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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Manganese (Mn) intoxication is known to induce parkinsonism. Mn-induced parkinsonism preferentially affect the globus pallidus in contrast to idiopathic parkinsonism where degeneration predominantly involves the nigral pars compacta. We describe a 51-year-old man who had been occupationally exposed to Mn. He had parkinsonian features including masked face, resting tremor, and bradykinesia. He also had a cock walk and a particular propensity to fall in a backward gait. There was no sustained therapeutic response to levodopa. A fluorodopa PET scan was normal. This case indicates that Mn-induced parkinsonism can be differentiated from idiopathic parkinsonism in that the former has unique clinical features and a normal fluorodopa PET scan.
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PMID:Manganese induced parkinsonism: a case report. 974 52

Tremor and seizures developed in a 2-year-old girl receiving total parenteral nutrition. T1-weighted images on MRI revealed areas of hyperintensity in the basal ganglia, brainstem and cerebellum. Blood manganese was elevated. The symptoms and MRI abnormalities disappeared after withdrawal of manganese administration. The recommendation of daily parenteral manganese intake was discussed.
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PMID:Tremor and seizures associated with chronic manganese intoxication. 1020 31

In 1987, a cross-sectional study in a dry-alkaline battery plant in Belgium revealed subclinical neurobehavioral dysfunctions associated with inhalation exposure to manganese dioxide (MnO2) particulate. The overall geometric mean of the time-weighted average concentration of manganese (Mn) in "total" dust (MnT) amounted, at that time, to 1 mg Mn/m3 and the duration of exposure was 5.5 years on average. An 8-year longitudinal investigation was conducted in this cohort (n = 92) in order to find out whether early effects on eye-hand coordination (EHC), hand steadiness (HST), and simple visual reaction time (VRT) were reversible when the airborne manganese concentration at the workplace was abated. During the observation period from 1988 to 1995, MnT monitoring was implemented on a monthly basis producing more than 1300 personal air samples, EHC tests were given yearly to assess the precision of the hand-forearm movement (PN1), and HST and VRT tests were carried out yearly since 1991. By the end of the study, the cohort size had dropped to 34 subjects. The model of unbalanced repeated measurements with unstructured covariance matrix and a time-varying covariate (log MnT) was the most appropriate to analyze the data. Wald chi 2 statistic was used for testing time-trends. The reduction of MnT over time was significantly associated with an improvement of the PN1 values (total cohort: Wald chi 2 = 8.5, p = 0.004; beta log MnT = -6.098 +/- 2.096). Like in the total cohort, time-trends were also found in the three exposure subgroups which could be identified in the cohort (average MnT over 1987-1992 were about 400, 600, and 2000 micrograms Mn/m3 for the low, medium, and high exposure subgroups, respectively). Only in the low exposure subgroup the PN1 value normalized when MnT (provisional estimates) decreased from about 400 to 130 micrograms Mn/m3 by the end of the study. Solely the reduction in MnT explained these findings on PN1, while a "healthy-worker-effect" mechanism was unlikely to have operated. The prognosis for the medium and high exposure subgroups remains uncertain as the improvement of their EHC performance may have been affected by past MnO2 exposure to such an extent that the persistence of a partial loss of EHC ability is suggested. The time courses of the HST and VRT test results, however, indicated the absence of any improvement, suggesting irreversible impairment of hand stability (postural tremor) and simple visual reaction time. A separate examination in a group of 39 control subjects, re-tested 10 years after the first test in 1987, virtually precluded age as confounding factor in this prospective study. The findings of the longitudinal study are corroborated by the outcome of a separate follow-up study in a group of 24 ex-Mn employees, who showed in 1996 a significant improvement of eye-hand coordination after at least three years with no MnO2 exposure; as to HST and VRT, there was no significant change in the deficit of these two neurobehavioral markers.
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PMID:Prospective study on the reversibility of neurobehavioral effects in workers exposed to manganese dioxide. 1038 89

Occupational exposure to manganese can cause early neurobehavioral effects in low- or a-symptomatic workers. A battery of neuropsychological tests was administered to a group of 61 ferroalloy male workers and 87 controls. The average (geometric mean) manganese concentrations in total dust at the plant have changed from 1981 to 1997 respectively from 1597.03 micrograms/m3 to 239 micrograms/m3 at the furnace area; from 151.53 to 255.76 micrograms/m3 at the casting area; from 167 to 54.7 micrograms/m3 at the maintenance (welding operations), yielding a current overall value of 54.25 micrograms/m3. A cumulative exposure index was calculated for each alloy worker and the average value (geometric mean) resulted to be 1204.87 micrograms/m3 x years, which divided by the average length of exposure (15.17 years), showed the concentration of 70.83 micrograms/m3 of manganese in total dust. Blood and urinary manganese geometric means resulted significantly higher in the exposed workers (9.18 micrograms/l and 1.53 micrograms/g creatinine, respectively) than in controls (5.74 micrograms/l and 0.40 microgram/g creatinine, respectively). A positive correlation was observed between the airborne manganese concentrations in total dust and blood manganese (n = 55; R = 0.36; R2 = 0.13; p = 0.0068), whereas no association resulted between cumulative exposure index and both blood manganese and urinary manganese. Higher prevalence of symptoms reporting was observed in the alloy workers concerning irritability, loss of equilibrium and rigidity. Tremor parameters including the central frequency and its dispersion, resulted to be statistically different in the exposed workers compared to the controls. Motor functions exploring the coordination of rapid and alternating movements and memory functions resulted to be impaired in the manganese workers. Dose-effect relationships were observed between the cumulative exposure index and some of the test results, whereas no relationship was found with the airborne manganese concentrations and the biological indicators of exposure. These findings are consistent with the existing knowledge of a cumulative mechanism of action of manganese, which must be carefully considered when setting safe exposure levels. In order to be protective for the entire working life, the average annual exposure level should be lower than 100 micrograms/m3.
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PMID:Long-term exposure to "low levels" of manganese oxides and neurofunctional changes in ferroalloy workers. 1038 91

