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

Toxic metals encountered industrially or environmentally may produce the following syndromes: 1) Peripheral neuropathy: which is mainly sensory in arsenic and entirely motor with inorganic lead, organophosphorus compounds and tallium produce a mixed form of peripheral neuropathy. 2) Encephalopathy: usually with lead poisoning where ataxia and hemiplegia or optic atrophy may occur. 3) Optic neuritis: transient or permanent impairment of vision in arsenic poisoning and blurring of vision followed by field fedects with thallium poisoning. 4) Cerebellar disturbances: in the form of ataxia in organic mercury. 5) Parkinsonism: extrapyramidal signs occurs in manganese poisoning shown as mask face and rigidity of muscles. 6) Mental changes: as acute psychosis in organic lead and erethism in organic mercury.
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PMID:Neurological syndromes produced by some toxic metals encountered industrially or environmentally. 35 38

Organic mercury compounds have greatest affinity to the central nervous system (cerebellar white matter, basal ganglia, occipital and frontal cortex). Anatomical changes observed in the brain are of degenerative type. Similar changes are found also in the myocardium, liver and kidneys. The authors observed for 2 years a family of three persons who contracted poisoning with organic mercury compounds after easting the meat of pigs and hens fed through negligence with wheat destined for sowing, containing methyl-mercurocyanoguanidine. The level of total mercury determined by the method of cold atomic absorption was in these patients four months after poisoning 650,500 and 175 ng/ml of blood (normal value from 1.56 to 18.72 ng/ml). During the observation it has been established that the severity of poisoning was related to the level of mercury found in the organism. Pharmacological treatment (Cuprenil, Thioctacid, vitamin B complex) and rehabilitation brough slight improvement after 2 years. Two patients with total blood mercury level 650 and 500 ng/ml were completely disabled due to encephalopathy with high grade ataxia, dysarthria and concentric narrowing of the field of vision. In the third patients with less severe poisoning (175 ng/ml) pathological manifestations disappeared completely after short treatment.
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PMID:[Encephalopathy after poisoning with organic mercury compounds]. 48 88

The clinical features of 49 children who had eaten bread contaminated with methylmercury in rural Iraq were reviewed. Symptoms and signs relating to the nervous system--varying degrees of ataxia, weakness, and visual and sensory changes--dominated the clinical picture. The severity of poisoning was related to the blood mercury concentration, as was the degree of recovery. Follow-up over two years showed that children who had had mild or moderate poisoning slowly but steadily improved, some of them recovering normal function, though all had a residual generalized hyperreflexia. In some patients ataxia and motor weakness disappeared. Visual changes also improved, though less completely, and of 17 blind children, only five had recovered partial sight by the end of two years. Seven of the 18 children who suffered very severe poisoning were left physically and mentally incapacitated. The degree of clinical progress shown by these children was better than that shown by some other groups of patients, possibly because the poisoning was relatively acute and mercury consumption was stopped immediately after its effects had become obvious.
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PMID:Methylmercury poisoning in Iraqi children: clinical observations over two years. 63 Feb 56

Young adult rabbits have been given methyl mercury salts by subcutaneous injections or by gastric intubation. After 3 daily doses of 7.5 mg/kg by the 8th day moderate to severe ataxia developed, and after 4 doses, severe ataxia. Some of these latter animals might die. This species, therefore, seems to be about twice as sensitive to the neurotoxic properties of methyl mercury salts as the laboratory rat. With the light microscope extensive degenerative changes were seen in primary sensory ganglion cells, in both Purkinje and granule cells of the cerebellum, and in certain cells in several regions of the forebrain. The earliest changes became visible microscopically about the fourth day after commencing dosing, and reached a maximum of severity from the 7th to 10th day. The pattern of neuronal damage more closely resembled that found in the cat and in man than that seen in the rat. No evidence of changes vascular permeability was detected.
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PMID:Some effects of methyl mercury salts on the rabbit nervous system. 116 65

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

Doses of 3, 8.4, 20, 46, 74 or 176 mug Hg/kg/day were fed to groups of 8--10 adult cats, either as methylmercuric chloride or as methylmercury-contaminated fish, 7 days/week for up to 2 years. Food consumption, body weight change, blood mercury levels, haematology, urine analysis, serum blood urea nitrogen (BUN) levels and neurological status were assessed regularly in all animals. Clinical signs of methylmercury toxicity -- consisting of ataxia, loss of balance and motor incorrdination -- occured in groups receiving 176 mug Hg/kg/day after 14 weeks of treatment. Pathological findings were confined to the nervous system and consisted of loss of nerve cells with replacement by reactive and fibrillary gloisis. Terminal blood and brain mercury levels were approx. 10 ppm. There were no differences in the time required to develop clinical signs of methylmercury toxicity, tissue mercury levels or pathology between the groups of cats receiving methylmercury as methylmercuric chloride or as methylmercury-contaminated fish, at either dose level. Blood mercury levels in the remaining doses groups appeared to plateau after 40 weeks of treatment. Groups receiving 46 mug Hg/kg/day began to show some neurological impairment after 60 weeks of treatment which did not progress in subsequent weeks. No treatment-related effects were present in groups receiving 20, 8.4 or 3 mug Hg/kg/day after 2 years.
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PMID:Chronic toxicity of methylmercury in the adult cat. Interim report. 126 72

