Studies of mercury related to ataxia, balance, tremor :

 

There was a strong association between learning disability* and autism spectrum disorder (often combined with hyperactivity disorder) on the one hand, and both simple and borderline 'ataxia' on the other

 

Ataxia, autism, and the cerebellum: a clinical study of 32 individuals with congenital ataxia.   Ahsgren I, Baldwin I, Goetzinger-Falk C, Erikson A, Flodmark O, Gillberg C.  Dev Med Child Neurol. 2005 Mar;47(3):193-8.

 

 

Those with autism and ataxia usually improve after metals detoxification.   Likewise is true for MS patients.  www.flcv.com/ms.html 

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(Mercury causes ataxia)  NIH Medline  Items 1 - 20 of 80

 

Mercury as a serious health hazard for children in gold mining areas  (ataxia,etc.)

Bose-O'Reilly S, Lettmeier B, Gothe RM, Beinhoff C, Siebert U, Drasch G.  Environ Res. 2008 May;107(1):89-97. Epub 2008 Mar 5

 

Long-term exposure to methylmercury and neurologic signs in Minamata and neighboring communities.  Yorifuji T, Tsuda T, Takao S, Harada M.  Epidemiology. 2008 Jan;19(1):3-9

 

Somatosensory disturbance by methylmercury exposure

Takaoka S, Kawakami Y, Fujino T, Oh-ishi F, Motokura F, Kumagai Y, Miyaoka T.  Environ Res. 2008 May;107(1):6-19. Epub 2007 Jul 20

 

High prevalence of extrapyramidal signs and symptoms in a group of Italian dental technicians

Fabrizio E, Vanacore N, Valente M, Rubino A, Meco G.  BMC Neurol. 2007 Aug 8;7:24

 

 

Elemental mercury poisoning probably causes cortical myoclonus.

Mov Disord. 2007 Oct 15;22(13):1964-8. Ragothaman M et al

 

 

Coordination deficits induced in young adult mice treated with methylmercury.

Int J Toxicol. 2007 Mar-Apr;26(2):115-21. Bellum S, Thuett KA, Grajeda R, Abbott LC.

 

A meta-analysis epidemiological assessment of neurodevelopmental disorders following vaccines administered from 1994 through 2000 in the United States. 

Neuro Endocrinol Lett. 2006 Aug;27(4):401-13. Geier DA, Geier MR.

 

Toxic effects seen in a herd of beef cattle following exposure to ash residues contaminated by lead and mercury.

Vet J. 2007 Jul;174(1):99-105. Epub 2006 Jun 5. Krametter-Froetscher R et al

 

Dose-dependent effects of methylmercury administered during neonatal brain spurt in rats.  Brain Res Dev Brain Res. 2004 Sep 17;152(2):171-6.  Sakamoto M, et al

 

Etc.

meta-analysis epidemiological assessment of neurodevelopmental disorders following vaccines administered from 1994 through 2000 in the United States.     Geier DA, Geier MR.  Neuro Endocrinol Lett. 2006 Aug;27(4):401-13.

The Institute for Chronic Illnesses, Inc., Silver Spring, MD 20905, USA. mgeier@comcast.net

BACKGROUND: Thimerosal is an ethylmercury-containing compound (49.6% mercury by weight) used as at the preservative level in vaccines (0.005% to 0.01%). METHODS: Statistical modeling in a meta-analysis epidemiological assessment of the Vaccine Adverse Event Reporting System (VAERS) for neurodevelopment disorders (NDs) reported following Diphtheria-Tetanus-whole-cell-Pertussis (DTP) vaccines in comparison to Diphtheria-Tetanus-whole-cell-Pertussis-Haemophilus Influenzae Type b (DTPH) vaccines (administered: 1994-1997) and following Thimerosal-containing Diphtheria-Tetanus-acellular-Pertussis (DTaP), vaccines in comparison to Thimerosal-free DTaP vaccines (administered: 1997-2000), was undertaken. RESULTS: Significantly increased adjusted (sex, age, vaccine type, vaccine manufacturer) risks of autism, speech disorders, mental retardation, personality disorders, thinking abnormalities, ataxia, and NDs in general, with minimal systematic error or confounding, were associated with TCV exposure. CONCLUSION: It is clear from the results of the present epidemiological study and other recently published data associating mercury exposure with childhood NDs, additional ND research should be undertaken in the context of evaluating mercury-associated exposures, especially from Thimerosal-containing vaccines.

