Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical signs of toxicosis, neurologic lesions, and elevated tissue residues of methylmercury (MM) were produced in 12 pigs by oral administration of 1.29, 0.86, 0.64, and 0.43 mg mercury/kg of body weight daily as methylmercuric hydroxide (MMH). Clinical signs which began on day 17 were ataxia, dysmetria, blindness, convulsions, paresis, and death. Time of onset of signs was inversely related to size of daily dose. Microscopic lesions were found in the cerebrum brain stem, and spinal cord, and correlated well with clinical signs. The cerebrum in which severity of lesions was directly related to length of exposure was the most severely affected region of the central nervous system (CNS). Lesions were neuronal necrosis, neuronophagia, cortical vacuolation, axon swelling, gliosis, leptomeningitis, and vascular fibrinoid necrosis. Neuronal necrosis was most extensive within mid and deep cerebrocortical laminae. Brain residues of MM were directly proportional to the size of daily dose, and statistically significant. Distribution of MM among different tissues was rather uniform with highest concentrations found in liver, followed by kidney, muscle, spleen, and brain.
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PMID:The pathology of subacute methylmerculialism in swine. 125 8

Ten carcasses and three vertebral columns from north Norwegian dairy goats, which had been killed due to clinical signs of severe neurologic disease, were received for necropsy. Pathological examination revealed nematodes and nematode ova in the central nervous system (CNS) of nine goats. Worms found by gross examination were identified as Elaphostrongylus rangiferi Mitskevich, 1960. Focal traumatic encephalomyelomalacia, apparently caused by migrating worms, perivascular cuffing, eosinophilic leptomeningitis and perineural infiltrations and granulomas, could be demonstrated in CNS sections from all 13 animals examined. Clinical signs reported were initial pruritus followed by motor weakness, lameness, paresis, reduced vision, circling, abnormal head position, bulging eyes and scoliosis. The disease occurred from September to January in regions with a considerable migrant reindeer population. It was concluded that the reported outbreaks of neurologic disease represented seasonal occurrence of cerebrospinal elaphostrongylosis caused by Elaphostrongylus rangiferi, the elaphostrongyloid nematode of reindeer (Rangifer tarandus tarandus).
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PMID:Cerebrospinal elaphostrongylosis in dairy goats in northern Norway. 179 88

A 25-year-old woman developed Nelson's syndrome, 3 years after successful bilateral adrenalectomy for Cushing's disease. Despite pituitary surgery and radiotherapy the tumour showed invasive growth, leading to visual disturbance, paresis of the oculomotor nerve and, 34 years after adrenalectomy, to death by widespread purulent leptomeningitis. Autopsy revealed a large adenohypophyseal carcinoma with a metastasis attached to the dura, both tumours showing immunocytochemical staining for ACTH and TSH. We review the literature on metastatic adenohypophyseal carcinoma in Cushing's disease and Nelson's syndrome and discuss the role of proliferation markers as indicators of malignant progression.
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PMID:Progression of a Nelson's adenoma to pituitary carcinoma; a case report and review of the literature. 1009 Jan 41