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Manganese toxicity, dopaminergic dysfunction and hepatic encephalopathy
R F Butterworth1, L Spahr, S Fontaine
1Neuroscience Research Unit, Hôpital Saint-Luc (University of Montreal), Quebec, Canada.
Metabolic Brain Disease
|December 1, 1995
Summary
Chronic liver disease causes manganese buildup in the brain, leading to abnormal MRI signals and movement disorders. Liver transplants can reverse these manganese-related brain changes.
Area of Science:
- Neurology
- Hepatology
- Radiology
Background:
- Chronic liver disease frequently causes pallidal signal hyperintensity on T1-weighted MRI (>75% incidence).
- This hyperintensity correlates with blood manganese levels and extrapyramidal symptoms.
- Manganese deposition is a primary cause of pallidal hyperintensity in T1-weighted MRI.
Purpose of the Study:
- To investigate the role of manganese deposition in pallidal hyperintensity in chronic liver disease patients.
- To explore the relationship between manganese, dopaminergic function, and extrapyramidal symptoms.
- To assess the effects of liver transplantation on these parameters.
Main Methods:
- Analysis of T1-weighted Magnetic Resonance Imaging (MRI) findings.
- Measurement of blood manganese levels.
- Autopsy studies measuring pallidal manganese and dopamine D2 binding sites.
- Evaluation of patients before and after liver transplantation.
Main Results:
- Patients with chronic liver disease show significant pallidal manganese deposition (2-7 fold increase) and reduced dopamine D2 binding sites.
- Pallidal MR signal hyperintensity correlates with blood manganese levels.
- Liver transplantation led to normalization of pallidal MR signals and blood manganese levels.
Conclusions:
- Pallidal MR signal hyperintensity in chronic liver disease is attributed to manganese deposition.
- Manganese-induced alterations in dopaminergic function may contribute to extrapyramidal symptoms in these patients.
- Liver transplantation effectively reverses manganese-related neurological changes.