Turjanski N, Lees A J, Brooks D J
MRC Cyclotron Unit, Hammersmith Hospital, London, UK.
Neurology. 1997 Sep;49(3):717-23. doi: 10.1212/wnl.49.3.717.
Dyskinesias are usually seen in Parkinson's disease (PD) patients after several years of L-dopa therapy. Their presence has been attributed to supersensitivity of striatal D1 and D2 receptors. We have used PET to assess striatal D2 receptor binding in untreated PD patients and striatal D1 and D2 binding in L-dopa-treated PD patients. Untreated patients showed a 14% increase in mean D2 receptor binding in the putamen contralateral to the more affected limbs (p < 0.02). Treated patients were segregated into subgroups according to the presence or absence of dyskinesias. There were no differences in mean caudate and putamen D1 and D2 binding between dyskinetic and nondyskinetic patients, matched for duration of clinical disease. Both dyskinetic and nondyskinetic PD subgroups showed a similar 16% reduction of mean caudate D2 binding (p < 0.01) with normal D2 binding in putamen. Mean caudate and putamen D1 binding potentials of both subgroups were reduced by 10% compared with those of controls, though this trend did not reach significance. Putamen D1 binding, however, showed a negative correlation with duration and L-dopa treatment (p < 0.03). These findings suggest that, while exposure of PD patients to L-dopa may be associated with reductions in caudate D2 and caudate and putamen D1 receptor, dyskinesias are unlikely to result from alterations in striatal dopamine receptor binding.
运动障碍通常在帕金森病（PD）患者接受左旋多巴治疗数年之后出现。其出现被归因于纹状体D1和D2受体的超敏反应。我们使用正电子发射断层扫描（PET）来评估未经治疗的PD患者的纹状体D2受体结合情况以及接受左旋多巴治疗的PD患者的纹状体D1和D2受体结合情况。未经治疗的患者中，与受影响更严重肢体对侧的壳核相比，平均D2受体结合增加了14%（p < 0.02）。根据是否存在运动障碍，将接受治疗的患者分为亚组。在临床疾病持续时间匹配的运动障碍患者和非运动障碍患者之间，尾状核和壳核的平均D1和D2受体结合没有差异。运动障碍型和非运动障碍型PD亚组均显示尾状核平均D2受体结合有相似的16%的降低（p < 0.01），而壳核的D2受体结合正常。与对照组相比，两个亚组的尾状核和壳核平均D1受体结合潜能均降低了10%，尽管这一趋势未达到统计学意义。然而，壳核D1受体结合与病程及左旋多巴治疗呈负相关（p < 0.03）。这些发现表明，虽然PD患者接触左旋多巴可能与尾状核D2受体以及尾状核和壳核D1受体的减少有关，但运动障碍不太可能是由纹状体多巴胺受体结合的改变导致的。
