Striatal D₂ receptor status in patients with Parkinson's disease, striatonigral degeneration, and progressive supranuclear palsy, measured with ¹¹C‐raclopride and positron emission tomography

TLDR

Striatal dopamine D2 receptor density can be quantified by the equilibrium striatal‑to‑cerebellar uptake ratio of the radiotracer 11C‑raclopride. The study employed 11C‑raclopride PET imaging to measure striatal uptake in 6 untreated Parkinson’s disease patients, 5 treated PD patients with fluctuating L‑dopa response, 10 striatonigral degeneration patients, and 9 progressive supranuclear palsy patients, while also assessing regional cerebral blood flow with 15O‑water. Results showed normal or increased D2 binding in untreated PD, significant reductions in treated PD and in SND and PSP (10–24% lower), with PSP also exhibiting reduced striatal and frontal blood flow, indicating that loss of D2 sites alone does not explain poor L‑dopa response in SND and PSP.

Abstract

Abstract Equilibrium striatal: cerebellar 11 C‐raclopride (RAC) uptake ratios reflect the density of striatal dopamine D 2 binding sites. Using positron emission tomographic scanning we have measured striatal RAC uptake in 6 untreated patients with Parkinson's disease (PD), 5 chronically treated patients with PD and a fluctuating response to L ‐dopa, 10 patients with striatonigral degeneration (SND), and 9 patients with progressive supranuclear palsy (PSP). Regional cerebral blood flow was determined also, with C 15 O 2 . Mean strital: cerebellar RAC uptake was not significantly different from normal in untreated patients with PD, though 2 of these 6 patients showed significantly increased putamen tracer binding. Mean caudate and putamen: cerebellar RAC uptake ratios of the group with PD and fluctuating response to L ‐dopa were significantly reduced by 30% and 18%, respectively. The patients with SND had lesser, but significant, 10% and 11% decreases in mean caudate and putamen: cerebellar RAC uptake ratios, respectively, whereas patients with PSP showed 24% and 9% reductions in caudate and putamen: cerebellar RAC binding. Striatal and frontal blood flow were significantly reduced in patients with PSP, but not in patients with PD or SND. In conclusion, striatal D 2 binding potential is normal or raised in untreated patients with PD, but reduced in patients with PD and a fluctuating response to L ‐dopa. Patients with SND and PSP show a decrease in striatal RAC binding, but to a lesser extent than patients with PD and a fluctuating response to treatment. Failure of patients with SND and PSP to respond well to L ‐dopa cannot therefore be due to losss of striatal D 2 sites alone, but must reflect loss of other basal ganglia connections.