[123I]FP-CIT单光子发射计算机断层扫描对早发性帕金森病多巴胺能功能障碍的成像

Imaging of dopaminergic dysfunction with [123I]FP-CIT SPECT in early-onset parkin disease.

作者信息

Varrone A, Pellecchia M T, Amboni M, Sansone V, Salvatore E, Ghezzi D, Garavaglia B, Brice A, Brunetti A, Bonavita V, De Michele G, Salvatore M, Pappatà S, Barone P

机构信息

Biostructure and Bioimaging Institute, National Research Council, Via S. Pansini, 5, 80131, Napoli, Italy.

出版信息

Neurology. 2004 Dec 14;63(11):2097-103. doi: 10.1212/01.wnl.0000145765.19094.94.

DOI:10.1212/01.wnl.0000145765.19094.94

PMID:15596756

Abstract

OBJECTIVE

To investigate whether the presence of parkin gene mutations is associated with different nigrostriatal impairment than other early-onset parkinsonism.

METHODS

Eighteen consecutive early-onset Parkinson disease (PD) patients (nine parkin and nine nonparkin patients) and six controls were studied with [123I]FP-CIT SPECT.

RESULTS

Parkin patients had longer disease duration (15 +/- 9 vs 6 +/- 2 years, p = 0.008) and higher Unified Parkinson's Disease Rating Scale (UPDRS) motor score (35.8 +/- 13.7 vs 22.8 +/- 7.9, p = 0.025) than nonparkin patients. Caudate and putamen DAT density were reduced by 60% and 79% in parkin and by 43% and 70% in nonparkin patients. Multiple regression analysis showed that the UPDRS and the presence of parkin gene mutations, but not the disease duration, were significantly correlated with the striatal DAT density. Parkin patients showed a more symmetric DAT loss in both caudate and putamen as compared with nonparkin patients.

CONCLUSIONS

Parkin-related disease may be associated with a higher degree of nigrostriatal impairment, independently of the clinical severity of the disease, and a more symmetric involvement as compared with non-parkin early-onset disease.

摘要

目的

研究帕金森基因（parkin）突变的存在是否与不同于其他早发性帕金森综合征的黑质纹状体损害相关。

方法

对18例连续的早发性帕金森病（PD）患者（9例携带parkin基因和9例不携带parkin基因的患者）及6名对照者进行[123I]FP - CIT单光子发射计算机断层扫描（SPECT）研究。

结果

与不携带parkin基因的患者相比，携带parkin基因的患者病程更长（15±9年 vs 6±2年，p = 0.008），统一帕金森病评定量表（UPDRS）运动评分更高（35.8±13.7 vs 22.8±7.9，p = 0.025）。携带parkin基因的患者尾状核和壳核多巴胺转运体（DAT）密度分别降低60%和79%，不携带parkin基因的患者分别降低43%和70%。多元回归分析显示，UPDRS和parkin基因突变的存在与纹状体DAT密度显著相关，而病程与之无关。与不携带parkin基因的患者相比，携带parkin基因的患者在尾状核和壳核均表现出更对称的DAT丢失。