Abstract

Short interval intracortical facilitation (SICF) may be elicited by a paired pulse transcranial magnetic stimulation (TMS) paradigm, whereby a suprathreshold first stimulus (S1) precedes a perithreshold second stimulus (S2). Other facilitatory circuits can be probed by TMS such as intracranial facilitation, however the cortical contributions to these circuits may lie partially outside of M1. SICF as such represents a unique analog to M1 inhibitory circuits such as short interveal intracortical circuits. The aim of the present study was to provide insight into the physiological processes underlying the development of SICF using the threshold tracking TMS technique which was recently demonstrated to have significant reliability. TMS studies were undertaken on 35 healthy controls, using either a 90 mm circular and 70 mm figure of eight coil, and one of two targets (0.2 and 1.0 mV) tracked. The motor evoked potential (MEP) responses were recorded from the abductor pollicis brevis. SICF was consistently evident between interstimulus intervals (ISI) of 1–5 ms (P < 0.001), with two peaks occurring ISIs 1.5 and 3 ms when using the circular coil. A significant SICF reduction (F = 5.631, P < 0.05) was evident with the higher tracking target, while SICF increased when stimulating with the figure of eight coil. While there was a correlation between SICF and CSP duration, there was no relationship between SICF and SICI or ICF. Age appeared to have no influence on SICF, SICI, or ICF. Findings from the present work suggest that SICF appears to be mediated by I-wave facilitation.

Highlights

  • Cortical excitability reflects a balance between inhibitory and facilitatory neuronal circuits projected through pyramidal tract output tracts (Di Lazzaro et al, 2008; Ni and Chen, 2008; Rusu et al, 2014)

  • The first threshold tracking Transcranial magnetic simulation (TMS) paradigm recorded short interval intracortical facilitation (SICF), which developed between interstimulus intervals (ISI) of 1–5 ms (Figure 2A)

  • The threshold changes evident for SICF at each ISI were significantly different from the resting motor threshold (X2 of 51.610, P < 0.001), a notion confirmed on post-hoc testing (P < 0.001), and there was a significant correlation of SICF recorded at each of the ISI levels (Table 1)

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Summary

Introduction

Cortical excitability reflects a balance between inhibitory and facilitatory neuronal circuits projected through pyramidal tract output tracts (Di Lazzaro et al, 2008; Ni and Chen, 2008; Rusu et al, 2014). Increasing the S1 intensity toward peri- and suprathreshold levels, followed by an S2 stimulus at perithreshold intensity, leads to synergistic levels of facilitation, a phenomenon termed short interval intracortical facilitation (SICF; Tokimura et al, 1996; Ziemann et al, 1996c). Facilitatory I-wave interactions produced by S1 and S2 stimulation within the motor cortex have been postulated as a likely physiological mechanism for SICF, a notion supported by epidural recordings (Di Lazzaro et al, 1999). It has been reported that disinhibition of neuronal circuits mediating I-wave generation could contribute to SICF development (Wagle-Shukla et al, 2009)

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