The Nigrostriatal Dopaminergic System Assessed In Vivo by Positron Emission Tomography in Healthy Volunteer Subjects and Patients With Parkinson's Disease

doi:10.1001/archneur.1990.00530120034007

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Vol. 47 No. 12, December 1990

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The Nigrostriatal Dopaminergic System Assessed In Vivo by Positron Emission Tomography in Healthy Volunteer Subjects and Patients With Parkinson's Disease

Klaus L. Leenders, MD; Eric P. Salmon, MD; Pippa Tyrrell, MD; Daniela Perani, MD; David J. Brooks, MD; Harvey Sager, MD; Terry Jones, DSc; C. David Marsden, MD; Richard S. J. Frackowiak, MD

Arch Neurol. 1990;47(12):1290-1298.

Abstract

• A group of healthy control subjects and patients withParkinson's disease were investigated using positron emissiontomography and two tracers as indicators of different specificproperties of the presynaptic dopaminergic system in caudatenucleus and putamen. The first tracer, 6-L-(¹⁸F)-fluorodopa,was used as an analog of levodopa to assess its regional brainuptake, conversion into, and retention as dopamine and furthermetabolites. The second tracer, (¹¹C)-nomifensine was employedas an indicator of striatal monaminergic reuptake sites thatare principally dopaminergic. We have used this tracer to assessdopaminergic nerve terminal density. In patients with Parkinson'sdisease, striatal uptake of both tracers was decreased, putamenbeing significantly more affected than caudate. Side-to-sidedifferences of uptake in putamen, but not caudate, correlatedwith corresponding left-right differences of scored clinicalmotor performance. Both 6-L(¹⁸F)-fluorodopa and (¹¹C)-nomifensinetracer uptake in putamen was decreased on average to 40% ofnormal values, suggesting that a substantial part of the cellularelements of the dopaminergic nigrostriatal system is still intactin living parkinsonian patients. This is in contrast to thegenerally extreme depletion of endogenous dopamine in the putamenof patients found at postmortem. Our results lend support tothe search for drug treatments that protect against furthernigrostriatal cell loss and that could be exhibited as soonas the disease manifests clinically. If successful, a sufficientstriatal nerve terminal pool would remain so that the effectivenessof levodopa as a dopamine repletor could persist.

Author Affiliations

From the MRC Cyclotron Unit, Hammersmith Hospital, London, England (Drs Leenders, Salmon, Tyrrell, Perani, Brooks, Jones, and Frackowiak); the Paul Scherrer Institute, Villigen, Switzerland (Dr Leenders); the Cyclotron Research Centre, Liege, Belgium (Dr Salmon), the Consiglio Nazionale Richerche, Milan, Italy (Dr Perani); the Royal Hallamshire Hospital, Sheffield, England (Dr Sagar); and the Institute of Neurology, The National Hospital, London, England (Dr Marsden).

Footnotes

Accepted for publication April 30, 1990.

Reprint requests to the Paul Scherrer Institute, CH-5232, Villigen,Switzerland (Dr Leenders).

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