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

Methyl mercury intoxication causes ataxia. Structural changes of cerebellar and peripheral nerve tissues have been described. However, it is still unclear whether the ataxia is of cerebellar or peripheral origin. To clarify this question further, the effects of methyl mercury intoxication on the numbers of granule and Purkinje cells and the volume of Purkinje cell perikarya have been evaluated with stereological methods. Rats were intoxicated with methyl mercury, at a dose of 2 mg/kg per day for 19 successive days, and the analysis was carried out 2.5 or 4.5 weeks later. The total numbers of cerebellar granule cells and Purkinje cells were estimated using an optical fractionator and the mean volume of the Purkinje cells was estimated by the vertical rotator technique. The volumes of the granular cell layer, the molecular layer and the white matter were estimated using the Cavalieri principle. The intoxicated animals developed hindlimb incoordination when held by the tail. Although pronounced axonal degeneration occurred in the peripheral nervous system, no changes were found in cerebellar cell numbers or cell sizes in either of the test groups. The absence of detectable light microscopic changes in the cerebellum indicates that the peripheral nervous system is affected prior to the cerebellum in rats intoxicated with organic mercury.
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PMID:Structural preservation of cerebellar granule cells following neurointoxication with methyl mercury: a stereological study of the rat cerebellum. 852 98

The first methylmercury poisoning by consumption of fish arose in Minamata, Japan, in 1953. Methylmercury dispersed from Minamata to the Shiranui Sea until 1968. Mercury concentration in the hair of residents on the coast of the Shiranui Sea was 10 to 20 times higher than that in nonpolluted people in Kumamoto Prefecture in 1960. People on the coast of the Shiranui Sea have consumed fish containing low-dose methylmercury without a ban over decades until 1968. We studied the effect of long-term consumption of methylmercury on those people 10 years later after the end of methylmercury dispersion. Our epidemiological study clarified that people in a fishing village (Ooura) on the coast of the Shiranui Sea showed a significantly higher frequency of neurological signs characteristic of methylmercury poisoning (hypoesthesia, ataxia, impairment of hearing, visual change, and dysarthria) in comparison with people in a nonpolluted fishing village (Ichiburi). The neurological disorders were still detected 10 years later in Ooura after the end of methylmercury dispersion from Minamata; hypoesthesia showed the highest frequency in Ooura. These results suggest that people on the coast of the Shiranui Sea were afected by long-term dietary exposure to methylmercury.
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PMID:Expansion of methylmercury poisoning outside of Minamata: an epidemiological study on chronic methylmercury poisoning outside of Minamata. 860 58

The major physical forms of mercury to which humans are exposed are mercury vapor, Hg0, and methylmercury compounds, Ch3HgX. Mercury vapor emitted from both natural and anthropogenic sources is globally distributed in the atmosphere. It is returned as a water-soluble form in precipitation and finds its way into bodies of fresh and ocean water. Land run-off also accounts for further input into lakes and oceans. Inorganic mercury, present in water sediments, is subject to bacterial conversion to methylmercury compounds that are bioaccumulated in the aquatic food chain to reach the highest concentration in predatory fish. Human exposure to mercury vapor is from dental amalgam and industries using mercury. Methylmercury compounds are found exclusively in seafood and freshwater fish. The health effects of mercury vapor have been known since ancient times. Severe exposure results in a triad of symptoms, erethism, tremor, and gingivitis. Today, we are concerned with more subtle effects such as preclinical changes in kidney function and behavioral and cognitive changes associated with effects on the central nervous system. Methylmercury is a neurological poison affecting primarily brain tissue. In adults, brain damage is focal affecting the function of such areas as the cerebellum (ataxia) and the visual cortex (constricted visual fields). Methylmercury also at high doses can cause severe damage to the developing brain. Today the chief concern is with the more subtle effects arising from prenatal exposure such as delayed development and cognitive changes in children.
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PMID:The toxicology of mercury. 928 45

Mercury exists in various chemical forms. The important forms from a toxicological viewpoint are the metallic form, also called the elemental form, the divalent inorganic forms and methylmercury compounds. Elemental (Hg0) mercury has a high vapor pressure and the vapor causes a number of cases of poisoning via inhalation. Classical mercury poisoning is characterized by a triad of signs, namely tremors, erethism and gingivitis. Mercurial erethism, which is characterized by behavioral and personality changes such as extreme shyness, excitability, loss of memory, and insomnia are also observed. Recently, the effects of mercury exposure at levels around 0.05 mg/m3 or lower have been of concern and may include minor renal tubular damage, increased complaints of tiredness, memory disturbance and other symptoms, subclinical finger tremor, abnormal EEG by computerized analysis and impaired performance in neurobehavioral or neuropsychological tests. Abnormal gait, dysarthria, ataxia, deafness and constriction of the visual field are typical of the symptoms of methylmercury poisoning observed in Minamata and Iraqi outbreaks, as well as in occupational methylmercury poisoning cases. Furthermore, an infant born to a mother with excessive methylmercury consumption showed various neurological disturbances and delayed development. Since several populations are believed to be still exposed to methylmercury through the consumption of fish and sea mammals, neurobehavioral deviations in children of these populations have recently been investigated.
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PMID:Occupational and environmental toxicology of mercury and its compounds. 1081 38

