11/28. Acute renal failure following ingestion of manganese-containing fertilizer. fertilizers are used to promote the survival and growth of plants and crops and have a good safety record when used properly. The basic elements in fertilizer include phosphorus, nitrite, and potassium. In addition, there are additive agents that vary for different crops and which may include some metals. Acute intoxication by ingesting fertilizer includes damage to various organ systems as well as severe cardiovascular or respiratory distress. We report the case of a 64-year-old man who ingested about 700 mL of fertilizer and suffered acute renal failure, hyperkalemia, and mild methemoglobinemia. After supportive care and emergent hemodialysis for hemodynamic instability due to hyperkalemia, the renal function of the patient recovered in four days. ( info) |
12/28. [18F]FDOPA PET and clinical features in parkinsonism due to manganism. Manganese exposure reportedly causes a clinically and pathophysiologically distinct syndrome from idiopathic Parkinson's disease (PD). We describe the clinical features and results of positron emission tomography with 6-[18F]fluorodopa ([18F]FDOPA PET) of a patient with parkinsonism occurring in the setting of elevated blood manganese. The patient developed parkinsonism associated with elevated serum manganese from hepatic dysfunction. [18F]FDOPA PET demonstrated relatively symmetric and severely reduced [18F]FDOPA levels in the posterior putamen compared to controls. The globus pallidum interna had increased signal on T1-weighted magnetic resonance imaging (MRI) images. We conclude that elevated manganese exposure may be associated with reduced striatal [18F]FDOPA uptake, and MRI may reveal selective abnormality within the internal segment of the pallidum. This case suggests that the clinical and pathophysiological features of manganese-associated parkinsonism may overlap with that of PD. ( info) |
13/28. Effective treatment of manganese-induced occupational Parkinsonism with p-aminosalicylic acid: a case of 17-year follow-up study. OBJECTIVE: Chronic manganese (Mn) intoxication induces syndromes resembling parkinson disease. The clinical intervention has largely been unsuccessful. We report a 17-year follow-up study of effective treatment of occupational Mn parkinsonism with sodium para-aminosalicylic acid (PAS). methods: The patient, female and aged 50 at the time of treatment, was exposed to airborne Mn for 21 years (1963-1984). The patient had palpitations, hand tremor, lower limb myalgia, hypermyotonia, and a distinct festinating gait. She received 6 g PAS per day through an intravenous drip infusion for 4 days and rested for 3 days as one therapeutic course. Fifteen such courses were carried out between March and June 1987. RESULTS: At the end of PAS treatment, her symptoms were significantly alleviated, and handwriting recovered to normal. Recent follow-up examination at age 67 years (in 2004) showed a general normal presentation in clinical, neurologic, brain magnetic resonance imaging, and handwriting examinations with a minor yet passable gait. CONCLUSIONS: This case study suggests that PAS appears to be an effective drug for treatment of severe chronic Mn poisoning with a promising prognosis. ( info) |
14/28. Occupational manganese neurotoxicity provoked by hepatitis c. Manganese neurotoxicity developed in a highly exposed worker after asymptomatic, moderate hepatic dysfunction from hepatitis c infection. Antiviral therapy was accompanied by resolution of increased blood manganese levels and neurologic improvement. Even asymptomatic hepatic dysfunction may impair manganese clearance and place highly exposed persons at risk for toxicity. ( info) |
| Two cases of chronic manganese poisoning were treated with sodium para-aminosalicylic acid (PAS-Na; 6 g/day in 500 ml of 10% glucose solution by intravenous drip). The results indicated that one had been clinically cured and that the other had obviously improved in clinical symptoms and signs. Thus PAS-Na appears to be an effective drug for treatment of serious chronic manganese poisoning. ( info) |
16/28. Manganese levels in a jaundiced long-term total parenteral nutrition patient: potentiation of haloperidol toxicity? Case report and literature review. Manganese is vital in human nutrition. When oral intake is precluded, the recommended parenteral supplementation is 0.15 to 0.8 mg/day. Manganese is excreted primarily in the bile; during cholestasis, serum manganese levels may rise, and manganese toxicity ensue. Neuropsychiatric symptoms are prominent. Phenothiazine-derivative drugs may potentiate manganese toxicity. serum or whole blood manganese levels should guide manganese therapy in jaundiced patients. ( info) |
17/28. Morvan's fibrillary chorea. A case with possible manganese poisoning. The clinical picture of Morvan's fibrillary chorea includes a. spontaneous muscular activity resulting from repetitive motor unit action potentials of peripheral origin (multiplets), b. autonomic dysregulation with profuse hyperhidrosis, and c. central nervous system involvement as shown by severe insomnia and hallucinosis. A case featuring all these symptoms is presented. Whereas known causative factors range from gold or mercury poisoning to autoimmune disorders, the presented case is the first one in which chronic manganese intoxication (occupational exposure) seems to be implicated. Manganese has been found to inhibit acetylcholine esterase, and, as a consequence, may produce peripheral and central cholinergic hyperactivity. ( info) |
18/28. Chronic manganese intoxication. We report six cases of chronic manganese intoxication in workers at a ferromanganese factory in taiwan. diagnosis was confirmed by assessing increased manganese concentrations in the blood, scalp, and pubic hair. In addition, increased manganese levels in the environmental air were established. The patients showed a bradykinetic-rigid syndrome indistinguishable from Parkinson's disease that responded to treatment with levodopa. ( info) |
19/28. Chronic manganese poisoning: a neuropathological study with determination of manganese distribution in the brain. An autopsy case of a 52-year-old man suffering from chronic manganese poisoning (CMP) is reported with determination of the manganese distribution in the brain. The patient had been working in a manganese ore crushing plant since 1965. In 1967 he began to complain of difficulties in walking and diminished libido. Later, he developed various neuropsychiatric symptoms including euphoria, emotional incontinence, masked face, monotonous speech, "cock-walk", increased muscle tone, weakness of upper and lower extremities, tremor of the eye lids, and exaggeration of knee jerks. The major neuropathological change was degeneration of the basal ganglia, in which the pallidum was severely affected. The pallidum disclosed a loss and degeneration of nerve cells, which was especially marked in the medial segment, a prominent decrease of myelinated fibers, and moderate astrocytic proliferation. The substantia nigra was intact. Distribution of manganese in the brain of the present case of CMP was determined using flameless atomic absorption spectrometry and compared with control cases and also a case of Parkinson's disease (PD). There was no significant difference between the control cases and the case of PD in average concentration of manganese and its distribution in the brain. The present case of CMP showed no elevation in average concentration of manganese in the brain. However, there were some changes in its distribution. Thus, the continuance of neurological disorders in CMP is not linked to an elevated manganese concentration itself in the brain. CMP appears to be different from PD in neuropathology and manganese behavior in brain. ( info) |
20/28. Emic accounts of a mystery illness: the Groote Eylandt syndrome. The Aboriginal people of Groote Eylandt, in the northern territory of australia, are suffering from an unusual disease complex having neurological, psychiatric and teratological features, which admits no ready explanation. The island people at various times blame it on the spirits, or accuse enemies, or take some responsibility upon themselves. In this paper, 'emic' accounts of the illness (those current among the members of the society) are described in order to compare them with 'etic' accounts of those who study the society from the outside. Since emic views regulate people's behaviours toward illness, it is suggested these views should complement and inform etic views of researchers and therapists. This principle might apply to all mysterious or poorly understood illness. ( info) |