Biology subjects

Wessel, J. R.

Publications and source records attributed to Wessel, J. R..

At least 19 recordsLinked to original sources

bioRxiv2026

A domain-general basal ganglia mechanism for inhibitory control during language comprehension

Whether controlled language processing involves domain-general or language-specific neural circuits is subject of controversial debate. We tested whether the inhibitory control of linguistic activity shares a common neural process with motor inhibition in twenty humans undergoing intra- and extracranial neural field potential recordings and deep-brain stimulation. Engaging motor and linguistic inhibition simultaneously resulted in a significant behavioral cost, suggesting a shared underlying neural process. Indeed, neural decoders trained during motor inhibition were able to decode linguistic inhibition and vice versa. Depth-electrode recordings from the subthalamic nucleus (STN), a key basal ganglia area for inhibitory control, showed increased {beta}-band (13-30 Hz) activity during both linguistic and motor inhibition. Finally, disrupting the STN via deep-brain stimulation impaired behavioral and neural signatures of both linguistic and motor inhibition. Together, these findings show that the inhibitory control of language and movement share a domain-general mechanism implemented via the subthalamic nucleus of the basal ganglia.

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bioRxiv2026

Two types of response inhibition failures in humans

Response inhibition is a key control function that allows humans to perform safe, goal-directed behaviors. The dominant behavioral-computational model holds that response inhibition fails when the inhibition process is too slow to intercept unwanted movements. However, many have hypothesized that some inhibitory failures instead result from a failure to launch the inhibition process altogether. Since no method exists to identify individual trigger failure (TF) trials, they are hitherto a largely hypothetical phenomenon. We combined Bayesian process-mixture modeling with likelihood ratio testing and jackknife resampling to identify TF trials in 253 humans. We find that TF indeed represent a separate category from other inhibitory failures. Unlike other inhibitory failures, TF do not result from premature responses. Furthermore, TF lack a stop-signal P3 event-related potential, a neural index of response inhibition. Surprisingly, TF do not result from perceptual/attentional lapses. Thus, TF are a qualitatively distinct class of executive failure during response inhibition.

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bioRxiv2026

Cortico-basal ganglia dynamics of global and selective response inhibition in humans

Response inhibition is an important cognitive control mechanism, which enables flexible behavior by stopping inappropriate actions. Intracranial recordings across species have identified a neural circuit that implements response inhibition via the subthalamic nucleus of the basal ganglia. However, this work has been limited to simple tasks, in which unequivocal, salient "stop"-signals require the inhibition of all ongoing responses. Notably, response inhibition in the real world is substantially different. Real-world response inhibition is selective: it occurs only after specific salient signals ( stimulus-selectivity) and stops only specific movements, while others continue ( response-selectivity). If and how the fronto-subthalamic system implements selective inhibition is largely unknown. Here, we recorded subthalamic local field potentials and scalp-EEG in humans performing a novel, selective inhibition task. Salient signals either required stopping all initiated responses (global inhibition), stopping only some responses (response-selective inhibition), or continuing all responses - i.e., ignoring the signal (which ensures stimulus-selectivity). All three signals initially triggered a common fronto-subthalamic inhibitory process, signified by a rapid increase in {beta}-burst activity. During global inhibition, subthalamic {beta}-bursting subsequently increased above baseline, persisting for over a second. During response-selective inhibition, this activity was delayed, which enabled a second bout of disinhibition and allowed appropriate responses to continue. Throughout this period, frontal cortical and subthalamic {beta}-band activity was tightly coupled. This shows that selective inhibition is implemented through rapid, context-dependent engagement and release of fronto-subthalamic inhibition. Moreover, subthalamic activity lasted substantially longer than assumed by classic behavioral-computational models. This supports recent theoretical models that assume protracted response inhibition during action-stopping.

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bioRxiv2025

Pupil dilation indexes - but does not causally influence - conscious error detection: a double-blind, placebo-controlled investigation of performance-monitoring using atomoxetine.

