Transpinal and Transcortical Stimulation Alter Corticospinal Excitability and Increase Spinal Output

Abstract

The objective of this study was to assess changes in corticospinal excitability and spinal output following noninvasive transpinal and transcortical stimulation in humans. The size of the motor evoked potentials (MEPs), induced by transcranial magnetic stimulation (TMS) and recorded from the right plantar flexor and extensor muscles, was assessed following transcutaneous electric stimulation of the spine (tsESS) over the thoracolumbar region at conditioning-test (C-T) intervals that ranged from negative 50 to positive 50 ms. The size of the transpinal evoked potentials (TEPs), induced by tsESS and recorded from the right and left plantar flexor and extensor muscles, was assessed following TMS over the left primary motor cortex at 0.7 and at 1.1× MEP resting threshold at C-T intervals that ranged from negative 50 to positive 50 ms. The recruitment curves of MEPs and TEPs had a similar shape, and statistically significant differences between the sigmoid function parameters of MEPs and TEPs were not found. Anodal tsESS resulted in early MEP depression followed by long-latency MEP facilitation of both ankle plantar flexors and extensors. TEPs of ankle plantar flexors and extensors were increased regardless TMS intensity level. Subthreshold and suprathreshold TMS induced short-latency TEP facilitation that was larger in the TEPs ipsilateral to TMS. Noninvasive transpinal stimulation affected ipsilateral and contralateral actions of corticospinal neurons, while corticocortical and corticospinal descending volleys increased TEPs in both limbs. Transpinal and transcortical stimulation is a noninvasive neuromodulation method that alters corticospinal excitability and increases motor output of multiple spinal segments in humans.

Transspinal constant-current long-lasting stimulation: a new method to induce cortical and corticospinal plasticity

“…MEP excitability is influenced by single-pulse transspinal conditioning stimuli, is decreased when EPSPs for MEPs and TEPs are summated (Knikou 2014), and is increased at intervals consistent with MEP facilitation by peripheral nerve . While LTP typically results from repetitive stimulus pairs timed with presynaptic potentials to arrive before postsynaptic potentials, non-Hebbian LTP in the thalamus, cerebellar circuits, and spinal lamina I neurons has been reported (Naka et al 2013;Piochon et al 2013;Sieber et al 2013).…”

“…Single TMS pulses over the left primary motor cortex were delivered with a Magstim 200 2 stimulator (Magstim) with a double-cone coil (diameter 110 mm) placed so the current of the coil flowed from a posterior to an anterior direction. Procedures were similar to those we have previously utilized (Hanna-Boutros et al 2015;Knikou 2014;Knikou et al 2013). The point where the lines between the inion and glabellum and the left and right ear tragus met was marked on an EEG cap.…”

“…The latency of the TA MEP and TEP of each muscle was measured based on the cumulative sum technique on the rectified waveform average (Brinkworth and Türker 2003;Ellaway 1978;Knikou 2014).…”

“…We have demonstrated that the transspinal stimulation-induced TEPs in arm and leg muscles are increased when the excitability of peripheral nerves is altered or when descending and ascending inputs are synchronized to meet at the spinal cord (Einhorn et al 2013;Knikou 2013aKnikou , 2013bKnikou , 2014. On the basis of these findings, we hypothesized that transspinal stimulation induces cortical, corticospinal, and spinal neuroplasticity.…”

“…Electrical stimulation delivered epidurally or transcutaneously to the spinal cord generates compound action potentials or transspinal evoked potentials (TEPs) in arm and leg muscles with distinct neurophysiological characteristics (Einhorn et al 2013;Knikou 2013aKnikou , 2013bKnikou , 2014Maruyama et al 1982). TEPs are mediated mostly by direct nonsynaptic activation of motoneurons and indirect transsynaptic excitation of descending projections and local spinal interneuron circuits (Maruyama et al 1982;Sharpe and Jackson 2014).…”