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A Fluorodopa F 18 Positron Emission Tomography Study

Stéphane Thobois, MD; Maria-Joao Ribeiro, MD, PhD; Ebba Lohmann, MD; Alexandra Dürr, MD, PhD; Pierre Pollak, MD; Olivier Rascol, MD, PhD; Stéphane Guillouet, PharmD; Elizabeth Chapoy, MD; Nicolas Costes, PhD; Yves Agid, MD, PhD; Philippe Remy, MD, PhD; Alexis Brice, MD; Emmanuel Broussolle, MD, PhD; for the French Parkinson's Disease Genetics Study Group

Arch Neurol. 2003;60:713-718.

Background  Mutations of the parkin gene are frequently encountered in patients with young-onset Parkinson disease (YOPD), but the effects of this mutation on the nigrostriatal dopaminergic degeneration are not well established.

Objective  To analyze, using positron emission tomography and fluorodopa F 18, the severity and profile of striatal dopaminergic metabolism in YOPD patients with and without parkin gene mutations.

Methods  We performed positron emission tomography with fluorodopa F 18 in 19 YOPD patients with parkin gene mutations (parkin patients), 6 YOPD patients without parkin gene mutations (nonparkin patients), and 9 healthy controls. Putamen and caudate nucleus fluorodopa F 18 uptake was assessed using regions of interest analysis.

Results  In parkin patients, the striatal fluorodopa F 18 uptake reduction was 36.3%, 51.3%, and 66.7%, respectively, for the caudate nucleus, anterior putamen, and posterior putamen compared with controls. In nonparkin patients, this reduction was 23.0%, 43.6%, and 73.0%, respectively. This reduction was asymmetrical according to the most affected hemibody for the anterior and posterior putamen in parkin patients and for the posterior putamen in nonparkin patients. A rostrocaudal gradient was observed with a severe decrease in fluorodopa F 18 uptake in the putamen and relative sparing of the caudate nucleus. There was no significant difference of striatal fluorodopa F 18 uptake between our 2 YOPD populations. In parkin patients, no significant correlation was found among fluorodopa F 18 uptake, motor disability, and the type of mutations. In nonparkin patients, there was a significant correlation between fluorodopa F 18 uptake and clinical severity.

Conclusions  The pattern of fluorodopa F 18 uptake in the striatum of YOPD patients is similar to that of patients with idiopathic Parkinson disease and does not depend on the presence or absence of mutations of the parkin gene.

From the Service de Neurologie D and CERMEP (Centre d'Exploration et de Recherche Médicales par Emission de Positions) (Cyclotron Unit), Hôpital Neurologique Pierre Wertheimer, Lyon (Drs Thobois, Guillouet, Chapoy, Costes, and Broussolle); URA CEA-CNRS (Unité de Recherche Commissariat à l'Energie Atomique–Centre National de la Recherche Scientifique) 2210, Service Hospitalier Frédéric Joliot, Orsay (Drs Ribeiro and Remy); Département de Génétique, Cytogénétique et Embryologie, Fédération de Neurologie, INSERM (Institut National de la Santé et de la Recherche Médicale) Unité 289, and Centre d'Investigation Clinique (Dr Agid), Hôpital de la Salpêtrière, AP-HP (Assistance Publique–Hôpitaux de Paris), Paris (Drs Lohmann, Dürr, and Brice); Service de Neurologie and INSERM Unité 318, CHU (Centre Hospitalier Universitaire), Grenoble (Dr Pollak); Service de Neurologie, Hôpital Purpan, Toulouse (Dr Rascol); and Département de Neurosciences, CHU Henri Mondor, Faculté de Medecine, Créteil (Dr Remy), France.

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