Meng Detao, Zhuang Ping, Hallett Mark, Zhang Yuqing, Li Jianyu, Hu Yongsheng, Li Yongjie
Beijing Institute of Functional Neurosurgery, Xuanwu Hospital, Capital Medical University and Key Laboratory of Neurodegenerative Diseases (Capital Medical University), Ministry of Education, Beijing, China.
Beijing Institute of Functional Neurosurgery, Xuanwu Hospital, Capital Medical University and Key Laboratory of Neurodegenerative Diseases (Capital Medical University), Ministry of Education, Beijing, China; Center of Parkinson's Disease, Beijing Institute for Brain Disorders, Beijing, China.
J Neurol Sci. 2020 Mar 15;410:116661. doi: 10.1016/j.jns.2019.116661. Epub 2019 Dec 30.
Excessive neuronal activity in the globus pallidus internus (GPi) is believed to promote parkinsonian akinesia/bradykinesia, but not tremor. Parkinsonian tremor is thought to result from dysfunction in the basal ganglia and cerebello-thalamo-cortical circuits. Whether the GPi is involved in tremorgenesis has not been fully elucidated. This study was designed to quantify the characteristics of oscillatory GPi neurons in patients with Parkinson's disease.
Nine patients undergoing surgery were studied. Microelectrode recordings in the GPi and electromyographic (EMG) activity in the limbs were recorded and the mean spontaneous firing rates (MSFRs) were calculated. Spectral analysis was used to assess neuronal oscillatory patterns. Coherence analysis was applied to explore the relationship between oscillatory neurons and EMG.
Of 79 GPi neurons, 50.6% oscillated at the tremor frequency; 25.3% oscillated at β frequency, and 24.1% did not oscillate. The MSFR of all neurons was 81.5 ± 7.4 spikes/s. Among neurons oscillating at tremor frequency, 40% were coherent with the tremor. In four neurons, the pattern changed from tremor frequency to β frequency or vice versa. It appeared that the tremor began before the GPi fired bursts.
Some neuronal activity in the GPi correlates with tremor and this correlation might be due to either feedback, maintenance, or initiation. Since there were examples of EMG tremor prior to GPi activity, initiation seems least likely. The data further support the prediction of the classic pathophysiology model of Parkinson's disease.
内侧苍白球(GPi)中神经元活动过度被认为会导致帕金森病的运动不能/运动迟缓,但不会导致震颤。帕金森病震颤被认为是基底神经节和小脑-丘脑-皮质回路功能障碍所致。GPi是否参与震颤的发生尚未完全阐明。本研究旨在量化帕金森病患者中振荡性GPi神经元的特征。
对9例接受手术的患者进行研究。记录GPi中的微电极记录和肢体的肌电图(EMG)活动,并计算平均自发放电率(MSFRs)。采用频谱分析评估神经元振荡模式。应用相干分析探讨振荡神经元与EMG之间的关系。
在79个GPi神经元中,50.6%以震颤频率振荡;25.3%以β频率振荡,24.1%不振荡。所有神经元的MSFR为81.5±7.4次/秒。在以震颤频率振荡的神经元中,40%与震颤相干。在4个神经元中,模式从震颤频率变为β频率,或反之亦然。似乎震颤在GPi发放爆发之前就开始了。
GPi中的一些神经元活动与震颤相关,这种相关性可能是由于反馈、维持或启动。由于在GPi活动之前有EMG震颤的例子,启动似乎最不可能。这些数据进一步支持了帕金森病经典病理生理学模型的预测。