Three siblings with inhaled elemental mercury toxicity are described, and the signs and symptoms of mercury toxicity, interpretation of mercury concentrations, and management of elemental mercury exposure are reviewed. A 4-year-old girl was admitted to the hospital with a history of fever and increasing irritability, fatigue, malaise, insomnia, headache, anorexia, and ataxia. She was discharged two days later with a diagnosis of acute cerebellar ataxia. During the following 18 days, the child's condition worsened, and she was rehospitalized. Meanwhile her 11-year-old sister was hospitalized for evaluation of fatigue, weakness, lower back pain, and ataxia. The older girl's blood mercury concentration, at 5.5 micrograms/dL, was in the toxic range. Twenty-four-hour urine mercury screening confirmed mercury intoxication in both children. Questioning revealed that the girls' brother had recently spilled 0.5-1 oz of elemental mercury in the house. All family members underwent blood and urine mercury testing. The brother underwent a dimercaprol challenge to determine his tissue mercury burden, which was found to be greater than 2.4 micrograms/dL. The sisters underwent two courses of chelation therapy with dimercaprol. Symptoms persisted in all three children, and they underwent five 10-day cycles of N-acetyl-D,L-penicillamine (NAP) therapy; the youngest underwent a third dimercaprol regimen. All siblings continued NAP chelation therapy because of extensive tissue mercury burden until the results of repeated urine mercury concentration determinations were normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elemental mercury poisoning. 174 59

In middle of Kii peninsula, one of the biggest mercury mine in Japan had been present until about 10 years ago. The mercury contents in water and fish are reported to be higher in this district. So we investigated the mercury in hair of patients and normal controls. In this study the subjects are 23 cases of ALS including 15 cases in Nara and Mie and 8 cases in other prefectures except in Kii peninsula, 14 cases with ataxia, 11 cases with other degenerative diseases like Parkinson's disease and Alzheimer's disease, 25 cases of cerebrovascular disease as compared to 26 normal controls. The hair are taken from 3 areas on head of patients and normal controls. They are washed in 2% sodium lauryl sulfate and stirred in distilled water several times, and they are soaked in acetone and dried in filter paper. They are inserted in fire and vaporized mercury are measured (Zeeman Effect Mercury Analyzer) in ppm. The hair mercury concentration is 2.81 ppm in ALS in total, 3.62 ppm in ALS in Nara and Mie and 1.39 ppm in outside of Kii Peninsula, 2.34 ppm in ataxia, 1.83 ppm in other degenerative diseases, 1.66 ppm in cerebrovascular disease and 1.44 ppm in normal controls. Statistically it is significant (p less than 0.05) between that in ALS in Nara and Mie and that in normal controls. 6 cases (40%) with ALS in Nara and Mie have the value above the mean +2 standard deviation of controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mercury in hair of patients with ALS]. 280 5

A number of neurotoxic drugs, when administered prenatally, induce neurobehavioral impairments and cause delay of the development of central nervous functions, without morphological malformations. Experiments were undertaken to clarify the behavioral teratogenicity of the fungicide methoxy-ethyl-mercury chloride (MEMC). CFY rat dams were treated with different doses of MEMC during 7th-15th days of gestation (2.0, 0.62 and 0.02 mg/kg daily), perorally. Development of gait, motor coordination, behavior patterns in an open field test, swimming, and conditioned avoidance learning were tested at different ages of rat pups. MEMC did not cause any mortality of dams, but there was a mild ataxia at the 2.0 mg/kg treatment. While birthweight, number of offspring, ear-eye opening and gait were normal, unexpectedly high mortality occurred perinatally. After weaning, open field behavior was nearly normal, there was a mild decrease of rearing, grooming and ambulation and an initial preference for the periphery of the open field decreased. Ambulation increased significantly in 90-day-old pups. Motor coordination on a rotorod decreased in 23- and 36-day-old pups, but increased in 90-day-old pups at the 2.0 mg/kg dose. There was no difference among groups in amphetamine sensitivity tested in a swim stress test. During avoidance conditioning, pups treated with the two higher doses performed poorly when compared to controls and the latency of the positive conditioned response was lengthened significantly. Our results show a dose-dependent behavioral teratogenicity of this organomercurial fungicide. The so called no effect level--as far as the neurobehavioral impairments due to prenatal exposure are concerned--is 0.02 mg/kg daily.
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PMID:Behavioral effects of prenatal methoxy-ethyl-mercury chloride exposure in rat pups. 315 34

In man the clinical patterns of inorganic and organic mercury toxicity are different. Inorganic mercuric chloride mainly affects the renal and gastrointestinal systems. The characteristic neurological feature is a fine tremor, particularly of the hands and fingers. In contrast organic methyl mercury toxicity results in an exclusively neurological disorder, the characteristic features being ataxia, dysarthria, paresthesia and tunnel vision. To study the action of these classes of mercury compounds on neurones small amounts of mercuric chloride or methyl mercuric acetate were injected or iontophoresed into the rat cerebrum. The ultrastructural changes which followed were identical. Progressive and often pronounced cytoplasmic swelling of neurones suggested a defect at the cell membrane level. Thus is spite of their distinctive clinical syndromes these 2 classes of mercury compounds are capable of inducing neuronal necrosis.
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PMID:Identity of ultrastructural effects of mercuric chloride and methyl mercury after intracerebral injection. 621 46


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