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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An outbreak of ataxia, blindness, respiratory disease and kerato-conjunctivitis occurred in October 1972 in a beef feedlot in Cyprus. Fifteen animals died and 10 that were severely ataxic were slaughtered; many animals became blind. There was no opportunity to isolate virus when the disease was active but in March and October 1973 infectious bovine rhinotracheitis (IBR) virus was isolated from cattle after they had been treated corticosteroids to stimulate virus excretion. It is probable that IBR virus caused the disease. This is the first report of the isolation of IBR virus from cattle in Cyprus.
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PMID:Use of corticosteroids to isolate IBR virus from cattle in Cyprus after respiratory disease and ataxia. 4 19

Neuroblastoma, which is primarily an extracranial disease, has remote manifestations which can be confusing. Neurologic signs and symptoms such as opsoclonus (dancing eyes), ataxia, blindness, and cord paralysis may precede by several months the manifestations of the primary tumor in a distant site such as the abdomen. Descriptions of nine cases demonstrate the various modes of presentation and some of the unusual aspects of this disease. The recent advent of computed tomography requires a reevaluation of the neuroradiologic approach to the evaluation of neuroblastoma.
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PMID:Remote effects of neuroblastoma. 9 12

A 49-year-old man developed ataxia, myoclonic jerks, cortical blindness, and dementia. In 3 1/2 months, he rapidly deteriorated and died. Clinical and autopsy diagnosis confirmed Creutzfeldt-Jakob disease. The eyes were examined and bilateral optic atrophy was noted. No other ocular changes were noted. Optic atrophy had not been noted before death.
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PMID:Creutzfeldt-Jakob disease and optic atrophy. 37 55

Twenty-seven dogs with lead poisoning were admitted to the University of Pennsylvania Veterinary Hospital from July, 1963, to April, 1975. The major source of the lead was paint. A common history was ingestion of plaster or paint scrapings during room renovation. Most of the dogs were less than 1 year old and had clinical signs referable to the gastrointestinal or the nervous system, or both. The gastrointestinal signs, in order of frequency, were vomiting, anorexia, tender abdomen, diarrhea, and constipation. The neurologic signs, in order of frequency, were hysteria, convulsions, ataxia, blindness, and mydriasis. The finding of many nucleated erythrocytes without severe anemia was nearly pathognomonic for lead poisoning. Of 14 affected dogs subjected to abdominal radiography, 9 had evidence of ingested radiopaque material. A mean blood lead concentration of 18.8 mug/100 ml, with a range of 0 to 50 mug/100 ml, was found for 26 dogs that were hospitalized for problems unrelated to lead poisoning. Of the 27 dogs with lead poisoning, 22 had their blood analyzed for lead. This group had blood lead values ranging from 40 to 530 mug/100 ml. Seven of the affected dogs were monitored throughout their period of treatment with calcium ethylenediaminetetraacetate. The concentration of lead in the blood decreased quickly after the initiation of treatment but leveled off after 2 or 3 days. The initial rapid phase probably corresponded to the removal of weakly bound or extracellular lead, whereas the slow phase probably corresponded to strongly bound or intracellular lead.
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PMID:Lead poisoning in dogs at the University of Pennsylvania Veterinary Hospital. 81 31

Clinical signs of toxicosis, neurologic lesions, and increased tissue residues of methylmercury (MM)were produced in 9 cats by oral administration of 1.29 and 0.86 mg of Hg/kg of body weight/day as methylmercuric hydroxide. Clinical signs, which began after 15 days of exposure, included anorexia, ataxia, hypermetria, proprioceptive impairment, blindness, vertical nystagmus, and grand mal convulsions. Significant lesions occurred in cerebrum, brainstem, and cerebellum and correlated well with clinical signs. Microscopic central nervous system lesions consisted of neuronal degeneration, necrosis and loss of neurons, swollen axons, demyelination, loss of nerve cell processes, vacuolation of neuropil, gliosis, neuronophagia, perivascular cuffs, endothelial hypertrophy and hyperplasia, leptomeningitis, and infrequent vascular necrosis. Overall distribution of central nervous system lesions was unrelated to daily dose, but more advanced lesions were produced by the smaller daily dose. Mean tissue residues of MM were generally directly related to daily dose, and the average distribution among tissues was constant, with highest concentrations in liver, followed by kidney, spleen, muscle, and brain. In utero exposure of kittens to MM, revealed transplacental accumulation.
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PMID:Pathology of subacute methylmercurialism in cats. 83 68