BackgroundConscious error detection is accompanied by error-related changes in phasic autonomic activity. This autonomic response is diminished in older age - accompanied by impairments in the conscious detection of action errors - i.e., increased error blindness. Indeed, the degree to which the autonomic response to errors declines across the lifespan is correlated with the increase in error blindness. However, the direction of causality - whether changes in autonomic reactivity are a consequence or cause of increased error blindness - is still debated. In the present study, we experimentally modulated the phasic autonomic response to action errors in healthy older adults while measuring their conscious error detection. MethodsAcross two sessions, thirty healthy older adults (60-80 years old) were given the sNRI atomoxetine or placebo in a double-blind fashion. In each session, they performed an anti-saccade task, which is commonly used to test conscious error detection. The autonomic response to errors was measured via changes in pupil dilation. A novelty-oddball task was also employed as a manipulation check. ResultsAtomoxetine reduced phasic pupil dilation to both novel stimuli in the novelty-oddball task and to action errors in the anti-saccade task. However, despite this blunting of the phasic autonomic response to errors, there were no significant differences in conscious error awareness between atomoxetine and placebo. Primary task performance was also unaffected. ConclusionsDespite its effects on phasic autonomic activity after errors, atomoxetine had no effect on conscious error detection in healthy older adults. This suggests that phasic autonomic activity is a consequence, rather than a contributing factor, to conscious error awareness. It also suggests that changes to phasic autonomic activity is unlikely to explain increased error blindness in older age.

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bioRxiv2025

Exploring neural mechanisms underlying error-related impairments in active working memory suggests an adaptive shielding of contents during cognitive control

Goal-directed behavior relies on cognitive flexibility - the ability to rapidly adapt ongoing thoughts and behaviors while preserving task-relevant information. The performance monitoring system optimizes such behavior by detecting and evaluating errors, while the working memory (WM) system maintains relevant information and protects it from interference. We investigated how these two systems interact. In prior work (Wessel et al., 2022), we found that motor errors impaired active WM maintenance (Error-Related Impairment of Active working Memory; ERIAM). Here, we aimed to identify the source of ERIAM by tracking a neurophysiological marker of visual WM maintenance - the contralateral delay activity (CDA) - throughout the error-making process. Forty-two human participants maintained visual information in WM while performing a motoric task during the delay period. Consistent with prior results, a significant ERIAM effect occurred: motor errors impaired WM performance. Critically, CDA amplitudes did not differ between motor correct and error trials before the flanker task, ruling out a general performance deficit. The CDA was also unaffected immediately after flankers, ruling out a perceptual interference explanation. Significant CDA differences only emerged after motor errors, supporting a genuinely error-related origin of the ERIAM effect. Contrary to prediction, however, CDA was more disrupted after correct responses than errors, and greater disruptions predicted a smaller ERIAM effect. These findings suggest that participants might store WM in multiple states to reduce interference from errors and that the CDA dynamics reflect these adaptive shielding strategies. These findings provide new insights into the source of error-related interference in active WM.

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bioRxiv2024

Common and unique neurophysiological signatures for the stopping and revising of actions reveal the temporal dynamics of inhibitory control

Inhibitory control is a crucial cognitive-control ability for behavioral flexibility that has been extensively investigated through action-stopping tasks. Multiple neurophysiological features have been proposed to represent signatures of inhibitory control during action-stopping, though the processes signified by these signatures are still controversially discussed. The present study aimed to disentangle these processes by comparing simple stopping situations with those in which additional action revisions were needed. Three experiments in female and male humans were performed to characterize the neurophysiological dynamics involved in action-stopping and - changing, with hypotheses derived from recently developed two-stage pause-then-cancel models of inhibitory control. Both stopping and revising an action triggered an early broad pause-process, marked by frontal EEG {beta}-bursts and non-selective suppression of corticospinal excitability. However, partial-EMG responses showed that motor activity was only partially inhibited by this pause, and that this activity can be further modulated during action-revision. In line with two-stage models of inhibitory control, subsequent frontocentral EEG activity after this initial pause selectively scaled depending on the required action revisions, with more activity observed for more complex revisions. This demonstrates the presence of a selective, effector-specific retune phase as the second process involved in action-stopping and -revision. Together, these findings show that inhibitory control is implemented over an extended period of time and in at least two phases. We are further able to align the most commonly proposed neurophysiological signatures to these phases and show that they are differentially modulated by the complexity of action-revision. Significance StatementInhibitory control is one of the most important control processes by which humans can regulate their behavior. Multiple neurophysiological signatures have been proposed to reflect inhibitory control. However, these play out on different time scales and appear to reflect different aspects of cognitive control, which are controversially debated. Recent two-stage models of inhibitory control have proposed that two phases implement the revisions of actions: pause and retune. Here, we provide the first empirical evidence for this proposition: Action revisions engendered a common initial low-latency pause, during which motor activity is broadly suppressed. Later activity, however, distinguishes between simple stopping of actions and more complex action revisions. These findings provide novel insights into the sequential dynamics of human action control.