Excessive manganese (Mn) has been associated with neurobehavioral deficits and neurological and/or neuropsychiatric illness, but the level at which this metal can cause adverse neurotoxic effects, particularly with long-term exposure, is still unknown. The objective of the present study was to assess nervous system functions in residents exposed to manganese from a variety of environmental sources. A random stratified sampling procedure was used to select participants; persons with a history of workplace exposure to Mn and other neurotoxic substances were excluded. A self-administered questionnaire provided data on socio-demographic variables. Blood samples were analyzed for total manganese (MnB), lead, mercury and serum iron. Nervous system assessment included computer and hand-administered neurobehavioral tests, computerized neuromotor tests, sensory evaluation and a neurological examination. The present analyses include 273 persons (151 women and 122 men); MnB range: 2.5 micrograms/L-15.9 micrograms/L (median: 7.3 micrograms/L). Multivariate analyses were used and neuro-outcomes were examined with respect to MnB, taking into account potential confounders and covariables. Results were grouped according to neurofunctional areas and MANOVA analyses revealed that higher MnB (7.5 micrograms/L) was significantly associated with changes in coordinated upper limb movements (Wilks' lambda = 0.92; p = 0.04) and poorer learning and recall (men: Wilks' lambda = 0.77; p = 0.002; women: Wilks' lambda = 0.86; p = 0.04). Further analyses revealed that with increasing log MnB (Simple regression: p < 0.05) performance on a pointing task was poorer, frequency dispersion of hand-arm tremor decreased, while harmonic index increased, and the velocity of a pronation/supination arm movement was slower. An Mn-age interaction was observed for certain motor tasks, with the poorest performance observed among those _50 y and in the higher MnB category. Differences between genders suggest that men may be at greater risk than women, although effects were also observed in women. These findings are consistent with the hypothesis that Mn neurotoxicity can be viewed on a continuum of dysfunction, with early, subtle changes at lower exposure levels.
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PMID:Manganese neurotoxicity, a continuum of dysfunction: results from a community based study. 1038 94

The effect of low level exposure to manganese (Mn) was examined in 297 subjects from southwest Quebec. Blood manganese (MnB) levels as well as other possibly relevant variables were obtained. We tested equipment and analysis procedures that we have developed to quantify aspects of motor function thought to be affected by exposure to toxins, in particular, rapid alternating movements, rapid and precise pointing movements, and tremor. (1) The eurythmokinesimeter measures timing and precision of contacts between a hand-held stylus and a pair of metal targets (proximal/distal). This roughly approximates the finger-to-nose test of the UPDRS. Characteristics quantifying speed, precision and regularity of the movements were calculated, as well as multiple contacts due to tremor and an index based on Fitts' Law eliminating the effect of the trade-off between speed and precision. (2) The diadochokinesimeter accurately measures rapid rotation of the forearms (pronation/supination). Characteristics quantifying the range, speed, period, shape and regularity of the oscillatory movements were calculated, as well as the smoothness of the movement on a fine scale and the coordination between the two hands. (3) Postural tremor of the arm and hand was measured using the accelerometry-based "TREMOR" system of Danish Product Development. We used the amplitude and frequency characteristics provided by the TREMOR system: intensity, center frequency, dispersion and harmonic index. Previous studies have shown that these tests are sufficiently sensitive to detect small differences in performance of different groups of subjects, with indications that some characteristics are also specific to particular conditions. In this study, significant though small effects related to age and gender were found in many of the characteristics. When effects of other variables are removed, low-level exposure to Mn was found to be associated with a decrease in ability to perform regular, rapid and precise pointing movements, a decrease in ability to attain high maximum rotation speeds in rapid alternating movements, and an increase in regularity of tremor oscillations. Moreover, the effects are age-related for levels of MnB 7.5, micrograms/L.
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PMID:Quantification of neuromotor function for detection of the effects of manganese. 1038 96