Sixty-six hospitalized patients suffering from chronic methylmercury poisoning were examined in Baghdad during 1972. The poisoning was attributed to consumption of home-made bread prepared from seed wheat treated with mercurial fungicide. The age incidence ranged between 4 and 70 years.Of the various clinical features encountered, neurological symptoms and signs were predominant and included muscular weakness, numbness, unsteady gait, paraesthesia, dysarthria, mental disturbances and, in severe cases, blindness, partial deafness, stupor, coma, and death. Involvement of the cardiovascular, urinary, gastrointestinal and haemopoietic systems, which was commonly encountered in ethylmercury poisoning in the 1960 outbreak in Iraq, was unusual.The severity of symptoms and signs was, broadly speaking, dose-dependent; high exposure led to severe clinical manifestations, but variations existed. Criteria, based on the clinical manifestations, were set for grading the severity of cases. The series included 2 asymptomatic cases, 20 mild, 20 moderate, 14 severe, and 10 very severe. In the latter group 5 patients died from failure of the central nervous system.The severely poisoned patients died irrespective of the medical treatment received. After 2 years of observation, most patients graded as mild or moderate cases lost their symptoms completely. Severe cases improved slowly, although ataxia, diminution of visual field and acuity and paraesthesia were still present. Thus, the previously accepted view that neurological signs were irreversible has been disproved.
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PMID:Intoxication due to alkylmercury-treated seed--1971-72 outbreak in Iraq: clinical aspects. 108 68

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

A 32-year-old male was admitted to our hospital complaining of dementia, gait disturbance and blindness. These symptoms developed at the early two decade and were progressive. On admission, his clinical features included dementia (IQ = 69), spasticity, accentuated deep tendon reflexes, ataxia and hypesthesias in his distal limbs. Brain CT scans showed diffuse cerebral atrophy. On light microscopy, many abnormal lipopigments resembling ceroid and lipofuscin were found in Schwann cells of sural nerve and histiocytes of colon. Ultrastructurally, these materials showed lamellar structure like Zebra bodies. Nine lysosomal enzymes, serum very long-chain fatty acids, serum amino acids and urinary oligosaccharides were all normal. Neuronal ceroid lipofuscinosis (NCL) of adult type was diagnosed on the basis of clinical features, radiological and pathological findings, and biochemical studies. Many previous studies suggested that NCL was a disorder with lysosomal dysfunction. We examined lysosomal protein degradation, using 125I-low density lipoprotein (LDL) in cultured fibroblasts from this patient. The degradation of LDL was normal, compared to control subjects. The activities of cathepsin and lysosomal glycosidases, were also normal. The amount of urinary dolichol has been reported to be elevated in the patients with infantile and late infantile types of NCL. However, no elevation was found in the urine of our patient.
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PMID:[Adult-onset neuronal ceroid lipofuscinosis--a case report with biological study]. 129 Nov 75

We reviewed the clinical and pathological data on 319 neuronal ceroid lipofuscinosis (NCL) cases to determine the degree of variability within the different forms and among and within families. Thirty-six cases (11.3%) were the infantile form; 116 cases (36.3%), late infantile; 163 cases (51.1%), juvenile; and four cases (1.3%), the adult form (Kufs disease). Clinical variability was found in all forms studied, but was most striking in the juvenile and late infantile forms of NCL. The expected initial findings of seizures, dementia, blindness, or motor impairment were evident in 255 cases (80%), and rarer, less typical initial neurological symptoms were seen mainly in the 64 cases (20%) of the juvenile form: behavior abnormalities (18/64), psychoses (12/64), neuropathy (2/64), involuntary movements (15/64), ataxia (9/64). Six juvenile and two adult cases had no detectable impairment of vision. All 319 NCL cases had skin or conjunctive biopsies or buffy coats that showed the characteristic ultrastructural abnormalities of NCL. Variability was evident in 16.7% in that a combination of fingerprint, curvilinear, and membranous profile inclusion bodies was observed in storage lysosomes, although one type of inclusion was distinctly predominant for each form. Postmortem examination of brains of 19 NCL cases (three with the infantile form, six with the late infantile form, nine with the juvenile form, and one with the adult form) revealed characteristic changes. Sixteen of the 19 NCL brains (84%) showed pathological variability in that they contained more than one kind of characteristic inclusion body in the neuronal lysosomal storage compartment. In all 19 NCL brains, small amounts of aging lipofuscin were also found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Variability in the clinical and pathological findings in the neuronal ceroid lipofuscinoses: review of data and observations. 131 16

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80


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