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 authors report results of treatment of 16 patients whose disease was caused by premeditated poisoning with thallium fluoride. The first signs of the disease appeared in 5 patients 30-38 hours and in the remaining 2-4 days after ingestion of poisoned food and were manifested by dyspepsia, leg pain. Then neurological symptoms of polyneuritis and encephalomyelitis prevailed. Within 1-3 weeks alopecia, xeroderma, herpetic phenomena appeared. Most patients showed disorders of the psycho-emotional sphere (intoxication encephalopathies of anxiety-paranoia type). Severe grades of thallitoxicosis were marked by involvement of the myocardium, liver and kidneys. Excretion of the nucleus is slow: with the urine (45%), with feces (55%). For correct diagnosis and for solution medical forensic problems examination of the content of thallium in the blood, urine, feces and hair is of importance. Treatment tactics are described in detail.
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PMID:[Clinical picture and treatment of acute thallium poisoning]. 275 99

Susac's syndrome (SS) consists of the triad of encephalopathy, branch retinal artery occlusions (BRAO), and hearing loss. It usually affects women aged 20 to 40, but men are also affected, and the age range extends from 9 to 72 years. It tends to be unrecognized, even in major academic centers. The complete triad may not be present at the onset, which makes diagnosis more difficult. However, since this disorder is treatable, early diagnosis is important. The encephalopathy is usually associated with headaches, multifocal neurologic manifestations, and psychiatric features (particularly paranoia). MRI shows a white matter disturbance that is frequently confused with multiple sclerosis and acute disseminated encephalomyelitis. During the encephalopathy, the corpus callosum is always affected and shows central involvement--small to large "snowballs" and linear defects, "spokes." As the acute changes (microinfarcts) resolve, central callosal "holes" develop, a pathognomonic finding. The deep gray matter (70%) and leptomeninges (33%) also may be involved. Dilated fundus examination will reveal branch retinal artery occlusions. Fluorescein angiography may disclose pathognomonic staining of the arterioles proximal to the occlusions and of nonoccluded arterioles. The cochlear hearing loss, sometimes associated with vertigo, is usually bilateral, and deafness becomes a major disabling problem. Brain biopsies, anatomic observations, and responses to immunosuppressive therapy suggest that SS represents an autoimmune endotheliopathy in the microvasculature of the brain, retina, and cochlea. Treatment requires immunosuppression. High-dose corticosteroid therapy is the mainstay, but additional therapies such as intravenous immunoglobulin, mycophenolate mofetil, and cyclophosphamide are often necessary. Rituximab is the newest therapy to consider. Treatment should be prompt, aggressive, and sustained to avoid the dreaded residuals of dementia, deafness, and blindness.
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PMID:Treatment of Susac's Syndrome. 1832 1