Effects of repetitive transcranial magnetic stimulation on recovery of function after spinal cord injury

Abstract

A major goal of rehabilitation strategies after spinal cord injury (SCI) is to enhance the recovery of function. One possible avenue to achieve this goal is to strengthen the efficacy of the residual neuronal pathways. Noninvasive repetitive transcranial magnetic stimulation (rTMS) has been used in patients with motor disorders as a tool to modulate activity of corticospinal, cortical, and subcortical pathways to promote functional recovery. This article reviews a series of studies published during the last decade that used rTMS in the acute and chronic stages of paraplegia and tetraplegia in humans with complete and incomplete SCI. In the studies, rTMS has been applied over the arm and leg representations of the primary motor cortex to target 3 main consequences of SCI: sensory and motor function impairments, spasticity, and neuropathic pain. Although some studies demonstrated that consecutive sessions of rTMS improve aspects of particular functions, other studies did not show similar effects. We discuss how rTMS parameters and postinjury reorganization in the corticospinal tract, motor cortical, and spinal cord circuits might be critical factors in understanding the advantages and disadvantages of using rTMS in patients with SCI. The available data highlight the limited information on the use of rTMS after SCI and the need to further understand the pathophysiology of neuronal structures affected by rTMS to maximize the potential beneficial effects of this technique in humans with SCI.

Keywords: Corticospinal tracts; Motor cortex; Neuroplasticity; Rehabilitation.

Conflict of interest statement

We have no conflicts of interest to disclose.

Copyright © 2015 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.

Figures

Figure 1.

Schematic illustration of the effects of high (A) and low (B) frequencies rTMS on corticospinal descending volleys. Top diagrams represent possible sites and structures of central circuits activated by TMS. Horizontal arrows represent excitatory inputs to the corticospinal cells from excitatory interneurons. Bottom trances indicate the epidural volleys elicited by TMS before (black) and after 5 Hz (red) and 1 Hz rTMS (green), respectively. Note that after 5 Hz rTMS the amplitude of D-wave is increased, the amplitude of the I3-wave is increased and a late I4-wave appears, and that after 1 Hz rTMS the amplitude of the later I-wave is reduced. (Modified with permission from Di Lazzaro et al., 2010).

Figure 2.

The effect of voluntary contraction on short-interval intracortical inhibition (SICI, A) and long-interval intracortical inhibition (LICI, B) in healthy controls and patients with SCI. Traces show MEPs of first dorsal interosseous muscle elicited at rest (top) and during 25% of maximal voluntary contraction (MVC, bottom). Black and red traces represent test MEP and conditioned (Cond.) MEP, respectively. Conditioning stimulation (CS, black arrows) preceded test stimulation (gray arrows) by 2 ms for SICI and 100 ms for LICI. On each bar graph, 25% of MVCADJ represents the condition in which the TMS intensity was adjusted so that the size of test MEP during 25% MVC was matched to rest. Note that LICI was decreased during voluntary contraction compared to at rest in healthy controls but not in SCI patients. SICI was decreased during voluntary contraction in both subject groups. (Modified with permission from Barry et al., 2013).

Figure 3.

A. The effect of 5 Hz rTMS over M1 on the soleus H-reflex. Note that the H-reflex was suppressed when the rTMS intensity was higher than 0.92 times the resting motor evoked potential (MEP) threshold (MT), and that the suppression of the H-reflex was gradually increased according to the rTMS intensity. B. The effect of rTMS on the heteronymous Ia facilitation of the soleus H-reflex. Traces show the control H-reflex (H, black), the H-reflex conditioned by rTMS (rTMS+H, gray), the size adjusted rTMS-conditioned H-reflex (rTMS+H1, blue), the H-reflex with preceded femoral nerve stimulation (FN+H, green), and the size adjusted rTMT-conditioned H-reflex with preceded femoral nerve stimulation (rTMS+FN+H1). Note that rTMS suppressed the soleus H-reflex (gray bar), and that the heteronymous Ia facilitation of the H-reflex (green bar) was attenuated by the conditioning rTMS (red bar). (Modified with permission from Perez et al., 2005).

Figure 4.

Motor evoked potentials elicited by cervicomedullary stimulation (CMEPs) during index finger abduction (black trace) and precision grip (red traces) in healthy controls and patients with SCI. Rectified traces of CMEPs are illustrated (A, C, E). The dotted vertical lines indicated the approximate time of CMEP onset and the CMEP responses diverge. Left figures represent data from the mean of all subjects (black bars) and individual subjects (open circles) (B, D, F). Note that the size of CMEPs decreased during precision grip compared to index finger abduction in healthy controls and in SCI patients with taking baclofen but remains unchanged in SCI patients without taking baclofen. (Modified with permission from Bunday et al., 2014).