Towards real-world generalizability of a circuit for action-stopping.

Two decades of cross-species neuroscience research on rapid action-stopping in the laboratory has provided motivation for an underlying prefrontal-basal ganglia circuit. Here we provide an update of key studies from the past few years. We conclude that this basic neural circuit is on increasingly firm ground, and we move on to consider whether the action-stopping function implemented by this circuit applies beyond the simple laboratory stop signal task. We advance through a series of studies of increasing 'real-worldness', starting with laboratory tests of stopping of speech, gait and bodily functions, and then going beyond the laboratory to consider neural recordings and stimulation during moments of control presumably required in everyday activities such as walking and driving. We end by asking whether stopping research has clinical relevance, focusing on movement disorders such as stuttering, tics and freezing of gait. Overall, we conclude there are hints that the prefrontal-basal ganglia action-stopping circuit that is engaged by the basic stop signal task is recruited in myriad scenarios; however, truly proving this for real-world scenarios requires a new generation of studies that will need to overcome substantial technical and inferential challenges.

Two modes of midfrontal theta suggest a role in conflict and error processing.

Midfrontal theta increases during scenarios when conflicts are successfully resolved. Often considered a generic signal of cognitive control, its temporal nature has hardly been investigated. Using advanced spatiotemporal techniques, we uncover that midfrontal theta occurs as a transient oscillation or "event" at single trials with their timing reflecting computationally distinct modes. Single-trial analyses of electrophysiological data from participants performing the Flanker (N = 24) and Simon task (N = 15) were used to probe the relationship between theta and metrics of stimulus-response conflict. We specifically investigated "partial errors", in which a small burst of muscle activity in the incorrect response effector occurred, quickly followed by a correction. We found that transient theta events in single trials could be categorized into two distinct theta modes based on their relative timing to different task events. Theta events from the first mode occurred briefly after the task stimulus and might reflect conflict-related processing of the stimulus. In contrast, theta events from the second mode were more likely to occur around the time partial errors were committed, suggesting they were elicited by a potential upcoming error. Importantly, in trials in which a full error was committed, this "error-related theta" occurred too late with respect to the onset of the erroneous muscle response, supporting the role of theta also in error correction. We conclude that different modes of transient midfrontal theta can be adopted in single trials not only to process stimulus-response conflict, but also to correct erroneous responses.

Failing to attend versus failing to stop: Single-trial decomposition of action-stopping in the stop signal task.

The capacity to stop impending or ongoing actions contributes to executive control over behavior. Action-stopping, however, is difficult to directly quantify. It is therefore assayed via computational modeling of behavior in the stop signal task to estimate the latency of stopping (stop signal reaction time, SSRT) and, more recently, the reliability of stopping in terms of the distribution of SSRTs (standard deviation, SD-SSRT) and the frequency with which one outright fails to react to a stop signal (trigger failures, TF). Critically, the validity of computational estimates remains unknown because we currently have no direct readouts of behavior against which to compare them. Here, we developed a method for providing single-trial behavioral readouts of SSRT and trigger failures. The method relies on an adaptation of the stop signal task in which participants respond by moving a computer mouse. In two online experiments, we used movement kinematics to quantify stopping performance (SSRT, SD-SSRT, and TF), and then applied the standard Race Model and recent BEESTS model in order to examine the convergent validity of the methods. Overall, we demonstrate good correspondence between kinematics- and model-based estimates of stopping performance at the group and individual level. We conclude that the new method provides valid estimates of stopping performance that, unlike model-based estimates, can be read out at the level of single trials. Our approach might therefore be useful for interrogating single-trial neurophysiological correlates of stopping and for large-scale, online studies of behavioral stopping.

Transient beta modulates decision thresholds during human action-stopping.

Action-stopping in humans involves bursts of beta oscillations in prefrontal-basal ganglia regions. To determine the functional role of these beta bursts we took advantage of the Race Model framework describing action-stopping. We incorporated beta bursts in three race model variants, each implementing a different functional contribution of beta to action-stopping. In these variants, we hypothesized that a transient increase in beta could (1) modulate decision thresholds, (2) change stop accumulation rates, or (3) promote the interaction between the Stop and the Go process. We then tested the model predictions using EEG recordings in humans performing a Stop-signal task. We found that the model variant in which beta increased decision thresholds for a brief period of time best explained the empirical data. The model parameters fitted to the empirical data indicated that beta bursts involve a stronger decision threshold modulation for the Go process than for the Stop process. This suggests that prefrontal beta influences stopping by temporarily holding the response from execution. Our study further suggests that human action-stopping could be multi-staged with the beta acting as a pause, increasing the response threshold for the Stop process to modulate behavior successfully. Overall, our approach of introducing transient oscillations into the race model and testing against human electrophysiological data provides a novel account of the puzzle of prefrontal beta in executive control.