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bioRxiv2024

Examining motor evidence for the pause-then-cancel model of action-stopping: Insights from motor system physiology

Stopping initiated actions is fundamental to adaptive behavior. Longstanding, single-process accounts of action-stopping have been challenged by recent, two-process, pause-then-cancel models. These models propose that action-stopping involves two inhibitory processes: 1) a fast Pause process, which broadly suppresses the motor system as the result of detecting any salient event, and 2) a slower Cancel process, which involves motor suppression specific to the cancelled action. A purported signature of the Pause process is global suppression, or the reduced corticospinal excitability (CSE) of task-unrelated effectors early on in action-stopping. However, unlike the Pause process, few (if any) motor system signatures of a Cancel process have been identified. Here, we used single- and paired-pulse TMS methods to comprehensively measure the local physiological excitation and inhibition of both responding and task-unrelated motor effector systems during action-stopping. Specifically, we measured CSE, short-interval intracortical inhibition (SICI), and the duration of the cortical silent period (CSP). Consistent with key predictions from the pause-then-cancel model, CSE measurements at the responding effector indicated that additional suppression was necessary to counteract Go-related increases in CSE during-action-stopping, particularly at later timepoints. Increases in SICI on Stop-signal trials did not differ across responding and non-responding effectors, or across timepoints. This suggests SICI as a potential source of global suppression. Increases in CSP duration on Stop- signal trials were more prominent at later timepoints. SICI and CSP duration therefore appeared most consistent with the Pause and Cancel processes, respectively. Our study provides further evidence from motor system physiology that multiple inhibitory processes influence action-stopping.

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bioRxiv2023

Biophysical modeling of frontocentral ERP generation links circuit-level mechanisms of action-stopping to a behavioral race model

Human frontocentral event-related potentials (FC-ERPs) are ubiquitous neural correlates of cognition and control, but their generating multiscale mechanisms remain mostly unknown. We used the Human Neocortical Neurosolver(HNN)s biophysical model of a canonical neocortical circuit under exogenous thalamic and cortical drive to simulate the cell and circuit mechanisms underpinning the P2, N2, and P3 features of the FC-ERP observed after Stop-Signals in the Stop-Signal task (SST). We demonstrate that a sequence of simulated external thalamocortical and cortico-cortical drives can produce the FC-ERP, similar to what has been shown for primary sensory cortices. We used this model of the FC-ERP to examine likely circuit-mechanisms underlying FC-ERP features that distinguish between successful and failed action-stopping. We also tested their adherence to the predictions of the horse-race model of the SST, with specific hypotheses motivated by theoretical links between the P3 and Stop process. These simulations revealed that a difference in P3 onset between successful and failed Stops is most likely due to a later arrival of thalamocortical drive in failed Stops, rather than, for example, a difference in effective strength of the input. In contrast, the same model predicted that early thalamocortical drives underpinning the P2 and N2 differed in both strength and timing across stopping accuracy conditions. Overall, this model generates novel testable predictions of the thalamocortical dynamics underlying FC-ERP generation during action-stopping. Moreover, it provides a detailed cellular and circuit-level interpretation that supports links between these macroscale signatures and predictions of the behavioral race model. Significance statementThe frontocentral event-related potential (FC-ERP) is an easily-measurable neural correlate of cognition and control. However, the cortical dynamics that produce this signature in humans are complex, limiting the ability of researchers to make predictions about its underlying mechanisms. In this study, we used the biophysical model included in the open-source Human Neocortical Neurosolver software to simulate and evaluate the likely cellular and circuit mechanisms that underlie the FC-ERP in the Stop-Signal task. We modeled mechanisms of the FC-ERP during successful and unsuccessful stopping, generating testable predictions regarding Stop-associated computations in human frontal cortex. Moreover, the resulting model parameters provide a starting point for simulating mechanisms of the FC-ERP and other frontal scalp EEG signatures in other task conditions and contexts.

