Subregional 6-[18F]fluoro-？-m-tyrosine Uptake in the Striatum in Parkinson's Disease

We assessed 101 patients with PD and 19 healthy volunteers. PD was diagnosed based on the UK Brain Bank criteria by two experts on movement disorders. Motor symptoms were measured with the Unified Parkinson's Disease Rating Scale (UPDRS). FMT uptake in the subregions of the striatum was analyzed using semi-automated software for region-of-interest demarcation on co-registered magnetic resonance images.In all PD patients, FMT uptake was decreased in the posterior putamen regardless of predominant motor symptoms and disease duration. Smaller uptake values were found in the putamen contralateral to the side with more affected limbs. The severity of bradykinesia, rigidity, and axial symptoms was correlated with the decrease of FMT uptake in the putamen, particularly in the anterior part. No significant correlation was observed between tremors and FMT uptake.Decrease of FMT uptake in the posterior putamen appears to be most sensitive in mild PD and uptake in the anterior putamen may reflect the severity of main motor symptoms, except for tremor.Cardinal motor symptoms such as bradykinesia, rigidity, and tremor in Parkinson's Disease (PD) become apparent after a depletion of dopamine in the striatum to approximately 20% of normal levels and a reduction in aromatic ？-amino acid decarboxylase (AADC) activity to 5%-20% of normal levels [1,2]. In PD, dopaminergic hypofunction in the striatum is not homogenous in association with the selective loss of ventral intermediate and lateral cell groups of the substantia nigra pars compacta that project to the posterior part of the striatum [3], although the reason for this selective vulnerability remains unknown.Positron emission tomography (PET) is valuable for assessing altered dopamine function in PD. The first tracer used to visualize and assess the integrity of dopamine presynaptic systems was 6-[18F]fluoro-？-dopa (FDOPA), a fluoro-analog of ？-dopa [4]. FDOPA is taken up into the dopaminergic axon terminals and decarboxylated by