A Unifying Pathophysiological Account for Post-stroke Spasticity and Disordered Motor Control
A Unifying Pathophysiological Account for Post-stroke Spasticity and Disordered Motor Control
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DOI：
10.3389/fneur.2019.00468
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发表时间：
2019-05-10
影响因子：
3.4
通讯作者：
Rymer, William Zev
中科院分区：
文献类型：
--
作者：
Li, Sheng;Chen, Yen-Ting;Rymer, William Zev
脑卒中后运动功能恢复过程中会发生皮质和皮质下的可塑性重组。同侧运动皮层的可塑性对运动功能的恢复起主要作用，而对侧运动皮层的作用尚不完全清楚。由于运动皮层及其下行通路的损伤以及随后的抑制作用的暴露，有证据表明对侧的网状脊髓束（reticulosporinal tract，简称CTST）兴奋性上调。动物研究和对中风幸存者的人体研究都表明并支持过度兴奋在中风后痉挛状态中的作用。动物实验的结果证明了过度兴奋在运动功能恢复中的代偿作用。相反，在中风幸存者中，过度兴奋似乎与异常的运动协同和运动控制障碍更相关。它不有助于恢复正常的运动功能。最近的动物研究强调了皮质网状投射的偏侧优势。特别是，存在上调同侧皮质网状投射从对侧运动前皮质（PM）和补充运动区（SMA）的内侧网状核。我们重新审视和修改以前的理论框架，并提出一个统一的帐户。该解释强调了卒中后抑制解除导致的对侧运动皮层的同侧PM/SMA-皮质-网状脊髓束过度兴奋的重要性。这一解释为脑卒中后痉挛和相关运动障碍，如运动协同异常和运动控制障碍提供了病理生理学基础。然而，需要进一步的研究来检查中风幸存者的这一途径，以更好地了解其潜在的作用，特别是在肌肉力量和运动恢复方面。这个帐户可以提供一个病理生理目标，发展神经调节干预，以管理痉挛，从而可能促进运动恢复。
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.