F145. Characterization of surround inhibition and SICI in the motor cortex by TMS-EEG

Introduction Short-latency cortical inhibition (or SICI) is mediated by GABA-A inhibition and can be investigated with paired pulses TMS. Motor surround inhibition (mSI) is supportive for the execution of selective finger movements. When TMS is delivered at movement onset, the motor evoked potential (MEP) recorded from a “surround” muscle that does not act as a synergist is reduced. TMS evokes cortical potentials that can be recorded by EEG (TEP). Past studies suggested that cortical GABA-A mediated inhibition may modulate TEP components of up to 45 ms latency, while component at 100 ms may be a marker of GABA-B inhibition. In this TMS-EEG exploratory study, we investigated the cortical correlates of SICI and mSI in healthy subjects. Methods We enrolled 17 right handed healthy volunteers (HVs). EMG was recorded from the first dorsal interosseous (FDI) and from the abductor digiti minimi (ADM). EEG was recorded from a 32 channel cap. TMS was delivered on the ADM hotspot, using S50 as the intensity for the TS and 80% of the resting motor threshold (RMT) as the CS. HVs were asked to press with the index finger. Three randomized conditions were tested (100 trials each): single pulse at rest (SP); SP at movement onset (index finger flexion 3 s after a tone) (Mov); paired pulses at rest (ISI: 2 ms) (PP). ADM MEPs were measured to calculate SICI (PP/SP) and mSI (Mov/SP). HVs were divided in a mSI and in a NO_mSI group using a cut-off value of 0.8. Average TEPs were calculated for each condition and for 5 predetermined regions of interest (ROI) on the scalp. Peak-to-peak amplitudes of P30, N45, P60, N100 and P180 were measured in each condition-ROI. Mixed design repeated-measures ANOVA was used for statistical analysis with factors Group, Condition, Component, and ROI Results EMG analysis showed that all but one subject showed SICI. 10 HVs showed mSI, 7 HVs were classified as NO_mSI. TEPs on the sensorimotor cortex showed that SICI was associated with a reduction in the excitatory components P30 and P60, and an increase in the inhibitory component N45. When all HVs were considered, movement onset was associated with a widespread N100 and P180 reduction, and a P30 reduction of the non-stimulated sensorimotor cortex. Movement-induced TEP modulation was different in people with and without mSI. Only in people with mSI, movement onset was associated with a P30 and P60 reduction and N45 increase of the stimulated sensorimotor cortex Conclusion At the level of sensorimotor cortex, SICI and mSI are associated with a similar modulation of cortical excitability that occurs in the first 60 ms after TMS. Such modulation is likely to be mediated by a GABA-A inhibition. N100 reduction at movement onset is likely related to a facilitatory state associated with a reduction in the GABA-B tone. Our findings can be used to develop new hypotheses to study the pathophysiological mechanisms underlying SICI and mSI abnormalities in patients with Parkinson disease and dystonia.