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

A 54-year-old man had a syndrome resembling amyotrophic lateral sclerosis after a brief but intense exposure to elemental mercury. The syndrome resolved as his urinary mercury levels fell. Mercury toxicity must be considered not only in individuals with recent anterior horn-cell dysfunction but also with otherwise unexplained peripheral neuropathy, tremor, ataxia, and a gamut of psychiatric symptoms including confusion and depression.
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PMID:Mercury intoxication simulating amyotrophic lateral sclerosis. 686 63

A male, born on December 8, 1956, during the period when many Minamata diseases broke out in a district. His parents who ate much fish and shell fish taken in Minamata Bay suffered from the light, incomplete Minamata disease showing sensory disturbance, the constriction of the visual field, muscular weakness, etc. He weighed 3,225 gr. upon the normal birth given 10 months after pregnancy. His abnormalities were noted since his head was not stabilized on the neck even six months after the birth. Because of the delay in the development of the motor function, he became barely able to sit, stand up and begin walking at the ages of 3, 5 and 6 respectively. In 1962 (at the age of 6), his congenital Minamata disease was diagnosed in view of his clinical symptoms and epidemiological conditions. The mercury value in the hair and blood upon the birth is not known because a considerable time had elapsed after the birth when his mercury poisoning was discovered. However, the clinical symptoms included intelligence disturbance, character change, dysarthria, primitive reflexes, strabismus, hypersalivation, ataxia and hyperkinesia, indicating a typical congenital Minamata disease. Until he became 13 years old (1969) or so, his mental and motor function developed, both gradually. In the same year, he was admitted to a special class for the handicapped. EEG examination revealed that there was a slow alpha activity in the basic pattern and that 6 Hz positive spike was found in the sleep EEG. The constriction of the visual field was classified through examination.2+
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PMID:[Congenital Minamata disease accompanied by arachnoid cyst (author's transl)]. 709 64

Lead, cadmium, mercury and arsenic are widely dispersed in the environment. Adults are primarily exposed to these contaminants in the workplace. Children may be exposed to toxic metals from numerous sources, including contaminated air, water, soil and food. The chronic toxic effects of lead include anemia, neuropathy, chronic renal disease and reproductive impairment. Lead is a carcinogen in three animal species. Cadmium causes emphysema, chronic renal disease, cancer of the prostate and possibly of the lung. Inorganic mercury causes gingivitis, stomatitis, neurologic impairment and nephrosis, while organic mercurials cause sensory neuropathy, ataxia, dysarthria and blindness. Arsenic causes dermatitis, skin cancer, sensory neuropathy, cirrhosis, angiosarcoma of the liver, lung cancer and possibly lymphatic cancer.
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PMID:Occupational and community exposures to toxic metals: lead, cadmium, mercury and arsenic. 716 33

Rats were fed on diets containing methyl mercury dicyandiamide (MMD) at concentrations of 1.5, 7.5 or 75 ppm, and observations made of their social and exploratory behaviour and of gross neurotoxicity (ataxia). Mercury concentration in the blood was monitored. MMD at 75 ppm (50 ppm Hg) for 24 days caused ataxia with a sudden onset at 21-27 days. Social behaviour was reduced at 16-17 days. In two experiments at 7.5 ppm MMD, activity was increased in observations of social behaviour after 2 to 17 days, and treated rats found water in an unfamiliar cage sooner than controls. No difference from controls was apparent from then until increased activity re-appeared after 9 mon of the diet (exp. 1) or after 7 days recovery from 31 or 45 days diet (exp. 2). Ataxia was not observed after 7.5 ppm MMD for up to 47 weeks or in 14 weeks recovery. No consistent effect was observed at 1.5 ppm MMD for 31-45 days. MMD, therefore, had a behavioural effect in rats, independent of gross neurotoxicity; its details were consistent with a hyperresponsiveness to stimuli. Tolerance occurred to this effect at a time when blood-mercury concentration was still rising, but the tolerance appeared to be subject to overload.
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PMID:Early change and adaptation in the social behaviour or rats given methyl mercury in the diet. 719 56

The ability of ethanol to affect hindlimb ataxia and body weight changes induced by methyl mercury was studied in rats. Animals treated with either water or ethanol increased in body weight during the experiment and showed no impairment of hindlimb movement. Rats treated with methyl mercury also increased in body weight but developed moderate hindlimb ataxia. Animals treated with ethanol and methyl mercury initially gained but subsequently lost weight and exhibited severe hindlimb ataxia. The results provide evidence that ethanol can potentiate methyl mercury toxicity in rats and, by implication, in humans.
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PMID:Ethanol potentiation of methyl mercury toxicity: a preliminary report. 728 7

