Hayase N, Miyashita N, Endo K, Narabayashi H
Neurological Clinic, Meguro, Tokyo, Japan.
Stereotact Funct Neurosurg. 1998;71(1):20-8. doi: 10.1159/000029643.
Microrecordings were performed during pallidotomy and thalamotomy for Parkinson's disease (PD). Neuronal activity in globus pallidus (GP) was in general agreement with previous studies of human and primate models of PD. Neuronal activity, where frequency of tremor appeared to oscillate independently from peripheral input, was encountered in GPi. In contrast, neuronal activity in Vim regarding frequency of firing also correlated with tremor and was passively driven by kinesthetic stimuli with a somatotopic arrangement. Pallidal lesions based on microrecording induced relative reductions of tremor, while small Vim lesions immediately alleviated tremor. Basal ganglia pathology due to dopamine depletion could generate oscillatory neuronal activity in GPi, which may cause tremor. However, peripheral feedback to the motor cortex via Vim is also significant for tremorgenesis, because Vim may be an excitatory driving source for motor cortical neurons. Thus, a Vim lesion could reduce excitability of the motor cortical neurons and abolish tremor.
在帕金森病（PD）的苍白球切开术和丘脑切开术期间进行了微记录。苍白球（GP）中的神经元活动总体上与先前关于人类和灵长类PD模型的研究一致。在苍白球内侧部（GPi）中遇到了神经元活动，其中震颤频率似乎独立于外周输入而振荡。相比之下，丘脑腹中间核（Vim）中关于放电频率的神经元活动也与震颤相关，并且由具有躯体定位排列的动觉刺激被动驱动。基于微记录的苍白球损伤导致震颤相对减轻，而小的Vim损伤立即缓解了震颤。多巴胺耗竭引起的基底神经节病理改变可在GPi中产生振荡性神经元活动，这可能导致震颤。然而，通过Vim向运动皮层的外周反馈对震颤的发生也很重要，因为Vim可能是运动皮层神经元的兴奋性驱动源。因此，Vim损伤可降低运动皮层神经元的兴奋性并消除震颤。