(more NLM Medline articles on mercury causing ataxia & ataxia improving after detox)

Neurodegeneration from mitochondrial insufficiency: nutrients, stem cells, growth factors, and prospects for brain rebuilding using integrative management.    Kidd PM.  Altern Med Rev. 2005 Dec;10(4):268-93   (mercury and other toxics cause mitochondrial damage, electron leakage)

Autopsy case of acute encephalopathy linked to familial hemiplegic migraine with cerebellar atrophy and mental retardation.  Neuropathology. 2005 Sep;25(3):228 (causes of such include mercury toxicity)

 

Retrospective and current risks of mercury to panthers in the Florida Everglades.

Ecotoxicology. 2004 Apr;13(3):223 (clinical symptoms, including ataxia and convulsions)

 

Brain sites of movement disorder: genetic and environmental agents in neurodevelopmental perturbations.  Neurotox Res. 2003;5(1-2):1-26  

(mercury can be a factor in ataxia disorders including autism, ADHD, parkinson’s, Frederrich’s ataxia, etc.)

 

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).

Sci Total Environ. 2003 May 20;307(1-3):71-82.

(mercury causes neurological problems including ataxia, which improve after mercury detoxification)

 

Clinical investigation of the lesions responsible for sensory disturbance in Minamata disease.

Tohoku J Exp Med. 2001 Nov;195(3):181-9  (mercury posioning)

 

Chronic neurobehavioural effects of mercury poisoning on a group of Zulu chemical workers.

Brain Inj. 2000 Sep;14(9):797-814.   (mercury causes ataxia/impaired motor function)

 

Effects of protein-deficient nutrition during rat pregnancy and development on developmental hindlimb crossing due to methylmercury intoxication.   Arch Toxicol. 2000 Jul;74(4-5):196-202

(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)

Occupational and environmental toxicology of mercury and its compounds.  Satoh H.    (mercury causes neurological conditions including ataxia and similar for infants born to mercury toxic moms)

MRI findings of Minamata disease--organic mercury poisoning.  Korogi Y, Takahashi M, Okajima T, Eto K.   (mercury toxicity from seafood with mercury causes neurological conditions including ataxia)

The toxicology of mercury.  Crit Rev Clin Lab Sci. 1997 Aug,  Clarkson TW.      (merucy vapor and organic mercury cause neurological problems including ataxia)

(these are the first page of studies documenting mercury causes ataxia and usually improves after mercury detox; there were several other pages in Medline  abstracts)

  

The toxicology of mercury.  Crit Rev Clin Lab Sci. 1997 Aug,  Clarkson TW.  

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.

 

 

[Trace elements in spinocerebellar degeneration]

Nippon Rinsho. 1996 Jan;54(1):129-33. Nakashima K.

Usually Parkinsonism was observed in manganese intoxication in man.

 

Parkinsonism in chronic occupational metallic mercury intoxication]

[Article in Polish]   Neurol Neurochir Pol. 2003;37 Suppl 5:31-8

Miller K, Ochudło S, Opala G, Smolicha W, Siuda J.

Poradnia Chorób Zawodowych, Szpital, Instytut Medycyny Pracy i Zdrowia Srodowiskowego w Sosnowcu.

Parkinson syndrome occurs in the course of chemical intoxication, especially Mn, CS2, CO. 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 occasions 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.

 

Coordination deficits induced in young adult mice treated with methylmercury.

Bellum S, Thuett KA, Grajeda R, Abbott LC.  Int J Toxicol. 2007 Mar-Apr;26(2):115-21

Safety Assessment, Merck Research Laboratories, West Point, Pennsylvania, USA.

Male and female C57BL/6J mice starting at postnatal (P) day 34 were exposed orally to five divided doses totaling 1.0 or 5.0 mg/kg of methylmercury (MeHg; given as methylmercuric chloride) or sterile deionized water in moistened rodent chow. After a 5-day waiting period, control and MeHg-treated mice were subjected to a standard battery of behavior tests for balance and motor coordination. Latency to falling on the accelerating rota-rod was significantly decreased in 5.0 mg/kg MeHg-exposed mice when compared to control mice. In the open field, horizontal exploration with respect to total distance traveled during the first 5 min on the first test day was significantly reduced in 1.0 mg/kg MeHg-exposed mice when compared to control mice. Rearing activity was not affected by MeHg treatment. In the footprint analysis, angle of foot placement measured in 1.0 mg/kg MeHg-treated mice was significantly greater compared to control mice. Base stance and stride length were unaffected by MeHg treatment. On the vertical pole test, 10 mice from each treatment group fell off the pole during the time the pole was shifted from a horizontal position to a vertical position, whereas none of the control mice fell. These results indicate that short-term, low to moderate doses of MeHg in young adult mice can be detrimental to motor coordination and balance.

