Dick J P, Cantello R, Buruma O, Gioux M, Benecke R, Day B L, Rothwell J C, Thompson P D, Marsden C D
Electroencephalogr Clin Neurophysiol. 1987 Mar;66(3):263-74. doi: 10.1016/0013-4694(87)90075-7.
Bereitschaftspotentials (BPs) prior to extension movements of the index finger were studied in normal subjects and in patients with Parkinson's disease. In both, BPs were studied before and after L-DOPA therapy; in addition, the normal subjects were studied after dopamine antagonists. In both patients and normal subjects, L-DOPA caused an increase in the amplitude of the early part of the BP and of the point of peak negativity, just prior to EMG onset (N1) but it did not cause an increase of the late lateralized part of the BP (NS' of Shibasaki); in normal subjects dopaminergic antagonists caused a decrease in the amplitude of the N1. Control experiments suggested that the change caused by L-DOPA was not the result of slower movement or poorer triggering when OFF drugs. For patients with Parkinson's disease there was no correlation between the change in their peak BP negativity (N1) after L-DOPA and their change in clinical mobility; in addition, there was no difference in the peak BP negativity of patients OFF therapy and that of age-matched normals, though there was a slight decrease in the amplitude of the early part of the BP for the patients with Parkinson's disease; this was the same part that had been enlarged by L-DOPA therapy. These findings suggest that the N1 is not affected by Parkinson's disease and that the effect of dopaminergic drugs on the N1 is mediated by actions on dopaminergic mechanisms elsewhere than in the striatum, perhaps in the cerebral cortex itself. The effect of L-DOPA will need to be taken into account in subsequent studies of the BP in Parkinson's disease.
对正常受试者和帕金森病患者食指伸展运动前的运动准备电位（BPs）进行了研究。在这两类人群中，均在左旋多巴治疗前后对BPs进行了研究；此外，还对正常受试者在使用多巴胺拮抗剂后进行了研究。在患者和正常受试者中，左旋多巴均使BP早期部分的幅度以及肌电图开始前（N1）的负峰点增加，但并未使BP后期的偏侧化部分（柴崎的NS'）增加；在正常受试者中，多巴胺能拮抗剂使N1的幅度降低。对照实验表明，左旋多巴引起的变化不是停药时运动变慢或触发能力变差的结果。对于帕金森病患者，左旋多巴治疗后其BP负峰（N1）的变化与临床运动能力的变化之间没有相关性；此外，未接受治疗的患者的BP负峰与年龄匹配的正常受试者的BP负峰没有差异，尽管帕金森病患者BP早期部分的幅度略有降低；这正是左旋多巴治疗使其增大的部分。这些发现表明，N1不受帕金森病影响，多巴胺能药物对N1的作用是通过对纹状体以外其他部位的多巴胺能机制起作用介导的，可能是在大脑皮层本身。在随后对帕金森病患者BP的研究中需要考虑左旋多巴的影响。
