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.

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.

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.

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.

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.

Controlling an inappropriate response tendency in the face of a reward-predicting stimulus likely depends on the strength of the reward-driven activation, the strength of a putative top–down control process, and their relative timing. We developed a rewarded go/no-go paradigm to investigate such dynamics. Participants made rapid responses (on go trials) to high versus low reward-predicting stimuli and sometimes had to withhold responding (on no-go trials) in the face of the same stimuli. Behaviorally, for high versus low reward stimuli, responses were faster on go trials, and there were more errors of commission on no-go trials. We used single-pulse TMS to map out the corticospinal excitability dynamics, especially on no-go trials where control is needed. For successful no-go trials, there was an early rise in motor activation that was then sharply reduced beneath baseline. This activation–reduction pattern was more pronounced for high- versus low-reward trials and in individuals with greater motivational drive for reward. A follow-on experiment showed that, when participants were fatigued by an effortful task, they made more errors on no-go trials for high versus low reward stimuli. Together, these studies show that, when a response is inappropriate, reward-predicting stimuli induce early motor activation, followed by a top–down effortful control process (which we interpret as response suppression) that depends on the strength of the preceding activation. Our findings provide novel information about the activation–suppression dynamics during control over reward-driven actions, and they illustrate how fatigue or depletion leads to control failures in the face of reward.

Everyday life, as well as psychiatric illness, is replete with examples where appetitive and aversive stimuli hijack the will, leading to maladaptive behavior. Yet the mechanisms underlying this phenomenon are not well understood. Here we investigate how motivational cues influence action tendencies in healthy individuals with a novel paradigm. Behaviorally, we observed that an appetitive cue biased go behavior (making a response), whereas an aversive cue biased no-go behavior (withholding a response). We hypothesized that the origin of this behavioral go/no-go bias occurs at the motor system level. To test this, we used single-pulse TMS as a motor system probe (rather than a disruptive tool) to index motivational biasing. We found that the appetitive cue biased the participants to go more by relatively increasing motor system excitability, and that the aversive cue biased participants to no-go more by relatively decreasing motor system excitability. These results show, first, that maladaptive behaviors arise from motivational cues quickly spilling over into the motor system and biasing behavior even before action selection and, second, that this occurs in opposing directions for appetitive and aversive cues.

Behavioral studies show that subjects respond more slowly to stimuli to which they previously stopped. This response slowing could be explained by “automatic inhibition” (i.e., the reinstantiation of motor suppression when a stimulus retrieves a stop association). Here we tested this using TMS. In Experiment 1, participants were trained to go or no-go to stimuli. Then, in a test phase, we compared the corticospinal excitability for go stimuli that were previously associated with stopping (no-go_then_go) with go stimuli that were previously associated with going (go_then_go). Corticospinal excitability was reduced for no-go_then_go compared with go_then_go stimuli at a mere 100 msec poststimulus. Although these results fit with automatic inhibition, there was, surprisingly, no suppression for no-go_then_no-go stimuli, although this should occur. We speculated that automatic inhibition lies within a continuum between effortful top–down response inhibition and no inhibition at all. When the need for executive control and active response suppression disappears, so does the manifestation of automatic inhibition. Therefore, it should emerge during go/no-go learning and disappear as performance asymptotes. Consistent with this idea, in Experiment 2, we demonstrated reduced corticospinal excitability for no-go versus go trials most prominently in the midphase of training but it wears off as performance asymptotes. We thus provide neurophysiological evidence for an inhibition mechanism that is automatically reinstantiated when a stimulus retrieves a learned stopping episode, but only in an executive context in which active suppression is required. This demonstrates that automatic and top–down inhibition jointly contribute to goal-directed behavior.

An important aspect of cognitive control is the ability to respond with restraint. Here, we modeled this experimentally by measuring the degree of response slowing that occurs when people respond to an imperative stimulus in a context where they might suddenly need to stop the initiated response compared with a context in which they do not need to stop. We refer to the RT slowing that occurs as the “response delay effect.” We conjectured that this response delay effect could relate to one or more neurocognitive mechanism(s): partial response suppression (i.e., “active braking”), prolonged decision time, and slower response facilitation. These accounts make different predictions about motor system excitability and brain activation. To test which neurocognitive mechanisms underlie the response delay effect, we performed two studies with TMS and we reanalyzed fMRI data. The results suggest that the response delay effect is at least partly explained by active braking, possibly involving a mechanism that is similar to that used to stop responses completely. These results further our understanding of how people respond with restraint by pointing to proactive recruitment of a neurocognitive mechanism heretofore associated with outright stopping.

Executive functions are likely mediated by interconnected circuits including frontal lobe and basal ganglia structures. We assessed the executive function of task switching in patients with early-stage Huntington's disease (HD), a neurodegenerative disease affecting the basal ganglia. In two experiments, the HD patients had greater difficulty when switching than when repeating a task than matched controls, and this was true even when scaling for the overall slowing of the patients. In the first experiment, HD patients had a switching deficit even in a “pure” condition where they had to switch, predictably, and with substantial preparation time, between stimuli having only one possible response, indicating a switching deficit different from that for patients with Parkinson's disease or frontal lobe trauma, and possibly relating to inadequate activation of stimulus-response links or “response set.” In the more elaborate second experiment, we could not account for the switching deficit of the patients in terms of inadequate preparation in advance of a switch, deficient suppression of taskset processing from the preswitch trial, or impaired suppression of interference due to the presence of a competing task set. Instead, we found that part of the switching deficit was due to elevated reaction time and errors on switch trials for a repeated response (same button press as on preswitch trial) relative to an alternated response (different button press from preswitch trial). We argue that this elevated “repetition effect” for the HD patients is due to excessive inhibition of the justperformed response in advance of a switch. Alterations in the “response-setting” process alone (Experiment 1) and both the response-setting and “response inhibition” process (Experiment 2) probably arise from striatal pathology in HD, thus accounting for the task-switching deficits and showing how basal ganglia implemented response processes may underpin executive function.