 

Tremor in workers with low exposure to metallic mercury.

Verberk MM, Sallé HJ, Kemper CH.  Am Ind Hyg Assoc J. 1986 Sep;47(9):559-62.

In a fluorescent lamp production factory, a newly developed lightweight balance-tremormeter was used to measure postural tremor of the finger in 21 workers (ages 28 to 61) exposed for 0.5-19 yr to metallic mercury. In addition, tremor was measured in an indirect way by means of a "hole-tremormeter." The excretion of mercury in urine was 9-53 (average 20) mumol/mol creatinine. With increasing mercury excretion, the following parameters increased: the acceleration of the tremor, the contribution of the neuromuscular component (8-12 Hz) to the power spectrum of the acceleration, the width of the power-spectrum and the score on the hole-tremormeter. The study indicates that exposure to metallic mercury below the current TLV (50 micrograms/m3) may increase the tremor of the finger.

 

Mercury as a serious health hazard for children in gold mining areas.

Bose-O'Reilly S, Lettmeier B, Gothe RM, Beinhoff C, Siebert U, Drasch G.  Environ Res. 2008 May;107(1):89-97. Epub 2008 Mar 5

Institute of Public Health, Medical Decision Making and Health Technology Assessment, UMIT-University for Health Sciences, Medical Informatics and Technology, Eduard Wallnoefer-Zentrum I, A-6060 Hall i.T., Austria. stephan.boeseoreilly@umit.at

In many developing countries, mercury is used to extract gold from ore in small-scale mining areas. Exposure through mercury in these small-scale mining communities is a serious health hazard, especially to the children living and working there. Many children begin working with immediate contact to mercury from the very early age of seven. In Indonesia and Zimbabwe, 166 children were clinically examined for mercury. The mercury concentration in the blood, urine, and hair was analyzed. Compared to the control groups, the exposed children showed typical symptoms of mercury intoxication, such as ataxia. The children working with mercury had high levels of this substance in the various biomonitors. The exposure derives mainly from the liquid mercury used to bind gold, forming an amalgam. The amalgam is heated and the smelting amalgam releases mercury vapor plus the wanted gold. Mercury vapor in contrast to liquid mercury is highly toxic. This elemental, vaporized mercury is the main form of exposure. Since in over 50 countries children live in small-scale gold mining areas and are exposed in a similar way to mercury, immediate action is needed to reduce this severe chemical health hazard for children. Child labor with hazardous substances such as mercury must be stopped.

 

Long-term exposure to methylmercury and neurologic signs in Minamata and neighboring communities.

Yorifuji T, Tsuda T, Takao S, Harada M.  Epidemiology. 2008 Jan;19(1):3-9

Department of Hygiene and Preventive Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. yorichan@md.okayama-u.ac.jp

BACKGROUND: It is well known that large-scale poisonings caused by methylmercury occurred in Japan (Minamata, in the 1950s) and Iraq. However, in contrast to Iraq, there have been few sound epidemiologic studies in Minamata. We evaluated the effect of methylmercury on neurologic signs using data from a 1971 population-based study. METHODS: Villages in 3 areas were selected for study: the Minamata area (a high-exposure area), the Goshonoura area (a medium-exposure area), and the Ariake area (a low-exposure area). We used place of residence as the exposure indicator. We examined associations between methylmercury exposure and the following neurologic signs measured on clinical examination: paresthesia of whole body, paresthesia of extremities, paresthesia around the mouth, ataxia, dysarthria, tremors, and pathologic reflexes. RESULTS: Total population was 1120 in the high-exposure villages, 1845 in the medium-exposure villages, and 1165 in the low-exposure villages. In the Minamata area, 87% (n=833) of the eligible population (age 10 years and older) participated in the 1971 investigations, in the Goshonoura area, 93% (n = 1450), and in the Ariake area, 77% (n = 755). Compared with subjects in the Ariake area, the subjects in the Minamata area manifested neurologic signs more frequently. The highest prevalence odds ratio was observed for paresthesia around the mouth (110; 95% confidence interval = 16-820). Although residents in the Goshonoura area had been exposed less heavily than those in the Minamata area, Goshonoura residents also had increased prevalence of neurologic signs. CONCLUSION: Long-term exposure to methylmercury has a strong adverse impact on neurologic signs among residents in a local community.