It was observed by Couper in 1837 that manganese dust produces a neurological syndrome characterized by muscle weakness, tremor, bent posture, whispered speech and excess salivation. The similarity of these symptoms to those of Parkinson's disease were not recognized for many years. In addition to its Parkinson-like effects, manganese produces behavioral symptoms in humans including nervousness, hallucinations, memory loss, cognitive problems, bizarre behaviors and flight of ideas. Despite these signs and symptoms, there have been few systematic attempts to study the effects of manganese on behavior using animal models. The need to better understand the effects of manganese on behavior is becoming more important due to the potential of increased environmental exposure to manganese due to its use, or proposed use as a gasoline additive in a number of countries. However, there is debate as to which manganese compounds should receive priority for testing, what route of administration should be used in this testing, what dosing regimens should be used, what species are appropriate for behavioral testing, and what behavioral tests should be selected. Research to answer these questions is needed so that the behavioral effects of manganese can be described comprehensively and the mechanisms underlying these effects can be understood.
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PMID:A brief history of the neurobehavioral toxicity of manganese: some unanswered questions. 1038 8

Positron emission tomography (PET) with [18F] 6-fluoro-L-dopa (18F-FDOPA) was performed in three South Korean patients with parkinsonism who developed after chronic manganese exposure. A 51-year-old man (patient 1) suffered from masked face, marked postural tremor of hands, dystonia in the neck and the upper extremities, severe retropulsion and lateropulsion which were typical for chronic manganese intoxication. 18F-FDOPA scan was normal. Other two patients, a 46-year-old man (patient 2) and a 47-year-old man (patient 3), showed tremor at rest and rigidity predominantly on the right side, bradykinesia, stooped posture and postural instability; all of these were typical for Parkinson's disease (PD). There was reduced uptake of 18F-FDOPA in the striatum, particularly in the posterior putamen predominant on the left side, in both patient 2 and 3. From these results, patient 1 was diagnosed as pure manganism, while patient 2 and 3 were primarily as PD, because loss of nigrostriatal fibers was obvious with asymmetry of affection in the putamen. PET with 18F-FDOPA provides valuable information for differentiation between PD and manganism, although it is not clear whether development of parkinsonian symptoms in patient 2 and 3 was modified by excessive manganese exposure.
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PMID:[Diagnostic utility of positron emission tomography for parkinsonism after chronic manganese exposure]. 1054 4

We describe a case of Wilson's disease with late psychiatric onset. Major depressive disorder was the first clinical manifestation at the age of 38 years. After pharmacotherapy with antidepressive agents, a manic episode was observed. Extrapyramidal hand tremor and micrography were the first neurological signs. Emotional lability occurred during worsening of extrapyramidal signs. Diagnosis was based on urinary and serum copper levels, ceruloplasmin serum level, Kayser-Fleischer ring, and liver biopsy that detected cirrhosis. Magnetic resonance imaging revealed basal ganglia hyperintensity on T1-weighted images, and hypodensity in the central part and hyperintensity in the peripheral part of the lentiform nucleus on T2-weighted images. Hyperintensity on T2-weighted images was also observed in the dorsal part of the midbrain. 123I-iodobenzamide single photon emission computed tomography (IBZM-SPECT) detected a normal distribution of the drug in the brain, with better signal in the right side and deficit of D2-dopaminergic receptors in the basal ganglia. Abnormal manganese erythrocyte level was observed. Treatment was based on penicillamine, zinc salts, low-copper diet, antidepressant agents, interpersonal psychotherapy and neurorehabilitation.
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PMID:Psychiatric symptoms as late onset of Wilson's disease: neuroradiological findings, clinical features and treatment. 1093 85

Manganese (Mn) is an essential metal that, in excess, causes an extrapyramidal syndrome consisting in tremor, rigidity and akinesia. Recently, Mn was found to accumulate in brains of cirrhotic patients who also present motor abnormalities. Manganese alters dopaminergic transmission promoting an increase in the turnover of dopamine (DA). In this study, we studied the changes in dopamine and its main metabolite homovanillic acid (HVA) to evaluate DA turnover following administration of manganese to bile-duct obstructed rats. Some groups of rats were treated with manganese chloride in two concentrations: 0.5 and 1 mg/ml of Mn2+ in their drinking water. Four weeks after surgery and treatment with manganese, striatal Mn, DA and HVA were assessed. Marked increases (P<0.05) of striatal manganese content were observed in cirrhotic rats treated and untreated with manganese, these augments were dependent on the Mn concentration in water. Striatal contents of DA in cirrhotic rats diminished by 30% (P<0.05), administration of 0.5 mg/ml of manganese in drinking water to these rats returned dopamine to the basal level and 1 mg/ml of manganese increased dopamine content by 27%. The relationship of Mn content and DA turnover (HVA:DA) in the same animal showed a positive and statically significant correlation (P<0.05), with differences in slope for sham (b1=0.1528) and cirrhotic rats (b1=0.0174). These results suggest that manganese brain accumulation observed in liver failure could be a key element to understand dopamine metabolism in cirrhotic condition of humans.
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PMID:Striatal manganese accumulation induces changes in dopamine metabolism in the cirrhotic rat. 1116 15


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