Burn D J, Rinne J O, Quinn N P, Lees A J, Marsden C D, Brooks D J
MRC Cyclotron Unit, Hammersmith Hospital, UK.
Brain. 1995 Aug;118 ( Pt 4):951-8. doi: 10.1093/brain/118.4.951.
The clinical differentiation of Parkinson's disease from the striatonigral degeneration (SND) type of multiple system atrophy (MSA) and Steele-Richardson-Olszewski syndrome (SRO) may be difficult. This is reflected by a 20-25% misdiagnosis rate in clinicopathological series of cases labelled as 'Parkinson's disease' in life. The caudate and putamen contain a high density of opioidergic neurons and receptors which have a close anatomical and physiological relationship with the dopaminergic system. We used [11C]diprenorphine with PET to investigate striatal opioid receptor binding in groups of patients with clinically defined Parkinson's disease (n = 8), SND (n = 7) and SRO (n = 6), compared with normal controls (n = 8). There was no significant difference between mean ligand binding in the putamen and caudate of Parkinson's disease cases when compared with normals. Mean putamen, but not caudate, opioid receptor binding was significantly reduced in the SND group, when compared with normals. By contrast, in the SRO group, both mean caudate and putamen opioid receptor binding was significantly reduced when compared with both normal and Parkinson's disease groups. When considering the individual patients, none of the eight Parkinson's disease cases (0%), none of the seven SND cases (0%), but four of the six SRO cases (67%) had caudate opioid receptor binding that was > 2.5 SDs below the normal mean. Corresponding figures for putamen opioid receptor binding were: none of the Parkinson's disease cases (0%); three of the SND cases (43%); and all of the SRO cases (100%). We conclude that there are differences in the pattern of opioid receptor binding in the striatum of Parkinson's disease, SND and SRO patients, as determined by [11C]diprenorphine PET. The different binding patterns may help to differentiate these akinetic-rigid syndromes in life.
帕金森病与多系统萎缩(MSA)的纹状体黑质变性(SND)型以及斯蒂尔-理查森-奥尔谢夫斯基综合征(SRO)在临床上进行鉴别可能存在困难。这一点在生前被诊断为“帕金森病”的临床病理系列病例中20%-25%的误诊率上得到了体现。尾状核和壳核含有高密度的阿片样物质能神经元和受体,它们与多巴胺能系统存在密切的解剖学和生理学关系。我们使用[11C]二丙诺啡和正电子发射断层扫描(PET)来研究临床确诊的帕金森病患者组(n = 8)、SND患者组(n = 7)和SRO患者组(n = 6)纹状体阿片受体结合情况,并与正常对照组(n = 8)进行比较。与正常对照组相比,帕金森病患者壳核和尾状核的平均配体结合无显著差异。与正常对照组相比,SND组壳核而非尾状核的阿片受体结合显著降低。相比之下,在SRO组中,与正常对照组和帕金森病患者组相比,尾状核和壳核的平均阿片受体结合均显著降低。在考虑个体患者时,8例帕金森病患者中无一例(0%)、7例SND患者中无一例(0%),但6例SRO患者中有4例(67%)的尾状核阿片受体结合低于正常均值2.5个标准差。壳核阿片受体结合的相应数据为:帕金森病患者无一例(0%);SND患者中有3例(43%);SRO患者全部(100%)。我们得出结论,通过[11C]二丙诺啡PET测定,帕金森病、SND和SRO患者纹状体中阿片受体结合模式存在差异。不同的结合模式可能有助于在生前鉴别这些运动不能-强直综合征。