Striatal D2 receptor status in patients with Parkinson's disease, striatonigral degeneration, and progressive supranuclear palsy, measured with 11C‐raclopride and positron emission tomography
Striatal D2 receptor status in patients with Parkinson's disease, striatonigral degeneration, and progressive supranuclear palsy, measured with 11C‐raclopride and positron emission tomography
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使用 11C-雷氯必利和正电子发射断层扫描测量帕金森病、纹状体黑质变性和进行性核上性麻痹患者的纹状体 D2 受体状态
DOI：
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发表时间：
1992
影响因子：
11.2
通讯作者：
Richard S. J. Frackowiak
中科院分区：
文献类型：
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作者：
D. Brooks;V. Ibáñez;G. Sawle;E. Playford;N. Quinn;C. Mathias;A. Lees;C. Marsden;R. Bannister;Richard S. J. Frackowiak
平衡纹状体：小脑11 C-雷氯必利（RAC）摄取比反映了纹状体多巴胺D2结合位点的密度。使用正电子发射断层扫描，我们测量了6例未经治疗的帕金森病（PD）患者，5例长期治疗的PD患者和对左旋多巴的反应波动，10例纹状体黑质变性（SND）患者和9例进行性核上性麻痹（PSP）患者的纹状体RAC摄取。还用C15 O2测定了局部脑血流量。平均strital：在未治疗的PD患者中，小脑RAC摄取与正常无显著差异，尽管这6例患者中有2例显示壳核示踪剂结合显著增加。平均尾状核和壳核：PD组和对左旋多巴反应波动组的小脑RAC摄取率分别显著降低30%和18%。SND患者的平均尾状核和壳核：小脑RAC摄取率分别降低了10%和11%，但降幅较小，而PSP患者的尾状核和壳核：小脑RAC结合率分别降低了24%和9%。PSP患者的纹状体和额叶血流量显著减少，但PD或SND患者则无此现象。总之，纹状体D2结合电位在未经治疗的PD患者中是正常或升高的，但在PD患者和对L-多巴反应波动的患者中降低。SND和PSP患者显示纹状体RAC结合减少，但程度低于PD患者和对治疗的反应波动。因此，SND和PSP患者对左旋多巴反应不佳不能仅归因于纹状体D2位点的丢失，而必须反映其他基底神经节连接的丢失。
Equilibrium striatal: cerebellar 11C‐raclopride (RAC) uptake ratios reflect the density of striatal dopamine D2 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 C15O2. 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 D2 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 D2 sites alone, but must reflect loss of other basal ganglia connections.