Evidence for a Window of Enhanced Plasticity in the Human Motor Cortex Following Ischemic Stroke.
Evidence for a Window of Enhanced Plasticity in the Human Motor Cortex Following Ischemic Stroke.
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DOI：
10.1177/1545968321992330
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发表时间：
2021-04
影响因子：
4.2
通讯作者：
Rothwell JC
中科院分区：
文献类型：
--
作者：
Hordacre B;Austin D;Brown KE;Graetz L;Pareés I;De Trane S;Vallence AM;Koblar S;Kleinig T;McDonnell MN;Greenwood R;Ridding MC;Rothwell JC
在临床前模型中，中风后早期的行为训练比延迟训练产生更大的收益。这种影响被认为是通过增加和广泛重组大脑中的突触连接来实现的。它被认为是一个自发的生物恢复期，在此期间突触可塑性增加。以寻找在缺血性中风后几周和几个月内人类大脑突触可塑性发生类似变化的证据。我们使用连续theta爆发式刺激(CTBS)来重复激活运动皮质中的突触。这启动了突触可塑性的早期阶段，暂时降低了皮质的兴奋性和运动诱发电位(MEP)的幅度。因此，CTB对MEP的影响越大，推测的突触可塑性水平就越高。数据是从不同的队列(澳大利亚和英国)收集的。在每个队列中，在中风后的几周到几个月内进行了一系列测量。对31例卒中幸存者(澳大利亚，66.6±17.8岁)的患侧运动皮质和29例卒中幸存者(英国，68.2±9.8岁)的对侧运动皮质进行了为期6个月的观察。CTBS对大脑皮质兴奋性的抑制在卒中后不久在对侧大脑半球最为显著，在随后的治疗中逐渐减弱(p=0.030)。在同侧大脑半球的12个月随访期内，CTBS的反应没有差别(p=0.903)。我们的结果首次提供了与中风后人脑突触可塑性增强时期一致的神经生理学证据。在此期间给予的行为训练可能在支持中风后恢复方面特别有效。
In pre-clinical models, behavioral training early after stroke produces larger gains compared with delayed training. The effects are thought to be mediated by increased and widespread reorganization of synaptic connections in the brain. It is viewed as a period of spontaneous biological recovery during which synaptic plasticity is increased. To look for evidence of a similar change in synaptic plasticity in the human brain in the weeks and months after ischemic stroke. We used continuous theta burst stimulation (cTBS) to activate synapses repeatedly in the motor cortex. This initiates early stages of synaptic plasticity that temporarily reduces cortical excitability and motor evoked potential (MEP) amplitude. Thus, the greater the effect of cTBS on the MEP, the greater the inferred level of synaptic plasticity. Data were collected from separate cohorts (Australia and UK). In each cohort, serial measurements were made in the weeks to months following stroke. Data were obtained for the ipsilesional motor cortex in 31 stroke survivors (Australia, 66.6±17.8 years) over 12 months and the contralesional motor cortex in 29 stroke survivors (UK, 68.2±9.8 years) over 6 months. Depression of cortical excitability by cTBS was most prominent shortly after stroke in the contralesional hemisphere and diminished over subsequent sessions (p=0.030). cTBS response did not differ across the 12 month follow-up period in the ipsilesional hemisphere (p=0.903). Our results provide the first neurophysiological evidence consistent with a period of enhanced synaptic plasticity in the human brain after stroke. Behavioral training given during this period may be especially effective in supporting post-stroke recovery.
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