Based on H-reflex data, spinal mechanisms are proposed to be responsible for the first 50-80 ms of the transcranial magnetic stimulation (TMS)-induced silent period. As several methodological issues can compromise H-reflex validity as a measure of motoneuron excitability, this study used transmastoid stimulation to elicit cervicomedullary motor evoked potentials (CMEPs) during the silent period. Eleven subjects made 1-3 visits which involved 32 or 44 brief (~3 s) isometric elbow flexor contractions at 25 % of maximal torque. During each contraction, transmastoid stimulation was delivered in isolation to elicit an unconditioned CMEP and at interstimulus intervals (ISIs) ranging from 50 to 150 ms after TMS to elicit a conditioned CMEP. Stimulus intensities for TMS and transmastoid stimulation were set to elicit a silent period of ~200 ms and an unconditioned CMEP of 15, 50, or 85 % of the maximal compound muscle action potential (M ), respectively. At all ISIs and intensities of transmastoid stimulation, the conditioned CMEP was significantly smaller than the unconditioned CMEP (p< 0.001). However, suppression of the conditioned CMEP was significantly less at 85 % compared to 15 or 50 % M (p = 0.001). Contrary to published H-reflex data, the conditioned CMEP did not recover within 50-80 ms, remaining significantly suppressed at the longest ISI tested (150 ms). These data suggest the spinal portion of the TMS-evoked silent period is considerably longer than reported previously. Transmastoid stimulation, unlike peripheral nerve stimulation, does not impact proprioceptive inflow to motoneurons. Hence, relative to the H-reflex, the CMEP will be subjected to greater afferent-mediated disfacilitation and inhibition due to the TMS-induced muscle twitch.

The cause of Adolescent Idiopathic Scoliosis (AIS) remains unclear, but one proposed cause of AIS is asymmetric vestibular function and the related descending drive to the spine musculature. The objective of this study was to determine if asymmetric vestibular function is present in individuals with AIS. Ten individuals with AIS (8F, 2M) and 10 healthy age- and sex-matched controls were exposed to 10s-long virtual rotations induced by monaural or binaural electrical vestibular stimulation (EVS), and 10s-long real rotations delivered by a rotating chair. Using a forced-choice paradigm, participants indicated their perceived rotation direction (right or left) to stimuli of varying intensity. A Bayesian adaptive algorithm adjusted the stimulus intensity and direction to identify a stimulus level, which we called the direction recognition threshold, at which participants correctly identified the rotation direction 69% of the time. For unilateral vestibular stimuli (monaural EVS), the direction recognition thresholds were more asymmetric in all participants with AIS compared to control participants [(0.22–1.00 mA) vs. (0.01–0.21 mA); p < 0.001]. For bilateral vestibular stimuli, however, the direction recognition thresholds did not differ between groups for either the real or virtual rotations (multiple p > 0.05). Previous reports of semicircular canal orientation asymmetry in individuals with AIS could not explain the magnitude of the vestibular function asymmetry we observed, suggesting a functional cause to the observed vestibular asymmetry. Thus, the present results suggest that a unilateral vestibular dysfunction is linked to AIS, potentially revealing a new path for the screening and monitoring of scoliosis in adolescents.

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