Li Sheng, Chen Yen-Ting, Francisco Gerard E, Zhou Ping, Rymer William Zev
Department of Physical Medicine and Rehabilitation, McGovern Medical School, University of Texas Health Science Center - Houston and TIRR Memorial Hermann Hospital, Houston, TX, United States.
Shirley Ryan Ability Lab, Chicago, IL, United States.
Front Neurol. 2019 May 10;10:468. doi: 10.3389/fneur.2019.00468. eCollection 2019.
Cortical and subcortical plastic reorganization occurs in the course of motor recovery after stroke. It is largely accepted that plasticity of ipsilesional motor cortex primarily contributes to recovery of motor function, while the contributions of contralesional motor cortex are not completely understood. As a result of damages to motor cortex and its descending pathways and subsequent unmasking of inhibition, there is evidence of upregulation of reticulospinal tract (RST) excitability in the contralesional side. Both animal studies and human studies with stroke survivors suggest and support the role of RST hyperexcitability in post-stroke spasticity. Findings from animal studies demonstrate the compensatory role of RST hyperexcitability in recovery of motor function. In contrast, RST hyperexcitability appears to be related more to abnormal motor synergy and disordered motor control in stroke survivors. It does not contribute to recovery of normal motor function. Recent animal studies highlight laterality dominance of corticoreticular projections. In particular, there exists upregulation of ipsilateral corticoreticular projections from contralesional premotor cortex (PM) and supplementary motor area (SMA) to medial reticular nuclei. We revisit and revise the previous theoretical framework and propose a unifying account. This account highlights the importance of ipsilateral PM/SMA-cortico-reticulospinal tract hyperexcitability from the contralesional motor cortex as a result of disinhibition after stroke. This account provides a pathophysiological basis for post-stroke spasticity and related movement impairments, such as abnormal motor synergy and disordered motor control. However, further research is needed to examine this pathway in stroke survivors to better understand its potential roles, especially in muscle strength and motor recovery. This account could provide a pathophysiological target for developing neuromodulatory interventions to manage spasticity and thus possibly to facilitate motor recovery.
皮质和皮质下的可塑性重组发生在中风后的运动恢复过程中。人们普遍认为，患侧运动皮质的可塑性主要有助于运动功能的恢复，而对侧运动皮质的作用尚未完全明确。由于运动皮质及其下行通路受损，以及随后抑制作用的解除，有证据表明对侧网状脊髓束（RST）兴奋性上调。动物研究和针对中风幸存者的人体研究均表明并支持RST兴奋性过高在中风后痉挛中的作用。动物研究结果表明RST兴奋性过高在运动功能恢复中具有代偿作用。相比之下，RST兴奋性过高似乎与中风幸存者的异常运动协同和运动控制紊乱关系更大。它对正常运动功能的恢复没有帮助。最近的动物研究突出了皮质网状投射的偏侧优势。特别是，从对侧运动前区（PM）和辅助运动区（SMA）到内侧网状核的同侧皮质网状投射存在上调。我们重新审视并修订了先前的理论框架，并提出了一个统一的解释。该解释强调了中风后去抑制导致对侧运动皮质同侧PM/SMA-皮质-网状脊髓束兴奋性过高的重要性。这一解释为中风后痉挛及相关运动障碍，如异常运动协同和运动控制紊乱，提供了病理生理学基础。然而，需要进一步研究来检查中风幸存者中的这条通路，以更好地了解其潜在作用，特别是在肌肉力量和运动恢复方面。这一解释可以为开发神经调节干预措施以管理痉挛并可能促进运动恢复提供一个病理生理学靶点。