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bioRxiv2022

Measuring the non-selective effects of motor inhibition using isometric force recordings

Inhibition is a key cognitive control mechanism. When rapidly exerted, inhibitory control has broad, non-selective motor effects, typically demonstrated using cortico-spinal excitability measurements (CSE) elicited by transcranial magnetic stimulation (TMS). For example, during rapid action-stopping, CSE is suppressed at both stopped and task-unrelated muscles. While such TMS-based CSE measurements provide crucial insights into the fronto-basal ganglia circuitry underlying non-selective inhibition, they have several downsides. TMS is contraindicated in many populations (e.g., epilepsy, deep-brain stimulation patients), has limited temporal resolution, produces distracting auditory and haptic stimulation, is difficult to combine with other imaging methods, and necessitates expensive, immobile equipment. Here, we attempted to measure the non-selective motor effects of inhibitory control using a method unaffected by these shortcomings. 30 participants exerted isometric force on a hand-held force transducer while performing a foot-response stop-signal task. Indeed, when foot movements were stopped, force output at the task-irrelevant hand was suppressed as well. Moreover, this non-selective reduction of isometric force was highly correlated with stop-signal performance and showed frequency dynamics similar to established inhibitory signatures typically found in neural and muscle recordings. Together, we demonstrate that isometric force recordings capture the non-selective effects of motor inhibition, enabling many applications that are impossible with TMS.

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bioRxiv2022

Beta bursts over frontal cortex track the surprise of unexpected events in auditory, visual, and tactile modalities

One of the fundamental ways in which the brain regulates and monitors behavior is by making predictions about the sensory environment and adjusting behavior when those expectations are violated. As such, surprise is one of the fundamental computations performed by the human brain. In recent years, it has been well-established that one key aspect by which behavior is adjusted during surprise is inhibitory control of the motor system. Moreover, since surprise automatically triggers inhibitory control without much proactive influence, it can provide unique insights into largely reactive control processes. Recent years have seen tremendous interest in burst-like {beta} frequency events in the human (and non-human) local field potential - especially over (pre)frontal cortex) - as a potential signature of inhibitory control. To date, {beta}-bursts have only been studied in paradigms involving a substantial amount of proactive control (such as the stop-signal task). Here, we used two cross-modal oddball tasks to investigate whether surprise processing is accompanied by increases in scalp-recorded {beta}-bursts. Indeed, we found that unexpected events in all tested sensory domains (haptic, auditory, visual) were followed by low-latency increases in {beta}-bursting over frontal cortex. Across experiments, {beta}-burst rates were positively correlated with estimates of surprise derived from Shannons information theory, a type of surprise that represents the degree to which a given stimulus violates prior expectations. As such, the current work clearly implicates frontal {beta}-bursts as a signature of surprise processing. We discuss these findings in the context of common frameworks of inhibitory and cognitive control after unexpected events.

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bioRxiv2022

Two types of motor inhibition after action errors in humans

Adaptive behavior requires the ability to appropriately react to action errors. Post-error slowing of response times (PES) is one of the most reliable phenomena in cognitive neuroscience. It has been proposed that PES is partially achieved through inhibition of the motor system. However, there is no direct evidence for this link - or indeed, that the motor system is physiologically inhibited after errors altogether. Here, we used transcranial magnetic stimulation and electromyography to measure cortico-spinal excitability (CSE) across four experiments using a Simon task, in which human participants sometimes committed errors. Errors were followed by reduced CSE at two different time points, and in two different modes. Shortly after error commission (250ms) CSE was broadly suppressed - i.e., even task-unrelated motor effectors were inhibited. During the preparation of the subsequent response, CSE was specifically reduced at task-related effectors only. This latter effect was directly related to PES, with stronger CSE suppression accompanying greater PES. This suggests that PES is achieved through increased inhibitory control during post-error responses. To provide converging evidence, we then re-analyzed an openly-available EEG dataset that contained both Simon- and Stop-signal tasks using independent component analysis. We found that the same neural source component that indexed action-cancellation in the stop-signal task also showed clear PES-related activity during post-error responses in the Simon task. Together, these findings provide clear evidence that post-error adaptation is partially achieved through motor inhibition. Moreover, inhibition is engaged in two modes (first non-selective, then selective), aligning with recent multi-stage theories of error processing.

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bioRxiv2022

Right inferior frontal cortex damage impairs the initiation of inhibitory control, but not its implementation

Inhibitory control is one of the most important control functions in the human brain. Much of our understanding of its neural basis comes from seminal work showing that lesions to the right inferior frontal cortex (rIFC) increase stop-signal reaction time (SSRT), a latent variable that expresses the speed of inhibitory control. However, recent work has identified substantial limitations of the SSRT method. Notably, SSRT is confounded by trigger failures: stop-signal trials in which inhibitory control was never initiated. Such trials inflate SSRT, but are typically indicative of attentional, rather than inhibitory deficits. Here, we used hierarchical Bayesian modeling to identify stop-signal trigger failures in human rIFC lesion patients, non-rIFC lesion patients, and healthy comparisons. Furthermore, we measured scalp-EEG to detect {beta}-bursts, a neurophysiological index of inhibitory control. rIFC lesion patients showed a more than five-fold increase in trigger failure trials and did not exhibit the typical increase of stop-related frontal {beta}- bursts. However, on trials in which such {beta}-bursts did occur, rIFC patients showed the typical subsequent upregulation of {beta} over sensorimotor areas, indicating that their ability to implement inhibitory control, once triggered, is intact. These findings suggest that the role of rIFC in inhibitory control has to be fundamentally reinterpreted.

