Reduced Uptake of FDOPA PET in End-stage Liver Disease With Elevated Manganese Levels | Hepatobiliary Disease | JAMA Neurology | JAMA Network
[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Mar 2012

Reduced Uptake of FDOPA PET in End-stage Liver Disease With Elevated Manganese Levels

Author Affiliations

Author Affiliations: Departments of Neurology (Drs Criswell, Perlmutter, Videen, and Racette, Mr Flores, and Ms Birke), Radiology (Drs Perlmutter, Videen, and Moerlein), Anatomy and Neurobiology (Dr Perlmutter), and Medicine (Dr Crippin) and Programs in Occupational Therapy (Dr Perlmutter) and Physical Therapy (Dr Perlmutter), Washington University School of Medicine, and American Parkinson Disease Association Advanced Center for Parkinson Research (Drs Criswell, Perlmutter, Videen, and Racette), St Louis, Missouri.

Arch Neurol. 2012;69(3):394-397. doi:10.1001/archneurol.2011.771

Objective To investigate whether manganese toxicity secondary to end-state liver disease is associated with nigrastriatal dysfunction as measured by 6-[18F]fluoro-L-DOPA (FDOPA) positron emission tomographic (PET) imaging.

Design Observational case report.

Setting The Movement Disorder Center at Washington University, St Louis, Missouri.

Patient An individual with manganese toxicity secondary to end-stage liver disease. His FDOPA PET was compared with those of 10 idiopathic Parkinson disease patients and 10 age- and sex-matched healthy controls.

Main Outcome Measure The average estimated net FDOPA uptake by Patlak graphical analysis for caudate, anterior putamen, and posterior putamen.

Results The FDOPA uptake for the patient with secondary manganese toxicity was reduced across all regions by more than 2 SDs compared with healthy controls: caudate (reduced 24.7%), anterior putamen (28.0%), and posterior putamen (29.3%). The ratio of uptake between the caudate/posterior putamen was 0.99 and was different from that of idiopathic Parkinson disease patients, in whom the greatest reduction of FDOPA was in the posterior putamen (mean [SD] ratio, 1.65 [0.41]).

Conclusions Reduce striatal uptake of FDOPA uptake indicates dysfunction of the nigrostriatal pathways in manganese toxicity secondary to end-stage liver disease. The pattern of striatal involvement with equal reduction of FDOPA uptake in the caudate compared with posterior putamen appears different from those previously reported in individuals with occupational manganese toxicity and idiopathic Parkinson disease and may be specific to manganese toxicity secondary to end-stage liver disease.