In humans, the primary motor cortex (M1) plays a crucial role in voluntary movement control. M1 receives basal ganglia and cerebellar output, and its activity is regulated by multiple inhibitory and excitatory intracortical (i.e., local) circuits (Di Lazzaro and Ziemann, 2013). In Parkinson’s disease (PD), paired-pulse transcranial magnetic stimulation (TMS) studies have demonstrated the impairment of specific intracortical M1 circuits, and these abnormalities are involved in the pathophysiology of motor dysfunction (Bologna et al., 2018, Guerra et al., 2021, 2019). The most reliable alterations are reduced effectiveness of short-interval intracortical inhibition (SICI), suggesting impaired GABA-A-ergic neurotransmission (Ammann et al., 2020, Berardelli et al., 2008), and abnormally enhanced short-interval intracortical facilitation (SICF), possibly reflecting increased synchronization and hyperexcitability of glutamatergic interneurons in M1 (Guerra et al., 2019, Ni et al., 2013, Shirota et al., 2019, Ziemann, 2020). Changes in long-interval intracortical inhibition (LICI) have also been reported (Berardelli et al., 2008, 1996).

在人类中，初级运动皮层 (M1) 在自主运动控制中起着至关重要的作用。M1 接收基底神经节和小脑输出，其活动受多个抑制性和兴奋性皮质内（即局部）回路的调节（Di Lazzaro 和 Ziemann，2013）。在帕金森病 (PD) 中，配对脉冲经颅磁刺激 (TMS) 研究表明特定皮质内 M1 回路受损，并且这些异常与运动功能障碍的病理生理学有关（Bologna 等，2018，Guerra 等。 , 2021, 2019)。最可靠的改变是短间隔皮质内抑制 (SICI) 的有效性降低，表明 GABA-A 能神经传递受损（Ammann 等人，2020；Berardelli 等人，2008），以及异常增强的短间隔皮质内促进（ SCF), 可能反映了 M1 中谷氨酸能中间神经元的同步性和过度兴奋性增加（Guerra 等，2019，Ni 等，2013，Shirota 等，2019，Ziemann，2020）。长间隔皮质内抑制 (LICI) 的变化也有报道（Berardelli 等人，2008 年，1996 年）。