 

Somatosensory disturbance by methylmercury exposure.

Takaoka S, Kawakami Y, Fujino T, Oh-ishi F, Motokura F, Kumagai Y, Miyaoka T.  Environ Res. 2008 May;107(1):6-19. Epub 2007 Jul 20

Minamata Kyoritsu Hospital, Minamata 867-0045, Japan. stakaoka@os.usen.ne.jp

Minamata disease is methylmercury poisoning from consuming fish and shellfish contaminated by industrial waste. The polluted seafood was widely consumed in the area around Minamata, but many individuals were never examined for or classified as having Minamata disease. Following the determination of the Supreme Court of Japan in October 2004 that the Japanese Government was responsible for spreading Minamata disease, over 13,000 residents came forward to be examined for Minamata disease. We studied 197 residents from the Minamata area who had a history of fish consumption during the polluted period to determine the importance of sensory symptoms and findings in making a diagnosis of Minamata disease. We divided the exposed subjects into non-complicated (E) and complicated (E+N) groups based on the absence or presence of other neurological or neurologically related disorders and compared them to residents in control area (C) after matching for age and sex. We quantitatively measured four somatosensory modalities (minimal tactile sense by Semmes-Weinstein monofilaments, vibration sense, position sense, and two-point discrimination) and did psychophysical tests of fine-surface-texture discrimination. Subjective complaints were higher in groups E and E+N than C. Over 90% of E+N and E subjects displayed a sensory disturbance on conventional neurological examination and 28% had visual constriction. About 50% of the E and E +N groups had upper and lower extremity ataxia and about 70% had truncal ataxia. The prevalence of these neurological findings was significantly higher in exposed subjects than controls. All sensory modalities were impaired in the E and E+N groups. All four quantitatively measured sensory modalities were correlated. The prevalence of complaints, neurological findings, and sensory impairment was similar or a little worse in group E+N than in group E. We conclude that sensory symptoms and findings are important in making the diagnosis of Minamata disease and that they can be determined even in the presence of neurological or neurologically related diseases.

 

High prevalence of extrapyramidal signs and symptoms in a group of Italian dental technicians.

Fabrizio E, Vanacore N, Valente M, Rubino A, Meco G.  BMC Neurol. 2007 Aug 8;7:24

Department of Neurological Sciences, La Sapienza University, Viale Universitŕ 3000185 Rome, Italy. edito@libero.it

BACKGROUND: Occupational and chronic exposure to solvents and metals is considered a possible risk factor for Parkinson's disease and essential tremor. While manufacturing dental prostheses, dental technicians are exposed to numerous chemicals that contain toxins known to affect the central nervous system, such as solvents (which contain n-hexane in particular) and metals (which contain mercury, iron, chromium, cobalt and nickel). METHODS: We performed an epidemiological and clinical study on all 27 dental technicians working in a school for dental technicians. We asked all the technicians to fill in a self-administered questionnaire on extrapyramidal symptoms, and the General Health Questionnaire (GHQ), a self-administered screening instrument, to detect any psychiatric disorders. Moreover, we invited all 27 dental technicians to undergo a neurological examination and provide a detailed occupational history in our clinic. RESULTS: Of the 14 subjects who underwent the neurological examination, four had postural tremor and one had a diagnosis of Parkinson's disease. CONCLUSION: We found a high prevalence of extrapyramidal signs and symptoms in this group of male dental technicians working in a state technical high school in Rome. We believe that this finding may be due to the presence of toxins in the dental technician's work.

 

Effects of mercury vapor exposure on neuromotor function in Chinese miners and smelters.

Iwata T, Sakamoto M, Feng X, Yoshida M, Liu XJ, Dakeishi M, Li P, Qiu G, Jiang H, Nakamura M, Murata K.   Int Arch Occup Environ Health. 2007 Apr;80(5):381-7. Epub 2006 Sep 22

Department of Environmental Health Sciences, Akita University School of Medicine, Akita, 010-8543, Japan.

