Manganese

Pathogenesis and Pathophysiology. Inhalation is the primary source of exposure. Neuropathologically, ganglion cells including cells of the pallidum show histological changes. Damage to the substantia nigra has also been seen, as have nerve cell alterations in the basal nuclei, frontal and parietal cortex, cerebellum, and hypothalamus.

Epidemiology and Risk Factors. The neurological syndrome manganism was first described in 1837. Since that time, hundreds of cases have been reported in the medical literature. Mining dust and industry are the primary sources of manganese (see Table,39:1 ). Like organic lead, manganese is also an antiknock additive in gasoline (MMT).

Outside the occupational setting, hospitalized patients receiving total parenteral nutrition (TPN) therapy that includes manganese can develop distinctive T1-weighted hyperintense patterns in the region of the globus pallidum. These apparent lesions disappear after cessation of TPN, but in some patients their presence correlates with clinical signs of parkinsonism and high blood levels of manganese.

Clinical Features and Associated Findings. The onset of symptoms is extremely variable from individual to individual and depends on the intensity of exposure, individual susceptibility, and possibly the type of ore involved. Symptoms may appear after only 1 or 2 months or after 20 years of exposure. The earliest signs of manganism include anorexia, asthenia, apathy, somnolence, headaches, and social withdrawal. Personality changes are common and consist of irritability, emotional lability, and periods of hyperexcitability (manganese psychosis). With continued exposure, moderate to high-level exposure symptoms characteristic of parkinsonism develop, including "masked facies" and bradykinesia). Speech is affected, becoming faint, monotonous, disjointed, occasionally unintelligible, and even mute. Other symptoms include weakness and fatigue, which increase until the worker is unable to go to work. Symptoms are generally confined to the extrapyramidal system, and gait difficulties are observed as retropulsion on rising and propulsion on walking, awkwardness and fine or coarse tremor of the hands, and gross rhythmical movements of the trunk and head. Micrographia in writing samples may also be evident. Whereas individuals with classic cases of severe manganism have more diffuse signs than those typical of Parkinson's disease, there are some concerns that chronic low or moderate exposure during occupations like welding could be a risk factor for typical Parkinson's disease.

Differential Diagnosis and Evaluation. Diagnosis requires a history of exposure to manganese in combination with physical findings. About 43 percent of the body burden of manganese is in the bone. Excretion is biphasic, consisting of a rapid phase with a half-life of 4 days and a second slower phase that has a half-life of 39 days. Methods of biological monitoring are poor, and individual manganese levels in blood and urine do not correlate with either present or past exposure. Diagnostic chelation with EDTA is not useful.

Management. Management involves removal of the patient from exposure. The chronic movement disorder may respond to the use of levodopa and 5-hydroxytryptophan. Patients studied by Mena and colleagues y responded well to levodopa doses of more than 3 g/day, showing a marked reduction in rigidity and all other symptoms except speech disorders. Traditional chelation therapy has not proved helpful.

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