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探究内源性配对联想刺激(ePAS)的干预参数。

Investigating the Intervention Parameters of Endogenous Paired Associative Stimulation (ePAS).

作者信息

Alder Gemma, Signal Nada, Vandal Alain C, Olsen Sharon, Jochumsen Mads, Niazi Imran Khan, Taylor Denise

机构信息

Health and Rehabilitation Research Institute, Auckland University of Technology, Auckland 0627, New Zealand.

Department of Statistics, University of Auckland, Auckland 1142, New Zealand.

出版信息

Brain Sci. 2021 Feb 12;11(2):224. doi: 10.3390/brainsci11020224.

DOI:10.3390/brainsci11020224
PMID:33673171
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7918620/
Abstract

Advances in our understanding of neural plasticity have prompted the emergence of neuromodulatory interventions, which modulate corticomotor excitability (CME) and hold potential for accelerating stroke recovery. Endogenous paired associative stimulation (ePAS) involves the repeated pairing of a single pulse of peripheral electrical stimulation (PES) with endogenous movement-related cortical potentials (MRCPs), which are derived from electroencephalography. However, little is known about the optimal parameters for its delivery. A factorial design with repeated measures delivered four different versions of ePAS, in which PES intensities and movement type were manipulated. Linear mixed models were employed to assess interaction effects between PES intensity (suprathreshold (Hi) and motor threshold (Lo)) and movement type (Voluntary and Imagined) on CME. ePAS interventions significantly increased CME compared to control interventions, except in the case of Lo-Voluntary ePAS. There was an overall main effect for the Hi-Voluntary ePAS intervention immediately post-intervention ( = 0.002), with a sub-additive interaction effect at 30 min' post-intervention ( = 0.042). Hi-Imagined and Lo-Imagined ePAS significantly increased CME for 30 min post-intervention ( = 0.038 and = 0.043 respectively). The effects of the two PES intensities were not significantly different. CME was significantly greater after performing imagined movements, compared to voluntary movements, with motor threshold PES (Lo) 15 min post-intervention ( = 0.012). This study supports previous research investigating Lo-Imagined ePAS and extends those findings by illustrating that ePAS interventions that deliver suprathreshold intensities during voluntary or imagined movements (Hi-Voluntary and Hi-Imagined) also increase CME. Importantly, our findings indicate that stimulation intensity and movement type interact in ePAS interventions. Factorial designs are an efficient way to explore the effects of manipulating the parameters of neuromodulatory interventions. Further research is required to ensure that these parameters are appropriately refined to maximise intervention efficacy for people with stroke and to support translation into clinical practice.

摘要

我们对神经可塑性理解的进展促使了神经调节干预的出现,这种干预可调节皮质运动兴奋性(CME),并具有加速中风恢复的潜力。内源性配对联想刺激(ePAS)涉及将单次外周电刺激(PES)脉冲与源自脑电图的内源性运动相关皮质电位(MRCPs)重复配对。然而,对于其最佳实施参数知之甚少。采用重复测量的析因设计实施了四种不同版本的ePAS,其中对PES强度和运动类型进行了操控。使用线性混合模型评估PES强度(阈上(Hi)和运动阈值(Lo))与运动类型(自主和想象)对CME的交互作用。与对照干预相比,ePAS干预显著增加了CME,但低强度自主ePAS除外。高强度自主ePAS干预在干预后即刻有总体主效应(P = 0.002),在干预后30分钟有次相加交互作用效应(P = 0.042)。高强度想象和低强度想象ePAS在干预后30分钟显著增加了CME(分别为P = 0.038和P = 0.043)。两种PES强度的效果无显著差异。在干预后15分钟,使用运动阈值PES(Lo)时,与自主运动相比,进行想象运动后CME显著更大(P = 0.012)。本研究支持了先前对低强度想象ePAS的研究,并通过说明在自主或想象运动期间给予阈上强度的ePAS干预(高强度自主和高强度想象)也会增加CME,扩展了这些发现。重要的是,我们的研究结果表明刺激强度和运动类型在ePAS干预中存在交互作用。析因设计是探索操控神经调节干预参数效果的有效方法。需要进一步研究以确保适当地优化这些参数,以使中风患者的干预效果最大化,并支持转化为临床实践。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/765b7477f82f/brainsci-11-00224-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/aef4c02ed3e9/brainsci-11-00224-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/6fbd9c78725b/brainsci-11-00224-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/4385c5ef799f/brainsci-11-00224-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/f15fbe7c6f08/brainsci-11-00224-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/e32d5e56b988/brainsci-11-00224-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/7fb8b7db4d9b/brainsci-11-00224-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/765b7477f82f/brainsci-11-00224-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/aef4c02ed3e9/brainsci-11-00224-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/6fbd9c78725b/brainsci-11-00224-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/4385c5ef799f/brainsci-11-00224-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/f15fbe7c6f08/brainsci-11-00224-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/e32d5e56b988/brainsci-11-00224-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/7fb8b7db4d9b/brainsci-11-00224-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d0/7918620/765b7477f82f/brainsci-11-00224-g007.jpg

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EMG- Versus EEG-Triggered Electrical Stimulation for Inducing Corticospinal Plasticity.
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