OBJECTIVES: Current risk assessment of elemental mercury vapor is based on the tremor toxicity. To clarify the neuromotor effects of occupational exposure to mercury vapor, hand tremor and postural sway were measured in 27 miners and smelters (i.e., exposed workers) and 52 unexposed subjects. METHODS: Urine samples were collected and total mercury and creatinine concentrations were determined. Data of the tremor and postural sway were analyzed using the fast Fourier transformation. RESULTS: The geometric means of the urinary mercury level (UHg) were 228 (range 22.6-4,577) microg/g creatinine for the exposed workers and 2.6 (1.0-17.4) microg/g creatinine for the unexposed subjects. Total tremor intensity and frequency-specific tremor intensities at 1-6 and 10-14 Hz were significantly larger in the exposed workers than in the unexposed subjects (P < 0.05), but they were not significantly related to the UHg among the exposed workers (P > 0.05). In contrast, there were no significant differences in any postural sway parameters between the above two groups (P > 0.05), but the transversal sway with eyes open was positively related to the UHg among the exposed workers in using multiple regression analysis (P < 0.05). CONCLUSIONS: These findings suggest that postural sway, as well as hand tremor, may be affected by elemental mercury vapor exposure, but the former test seems to be less sensitive to mercury than the latter one.

 

Neuromotor functions in Inuit preschool children exposed to Pb, PCBs, and Hg.

Després C, Beuter A, Richer F, Poitras K, Veilleux A, Ayotte P, Dewailly E, Saint-Amour D, Muckle G.  Neurotoxicol Teratol. 2005 Mar-Apr;27(2):245-57. Epub 2005 Jan 11

Cognitive Neuroscience Center, University of Quebec at Montreal, Montreal, Quebec, C.P. 8888 (Succ Centre Ville), Canada H3C 3P8.

The aim of this study was to examine the effects of prenatal and postnatal chronic exposure to mercury (Hg), polychlorinated biphenyls (PCBs) and lead (Pb) on the neuromotor development of preschool children. The study population consisted of 110 preschool Inuit children from Nunavik (Canada). Blood Hg, PCBs and Pb concentrations were measured at birth (cord blood) and at the time of testing. Gross motor functions were evaluated and a neurological examination was performed. Fine neuromotor performance was assessed using quantitative measures of postural hand tremor, reaction time, sway oscillations, as well as alternating and pointing movements. Potential covariates were documented including demographic and familial characteristics, other prenatal neurotoxicants (alcohol, tobacco) and nutrients (selenium (Se), Omega-3 polyunsaturated fatty acids (n-3 PUFA)). Hierarchical multivariate regression analyses were performed, controlling for significant covariates. Gross motor development was not linked to prenatal exposures. However, significant associations were observed between blood Pb concentration at testing time and changes in reaction time, sway oscillations, alternating arm movements and action tremor. For some of these outcomes, neuromotor effects of Pb exposure are observed at blood concentrations below 10 microg/dl. Negative effects of PCBs on neuromotor development were not clearly observed, neither were the potential beneficial effects of n-3 PUFA and selenium. Tremor amplitude was related to blood Hg concentrations at testing time, which corroborate an effect already reported among adults.

 

Low-level methylmercury exposure as a risk factor for neurologic abnormalities in adults.

Auger N, Kofman O, Kosatsky T, Armstrong B. Neurotoxicology. 2005 Mar;26(2):149-57.

Department of Epidemiology, Biostatistics, and Occupational Health, McGill University, Montreal, Que., Canada. nauger@santepub-mtl.qc.ca

Methylmercury is a neurotoxicant that bio-accumulates in the aquatic food chain and is present in all fish. Little is known about the effects of long-term low-dose exposure to methylmercury in adults. The aim of this study was to determine whether a dose-response relationship exists between long-term methylmercury exposure and neurological abnormalities in aboriginal Quebec Cree adults for whom fish is a dietary staple. We re-analysed data from a 1977 cross-sectional study conducted by Kofman and collaborators on a group of Quebec Cree individuals claiming ill health from local fish consumption. In the original 1977 study, 306 adult participants aged 18-82 years were assessed for methylmercury exposure. Tremor and other neurologic outcomes were assessed with a clinical examination. The investigators did not find clinical evidence of methylmercury intoxication based on an analysis of covariance. We used ordinal regression to obtain odds ratios for the relationship between total hair mercury levels and neurologic abnormalities. Hair mercury concentrations ranged from 0.5 to 46 ppm (parts per million). A 6 ppm increase in hair mercury was associated with increasing levels of tremor (OR, 2.22; 95% CI, 1.15-4.26) in adults under 40 years of age. There was no association with nine other outcomes considered, nor with tremor among older persons. Odds ratios were not influenced by gender, smoking, alcohol use, or co-morbidity. CONCLUSION:: Dose-dependent effects of methylmercury on tremor may occur below the commonly accepted 50 ppm threshold, particularly in young adults. These effects may be detectable by clinical examination. However, the results should be interpreted with caution given that alcohol use was probably under-reported and that multiple outcomes were studied.