Pregnant rats were fed either a control (20% protein) or low (3.5%) protein diet during gestation and lactation. The pups were separated from their mothers on postnatal day 21, and were given the same diet as their corresponding mothers. The groups of pups from each diet group were treated on either postnatal day 21 or postnatal day 60 with 7.5 mg methylmercury chloride (MeHgCl) per kg b.w. once daily by gavage for 10 consecutive days, and the development of ataxia (hind-limb crossing) was monitored. The offspring from mothers on the protein-deficient diet were found to be more sensitive to MeHg-induced ataxia than those on the protein-sufficient diet. The former accumulated more mercury in different brain regions than the latter. The rates of protein synthesis in different brain regions of the offspring fed the protein-deficient diet were significantly reduced compared with the rates in those fed the protein-sufficient diet. However, MeHg treatment did not significantly modify the rates of such protein synthesis further in protein-deficient rats. Thus, a significantly much higher inhibition of the intrinsic rates of protein synthesis in different brain regions due to severe protein deficiency, as observed in this study, may be partly responsible for the increased susceptibility of developing rats fed a protein-deficient diet to MeHg-induced ataxia, or hindlimb crossing, although other factor(s) might also be involved.
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PMID:Effects of protein-deficient nutrition during rat pregnancy and development on developmental hindlimb crossing due to methylmercury intoxication. 1095 92

Thiophene is a sulfur-containing heterocyclic hydrocarbon that has been detected in a number of environmental sources as various derivatives. Previous studies with rats have shown that thiophene induces selective degeneration of granule cells in the cerebellum, as observed with methyl mercury. To study the neurotoxicity of thiophene, Wistar rats received daily intramuscular injections of 0.2 mL thiophene for 3 days. Ataxia and convulsions were noted in all animals within 24 h after the final dose. Histologically, multiple foci of necrosis were observed in the cerebellum, predominantly in the granular layer. Neuronal damage was also found in the cerebral cortex, inferior colliculus and inferior olive. These findings suggest that thiophene causes widespread neuronal degeneration in rats and that the regional distribution of brain lesions induced by thiophene is different from that caused by methyl mercury poisoning.
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PMID:Thiophene, a sulfur-containing heterocyclic hydrocarbon, causes widespread neuronal degeneration in rats. 1121 Oct 52

Ninty-five inhabitants of the gold mining area of Mt. Diwata (on Mindanao, Philippines), who were diagnosed to be mercury (Hg) intoxicated, were orally treated with 2 x 200 mg of the chelating agent DMPS (Dimaval, Co. Heyl, Germany) for 14 days in the course of a UNIDO project focusing on mercury pollution abatement. Blood and urine samples before and after treatment, urine after the first application of DMPS and a hair sample were collected and analyzed for Hg. Before and after treatment extensive anamnestic data were collected, medical and neurological investigations and some neuro-psychological tests were performed. In spite of the short time of treatment most of the patients reported a marked improvement of the complaints which were stated by them before the therapy and which are characteristic for a chronic Hg intoxication, for example tremor, loss of memory, sleeplessness, metallic taste, etc. But even in some of the objective neurological parameters like hypo-mimia, Romberg test and tests for tremor/ataxia a statistical significant improvement could be found. Significant improvements could also be found in two neuro-psychological tests (pencil tapping and Frostig). In some cases an extreme high urinary Hg excretion was found under the chelating therapy with DMPS, and by this a distinct reduction of the Hg body burden. Nevertheless, in most cases Hg in blood and urine was not markedly decreased by the treatment. This shows that the duration of the treatment (14 days) was not sufficient for a permanent decrease in Hg. As DMPS excretes Hg mainly through the kidney, it can be concluded that in most cases even after 14 days of treatment there was an ongoing redistribution of Hg from other tissues to the kidney. In conclusion, this study proves that a chelating therapy with DMPS is highly effective even in the case of a mixed chronic and acute intoxication with an unknown combination of Hg vapor, inorganic Hg and organic Hg=methylmercury (MeHg), as characteristic for gold mining areas in the third world. Adverse side effects were rarely reported. Only in one case the medication had to be terminated after the first application due to an allergic skin reaction.
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PMID:The Mt. Diwata study on the Philippines 2000-treatment of mercury intoxicated inhabitants of a gold mining area with DMPS (2,3-dimercapto-1-propane-sulfonic acid, Dimaval). 1271 26

