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Striatal D 2 receptor status in patients with Parkinson's disease, striatonigral degeneration, and progressive supranuclear palsy, measured with 11 C‐raclopride and positron emission tomography
Author(s) -
Brooks D. J.,
Ibanez V.,
Sawle G. V.,
Playford E. D.,
Quinn N.,
Mathias C. J.,
Lees A. J.,
Marsden C. D.,
Bannister R.,
Frackowiak R. S. J.
Publication year - 1992
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410310209
Subject(s) - putamen , progressive supranuclear palsy , raclopride , parkinson's disease , caudate nucleus , medicine , binding potential , striatum , nuclear medicine , positron emission tomography , endocrinology , cerebral blood flow , chemistry , dopamine , pathology , disease
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.