), depends upon the initial appearance of the optic disc (in AION either hyperemia due to reperfusion, or swelling and pallor if total infarction has occurred). The authors have described children with abrupt loss of vision during renal dialysis, whose risk factors for AION included systemic hypotension and intra ocular hypertension. Children with vigorous treatment of accelerated hypertension, and children with migraine and pro thrombotic disorders have also incurred AION. Thus, AION should be suspected when acute loss of vision occurs in association with certain ocular and systemic risk factors. In children capable of cooperating for visual field examination, the typical change in AION is an altitudinal defect, while optic neuritis it is a central scotoma. The association of optic neuritis with multiple sclerosis, DeVic disease, and with acute demyelinating1 encephalomyelitis require special consideration in regard to treatment and prognosis. Acute loss of vision due to cerebral cortical insults involves a large differential diagnosis which includes vascular, metabolic and infective disease; as well as disorders causing transitory blindness such as seizures and migraine
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PMID:[Acute loss of vision in children]. 1259 57

Oxidative stress and mitochondrial dysfunction appear to contribute to neurodegenerative processes during multiple sclerosis (MS). Thus, antioxidants may represent a therapeutic option for MS. The antioxidant idebenone was proven to be beneficial in Friedreich's ataxia and Leber's hereditary optic neuropathy, two disorders caused by mitochondrial alterations. Here we showed that idebenone protected neuronal HT22 cells from glutamate-induced death in vitro. However, in experimental autoimmune encephalomyelitis, idebenone failed to affect disease incidence or onset when applied preventively, or to reduce disease severity when applied therapeutically. Histopathological examination of CNS from idebenone treated mice showed no improvement in inflammation, demyelination, or axonal damage. Thus, we hypothesize that idebenone treatment will likely not benefit patients with MS.
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PMID:The antioxidant idebenone fails to prevent or attenuate chronic experimental autoimmune encephalomyelitis in the mouse. 2387 88