Huang Chin-Chang, Weng Yi-Hsin, Lu Chin-Song, Chu Nai-Shin, Yen Tzu-Chen
Dept. of Neurology, Chang Gung Memorial Hospital, 199, Tung-Hwa North Road, Taipei, Taiwan.
J Neurol. 2003 Nov;250(11):1335-9. doi: 10.1007/s00415-003-0214-1.
Chronic exposure to manganese may induce parkinsonism similar to idiopathic Parkinson's disease (PD). However, clinical manifestations of manganism also have some features different from PD. The mechanisms of manganese-induced parkinsonism remain not fully understood. (99m)Tc-TRODAT-1 is a cocaine analogue that can bind to the dopamine transporter (DAT) site reflecting the function of presynaptic dopaminergic terminals. The purpose of this study was to evaluate DAT function using (99m)Tc-TRODAT-1 to investigate the integrity of the presynaptic dopaminergic terminals in manganese-induced parkinsonism. Brain (99m)Tc-TRODAT-1 single photon emission computed tomography was performed in 4 patients with chronic manganese intoxication in a ferromanganese smelting plant in Taiwan. Twelve PD patients and 12 healthy volunteers served as abnormal and normal controls, respectively. Clinically, all manganism patients had a bradykinetic-rigid syndrome. The scores of the Unified Parkinson's Disease Rating Scale ranged between 19 and 64. The uptake values of the (99m)Tc-TRODAT-1 were 0.868+/-0.136 in the right corpus striatum and 0.865+/-0.118 in the left, as compared with 0.951+/-0.059 and 0.956+/-0.058, respectively for the normal controls. The data were significantly higher than 0.250+/-0.070 and 0.317+/-0.066 respectively for the PD patients. Interestingly, there was a mild decrease in the uptake of (99m)Tc-TRODAT-1 in the putamen and the ratio of putamen and caudate when compared with the normal controls. Although the DAT shows a slight decrease in the putamen of manganism patients as compared with that of the normal controls, the data indicate that the presynaptic dopaminergic terminals are not the main target of chronic manganese intoxication. In addition (99m)Tc-TRODAT-1 SPECT can provide a useful, convenient and inexpensive tool for differentiation between chronic manganism and PD.
长期接触锰可能会诱发类似于特发性帕金森病（PD）的帕金森综合征。然而，锰中毒的临床表现也有一些与PD不同的特征。锰诱导帕金森综合征的机制仍未完全明确。（99m）Tc-TRODAT-1是一种可卡因类似物，可与多巴胺转运体（DAT）位点结合，反映突触前多巴胺能终末的功能。本研究旨在使用（99m）Tc-TRODAT-1评估DAT功能，以研究锰诱导帕金森综合征中突触前多巴胺能终末的完整性。对台湾一家锰铁冶炼厂的4例慢性锰中毒患者进行了脑部（99m）Tc-TRODAT-1单光子发射计算机断层扫描。分别以12例PD患者和12名健康志愿者作为异常对照和正常对照。临床上，所有锰中毒患者均有运动迟缓-强直综合征。统一帕金森病评定量表评分在19至64分之间。（99m）Tc-TRODAT-1在右侧纹状体的摄取值为0.868±0.136，左侧为0.865±0.118，而正常对照分别为0.951±0.059和0.956±0.058。这些数据显著高于PD患者的0.250±0.070和0.317±0.066。有趣的是，与正常对照相比，壳核中（99m）Tc-TRODAT-1的摄取以及壳核与尾状核的比值有轻度下降。虽然与正常对照相比，锰中毒患者壳核中的DAT略有下降，但数据表明突触前多巴胺能终末不是慢性锰中毒的主要靶点。此外，（99m）Tc-TRODAT-1单光子发射计算机断层扫描可为慢性锰中毒和PD的鉴别提供一种有用、便捷且廉价的工具。
