Department of Medicine, University of Auckland , Auckland , New Zealand.
J Neurophysiol. 2018 Dec 1;120(6):2858-2867. doi: 10.1152/jn.00472.2018. Epub 2018 Oct 3.
Bilateral priming is a rehabilitation adjuvant that can improve upper limb motor recovery poststroke. It uses a table-top device to couple the upper limbs together such that active flexion and extension of one wrist leads to passive movement of the opposite wrist in a mirror symmetric pattern. Bilateral priming increases corticomotor excitability (CME) in the primary motor cortex (M1) of the passively driven wrist; however, the neurophysiological mechanisms underlying this increase remain unclear. This study explored these mechanisms by using transcranial magnetic stimulation over the right M1 and recording motor-evoked potentials from the passively driven left extensor carpi radialis of healthy adults. Intracortical measures were recorded before and 5 and 35 min after a single 15-min session of priming. One-millisecond short-interval intracortical inhibition, long-interval intracortical inhibition, late cortical disinhibition (LCD), and intracortical facilitation were recorded with a posterior-anterior (PA) intracortical current, whereas CME and short-interval intracortical facilitation (SICF) were recorded with both PA and anterior-posterior (AP) currents. CME with PA stimulation was also recorded ~1 h postpriming. PA CME was elevated 35 min postpriming and remained elevated ~1 h postpriming. LCD decreased, and AP SICF increased at both 5 and 35 min postpriming. However, these changes in LCD and AP SICF are unlikely to be the cause of the increased PA CME because of the differing timelines of their effects and AP and PA currents activating separate interneuron circuits. These results suggest that bilateral priming does not increase CME through alterations of the intracortical circuits investigated here. NEW & NOTEWORTHY This is the first study to measure how bilateral priming modulates corticomotor excitability with posterior-anterior and anterior-posterior intracortical currents, 1-ms short-interval intracortical inhibition, late cortical disinhibition, intracortical facilitation, and short-interval intracortical facilitation. We found corticomotor excitability with a posterior-anterior current increased by 35 min until ~1 h postpriming. Short-interval intracortical facilitation with an anterior-posterior current was greater for at least 35 min postpriming. This provides further insight into the neurophysiological mechanisms underlying bilateral priming.
双侧启动是一种康复辅助手段，可以改善脑卒中后上肢运动功能的恢复。它使用桌面设备将上肢连接在一起，使得一只手腕的主动屈伸导致对侧手腕以镜像对称的模式被动运动。双侧启动会增加被驱动手腕的初级运动皮层（M1）中的运动皮质兴奋性（CME）；然而，这种增加的神经生理机制尚不清楚。本研究通过使用经颅磁刺激对右侧 M1 进行刺激，并记录健康成年人被驱动的左侧桡侧腕伸肌的运动诱发电位，来探索这些机制。在单次 15 分钟的启动治疗后 5 分钟和 35 分钟记录皮质内测量值。使用后前（PA）皮质内电流记录 1 毫秒短间隔皮质内抑制、长间隔皮质内抑制、晚期皮质去抑制（LCD）和皮质内易化，而使用 PA 和前后（AP）电流记录 CME 和短间隔皮质内易化（SICF）。用 PA 刺激记录 CME 也在启动后约 1 小时记录。PA CME 在启动后 35 分钟升高，并在启动后约 1 小时保持升高。LCD 在启动后 5 分钟和 35 分钟时降低，AP SICF 在启动后 5 分钟和 35 分钟时升高。然而，由于它们的作用时间不同，以及 AP 和 PA 电流激活不同的中间神经元回路，这些 LCD 和 AP SICF 的变化不太可能是导致 PA CME 增加的原因。这些结果表明，双侧启动不会通过改变此处研究的皮质内回路来增加 CME。本研究首次使用后前和前后皮质内电流、1 毫秒短间隔皮质内抑制、晚期皮质去抑制、皮质内易化和短间隔皮质内易化测量双侧启动如何调节运动皮质兴奋性。我们发现，使用后前电流时，CME 在启动后 35 分钟增加，直到启动后约 1 小时。使用前后电流时，SICF 在启动后至少 35 分钟内增加。这为双侧启动的神经生理机制提供了进一步的深入了解。
