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

• D. J. Brooks

• V. Ibanez

• G. V. Sawle

• E. D. Playford

• N. Quinn

• C. J. Mathias

• A. J. Lees

• C. D. Marsden

• R. Bannister

• R. S. J. Frackowiak

抄録

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.

収録刊行物

• Annals of Neurology

  Annals of Neurology 31 (2), 184-192, 1992-02

  Wiley

キーワード

• Neurology (clinical)
• Neurology

詳細情報

• CRID: 1360011144549415296
• NII論文ID: 30008832543
• DOI: 10.1002/ana.410310209
• ISSN: 15318249
• ISSN: 03645134
• Web Site: https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1002%2Fana.410310209
• Web Site: https://onlinelibrary.wiley.com/doi/pdf/10.1002/ana.410310209
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