Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A shipyard worker was poisoned by hydrogen sulfide (H2S), and rescued after 15-20 min. He regained consciousness after 2 days. Three days later his condition deteriorated, and he was more or less comatose for a month. When he woke up, he was amnesic, nearly blind, had reduced hearing, and had a moderate spastic tetraparesis and ataxia. Two months after the accident, he had greatly improved. Audiograms showed hearing loss with maximum at 2000 Hz and significantly poorer speech discrimination. EEG showed generalized dysrhythmia. At follow-up 5 years later he had not been able to resume his work, and had slight motor, memory and visual symptoms. CT and MRI showed slight cerebral atrophy. EEG and evoked responses were normal.
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PMID:Delayed neuropsychiatric sequelae after acute hydrogen sulfide poisoning: affection of motor function, memory, vision and hearing. 177 8

Two groups of 3 120-160-kg Holstein steers were fed a diet high in carbohydrate and low in long fiber and either with or without added sodium sulfate. Prior to and during the course of feeding the experimental diet, the concentrations of rumen hydrogen sulfide gas and rumen fluid sulfide were determined by a simple sulfide detector tube method and by sulfide-selective electrode, respectively. Other measurements included rumen fluid pH, blood creatine kinase, and blood sulfhemoglobin. Two of the 3 steers fed the high-sulfate diet developed signs and lesions of polioencephalomalacia. Clinical signs included episodic ataxia and blunted or absent menace reaction. Increased ruminal H2S gas concentrations occurred in all 3 steers consuming the diet with added sulfate. The onset of clinical signs coincided with the onset of elevated H2S concentrations. These increases were 40-60 times the values measured in the steers consuming the diet without added sulfate. In contrast, increases in rumen fluid sulfide concentrations usually rose to 4 times that of control steers. The steers fed an identical diet but without added sulfate exhibited no signs or lesions of polioencephalomalacia and no elevations of sulfide in rumen gas or fluid. All steers had a modest decrease in rumen fluid pH associated with the transition to the concentrate diet. No significant changes were observed in any of the blood measurements of any of the steers. An additional pair of steers was fed the experimental diet with or without added sulfate to compare the ruminal H2S gas concentrations estimated by H2S detector tubes with those estimated by a different method of analysis utilizing charcoal trapping of H2S, conversion to sulfate, and measurement of the sulfate. Both methods yielded comparable estimates of H2S concentration. Overall, these data indicate that changes in rumen gas cap H2S concentrations are larger than changes in rumen fluid sulfide concentration and the estimation of rumen gas cap H2S concentration may be a practical approach to detecting pathologic increases in ruminal H2S gas. This simple, rapid, minimally invasive method should be useful for estimating the H2S content of ruminal gas under field conditions.
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PMID:In vivo indicators of pathologic ruminal sulfide production in steers with diet-induced polioencephalomalacia. 908 29

A red deer herd of 150 mixed-age hinds, 48 stags and 102 weaners was identified as severely copper deficient during an observational study of 15 deer farms in the lower North Island of New Zealand during 1992 and 1993. Severe lameness was observed in nine weaners in 1992 (8.8% prevalence) and 15 in 1993 (12% prevalence). Typical abnormalities included swollen hocks and carpal joints and outward rotation of hind legs with hocks touching. At postmortem examination, there were epiphyseal fractures of the femoral head, severe degenerative arthropathy of the coxo-femoral joints and erosions of cartilage in many other limb joints. Osteochondrosis was confirmed histologically. Concurrently, three adult hinds and one adult stag developed into-ordination typical of enzootic ataxia which was confirmed histologically. Blood and liver copper concentrations in untreated affected weaner deer ranged from undetectable to 16.0 micromol/l (mean 7.6 micromol/l) and 25 to 53 micromol/kg (mean 39 micromol/kg), respectively. Mean blood copper concentrations in unaffected weaners in March 1992 and 1993 were 5.3 micromol/l and 4.4 micromol/l, respectively. The mean blood copper concentration in seven hinds in September 1992, prior to onset of clinical signs of enzootic ataxia, was 1.5 micromol/l (range 1.0-2.4 micromol/l). At other times of the year, mean blood copper concentrations ranged up to 12.5 micromol/l in adults and 8.9 micromol/l in weaners before treatment began in 1993. Pasture analyses showed copper contents of 6-11 ppm in 11 samples collected during 1992 and 1993. Sulphur ranged from 0.18 to 0.37%, molybdenum from 0.51 to 3.56 ppm and iron from 130 to 2886 ppm. These measurements supported a diagnosis of secondary copper deficiency. Supplementation with oral oxidised copper wire particles was undertaken from December 1992, resulting in an improvement in blood copper concentrations in some classes of deer. No further clinical abnormalities have been observed.
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PMID:Osteochondrosis, skeletal abnormalities and enzootic ataxia associated with copper deficiency in a farmed red deer (Cervus elaphus) herd. 1603 12