Neurorehabilitation and Neural Repair ( IF 4.2 ) Pub Date : 2021-02-12 , DOI: 10.1177/1545968321992330 Brenton Hordacre 1 , Duncan Austin 2 , Katlyn E Brown 2 , Lynton Graetz 3 , Isabel Pareés 4, 5 , Stefania De Trane 6, 7, 8 , Ann-Maree Vallence 9, 10, 11 , Simon Koblar 3, 12 , Timothy Kleinig 3, 12 , Michelle N McDonnell 13 , Richard Greenwood 8 , Michael C Ridding 1 , John C Rothwell 2
Background
In preclinical 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.
Objective
To look for evidence of a similar change in synaptic plasticity in the human brain in the weeks and months after ischemic stroke.
Methods
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 amplitude. Thus, the greater the effect of cTBS on the motor-evoked potential, 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.
Results
Depression of cortical excitability by cTBS was most prominent shortly after stroke in the contralesional hemisphere and diminished over subsequent sessions (P = .030). cTBS response did not differ across the 12-month follow-up period in the ipsilesional hemisphere (P = .903).
Conclusions
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 poststroke recovery.
中文翻译:
缺血性中风后人类运动皮层可塑性增强的窗口的证据
背景
在临床前模型中,与延迟训练相比,中风后早期的行为训练能产生更大的收益。这种效应被认为是通过大脑中突触连接的增加和广泛重组来介导的。它被视为自发生物恢复的时期,在此期间突触可塑性增加。
客观的
寻找缺血性中风后数周和数月内人脑突触可塑性发生类似变化的证据。
方法
我们使用连续θ爆发刺激(cTBS)来重复激活运动皮层中的突触。这启动了突触可塑性的早期阶段,暂时降低了皮质兴奋性和运动诱发电位振幅。因此,cTBS 对运动诱发电位的影响越大,推断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,在中风后数周至数月内进行连续测量。我们获得了 31 名中风幸存者(澳大利亚,66.6 ± 17.8 岁)12 个月内的同侧运动皮层数据和 29 名中风幸存者(英国,68.2 ± 9.8 岁)6 个月内的对侧运动皮层数据。
结果
cTBS 对皮质兴奋性的抑制在中风后不久对侧半球最为明显,并在随后的疗程中减弱 ( P = .030)。在 12 个月的随访期内,同病半球的 cTBS 反应没有差异 ( P = .903)。
结论
我们的研究结果提供了第一个神经生理学证据,与中风后人脑突触可塑性增强的时期一致。在此期间进行的行为训练可能对支持中风后恢复特别有效。