Zmeykina, E. | Search bioRxiv

bioRxiv2020

Inhibiting corticospinal excitability by entraining ongoing mu-alpha rhythm in motor cortex

AbstractsSensorimotor mu-alpha rhythm reflects the state of cortical excitability. Repetitive transcranial magnetic stimulation (rTMS) can modulate neural synchrony by inducing periodic electric fields (E-fields) in the cortical networks. We hypothesized that the increased synchronization of mu-alpha rhythm would inhibit the corticospinal excitability reflected by decreased motor evoked potentials (MEP). In seventeen healthy participants, we applied rhythmic, arrhythmic, and sham rTMS over the left M1. The stimulation intensity was individually adapted to 35 mV/mm using prospective E-field estimation. This intensity corresponded to ca. 40% of the resting motor threshold. We found that rhythmic rTMS increased the synchronization of mu-alpha rhythm, increased mu-alpha/beta power, and reduced MEPs. On the other hand, arrhythmic rTMS did not change the ongoing mu-alpha synchronization or MEPs, though it increased the alpha/beta power. We concluded that low intensity, rhythmic rTMS can synchronize mu-alpha rhythm and modulate the corticospinal excitability in M1. HighlightsO_LIWe studied the effect of rhythmic rTMS induced E-field at 35 mV/mm in the M1 C_LIO_LIProspective electric field modeling guided the individualized rTMS intensities C_LIO_LIRhyhtmic rTMS entrained mu-alpha rhythm and modulated mu-alpha/beta power C_LIO_LIArrhythmic rTMS did not synchronize ongoing activity though increased mu-alpha/beta power. C_LIO_LIRhythmic but not arrhythmic or sham rTMS inhibited the cortical excitability in M1 C_LI

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bioRxiv2020

Short-lived alpha power suppression induced by low-intensity arrhythmic rTMS

This study was conducted to provide a better understanding of the role of electric field strength in the production of aftereffects in resting state scalp electroencephalography by repetitive transcranial magnetic stimulation (rTMS) in humans. We conducted two separate experiments in which we applied rTMS over the left parietal-occipital region. Prospective electric field simulation guided the choice of the individual stimulation intensities. In the main experiment, 16 participants received rhythmic and arrhythmic rTMS bursts at between ca. 20 and 50 mv/mm peak absolute electric field intensities. In the control experiment, another group of 16 participants received sham rTMS. To characterize the aftereffects, we estimated the alpha power (8-14 Hz) changes recorded in the inter-burst intervals, i.e., from 0.2 to 10 seconds after rTMS. We found aftereffects lasting up to two seconds after stimulation with ca. 35 mV/mm. Relative to baseline, alpha power was significantly reduced by the arrhythmic protocol, while there was no significant change with the rhythmic protocol. However, we found no significant long-term, i.e., up to 10-second, differences between the rhythmic and arrhythmic stimulation, or between the rhythmic and sham protocols. Weak arrhythmic rTMS induced short-lived alpha suppression during the inter-burst intervals.

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