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Editorial |

Progression of Parkinson Disease:  Are We Making Progress in Charting the Course?

Joseph Jankovic, MD
Arch Neurol. 2005;62(3):351-352. doi:10.1001/archneur.62.3.351.
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While progressive motor and nonmotor decline is the expected natural course of Parkinson disease (PD), there is a remarkable paucity of data on what determines the rate of progression before and after the onset of symptoms. Using serial fluorodopa F 18 ([18F]fluorodopa) positron emission tomography (PET) in a prospective, longitudinal study of 31 patients with PD observed for more than 5 years, Hilker et al1 found an annual decline in striatal [18F]fluorodopa ranging from 4.4% (caudate) to 6.3% (putamen). This is similar to other longitudinal studies of PD progression, using imaging ligands that either measure dopamine metabolism ([18F]fluorodopa PET) or target dopamine transporter (β-carboxymethyoxy-3-β-[4-iodophenyl] tropane single-photon emission computed tomography), demonstrating an annualized rate of reduction in these striatal markers of about 4% to 13% in patients with PD compared with 0% to 2.5% change in healthy controls.25 These imaging studies are consistent with pathological studies showing that the rate of nigral degeneration in patients with PD is 8- to 10-fold higher than that in healthy age-matched controls.

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Hypothetical dopaminergic and nondopaminergic progression and compensatory mechanisms postulated for Parkinson disease (PD) and other presynaptic (congenital or genetic) parkinsonian disorders. DA indicates dopamine; SN, substantia nigra.

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