Temporal Dynamics of Proactive and Reactive Motor Inhibition

Abstract

Proactive motor inhibition refers to endogenous preparatory mechanisms facilitating action inhibition, whereas reactive motor inhibition is considered to be a sudden stopping process triggered by external signals. Previous studies were inconclusive about the temporal dynamics of involved neurocognitive processes during proactive and reactive motor control. Using electroencephalography (EEG), we investigated the time-course of proactive and reactive inhibition, measuring event-related oscillations and event-related potentials (ERPs). Participants performed in a cued go/nogo paradigm with cues indicating whether the motor response might or might not have to be inhibited. Based on the dual mechanisms of control (DMC) framework by Braver, we investigated the role of attentional effects, motor preparation in the sensorimotor cortex and prefrontal cognitive control mechanisms, separating effects before and after target onset. In the cue-target interval, proactive motor inhibition was associated with increased attention, reflected in reduced visual alpha power and an increased contingent negative variation (CNV). At the same time, motor inhibition was modulated by reduced sensorimotor beta power. After target onset, proactive inhibition resulted in an increased N1, indicating allocation of attention towards relevant stimuli, increased prefrontal beta power and a modulation of sensorimotor mu activity. As in previous studies, reactive stopping of motor actions was associated with increased prefrontal beta power and increased sensorimotor beta activity. The results stress the relevance of attentional mechanisms for proactive inhibition and speak for different neurocognitive mechanisms being involved in the early preparation for and in later implementation of motor inhibition.

Combining Movement-Related Cortical Potentials and Event-Related Desynchronization to Study Movement Preparation and Execution

“…Bereitschaftspotential (BP) ( 14 ) is the early subcomponent of MRCPs and is believed to be generated by the supplementary motor area (SMA) ( 15 ), motor cortex, and cingulate gyrus ( 14 , 16 ) and represents the motor preparation stage of movement. In addition to BP, a contingent negative variation (CNV) was reported to present in movement preparation stage ( 17 , 18 ) and reflects motor expectancy and preparation. The late subcomponent, the motor potential (MP), has been proposed to be generated from the underlying motor cortex and partly due to afferents excited by the movement ( 14 ).…”

Methylphenidate promotes the interaction between motor cortex facilitation and attention in healthy adults: A combined study using event‐related potentials and transcranial magnetic stimulation

“…The CNV is a gradient, negative slow ERP to cue stimuli (Walter, Cooper, Aldridge, McCallum, & Winter, ), which ceases at the presentation of a target stimulus (Bekker, Kenemans, & Verbaten, ). The neuronal source of both CNV and N1 is assumed to be located in the extrastriate cortex (Hillyard & Anllo‐Vento, ; Liebrand, Pein, Tzvi, & Kramer, ). N2 and P3 differ between go and nogo tasks, with a longer latency and more anterior topography for the nogo‐P3 and a more negatively and frontocentral topography for nogo N2 (Falkenstein, Hoormann, & Hohnsbein, ; Spronk, Jonkman, & Kemner, ).…”

Mobile EEG reveals functionally dissociable dynamic processes supporting real-world ambulatory obstacle avoidance: Evidence for early proactive control

“…The beta rebound is typically observed generally over sensorimotor areas after motor execution or motor imagery (Pfurtscheller et al, 2005;Pfurtscheller & Solis-Escalante, 2009) and it is believed to reflect an active recalibration process that takes place after a change in the state of the motor system (Pfurtscheller et al, 1996;Engel & Fries, 2010;Kilavik et al, 2013). Notably, the beta rebound over prefrontal and sensorimotor areas is considered a possible index of reactive control (Cooper et al, 2019;Liebrand et al, 2017). Accordingly, the presence of the beta rebound in our study only after a gait adjustment was required in order to step over an obstacle, provides a marker of the reactive process that needs to take place in order to restore the motor system to its previous state.…”

“…There is, however, wider evidence for reactive control mechanisms after movement. In particular, EEG studies have revealed post-movement increases of beta power (13-30 Hz), described as the beta rebound, as a marker of reactive control (Liebrand et al, 2017). Beta oscillatory activity over sensory motor regions is enhanced when the predictions of an incoming stimulus are violated (Arnal et al, 2011) and after forcibly interrupted movements (Alegre et al, 2008;Heinrichs-Graham et al, 2017), suggesting a mechanism that re-calibrates the motor system after a movement (Pfurtscheller et al, 1996;Engel & Fries, 2010;Kilavik et al, 2013).…”