71.: Modification of transcranial magnetic stimulation-evoked potentials by cerebellar theta burst stimulation

Abstract

Repetitive transcranial magnetic stimulation (rTMS) is a potential treatment for neurological disease. Combined transcranial magnetic stimulation and electroencephalography (TMS-EEG) is a relatively new approach to the study of cortical excitability in neurological disease, with the N100 component of the TMS-evoked potential being a marker of intracortical inhibition. Intermittent theta burst stimulation (iTBS) of the cerebellum increases corticospinal excitability in the contralateral primary motor cortex and continuous theta burst stimulation (cTBS) decreases excitability, as reflected in motor evoked potentials (MEP). The purpose of this study was to compare the effects of cTBS on the MEP and N100 potential. TMS-EEG was carried out in 16 healthy volunteers, aged 21–30 years. In each session, MEP were recorded from the left motor cortex. Single TMS pulses were then applied before and after 30 Hz iTBS, cTBS or sham stimulation of the right cerebellar hemisphere stimulus intensity of 80% or 90% of active motor threshold. Further MEP were then recorded. EEG recordings were analysed offline and independent component analysis was used to remove artefact. Mean N100 amplitudes after the three treatments were compared using mixed model analysis of variance, with the pre-treatment N100 amplitudes as covariates. Using a stimulus intensity of 90%, there was an effect of TBS protocol on amplitude of the resting MEP, which was significantly lower after cTBS than sham TBS, F(2, 14) = 4.28, p = 0.035. Cortical silent period (CSP) was increased following iTBS, compared to sham, F(2, 13) = 4.87, p = 0.026), but were not significant for 80% TBS. Combining results of 80% and 90% stimulus intensities, the mean N100 amplitude was significantly greater after iTBS than sham TBS, F(2, 27) = 3.52, p = 0.044. The augmentation of the N100 potential by iTBS is consistent with the increase in the CSP, also a marker of inhibition. Unexpectedly, the reduction in the amplitude of the resting MEP by cTBS was not accompanied by an increase in either the CSP or the N100 amplitude suggesting it arises from decreased facilitation rather than increased intracortical inhibition. These findings are important for predicting the effects of cerebellar rTMS in disease.