Cases reported "Manganese Poisoning"

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1/28. Manganese intoxication during total parenteral nutrition: report of two cases and review of the literature.

    We report two cases of manganese (Mn) intoxication during total parenteral nutrition including manganese (Mn). Both patients showed parkinsonism with psychiatric symptoms and elevated serum Mn levels. T1-weighted magnetic resonance images (MRI) revealed symmetrical high intensity lesions in the globus pallidus. Discontinuation of Mn supplementation and levodopa treatment improved the symptoms and MRI abnormalities in the both patients. Thus, careful attention should be paid to the long-term intravenous administration of Mn. ( info)

2/28. tremor and seizures associated with chronic manganese intoxication.

    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. ( info)

3/28. Rapid progression of parkinsonism associated with an increase of blood manganese.

    In this paper, we report a 72-year-old man whose parkinsonian pictures accelerated rapidly after an ingestion of unknown herb pills. His serum manganese and aluminum level increased 2-fold and 5-fold over physiological level respectively. A reverse of his parkinsonian deterioration was accompanied with a normalization of these metals. Exclusive heavy metals have been widely mentioned in parkinsonism. While industrial source of these metals has extensively been sought, pharmacology is rarely mentioned in this aspect, especially of herb medicine origin. We suggest that an acceleration of parkinsonian pictures should raise the need to re-evaluate the possibility of heavy metal intoxication in parkinsonism. Besides of industrial contamination, we should be alert for the nonindustrial source in our population. ( info)

4/28. Idiopathic parkinsonism with superimposed manganese exposure: utility of positron emission tomography.

    It is difficult to distinguish manganism from idiopathic parkinsonism by clinical signs only. Case history and examination: A 48-year-old welder for over 10 years complained of masked face, right side (arm and leg) resting tremor, and bradykinesia for over one year. magnetic resonance imaging (MRI) findings showed symmetrical high signal intensities in the globus pallidus on T1 weighted image. These intensities disappeared almost completely six months after cessation of exposure. 18F-6-fluorodopa (18F-dopa) positron emission tomography (PET) findings showed reduced 18F-dopa uptake in the left putamen, findings which appear in idiopathic parkinsonism. A PET study is necessary to distinguish manganism from idiopathic parkinsonism, especially in a working environment with elevated Mn concentrations, such as welding. ( info)

5/28. Occupational Mn parkinsonism: magnetic resonance imaging and clinical patterns following CaNa2-EDTA chelation.

    We report a case of occupational parkinsonism due to manganese exposure in which professional exposure has been documented both by the high blood and urinary levels of the metal and by its presence in the materials used. A strong relation was evident among chelating treatment, cessation of exposure and clinical improvement. MRI confirmed the evolution of clinical pattern by means of reduction of heavy metal deposition in basal ganglia. These findings also agree with the few experimental and human studies published. This case study points to the need for an accurate occupational history collection and suggests the possibility of useful chelating therapy with CaNa2EDTA. ( info)

6/28. Manganese intoxication during intermittent parenteral nutrition: report of two cases.

    BACKGROUND AND methods: The administration of trace elements is thought to be needed in patients receiving long-term parenteral nutrition. Recently, manganese intoxication or deposition was documented in such patients. We report two cases of manganese intoxication during intermittent parenteral nutrition including manganese. Manganese had been administered for 4 years at a frequency of one or two times per week in one case and for 5 years at a frequency of one or two times per month in the other case. Both cases showed mild symptoms with headache and dizziness. One case had mild hepatic dysfunction and the other did not. The whole-blood manganese level increased in one case, but not in the other case. T1-weighted magnetic resonance images revealed symmetrical high-intensity areas in basal ganglia and thalamus in both cases. After the administration of manganese was stopped, these symptoms all disappeared and the magnetic resonance images abnormalities gradually improved in both patients. Mild long-term manganese intoxication is thus considered to occur regardless of the frequency of using a manganese supplement. CONCLUSIONS: patients should be carefully monitored when receiving long-term parenteral nutrition including manganese, even when the manganese dose is small and the frequency of receiving a manganese supplement is low. ( info)

7/28. Myoclonic involuntary movement associated with chronic manganese poisoning.

    We report a 17-year-old man showing myoclonic involuntary movement (IVM) associated with chronic manganese (Mn) poisoning. The patient, a welder, showed myoclonic IVM mainly in the right upper and lower extremities, elevated levels of Mn in the blood and hair and high-intensity signals in the globus pallidus on T1-weighted MR images. chelation therapy resulted in improvement of the myoclonic IVM and MRI abnormalities. This is the first report of Mn poisoning characterized by myoclonic IVM without parkinsonism. ( info)

8/28. Lethal manganese-cadmium intoxication. A case report.

    A case of a lethal manganese-cadmium (Mn-Cd) intoxication is reported. The postmortem examination revealed a noticeable reddish-violet discolouration of the serous cutes of all body cavities, but there was no indication of any corrosive burns of the mucous membranes of the gastrointestinal tract. An Mn concentration of 899 micro g/l blood and a Cd concentration of 238 micro g/l blood were found in the deceased woman. These concentrations are higher than normal levels by a factor of about 100. A subacute or chronic manganese-cadmium absorption must be assumed. ( info)

9/28. Secondary progressive chronic manganism associated with markedly decreased striatal D2 receptor density.

    We describe a patient with chronic manganism due to intoxication 40 years ago. Whereas previous reports on acute or subacute intoxication have shown no or only small reductions in striatal D2 receptor density, we found markedly decreased D2 receptor density using (18)F-methylspiperone PET in this very late stage of chronic manganism, supporting the hypothesis that manganese intoxication may trigger a neurodegenerative disease process. ( info)

10/28. Manganese intoxication: the cause of an inexplicable epileptic syndrome in a 3 year old child.

    Excess manganese (Mn) can cause several neurotoxic effects, however only a few studies have reported epileptic syndromes related to manganese intoxication. We describe an epileptic syndrome due to manganese intoxication in a 3 year old male child. His blood manganese was elevated, but no other abnormal values or toxic substances were found in blood or urine. The electroencephalogram (EEG) showed a picture of progressive encephalopathy, while brain magnetic resonance was normal. The patient's conditions rapidly worsened to epileptic status despite the use of antiepileptic drugs. Chelating treatment with CaNa(2)EDTA was initiated to remove excess manganese and promptly succeeded in reverting epileptic symptoms. Concurrently, manganese blood levels and electroencephalogram progressively normalized. Thereafter it has been possible to discontinue antiepileptic treatment, and the patient remains in excellent conditions without any treatment. ( info)
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