Motor cortex oscillates at its intrinsic post-movement beta rhythm following real (but not sham) single pulse, rhythmic and arrhythmic transcranial magnetic stimulation.

We aimed to test the idea that rhythmic transcranial magnetic stimulation (TMS) entrains cortical oscillations. To do this, we examined oscillatory responses in the electroencephalogram (EEG) to TMS over primary motor cortex. In particular, we contrasted responses to real TMS with those to sham TMS in order to dissociate the contributions of direct (transcranial) activation and indirect activation (via auditory/sensory input) of the brain. We first showed that real single pulse TMS elicited a brief (∼200 ms) increase in sensorimotor beta power whose frequency closely matched that of each individual's post-movement beta rebound (PMBR, ∼18 Hz). Sham TMS triggered minimal oscillatory activity. Together this implies that real TMS interacts with endogenous oscillations via direct brain activation. We then showed that although trains of real rhythmic TMS delivered at each individuals PMBR frequency produced a brief increase in beta power at the same frequency, real arrhythmic TMS also elicited an equivalent increase in beta. The implication is that the oscillatory response is independent of the rhythm of stimulation. By contrast, sham stimulation elicited minimal activity in the beta band, and the responses to rhythmic and arrhythmic sham TMS were broadly similar, showing that sham rhythmic stimulation did not produce entrainment via sensory rhythms. Together, the data demonstrate that the beta oscillatory response of M1 to real TMS predominantly reflects direct activation of the underlying cortex. However, the data do not support the notion of rhythmic TMS enhancing oscillatory activity via entrainment-like mechanisms, at least within the constraints of the current experimental set-up.

Mind Wandering Impedes Response Inhibition by Affecting the Triggering of the Inhibitory Process.

Mind wandering is a state in which our mental focus shifts toward task-unrelated thoughts. Although it is known that mind wandering has a detrimental effect on concurrent task performance (e.g., decreased accuracy), its effect on executive functions is poorly studied. Yet the latter question is relevant to many real-world situations, such as rapid stopping during driving. Here, we studied how mind wandering would affect the requirement to subsequently stop an incipient motor response. In healthy adults, we tested whether mind wandering affected stopping and, if so, which component of stopping was affected: the triggering of the inhibitory brake or the implementation of the brake following triggering. We observed that during mind wandering, stopping latency increased, as did the percentage of trials with failed triggering. Indeed, 67% of the variance of the increase in stopping latency was explained by increased trigger failures. Thus, mind wandering primarily affects stopping by affecting the triggering of the brake.

Behavioral Induction of a High Beta State in Sensorimotor Cortex Leads to Movement Slowing.

The sensorimotor beta rhythm (∼13-30 Hz) is commonly seen in relation to movement. It is important to understand its functional/behavioral significance in both health and disease. Sorting out competing theories of sensorimotor beta is hampered by a paucity of experimental protocols in humans that manipulate/induce beta oscillations and test their putative effects on concurrent behavior. Here, we developed a novel behavioral paradigm to generate beta and then test its functional relevance. In two human experiments with scalp EEG (n = 11 and 15), we show that a movement instruction generates a high beta state (postmovement beta rebound), which then slows down subsequent movements required during that state. We also show that this high initial beta rebound related to reduced mu-beta desynchronization for the subsequent movement and, further, that the temporal features of the beta state, that is, the beta bursts, related to the degree of slowing. These results suggest that increased sensorimotor beta in the postmovement period corresponds to an inhibitory state-insofar as it retards subsequent movement. By demonstrating a behavioral method by which people can proactively create a high beta state, our paradigm provides opportunities to test the effect of this state on sensations and affordances. It also suggests related experiments using motor imagery rather than actual movement, and this could later be clinically relevant, for example, in tic disorder.

Unwanted Memory Intrusions Recruit Broad Motor Suppression.

