Shinotoh H, Snow B J, Chu N S, Huang C C, Lu C S, Lee C, Takahashi H, Calne D B
Neurodegenerative Disorders Centre, University of British Columbia, Vancouver, Canada.
Neurology. 1997 Apr;48(4):1053-6. doi: 10.1212/wnl.48.4.1053.
We performed PET on four patients with chronic industrial Mn intoxication; presynaptic and postsynaptic dopaminergic function were measured with [18F]6-fluoro-L-dopa (6FD) and [11C]raclopride (RAC). All patients had a rigid-akinetic syndrome; they had no sustained benefit from L-dopa. Influx constants (Ki) of 6FD were normal in the caudate and putamen. RAC binding was mildly reduced in the caudate and normal in the putamen. We conclude that nigrostriatal dopaminergic dysfunction is not responsible for the parkinsonism caused by chronic Mn intoxication. The pathology is likely to be downstream of the dopaminergic projection.
我们对4例慢性工业性锰中毒患者进行了正电子发射断层扫描（PET）；用[18F]6-氟-L-多巴（6FD）和[11C]雷氯必利（RAC）测量突触前和突触后多巴胺能功能。所有患者均有强直-运动不能综合征；他们未从左旋多巴中获得持续益处。尾状核和壳核中6FD的流入常数（Ki）正常。尾状核中RAC结合轻度降低，壳核中正常。我们得出结论，黑质纹状体多巴胺能功能障碍不是慢性锰中毒所致帕金森症的原因。其病理可能位于多巴胺能投射的下游。
