Department of Exercise Sciences, University of Auckland, Auckland, New Zealand.
Centre for Brain Research, University of Auckland, Auckland, New Zealand.
J Neurophysiol. 2020 May 1;123(5):1775-1790. doi: 10.1152/jn.00561.2019. Epub 2020 Mar 18.
Stroke is a leading cause of death and disability worldwide with many people left with impaired motor function. Evidence from experimental animal models of stroke indicates that reducing motor cortex inhibition may facilitate neural plasticity and motor recovery. This study compared primary motor cortex (M1) inhibition measures over the first 12 wk after stroke with a cohort of age-similar healthy controls. The excitation-inhibition ratio and gamma-aminobutyric acid (GABA) neurotransmission within M1 were assessed using magnetic resonance spectroscopy and threshold hunting paired-pulse transcranial magnetic stimulation respectively. Upper limb impairment and function were assessed with the Fugl-Meyer Upper Extremity Scale and Action Research Arm Test. Patients with a functional corticospinal pathway had motor-evoked potentials on the paretic side and exhibited better recovery from upper limb impairment and recovery of function than patients without a functional corticospinal pathway. Compared with age-similar controls, the neurochemical balance in terms of the excitation-inhibition ratio was greater within contralesional M1 in patients with a functional corticospinal pathway. There was evidence for elevated long-interval inhibition in both ipsilesional and contralesional M1 compared with controls. Short-interval inhibition measures differed between the first and second phases, with evidence for elevation of the former only in ipsilesional M1 and no evidence of disinhibition for the latter. Overall, findings from transcranial magnetic stimulation indicate an upregulation of GABA-mediated tonic inhibition in M1 early after stroke. Therapeutic approaches that aim to normalize inhibitory tone during the subacute period warrant further investigation. Magnetic resonance spectroscopy indicated higher excitation-inhibition ratios within motor cortex during subacute recovery than age-similar healthy controls. Measures obtained from adaptive threshold hunting paired-pulse transcranial magnetic stimulation indicated greater tonic inhibition in patients compared with controls. Therapeutic approaches that aim to normalize motor cortex inhibition during the subacute stage of recovery should be explored.
中风是全球范围内导致死亡和残疾的主要原因，许多患者遗留运动功能障碍。中风实验动物模型的证据表明，减少运动皮层抑制可能促进神经可塑性和运动功能恢复。本研究比较了中风后前 12 周内初级运动皮层（M1）抑制测量值与一组年龄相似的健康对照组。使用磁共振波谱和阈上钩双边脉冲经颅磁刺激分别评估 M1 内的兴奋-抑制比和γ-氨基丁酸（GABA）神经传递。使用 Fugl-Meyer 上肢量表和动作研究上肢测试评估上肢损伤和功能。有功能皮质脊髓束的患者在瘫痪侧有运动诱发电位，表现出比无功能皮质脊髓束的患者更好的上肢损伤恢复和功能恢复。与年龄相似的对照组相比，有功能皮质脊髓束的患者对侧 M1 内的神经化学平衡方面的兴奋-抑制比更大。与对照组相比，双侧 M1 均存在长潜伏期抑制升高的证据。与对照组相比，短潜伏期抑制测量值在第一和第二阶段之间存在差异，仅在同侧 M1 中存在前者的升高，而后者没有抑制作用的证据。总的来说，经颅磁刺激的结果表明，中风后早期 M1 中 GABA 介导的紧张性抑制上调。旨在亚急性期正常化抑制作用的治疗方法值得进一步研究。磁共振波谱显示，亚急性恢复期运动皮层的兴奋-抑制比高于年龄相似的健康对照组。自适应阈上钩双边脉冲经颅磁刺激获得的测量值表明，患者的紧张性抑制比对照组更大。旨在亚急性期恢复期间正常化运动皮层抑制的治疗方法应进行探索。