Quickly preventing the retrieval of (inappropriate) long-term memories might recruit a similar control mechanism as rapid action-stopping. A very specific characteristic of rapid action-stopping is "global motor suppression": When a single response is rapidly stopped, there is a broad skeletomotor suppression. This is shown by the technique of TMS placed over a task-irrelevant part of the primary motor cortex (M1) to measure motor-evoked potentials. Here, we used this same TMS method to test if rapidly preventing long-term memory retrieval also shows this broad skeletomotor suppression effect. Twenty human participants underwent a Think/No-Think task. In the first phase, they learned word pairs. In the second phase, they received the left-hand word as a cue and had to either retrieve the associated right-hand word ("Think") or stop retrieval ("No-Think"). At the end of each trial, they reported whether they had experienced an intrusion of the associated memory. Behaviorally, on No-Think trials, they reported fewer intrusions than Think trials, and the reporting of intrusions decreased with practice. Physiologically, we observed that the motor-evoked potential, measured from the hand (which was irrelevant to the task), was reduced on No-Think trials in the time frame of 300-500 msec, especially on trials where they did report an intrusion. This unexpected result contradicted our preregistered prediction that we would find such a decrease on No-Think trials where the intrusion was not reported. These data suggest that one form of executive control over (inappropriate) long-term memory retrieval is a rapid and broad stop, akin to action-stopping, that is triggered by the intrusion itself.

Fronto-subthalamic phase synchronization and cross-frequency coupling during conflict processing.

Growing evidence suggests that both the medial prefrontal cortex (mPFC) and the subthalamic nucleus (STN) play crucial roles in conflict processing, but how these two structures coordinate their activities remains poorly understood. We simultaneously recorded electroencephalogram from the mPFC and local field potentials from the STN using deep brain stimulation electrodes in 13 Parkinson's disease patients while they performed a Stroop task. Both mPFC and STN showed significant increases in theta activities (2-8 Hz) in incongruent trials compared to the congruent trials. The theta activity in incongruent trials also demonstrated significantly increased phase synchronization between mPFC and STN. Furthermore, the amplitude of gamma oscillation was modulated by the phase of theta activity at the STN in incongruent trials. Such theta-gamma phase-amplitude coupling (PAC) was much stronger for incongruent trials with faster reaction times than those with slower reaction times. Elevated theta-gamma PAC in the STN provides a novel mechanism by which the STN may operationalize its proposed "hold-your-horses" role. The co-occurrence of mPFC-STN theta phase synchronization and STN theta-gamma PAC reflects a neural substrate for fronto-subthalamic communication during conflict processing. More broadly, it may be a general mechanism for neuronal interactions in the cortico-basal ganglia circuits via a combination of long-range, within-frequency phase synchronization and local cross-frequency PAC.

Double-blind disruption of right inferior frontal cortex with TMS reduces right frontal beta power for action stopping.

Stopping action depends on the integrity of the right inferior frontal gyrus (rIFG). Electrocorticography from the rIFG shows an increase in beta power during action stopping. Scalp EEG shows a similar right frontal beta increase, but it is unknown whether this beta modulation relates to the underlying rIFG network. Demonstrating a causal relationship between the rIFG and right frontal beta in EEG during action stopping is important for putting this electrophysiological marker on a firmer footing. In a double-blind study with a true sham coil, we used fMRI-guided 1-Hz repetitive transcranial magnetic stimulation (rTMS) to disrupt the rIFG and to test whether this reduced right frontal beta and impaired action stopping. We found that rTMS selectively slowed stop signal reaction time (SSRT) (no effect on Go) and reduced right frontal beta (no effect on sensorimotor mu/beta related to Go); it also reduced the variance of a single-trial muscle marker of stopping. Surprisingly, sham stimulation also slowed SSRTs and reduced beta. Part of this effect, however, resulted from carryover of real stimulation in participants who received real stimulation first. A post hoc between-group comparison of those participants who received real first compared with those who received sham first showed that real stimulation reduced beta significantly more. Thus, real rTMS uniquely affected metrics of stopping in the muscle and resulted in a stronger erosion of beta. We argue that this causal test validates right frontal beta as a functional marker of action stopping.NEW & NOTEWORTHY Action stopping recruits the right inferior frontal gyrus (rIFG) and elicits increases in right frontal beta. The present study now provides causal evidence linking these stopping-related beta oscillations to the integrity of the underlying rIFG network. One-hertz transcranial magnetic stimulation (TMS) over the rIFG impaired stopping and reduced right frontal beta during a stop-signal task. Furthermore, the effect on neural oscillations was specific to stopping-related beta, with no change in sensorimotor mu/beta corresponding to the Go response.

