@article {Goldstein1479, author = {David S. Goldstein and Courtney Holmes and LaToya Sewell and Irwin J. Kopin}, title = {Hypertension Increases Cerebral 6-18F-Fluorodopa{\textendash}Derived Radioactivity}, volume = {50}, number = {9}, pages = {1479--1482}, year = {2009}, doi = {10.2967/jnumed.109.062869}, publisher = {Society of Nuclear Medicine}, abstract = {6-18F-fluorodopa PET depicts the striatal dopaminergic lesion characterizing Parkinson disease (PD); however, striatal uptake of 6-18F-fluorodopa{\textendash}derived radioactivity can be normal. Supine hypertension (SH) might increase 6-18F-fluorodopa uptake. Methods: We measured putamen, caudate, and occipital cortex 6-18F-fluorodopa{\textendash}derived radioactivity and supine blood pressure in patients with PD + SH (systolic pressure >= 180 mm Hg, n = 8), patients with PD without SH (PD - SH, n = 19), patients with pure autonomic failure (n = 8), and controls (n = 16). Results: Peak putamen radioactivity correlated with supine systolic pressure across all subjects and among PD patients and was higher in PD + SH than in PD - SH (P = 0.01). Both subgroups had rapid fractional declines in radioactivity between the peak and late values (P \< 0.0001, compared with controls). Arterial 6-18F-fluorodopa concentrations were similar in the compared groups. Conclusion: In PD, SH is associated with augmented striatal 6-18F-fluorodopa{\textendash}derived radioactivity. Regardless of SH, retention of 6-18F-fluorodopa{\textendash}derived radioactivity is markedly reduced. A model-independent approach can identify striatal dopaminergic denervation in PD.}, issn = {0161-5505}, URL = {https://jnm.snmjournals.org/content/50/9/1479}, eprint = {https://jnm.snmjournals.org/content/50/9/1479.full.pdf}, journal = {Journal of Nuclear Medicine} }