An opportunity to study the effects of methylmercury poisoning in humans was provided by the large outbreak in Iraq in 1971-2. In adults, poisoning resulted from the ingestion of home-made bread prepared from methylmercury-treated seed grain and there was a highly significant correlation between the amount of bread ingested and blood mercury levels. Poisoning in infants resulted either from prior exposure in utero or from suckling or both. Blood mercury levels were higher in infants and children than in adults. There was no increased incidence of congenital defects. Symptoms and signs of poisoning and histopathological changes were mainly confined to the CNS. Symptoms developed, on average, 1-2 months after exposure. In children there was mental retardation with delayed onset of speech and impaired motor, sensory and autonomic function. Severely affected children were blind and deaf. In adults, the clinical picture could be classified as 1, mild (mainly of sensory symptoms) 2, moderate (sensory symptoms accompanied by cerebellar signs) and 3, severe (gross ataxia with marked visual and hearing loss which, in some cases, progressed to akinetic mutism followed by coma). Grades 1 and 2 carried a better prognosis thant grade 3. Interference with transmission at the myoneural junction was found in 14% of patients studied. There was no evidence of peripheral nerve involvement per se and sensory symptoms may be of central origin. The clinical differences between the Iraqi and Japanese outbreaks may be a result, in part at least, of the severe, prolonged and continuous exposure which occurred in the latter outbreak. Improvement was observed among the mild and moderate group. Treatment with chelating agents, thiol resin, haemodialysis and exchange transfusion lowered blood mercury concentrations but produced no convincing clinical benefit. To be effective, treatment may need to be instituted soon after exposure.
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PMID:Clinical and epidemiological aspects of methylmercury poisoning. 738 45

Pigeons were trained on a fixed consecutive number schedule of reinforcement, pecking eight or nine times on one key (a run) before making the single response on a second key that was reinforced if the number requirement had been met. A run of fewer than eight or more than nine responses reset the response requirement. They then were given methylmercury chronically until behavioral signs of poisoning occurred. Where possible, recovery was followed. Percentage of reinforcers earned and rate at which the birds pecked both decreased whereas variability of run length increased after enough methylmercury had been given to produce blood mercury concentrations between 13 and 27 ppm. Some birds also showed consistent shortening of run length throughout the time of maximum poisoning. Because ataxia was a common accompaniment of the changes in operant behavior, other methods of producing ataxia (hobbling one foot or dosing with ethanol) were also studied in some birds. The pattern of changes induced with these methods did not match that seen after methylmercury.
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PMID:Methylmercury-induced changes in operant discrimination by the pigeon. 740 Sep 64

The clinical and pathologic features of a male patient with generalized glutathione deficiency and pyroglutamic aciduria are presented. The patient died at the age of 28 years. He was mentally retarded from infancy and developed progressive tremor, retardation of movement, and ataxia as from the age of 16. Neuropathologic examination of the brain disclosed a selective atrophy of the granule cell layer of the cerebellum and focal lesions in the visual cortex and the thalamus. The type and distribution of the lesions resembled those seen after mercury intoxication. However, in our patient the damage was probably caused by the lack of protection of glutathione against oxidative damage in the brain. Possible treatment of this rare metabolic disorder might include external supply of an antioxidant, e.g., a thiol capable of penetrating the blood brain barrier.
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PMID:The cerebral lesions in a patient with generalized glutathione deficiency and pyroglutamic aciduria (5-oxoprolinuria). 744 86

In the past, methylmercury compounds were manufactured as fungicides or appeared as unwanted byproducts of the chemical industry, but today the methylation of inorganic mercury in aquatic sediments and soils is the predominant if not the sole source of methylmercury. This form of mercury is bioaccumulated to a high degree in aquatic food chains to attain its highest concentrations in edible tissues in long-lived predatory fish living in both fresh and ocean waters. It is well absorbed from the diet and distributes within a few days to all tissues in the body. It crosses without hindrance the blood-brain and placental barriers to reach its principal target tissue, the brain. It is eliminated chiefly in the feces after conversion to inorganic mercury. The biological half-time of methylmercury in human tissues is about 50 days, but there is wide individual variation. Adult poisoning is characterized by focal damage to discrete anatomical areas of the brain such as the visual cortex and granule layer of the cerebellum. A latent period of weeks or months may ensue before the appearance of signs and symptoms of poisoning. The latter manifest themselves as paresthesia, ataxia, constriction of the visual fields, and hearing loss. The prenatal period is the most sensitive stage of the life cycle to methylmercury. Prenatally poisoned infants exhibit a range of effects from severe cerebral palsy to subtle developmental delays. Methylmercury is believed to inhibit those processes in the brain specially involved in development and growth such as neuronal cell division and migration.
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PMID:Mercury: major issues in environmental health. 835 79

Toxic chemicals in the environment can cause a wide range of neurological disease. High-dose exposures to environmental neurotoxicants have produced encephalopathy in children ingesting chips of lead-based paint, blindness in persons who ingested methanol, blindness and ataxia in persons who consumed organic mercury, spinal cord degeneration and peripheral neuropathy in persons exposed to tri-ortho-cresyl phosphate (TOCP), and Parkinsonism in persons exposed to MPTP or to manganese. Environmental neurotoxicants have also been shown to produce a wide range of subclinical neurotoxic effects, including reduction in intelligence, impairment in reasoning ability, shortening of attention span, and alternation of behavior. The first step in the prevention of environmental neurotoxicity is to test chemicals for their toxic potential. More than 70,000 chemicals are currently in commerce. However, except for pharmaceuticals, fewer than 10% of these chemicals have been tested for neurotoxicity. A logical approach to neurotoxicologic assessment of chemical substances will build on and extend currently available test systems. It will have a tiered structure. The first or screening tier will consist of tests to measure obvious structural and functional changes, often a functional observational battery. Subsequent levels of testing will be guided by the results of initial screening. Toxicologic testing must be supplemented by epidemiologic surveillance of populations exposed to known and suspect neurotoxicants. Screening programs in these populations designed to detect excessive absorption of a neurotoxic agent or subclinical neurological dysfunction can be useful in identifying affected individuals before severe disability occurs.
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PMID:Strategies for the prevention of environmental neurotoxic illness. 847 70


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