Table of Contents Author Guidelines Submit a Manuscript
Neural Plasticity
Volume 2018, Article ID 8265427, 9 pages
https://doi.org/10.1155/2018/8265427
Research Article

Corticospinal and Spinal Excitabilities Are Modulated during Motor Imagery Associated with Somatosensory Electrical Nerve Stimulation

INSERM UMR1093-CAPS, UFR des Sciences du Sport, Université Bourgogne Franche-Comté, 21000 Dijon, France

Correspondence should be addressed to E. Traverse; rf.engogruob-u@esrevart.eidole

Received 12 December 2017; Revised 20 March 2018; Accepted 27 March 2018; Published 23 April 2018

Academic Editor: Ambra Bisio

Copyright © 2018 E. Traverse et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Motor imagery (MI), the mental simulation of an action, influences the cortical, corticospinal, and spinal levels, despite the lack of somatosensory afferent feedbacks. The aim of this study was to analyze the effect of MI associated with somatosensory stimulation (SS) on the corticospinal and spinal excitabilities. We used transcranial magnetic stimulation and peripheral nerve stimulation to induce motor-evoked potentials (MEP) and H-reflexes, respectively, in soleus and medialis gastrocnemius (MG) muscles of the right leg. Twelve participants performed three tasks: (1) MI of submaximal plantar flexion, (2) SS at 65 Hz on the posterior tibial nerve with an intensity below the motor threshold, and (3) MI + SS. MEP and H-reflex amplitudes were recorded before, during, and after the tasks. Our results confirmed that MI increased corticospinal excitability in a time-specific manner. We found that tended to potentiate MEP amplitude of the MG muscle compared to MI alone. We confirmed that SS decreased spinal excitability, and this decrease was partially compensated when combined with MI, especially for the MG muscle. The increase of CSE could be explained by a modulation of the spinal inhibitions induced by SS, depending on the amount of afferent feedbacks.