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Hypertension Increases Cerebral 6-¹⁸F-Fluorodopa–Derived Radioactivity

Clinical Neurocardiology Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland

Correspondence: For correspondence or reprints contact: David S. Goldstein, Clinical Neurocardiology Section, CNP/DIR/NINDS/NIH, Building 10, Room 6N252, 10 Center Dr., MSC-1620 Bethesda, MD 20892-1620. E-mail: goldsteind{at}ninds.nih.gov

6-¹⁸F-fluorodopa PET depicts the striatal dopaminergic lesion characterizing Parkinson disease (PD); however, striatal uptake of 6-¹⁸F-fluorodopa–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–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–derived radioactivity. Regardless of SH, retention of 6-¹⁸F-fluorodopa–derived radioactivity is markedly reduced. A model-independent approach can identify striatal dopaminergic denervation in PD.

Key Words: fluorodopa • Parkinson • pure autonomic failure • orthostatic hypotension • supine hypertension

COPYRIGHT © 2009 by the Society of Nuclear Medicine, Inc.

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