Beta Oscillations in Working Memory, Executive Control of Movement and Thought, and Sensorimotor Function.

Beta oscillations (∼13 to 30 Hz) have been observed during many perceptual, cognitive, and motor processes in a plethora of brain recording studies. Although the function of beta oscillations (hereafter "beta" for short) is unlikely to be explained by any single monolithic description, we here discuss several convergent findings. In prefrontal cortex (PFC), increased beta appears at the end of a trial when working memory information needs to be erased. A similar "clear-out" function might apply during the stopping of action and the stopping of long-term memory retrieval (stopping thoughts), where increased prefrontal beta is also observed. A different apparent role for beta in PFC occurs during the delay period of working memory tasks: it might serve to maintain the current contents and/or to prevent interference from distraction. We confront the challenge of relating these observations to the large literature on beta recorded from sensorimotor cortex. Potentially, the clear-out of working memory in PFC has its counterpart in the postmovement clear-out of the motor plan in sensorimotor cortex. However, recent studies support alternative interpretations. In addition, we flag emerging research on different frequencies of beta and the relationship between beta and single-neuron spiking. We also discuss where beta might be generated: basal ganglia, cortex, or both. We end by considering the clinical implications for adaptive deep-brain stimulation.

Temporally-precise disruption of prefrontal cortex informed by the timing of beta bursts impairs human action-stopping.

Human action-stopping is thought to rely on a prefronto-basal ganglia-thalamocortical network, with right inferior frontal cortex (rIFC) posited to play a critical role in the early stage of implementation. Here we sought causal evidence for this idea in experiments involving healthy human participants. We first show that action-stopping is preceded by bursts of electroencephalographic activity in the beta band over prefrontal electrodes, putatively rIFC, and that the timing of these bursts correlates with the latency of stopping at a single-trial level: earlier bursts are associated with faster stopping. From this we reasoned that the integrity of rIFC at the time of beta bursts might be critical to successful stopping. We then used fMRI-guided transcranial magnetic stimulation (TMS) to disrupt rIFC at the approximate time of beta bursting. Stimulation prolonged stopping latencies and, moreover, the prolongation was most pronounced in individuals for whom the pulse appeared closer to the presumed time of beta bursting. These results help validate a model of the neural architecture and temporal dynamics of action-stopping. They also highlight the usefulness of prefrontal beta bursts to index an apparently important sub-process of stopping, the timing of which might help explain within- and between-individual variation in impulse control.

Preventing a Thought from Coming to Mind Elicits Increased Right Frontal Beta Just as Stopping Action Does.

In the stop-signal task, an electrophysiological signature of action-stopping is increased early right frontal beta band power for successful vs. failed stop trials. Here we tested whether the requirement to stop an unwanted thought from coming to mind also elicits this signature. We recorded scalp EEG during a Think/No-Think task and a subsequent stop signal task in 42 participants. In the Think/No-Think task, participants first learned word pairs. In a second phase, they received the left-hand word as a reminder and were cued either to retrieve the associated right-hand word ("Think") or to stop retrieval ("No-Think"). At the end of each trial, participants reported whether they had experienced an intrusion of the associated memory. Finally, they received the left-hand reminder word and were asked to recall its associated target. Behaviorally, there was worse final recall for items in the No-Think condition, and decreased intrusions with practice for No-Think trials. For EEG, we reproduced increased early right frontal beta power for successful vs. failed action stopping. Critically, No-Think trials also elicited increased early right frontal beta power and this was stronger for trials without intrusion. These results suggest that preventing a thought from coming to mind also recruits fast prefrontal stopping.

The Functional Role of Response Suppression during an Urge to Relieve Pain.

