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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
PubMed

Insights

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.

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