Prior intention can locally tune inhibitory processes in the primary motor cortex: direct evidence from combined TMS‐EEG

Abstract

Human subjects are able to prepare cognitively to resist an involuntary movement evoked by a suprathreshold transcranial magnetic stimulation (TMS) applied over the primary motor cortex (M1) by anticipatory selective modulation of corticospinal excitability. Uncovering how the sensorimotor cortical network is involved in this process could reveal directly how a prior intention can tune the intrinsic dynamics of M1 before any peripheral intervention. Here, we used combined TMS-EEG to study the cortical integrative processes that are engaged both in the preparation to react to TMS (Resist vs. Assist) and in the subsequent response to it. During the preparatory period, the contingent negative variation (CNV) amplitude was found to be smaller over central electrodes (FC1, C1, Cz) when preparing to resist compared with preparing to assist the evoked movement whereas alpha-oscillation power was similar in the two conditions. Following TMS, the amplitude of the TMS evoked-N100 component was higher in the Resist than in the Assist condition for some central electrodes (FCz, C1, Cz, CP1, CP3). Moreover, for six out of eight subjects, a single-trial-based analysis revealed a negative correlation between CNV amplitude and N100 amplitude. In conclusion, prior intention can tune the excitability of M1. When subjects prepare to resist a TMS-evoked movement, the anticipatory processes cause a decreased cortical excitability by locally increasing the inhibitory processes.

Cortical inhibition in attention deficit hyperactivity disorder: new insights from the electroencephalographic response to transcranial magnetic stimulation

“…TMS-evoked N100 occurred already at subthreshold TMS intensities with highly reliable amplitudes (Bender et al, 2005a). This supports previous evidence that TMS-evoked N100 adds additional and independent information to measures based on MEP amplitudes and may be a marker of cortical inhibition (Bender et al, 2005a;Bonnard et al, 2009;Ilmoniemi et al, 2010). We found that less TMS-evoked N100 reduction (i.e.…”

“…In contrast to MEPs, which are potentially affected by a combination of cortical, subcortical and spinal mechanisms (Kiers et al, 1993), the TMS-evoked N100 directly assesses cortical responses to TMS without influences of spinal inhibitory mechanisms (Nikulin et al, 2003;Bender et al, 2005a;Ilmoniemi and Kicic, 2010). In healthy subjects, the TMS-evoked N100 component decreases during motor cortex disinhibition related to movement execution (Nikulin et al, 2003) and motor response preparation (Bender et al, 2005a) and increases during response inhibition (Bonnard et al, 2009). Therefore, the TMS-evoked N100 is considered to be a marker of motor cortex inhibition influenced by cortico-striato-thalamo-cortical loops (Bender et al, 2005a).…”

Intracortical Inhibition Assessed with Paired-Pulse Transcranial Magnetic Stimulation is Modulated during Shortening and Lengthening Contractions in Young and Old Adults

“…In contrast to SP duration, our findings demonstrate that LICI in young subjects was greater during both shortening and lengthening contractions, suggesting increased GABAB mediated inhibition within M1 during movement in healthy young subjects. This increase in LICI is consistent with a previous report that the EEG derived N100 response is greater during movement preparation in young subjects [48]. Despite this, LICI in old subjects was unaffected by contraction type, suggesting that the ageing process results in reduced modulation of intracortical GABAB-mediated circuitry during movement.…”

Transcranial Magnetic Stimulation-Electroencephalography Responses in Recovered and Symptomatic Mild Traumatic Brain Injury

“…Converging evidence from several studies, however, shows that direct effects of TMS to the N100-P200 are substantial, probably more important than sensory stimulation. 19,25,26,33,34 The N100 is sensitive to certain clinical conditions, including ADHD 35 and mild cognitive impairment, 27 where reduced N100 amplitudes have been found. The balance of cortical inhibitory and facilitatory circuits in paired-pulse TMS-EEG is also reflected in latencies.…”