Being in the state of having both a strong impulse to act and a simultaneous need to withhold is commonly described as an "urge." Although urges are part of everyday life and also important to several clinical disorders, the components of urge are poorly understood. It has been conjectured that withholding an action during urge involves active response suppression. We tested that idea by designing an urge paradigm that required participants to resist an impulse to press a button and gain relief from heat (one hand was poised to press while the other arm had heat stimulation). We first used paired-pulse TMS over motor cortex (M1) to measure corticospinal excitability of the hand that could press for relief, while participants withheld movement. We observed increased short-interval intracortical inhibition, an index of M1 GABAergic interneuron activity that was maintained across seconds and specific to the task-relevant finger. A second experiment replicated this. We next used EEG to better "image" putative cortical signatures of motor suppression and pain. We found increased sensorimotor beta contralateral to the task-relevant hand while participants withheld the movement during heat. We interpret this as further evidence of a motor suppressive process. Additionally, there was beta desynchronization contralateral to the arm with heat, which could reflect a pain signature. Strikingly, participants who "suppressed" more exhibited less of a putative "pain" response. We speculate that, during urge, a suppressive state may have functional relevance for both resisting a prohibited action and for mitigating discomfort.

Preparing to Stop Action Increases Beta Band Power in Contralateral Sensorimotor Cortex.

How do we prepare to stop ourselves in the future? Here, we used scalp EEG to test the hypothesis that people prepare to stop by putting parts of their motor system (specifically, here, sensorimotor cortex) into a suppressed state ahead of time. On each trial, participants were cued to prepare to stop one hand and then initiated a bimanual movement. On a minority of trials, participants were instructed to stop the cued hand while continuing quickly with the other. We used a guided multivariate source separation method to examine oscillatory power changes in presumed sensorimotor cortical areas. We observed that, when people prepare to stop a hand, there were above-baseline beta band power increases (12-24 Hz) in contralateral cortex up to a second earlier. This increase in beta band power in the proactive period was functionally relevant because it predicted, trial by trial, the degree of selectivity with which participants subsequently stopped a response but did not relate to movement per se. Thus, preparing to stop particular response channels corresponds to increased beta power from contralateral (sensorimotor) cortex, and this relates specifically to subsequent stopping. These results provide a high temporal resolution and frequency-specific electrophysiological signature of the preparing-to-stop state that is pertinent to future studies of mitigating provocation, including in clinical disorders. The results also highlight the utility of guided multivariate source separation for revealing the cortical dynamics underlying both movement and response suppression.

Event-related deep brain stimulation of the subthalamic nucleus affects conflict processing.

OBJECTIVE: Many lines of evidence suggest that response conflict recruits brain regions in the cortical-basal ganglia system. Within the basal ganglia, deep brain recordings from the subthalamic nucleus (STN) have shown that conflict triggers a transient increase in low-frequency oscillations (LFOs; 2-8Hz). Here, we deployed a new method of delivering short trains of event-related deep brain stimulation (DBS) to the STN to test the causal role of the STN and its associated circuits in conflict-related processing. METHODS: In a double-blind design, we stimulated the STN in patients with Parkinson disease by locking brief trains of DBS to specific periods of the trial within a Stroop task. RESULTS: Stimulation had a specific effect on conflict compared to nonconflict trials by relatively speeding responses on conflict trials (ie, reducing the Stroop effect, defined as the difference in reaction time between conflict and nonconflict trials) when it was delivered in the preresponse period in the preparation phase. Stimulation also increased errors when it was delivered early in the response window. This latter result corresponded to the timing of the conflict-induced increase in LFOs observed in the absence of stimulation but was not directly related to the reduction in the Stroop effect. INTERPRETATION: These results support the theory that the time of LFO increase recorded from the STN corresponds to a conflict-processing function. They also provide one of the first demonstrations of event-related DBS of the STN in humans during a cognitive control paradigm. Ann Neurol 2018;84:515-526.

Establishing a Right Frontal Beta Signature for Stopping Action in Scalp EEG: Implications for Testing Inhibitory Control in Other Task Contexts.

