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Long-term progression in chronic manganism: ten years of follow-up
1Department of Neurology, Chang Gung Memorial Hospital and Medical College, Taipei, Taiwan.
Abstract:
We studied the long-term clinical course of five patients with chronic manganese intoxication. The mean scores of the King's College Hospital Rating Scale for Parkinson's disease increased from 15.0 +/- 4.2 in 1987 to 28.3 +/- 6.70 in 1991 and then to 38.1 +/- 12.9 in 1995. The deterioration was most prominent in gait, rigidity, speed of foot tapping, and writing. Tissue concentrations of manganese in blood, urine, scalp hair, and pubic hair returned to normal. Follow-up MRIs did not show paramagnetic high-signal intensity on T1-weighted images. The data indicate that clinical progression in patients with manganese parkinsonism continues even 10 years after cessation of exposure.
Insights
Chronic manganese intoxication can lead to progressive parkinsonism years after exposure ends. Symptoms like gait and writing difficulties worsen over time, even as manganese levels normalize.
Area of Science:
- Neuroscience
- Toxicology
- Neurology
Background:
- Chronic manganese intoxication is a known cause of parkinsonism.
- The long-term clinical progression after exposure cessation is not well-documented.
Purpose of the Study:
- To investigate the long-term clinical course of patients with chronic manganese intoxication.
Main Methods:
- Longitudinal study of five patients with chronic manganese intoxication.
- Clinical assessment using the King's College Hospital Rating Scale for Parkinson's disease.
- Monitoring of manganese levels in blood, urine, and hair.
- Follow-up Magnetic Resonance Imaging (MRI).
Main Results:
- Parkinsonism scores significantly worsened over a decade (1987-1995).
- Deterioration was most evident in gait, rigidity, foot tapping speed, and writing.
- Manganese levels in tissues normalized, and MRI findings did not show persistent abnormalities.
Conclusions:
- Clinical progression of manganese parkinsonism can continue for at least 10 years after exposure cessation.
- This suggests a persistent neurotoxic effect or ongoing pathological processes.
- Further research is needed to understand the mechanisms underlying long-term progression.