We thank Fernandez and Friedman for their comments. Although the results they mention were obtained in a small number of subjects, they point out an unresolved question: whether patients with PD can have normal findings on 18F-dopa PET scans. From our results, one could extrapolate that the compensatory increase of the dopa decarboxylase might produce normal 18F-dopa PET scan findings despite the disappearance of 20% or 30% of the dopaminergic neurons. However, the study showing that 18F-dopa uptake is highly correlated to motor function suggests that when this uptake is normal, the motor performance is nearly normal. Finally, abnormal results on 18F-dopa PET scans have occurred in asymptomatic co-twins of patients with PD.1 Although this type of PD is probably genetic and may be different from the idiopathic form, this finding argues against the likelihood of PD symptoms without abnormal 18F-dopa PET scan findings. Finally, technical parameters for image acquisition and analysis might influence the ability to discriminate between normal and abnormal results on these scans. Consequently, reporting and following cases of PD that demonstrate normal findings on 18F-dopa PET scans and abnormal results on examinations using DAT ligands is of major interest.
Ribeiro M, Vidailhet M, Remy P. In reply. Arch Neurol. 2002;59(12):1973–1974. doi:https://doi.org/
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