Somatosensory input in the context of transcranial magnetic stimulation coupled with electroencephalography: An evidence-based overview

Changes in Cortical Activation by Transcranial Magnetic Stimulation Due to Coil Rotation Are Not Attributable to Cranial Muscle Activation

“…By contrast, the topography of significant differences between M1 standard and M1 emg , both in the time and time/frequency domains, is lateralized and, thus, likely driven by a different direct cortical activation due to TMS. This is further indirectly supported by the similar VAS scores for discomfort in the two conditions, which is highly correlated with cranial muscle twitches [16,60]; this result probably indicates that the difference in muscle activation was not large enough to generate a different percept and, by extension, a different multimodal vertex potential due to saliency of stimulation [33]. Finally, it is interesting to note that the two processing pipelines did not produce exactly the same effects on the data, indicating that they are not equivalent.…”

“…A possible overlap between somatosensory evoked responses (SEPs) and TEPs may represent a more pertinent problem in the present experimental setting. Since it has been suggested that afferent input due to cranial muscle contraction may induce measurable EEG responses [16], it is conceivable that the larger muscle twitch in the M1 standard condition may have driven the observed differences in TMS-induced signals. However, it has been suggested that somatosensory input due to cranial muscle twitches induces a multimodal vertex N100/P200, similar to AEPs, rather than a lateralized signal compatible with the modality-specific activation of the somatosensory cortex [16,59].…”

“…Since it has been suggested that afferent input due to cranial muscle contraction may induce measurable EEG responses [16], it is conceivable that the larger muscle twitch in the M1 standard condition may have driven the observed differences in TMS-induced signals. However, it has been suggested that somatosensory input due to cranial muscle twitches induces a multimodal vertex N100/P200, similar to AEPs, rather than a lateralized signal compatible with the modality-specific activation of the somatosensory cortex [16,59]. By contrast, the topography of significant differences between M1 standard and M1 emg , both in the time and time/frequency domains, is lateralized and, thus, likely driven by a different direct cortical activation due to TMS.…”

“…One of the main technical issues of TMS-EEG is the activation of cranial muscle by TMS; this may contaminate TMS-EEG responses either directly, as it can induce an early, TMS-locked EMG signal [12][13][14][15], or indirectly, due to somatosensory input caused by muscle twitches [16]. A possible way to address this problem is to remove the EMG signal offline with blind source separation techniques, such as independent component analysis (ICA) or signal-space projection with source-informed reconstruction (SSP-SIR) [13,17,18].…”

Methodological choices matter: A systematic comparison of TMS-EEG studies targeting the primary motor cortex

“…For example, a clear N100-P180 response was observed in a deaf individual, when stimulation was delivered in proximity to the scalp [25]. In this case, the N100-P180 was most likely produced by stimulation-induced excitation of skin receptors and peripheral axons contributing to somatosensation [27]. Importantly, no N100-P180 response was seen when the coil was positioned further away from the head, effectively eliminating the somatosensory stimulation by the TMS pulse [25].…”