Tracking markers of response inhibition in electroencephalographic data: why should we and how can we go beyond the N2 component?

Abstract

Response inhibition is a pivotal component of executive control, which is especially difficult to assess. Indeed, it is a substantial challenge to gauge brain-behavior relationships because this function is precisely intended to suppress overt measurable behaviors. A further complication is that no single neuroimaging method has been found that can disentangle the accurate time-course of concurrent excitatory and inhibitory mechanisms. Here, we argue that this objective can be achieved with electroencephalography (EEG) on some conditions. Based on a systematic review, we emphasize that the standard event-related potential N2 (N200) is not an appropriate marker of prepotent response inhibition. We provide guidelines for assessing the cortical brain dynamics of response inhibition with EEG. This includes the combined use of inseparable data processing steps (source separation, source localization, and single-trial and time-frequency analyses) as well as the amendment of the classical experimental designs to enable the recording of different kinds of electrophysiological activity predicted by different models of response inhibition. We conclude with an illustration based on recent findings of how fruitful this approach can be.

Exposing an “Intangible” Cognitive Skill Among Collegiate Football Players: III. Enhanced Reaction Control to Motion

“…This speculation is consistent with a growing literature that argues for blurred distinctions between automatic and controlled processing in elite athletic performance (see discussion in Bashore et al, 2018). However, on the basis of findings from a meta-analysis, Albares et al (2015) offered a set of penetrating methodological, technical, and analytical criticisms to argue that the N200 does not serve as either a reliable or valid index of response inhibition. With these criticisms in mind, our view is that the pattern of ERP activity observed by Nakamoto and Mori (2012) suggests that players recognize target movement deceleration more quickly (N200 latency) and re-calibrate the level of activation of the prepared movement to it more effectively (P300 amplitude) than do controls, while concurrently slowing translation of the stimulus input (i.e., change in target speed) into the designated response output (button press) until the time of target arrival with greater proficiency than do controls (P300 latency; see Verleger et al, 2005;Bashore et al, 2013, for discussions of the putative relationship between P300 latency and S-R translation).…”

Clonidine modulates the activity of the subthalamic‐supplementary motor loop: evidence from a pharmacological study combining deep brain stimulation and electroencephalography recordings in Parkinsonian patients

“…Guidelines for assessing the cortical brain dynamics of response inhibition with EEG are summarized in Albares et al . (). In sum, we compared the mean power of the 500 ms pre‐stimulus period to the mean power of the 100 ms pre‐RT period on a single‐trial basis (aggregate data) by means of Kruskal–Wallis tests and post hoc testing ( p < 0.05 Tukey‐Cramer corrected).…”

“…), (ii) apply group Blind Source Separation (gBSS), a method that directly identifies the components that are consistently expressed in the population (Lio and Boulinguez ; Albares et al . ; Huster et al . ).…”

“…; revised), to separate/localize significant sources on the basis of the mixed signal recorded on the scalp (Lio and Boulinguez , ), and to apply advanced signal processing methods to unravel the time course of concurrent excitatory and inhibitory activity (Albares et al . ).…”

Passive perceptual learning modulates motor inhibitory control in superior frontal regions

“…We quantified the P2 in the time window between 170 and 200 ms in GO and NOGO trials for the “stimulation group” and 210–240 ms in GO and NOGO trials for the “no‐stimulation group.” The mean amplitude in the N2 time window was quantified at electrode Cz in the time range from 350 to 380 ms in GO trials for both groups and time points. This time window might seem late for this component, yet the N2 component can occur between 200 and 400 ms after stimulus onset (Albares, Lio, & Boulinguez, ) and the chosen time window is still within this range. In NOGO trials, the time window from 260 to 290 ms was used for the “stimulation group” for both time points.…”