Parkinson syndrome occurs in the course of chemical intoxication, especially Mn, CS2, CO. It is rarely caused by chronic mercury intoxication. We present the case of 55 year old man who was exposed to metallic mercury vapor during 33 years of working in the chemical plant at the production of chlorine. On several occassions patient was removed from contact with Hg because of the symptoms of increased Hg absorption. At the age of 52 he developed hand tremor, balance and gait disturbance with bradykinesia, paresthesias of the upper extremities, neurobehavioral abnormalities, slight memory loss, and spatial disorientation. Psychoneurological examination revealed dementia, Parkinson's syndrome and ataxia of the lower limbs. Mercury excretion in the urine, which equaled 18.3 mu\g creatinine, confirmed exposure to Hg. MRI of the head revealed cortical and cerebellar atrophy. Electroneurography examination found features of subclinical peripheral sensory axonopathy of the upper limbs. Despite atypical clinical course (parkinsonismus) chronic mercury encephalopathy was diagnosed based on documented occupational exposure and diagnostic test results.
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PMID:[Parkinsonism in chronic occupational metallic mercury intoxication]. 1509 29

Florida panthers are an endangered species inhabiting south Florida. Hg has been suggested as a causative factor for low populations and some reported panther deaths, but a quantitative assessment of risks has never been performed. This study quantitatively evaluated retrospective (pre-1992) and current (2002) risks of chronic dietary Hg exposures to panthers in the Florida Everglades. A probabilistic assessment of Hg risks was performed using a dietary exposure model and Latin Hypercube sampling that incorporated the variability and uncertainty in ingestion rate, diet, body weight, and mercury exposure of panthers. Hazard quotients (HQs) for retrospective risks ranged from less than 0.1-20, with a 46% probability of exceeding chronic dietary thresholds for methylmercury. Retrospective risks of developing clinical symptoms, including ataxia and convulsions, had an HQ range of <0.1-5.4 with a 17% probability of exceeding an HQ of 1. Current risks were substantially lower (4% probability of exceedences; HQ range <0.1-3.5) because of an estimated 70-90% decline in Hg exposure to panthers over the last decade. Under worst case conditions of panthers consuming only raccoons from the most contaminated area of the Everglades, current risks of developing clinical symptoms that may lead to death was 4.6%. Current risks of mercury poisoning of panthers with a diversified diet was 0.1% (HQ range of <0.1-1.4). The results of this assessment indicate that past Hg exposures likely adversely affected panthers in the Everglades, but current risks of Hg are low.
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PMID:Retrospective and current risks of mercury to panthers in the Florida Everglades. 1521 46

Rapid brain growth occurs primarily during the third trimester in humans, whereas in rats it occurs after parturition. Therefore, we hypothesized that the effects of methylmercury (MeHg) on the postnatal developing rat nervous system may help in understanding the neurotoxicity on the human fetal brain when the brain is most vulnerable. In the present experiment, the dose-response effects of MeHg treatment during the postnatal developing phase in rats were studied. Male Wistar rats were orally administered 0, 1, 3, and 5 mg/kg/day methylmercury chloride (MMC), respectively, on postnatal day 1 and for 30 consecutive days. The body weight decline began from day 25 and typical symptoms, such as hind-limb crossing and ataxia, were observed in rats treated with 5 mg/kg/day MMC. The weight loss and typical symptoms were not observed in rats treated with 1 and 3 mg/kg/day. Mercury (Hg) concentrations in the brain were 2.6, 4.5, and 9.6 microg/g in the rats treated with 1, 3, and 5 mg/kg/day, respectively, on the day after the final MMC treatment. At 5 to 6 weeks of age, dose-dependent deficits of motor coordination in the rotarod test and learning disability in the passive avoidance response test were observed. Histopathological examination of a proportion of the MeHg-treated rats revealed widespread neuronal degeneration manifested by neuron loss and astrocytosis in the cerebral cortex, striatum, and cerebellum, where severity of the lesions seemed to increase in proportion to the administered dose of MMC. These findings using neonatal rats will be useful for better understanding of the effects of MeHg in the developing human brain during gestation.
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PMID:Dose-dependent effects of methylmercury administered during neonatal brain spurt in rats. 1535 5


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