Physical and Rehabilitation Medicine Institute, General Hospital, Medical School of the University of Sao Paulo, Sao Paulo, Brazil.
Neuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Clin Neurophysiol. 2020 Aug;131(8):1806-1814. doi: 10.1016/j.clinph.2020.04.166. Epub 2020 May 22.
The gait recovery in spinal cord injury (SCI) seems to be partially related to the reorganization of cerebral function; however, the neural mechanisms and the respective biomarkers are not well known. This study tested the hypothesis that enhanced beta-band oscillations may be a marker of compensatory neural plasticity during the recovery period in SCI. We tested this hypothesis at baseline in SCI subjects and also in response to cortical stimulation with transcranial direct current stimulation (tDCS) combined with robotic-assisted gait training (RAGT).
In this neurophysiological analysis of a randomized controlled trial, thirty-nine patients with incomplete SCI were included. They received 30 sessions of either active or sham anodal tDCS over the primary motor area for 20 min combined with RAGT. We analyzed the Electroencephalography (EEG) power spectrum and task-related power modulation of EEG oscillations, and their association with gait function indexed by Walk Index for Spinal Cord Injury (WISCI-II). Univariate and multivariate linear/logistic regression analyses were performed to identify the predictors of gait function and recovery.
Consistent with our hypothesis, we found that in the sensorimotor area: (1) Anodal tDCS combined with RAGT can modulate high-beta EEG oscillations power and enhance gait recovery; (2) higher high-beta EEG oscillations power at baseline can predict baseline gait function; (3) high-beta EEG oscillations power at baseline can predict gait recovery - the higher power at baseline, the better gait recovery; (4) decreases in relative high-beta power and increases in beta power decrease during walking are associated with gait recovery.
Enhanced EEG beta oscillations in the sensorimotor area in SCI subjects may be part of a compensatory mechanism to enhance local plasticity. Our results point to the direction that interventions enhancing local plasticity such as tDCS combined with robotic training also lead to an immediate increase in sensorimotor cortex activation, improvement in gait recovery, and subsequent decrease in high-beta power. These findings suggest that beta-band oscillations may be potential biomarkers of gait function and recovery in SCI.
These findings are significant for rehabilitation in SCI patients, and as EEG is a portable, inexpensive, and easy-to-apply system, the clinical translation is feasible to follow better the recovery process and to help to individualize rehabilitation therapies of SCI patients.
脊髓损伤（SCI）患者的步态恢复似乎与大脑功能的重组部分相关；然而，神经机制和相应的生物标志物尚不清楚。本研究假设增强的β波段振荡可能是 SCI 恢复期代偿性神经可塑性的标志物，并对此进行了测试。我们在 SCI 患者的基线和经颅直流电刺激（tDCS）联合机器人辅助步态训练（RAGT）后的皮质刺激时对此假设进行了测试。
在这项针对随机对照试验的神经生理学分析中，纳入了 39 名不完全性 SCI 患者。他们接受了 30 次真/假阳极 tDCS 治疗，每次 20 分钟，刺激部位为初级运动区，同时接受 RAGT。我们分析了脑电图（EEG）频谱和与任务相关的 EEG 振荡的功率调制，并将其与脊髓损伤步行指数（WISCI-II）评估的步态功能相关联。采用单变量和多变量线性/逻辑回归分析来确定步态功能和恢复的预测因素。
与我们的假设一致，我们发现：（1）tDCS 联合 RAGT 可以调节感觉运动区的高β EEG 振荡功率，并增强步态恢复；（2）基线时较高的高β EEG 振荡功率可以预测基线步态功能；（3）基线时的高β EEG 振荡功率可以预测步态恢复-基线时的功率越高，步态恢复越好；（4）步行时相对高β功率的降低和β功率的增加与步态恢复相关。
SCI 患者感觉运动区增强的 EEGβ 振荡可能是增强局部可塑性的代偿机制的一部分。我们的研究结果表明，增强局部可塑性的干预措施，如 tDCS 联合机器人训练，也会导致感觉运动皮层激活的即时增加，步态恢复的改善，以及随后的高β功率降低。这些发现表明，β 波段振荡可能是 SCI 患者步态功能和恢复的潜在生物标志物。
这些发现对 SCI 患者的康复具有重要意义，由于 EEG 是一种便携式、廉价且易于应用的系统，因此临床转化是可行的，可以更好地跟踪恢复过程，并帮助对 SCI 患者的康复治疗进行个体化。
