Fridman Esteban A, Hanakawa Takashi, Chung Melissa, Hummel Friedhelm, Leiguarda Ramon C, Cohen Leonardo G
Human Cortical Physiology Section, NINDS, NIH, Bethesda, MD 20892-1428, USA.
Brain. 2004 Apr;127(Pt 4):747-58. doi: 10.1093/brain/awh082. Epub 2004 Jan 28.
The substrates that mediate recovery of motor function after stroke are incompletely understood. Several primate and human studies proposed the involvement of the premotor cortex of the lesioned hemisphere. Here, we studied four chronic stroke patients with focal subcortical lesions affecting the corticospinal outflow originating in the primary motor cortex (M1) and good motor recovery. We tested the hypothesis that, in these patients, disruption of activity in the premotor cortex of the lesioned hemisphere by transcranial magnetic stimulation (TMS) would result in degraded behaviour in the paretic hand. TMS was applied to the primary motor cortex, dorsal premotor cortex (PMd) and ventral premotor cortex (PMv) of the affected (M1AH, PMdAH, PMvAH) and intact (M1IH, PMdIH, PMvIH) hemispheres of patients and healthy controls in the setting of a simple reaction time (SRT) paradigm performed with the hand contralateral to the stimulated hemisphere. TMS applied to M1 led to substantial contralateral SRT delays in both groups. TMS applied to PMdAH of patients elicited clear delays in contralateral SRT in the paretic hand, whereas TMS applied to PMdIH of patients or healthy volunteers did not. Motor evoked potentials after stimulation of PMdAH were, on average, larger and had, on average, shorter latency than after stimulation of M1AH. These results indicate that PMdAH participates as a substrate mediating functional recovery of executive motor function in patients with focal lesions of corticospinal outflow originating in M1 and good motor recovery. Our results are consistent with the hypothesis that the dorsal premotor cortex of the affected hemisphere can reorganize to control basic parameters of movement usually assigned to M1 function.
中风后介导运动功能恢复的底物尚未完全明确。一些灵长类动物和人类研究表明，受损半球的运动前区皮质参与其中。在此，我们研究了4例慢性中风患者，他们患有局灶性皮质下病变，影响起源于初级运动皮层（M1）的皮质脊髓传出通路，且运动功能恢复良好。我们测试了这样一个假设：在这些患者中，经颅磁刺激（TMS）破坏受损半球运动前区皮质的活动会导致患侧手的行为能力下降。在对与受刺激半球对侧的手进行简单反应时间（SRT）范式测试时，将TMS分别应用于患者和健康对照的患侧（M1AH、PMdAH、PMvAH）和健侧（M1IH、PMdIH、PMvIH）半球的初级运动皮层、背侧运动前区皮质（PMd）和腹侧运动前区皮质（PMv）。对M1施加TMS导致两组对侧SRT均显著延迟。对患者的PMdAH施加TMS会使患侧手的对侧SRT明显延迟，而对患者或健康志愿者的PMdIH施加TMS则不会。刺激PMdAH后的运动诱发电位平均而言比刺激M1AH后更大，且潜伏期更短。这些结果表明，PMdAH作为一种底物参与介导了起源于M1且运动功能恢复良好的皮质脊髓传出通路局灶性病变患者的执行运动功能的功能恢复。我们的结果与以下假设一致：即受损半球的背侧运动前区皮质可以重新组织，以控制通常由M1功能负责的运动基本参数。