Many studies have examined the rapid stopping of action as a proxy of human self-control. Several methods have shown that a critical focus for stopping is the right inferior frontal cortex. Moreover, electrocorticography studies have shown beta band power increases in the right inferior frontal cortex and in the BG for successful versus failed stop trials, before the time of stopping elapses, perhaps underpinning a prefrontal-BG network for inhibitory control. Here, we tested whether the same signature might be visible in scalp electroencephalography (EEG)-which would open important avenues for using this signature in studies of the recruitment and timing of prefrontal inhibitory control. We used independent component analysis and time-frequency approaches to analyze EEG from three different cohorts of healthy young volunteers (48 participants in total) performing versions of the standard stop signal task. We identified a spectral power increase in the band 13-20 Hz that occurs after the stop signal, but before the time of stopping elapses, with a right frontal topography in the EEG. This right frontal beta band increase was significantly larger for successful compared with failed stops in two of the three studies. We also tested the hypothesis that unexpected events recruit the same frontal system for stopping. Indeed, we show that the stopping-related right-lateralized frontal beta signature was also active after unexpected events (and we accordingly provide data and scripts for the method). These results validate a right frontal beta signature in the EEG as a temporally precise and functionally significant neural marker of the response inhibition process.

Topography and timing of activity in right inferior frontal cortex and anterior insula for stopping movement.

Stopping incipient action activates both the right inferior frontal cortex (rIFC) and the anterior insula (rAI). Controversy has arisen as to whether these comprise a unitary cortical cluster-the rIFC/rAI-or whether rIFC is the primary stopping locus. To address this, we recorded directly from these structures while taking advantage of the high spatiotemporal resolution of closely spaced stereo-electro-encephalographic (SEEG) electrodes. We studied 12 patients performing a stop-signal task. On each trial they initiated a motor response (Go) and tried to stop to an occasional stop signal. Both the rIFC and rAI exhibited an increase in broadband gamma activity (BGA) after the stop signal and within the time of stopping (stop signal reaction time, SSRT), regardless of the success of stopping. The proportion of electrodes with this response was significantly greater in the rIFC than the rAI. Also, the rIFC response preceded that in the rAI. Last, while the BGA increase in rIFC occurred mainly prior to SSRT, the rAI showed a sustained increase in the beta and low gamma bands after the SSRT. In summary, the rIFC was activated soon after the stop signal, prior to and more robustly than the rAI, which on the other hand, showed a more prolonged response after the onset of stopping. Our results are most compatible with the notion that the rIFC is involved in triggering outright stopping in concert with a wider network, while the rAI is likely engaged by other processes, such as arousal, saliency, or behavioral adjustments. Hum Brain Mapp 39:189-203, 2018. © 2017 Wiley Periodicals, Inc.

High Working Memory Load Increases Intracortical Inhibition in Primary Motor Cortex and Diminishes the Motor Affordance Effect.

UNLABELLED: Motor affordances occur when the visual properties of an object elicit behaviorally relevant motor representations. Typically, motor affordances only produce subtle effects on response time or on motor activity indexed by neuroimaging/neuroelectrophysiology, but sometimes they can trigger action itself. This is apparent in "utilization behavior," where individuals with frontal cortex damage inappropriately grasp affording objects. This raises the possibility that, in healthy-functioning individuals, frontal cortex helps ensure that irrelevant affordance provocations remain below the threshold for actual movement. In Experiment 1, we tested this "frontal control" hypothesis by "loading" the frontal cortex with an effortful working memory (WM) task (which ostensibly consumes frontal resources) and examined whether this increased EEG measures of motor affordances to irrelevant affording objects. Under low WM load, there were typical motor affordance signatures: an event-related desynchronization in the mu frequency and an increased P300 amplitude for affording (vs nonaffording) objects over centroparietal electrodes. Contrary to our prediction, however, these affordance measures were diminished under high WM load. In Experiment 2, we tested competing mechanisms responsible for the diminished affordance in Experiment 1. We used paired-pulse transcranial magnetic stimulation over primary motor cortex to measure long-interval cortical inhibition. We found greater long-interval cortical inhibition for high versus low load both before and after the affording object, suggesting that a tonic inhibition state in primary motor cortex could prevent the affordance from provoking the motor system. Overall, our results suggest that a high WM load "sets" the motor system into a suppressed state that mitigates motor affordances. SIGNIFICANCE STATEMENT: Is an irrelevant motor affordance more likely to be triggered when you are under low or high cognitive load? We examined this using physiological measures of the motor affordance while working memory load was varied. We observed a typical motor affordance signature when working memory load was low; however, it was abolished when load was high. Further, there was increased intracortical inhibition in primary motor cortex under high working memory load. This suggests that being in a state of high cognitive load "sets" the motor system to be imperturbable to distracting motor influences. This makes a novel link between working memory load and the balance of excitatory/inhibitory activity in the motor cortex and potentially has implications for disorders of impulsivity.