Brown Peter, Mazzone Paolo, Oliviero Antonio, Altibrandi Maria Grazia, Pilato Fabio, Tonali Pietro A, Di Lazzaro Vincenzo
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London WCIN 3BG, UK.
Exp Neurol. 2004 Aug;188(2):480-90. doi: 10.1016/j.expneurol.2004.05.009.
The pattern of neuronal discharge within the basal ganglia is disturbed in Parkinson's disease (PD). In particular, there is a tendency for neuronal elements to synchronise at around 20 Hz in the absence of dopaminergic treatment, whereas this activity can be replaced by spontaneous synchronisation at much higher frequencies (>70 Hz) following dopaminergic treatment [J. Neurosci. 21 (2001) 1033; Brain 126 (2003) 2153]. In two PD patients (3 sides), we show that stimulating the subthalamic area at around 20 Hz exacerbates synchronisation at similar frequencies in the globus pallidus interna, the major output structure of the human basal ganglia. In contrast, stimulating the subthalamic area at >70 Hz suppresses pallidal activity at about 20 Hz. Clinically, stimulation of the subthalamic area at similar high frequencies reverses parkinsonism and forms the basis of therapeutic deep brain stimulation in PD. The results point to a possible common mechanism by which both dopaminergic treatment associated synchronisation of subthalamic activity at very high frequency and synchronisation imposed by therapeutic stimulation of the subthalamic area inhibit an abnormal and potentially deleterious synchronisation of basal ganglia output at around 20 Hz. If this activity is unchecked by synchronisation at higher frequency, then pathological 20-Hz oscillations may cascade through the basal ganglia, increasing at subsequent levels of processing.
帕金森病（PD）患者基底神经节内的神经元放电模式会受到干扰。特别是，在未进行多巴胺能治疗时，神经元成分有在约20赫兹同步的倾向，而在多巴胺能治疗后，这种活动可被更高频率（>70赫兹）的自发同步所取代[《神经科学杂志》21卷（2001年）第1033页；《大脑》126卷（2003年）第2153页]。在两名帕金森病患者（共3侧）中，我们发现以约20赫兹刺激丘脑底区域会加剧苍白球内侧部（人类基底神经节的主要输出结构）中类似频率的同步。相反，以>70赫兹刺激丘脑底区域会抑制约20赫兹的苍白球活动。临床上，以类似高频刺激丘脑底区域可逆转帕金森症状，这也是帕金森病治疗性脑深部刺激的基础。这些结果指出了一种可能的共同机制，即多巴胺能治疗相关的丘脑底活动在非常高频率下的同步以及丘脑底区域治疗性刺激所施加的同步，均抑制了基底神经节输出在约20赫兹时异常且可能有害的同步。如果这种活动未被更高频率的同步所抑制，那么病理性的20赫兹振荡可能会在基底神经节中逐级放大，在后续处理水平上增强。
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