A positron emission tomography study on the role of nigral lesions in parkinsonism in patients with amyotrophic lateral sclerosis
A positron emission tomography study on the role of nigral lesions in parkinsonism in patients with amyotrophic lateral sclerosis
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DOI：
10.1001/archneur.63.12.1719
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发表时间：
2006-12-01
影响因子：
--
通讯作者：
Kwak, Shin
中科院分区：
文献类型：
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作者：
Hideyama, Takuto;Momose, Toshimitsu;Kwak, Shin
背景资料：肌萎缩侧索硬化症（ALS）患者有时会表现出帕金森综合征，但导致帕金森综合征的病变尚未得到广泛研究。目的：检测黑质纹状体系统功能障碍是否是ALS患者帕金森综合征的原因。设计：在过去10年中，我们神经科病房收治了182名ALS患者，我们抽取了所有符合帕金森综合征和ALS标准的患者。地点：东京大学医院。方法：我们进行了[F-18] L-多巴和[C-11] N-甲基螺哌隆正电子发射断层扫描和Tc-99 m六甲基丙烯胺肟单，对5例表现为明显帕金森综合征的ALS患者进行了光子发射计算机断层扫描研究。两名男性和3名女性患者（平均年龄63.2 ± 5.8岁）平均患有ALS 28.6 ± 21.5个月，平均患有帕金森症15.2 ± 11.4个月。他们的帕金森症的特点是突出的运动迟缓，没有静止性震颤或痴呆。正电子发射断层扫描研究结果表明黑质纹状体功能正常，但单光子发射计算机断层扫描结果显示额颞叶皮质血流量减少。结论：ALS中的帕金森病可能是由于皮质病变而不是黑质纹状体功能障碍造成的，这两种症状都是额颞叶痴呆伴运动神经元疾病（包括经典ALS）的临床表现。
Background: Patients with amyotrophic lateral sclerosis (ALS) sometimes exhibit parkinsonism, but the lesion responsible for parkinsonism has not been extensively studied.Objective: To test whether nigrostriatal system dysfunction is responsible for parkinsonism in ALS.Design: From the 182 ALS patients who were admitted to our neurology ward during the past 10 years, we extracted all the patients who satisfied the criteria of both parkinsonism and ALS.Setting: The University of Tokyo Hospital.Methods: We conducted [F-18]L-dopa and [C-11]N-methylspiperone positron emission tomography and technetium Tc99m hexamethylpropyleneamine oxime single-photon emission computed tomography studies on 5 patients with ALS manifesting overt parkinsonism.Results: Two male and 3 female patients (average age, 63.2 +/- 5.8 years) had ALS for an average of 28.6 +/- 21.5 months and had parkinsonism for an average of 15.2 +/- 11.4 months. Features of their parkinsonism were characterized by outstanding bradykinesia without resting tremor or dementia. The results of positron emission tomography studies indicated normal nigrostriatal function, but those of single-photon emission computed tomography demonstrated decreased blood flow in the frontotemporal cortices.Conclusion: It is likely that parkinsonism in ALS is due to cortical lesions rather than nigrostriatal dysfunction and that both symptoms are the clinical manifestation of frontotemporal dementia with motor neuron diseases, including classic ALS.