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
(Mercury causes ataxia) NIH Medline Items 1 - 20 of 80
Mercury as a serious health hazard for children in gold mining areas (ataxia,etc.)
Somatosensory disturbance by methylmercury exposure
High prevalence of extrapyramidal signs and symptoms in a group of Italian dental technicians
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.
epidemiological assessment of neurodevelopmental
disorders following vaccines administered from 1994 through 2000 in the
Neuro Endocrinol Lett. 2006 Aug;27(4):401-13.
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
The Institute for Chronic Illnesses, Inc.,
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.
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.)
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)
The toxicology of mercury. Crit Rev Clin Lab Sci. 1997 Aug,
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]
Usually Parkinsonism was observed in manganese intoxication in man.
[Article in Polish] Neurol Neurochir Pol. 2003;37 Suppl -8
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.
Safety Assessment, Merck Research
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.
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.
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
Department of Hygiene and
BACKGROUND: It is well known that large-scale poisonings
caused by methylmercury occurred in
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.
Department of Neurological
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
Department of Environmental Health
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.
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
Department of Epidemiology,
Biostatistics, and Occupational Health,
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.