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bioRxiv2022

Lingering neural representations of past task features adversely affect future behavior

During goal-directed behavior, humans purportedly form and retrieve so called event files - conjunctive representations that link context-specific information about stimuli, their associated actions, and the expected action-outcomes. The automatic formation - and later retrieval - of such conjunctive event file representations can substantially facilitate efficient action selection. However, recent behavioral work suggests that these event-files may also adversely affect future behavior, especially when action requirements have changed between successive instances of the same task context (e.g., during task-switching). Here, we directly tested this hypothesis through a recently developed method that allows measuring the strength of the neural representations of context-specific stimulus-action conjunctions (i.e., event files). Thirty-five male and female adult humans performed a task-switching paradigm while undergoing EEG recordings. Replicating previous behavioral work, we found that changes in action requirements between two spaced repetitions of the same task incurred a significant reaction time cost. By combining multi-variate pattern analysis and representational similarity analysis of the EEG recordings with linear mixed-effects modeling of trial-to-trial behavior, we then found that the magnitude of this behavioral cost was directly proportional to the strength of the conjunctive representation formed during the most recent previous exposure to the same task - i.e., the most recent event file. This confirms that the formation of conjunctive representations of specific task contexts, stimuli, and actions in the brain can indeed adversely affect future behavior. Moreover, these findings demonstrate the potential of neural decoding of complex task set representations towards the prediction of behavior beyond the current trial.

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bioRxiv2021

Towards a two-stage model of action-stopping: Attentional capture explains motor inhibition during early stop-signal processing

The ability to stop an already initiated action is paramount to adaptive behavior. Most scientific debate in the field of human action-stopping currently focuses on two interrelated questions. First: Which mental and neural processes underpin the implementation of inhibitory control, and which reflect the attentional detection of salient stop-signals instead? Second: Why do physiological signatures of inhibition occur at two different latencies after stop-signals (for visual signals, either before or after [~]150ms)? Here, we address both questions via two pre-registered experiments that combined transcranial magnetic stimulation, electromyography, and multi-variate pattern analysis of whole-scalp electroencephalography. Using a stop-signal task that also contained a second type of salient signal that did not require stopping, we found that both signals induced equal amounts of early-latency inhibitory activity, whereas only later signatures (after 175ms) distinguished the two. These findings resolve ongoing debates in the literature and strongly suggest a two-step model of action-stopping.

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bioRxiv2021

Cortico-subcortical β burst dynamics underlying movement cancellation in humans

Dominant neuroanatomical models hold that humans regulate their movements via loop-like cortico-subcortical networks, including the subthalamic nucleus (STN), thalamus, and sensorimotor cortices (SMC). Inhibitory commands across these networks are purportedly sent via transient, burst-like signals in the {beta} frequency (15-29Hz). However, since human depth-recording studies are typically limited to one recording site, direct evidence for this proposition is hitherto lacking. Here, we present simultaneous multi-site depth-recordings from SMC and either STN or thalamus in humans performing the stop-signal task. In line with their purported function as inhibitory signals, subcortical {beta}-bursts were increased on successful stop-trials and were followed within 50ms by increased {beta}-bursting over SMC. Moreover, between-site comparisons (including in a patient with simultaneous recordings from all three sites) confirmed that {beta}-bursts in STN precede thalamic {beta}-bursts. This provides first empirical evidence for the role of {beta}-bursts in conveying inhibitory commands along long-proposed cortico-subcortical networks underlying movement regulation in humans.

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bioRxiv2020

Latency and amplitude of the stop-signal P3 event-related potential are related to inhibitory GABAa activity in primary motor cortex

By stopping actions even after their initiation, humans can adapt their ongoing behavior rapidly to changing environmental circumstances. The neural processes underlying the implementation of rapid action-stopping are still controversially discussed. In the early 1990s, a fronto-central P3 event-related potential (ERP) was identified in the human EEG response following stop-signals in the classic stop-signal task, accompanied by the proposal that this ERP reflects the "inhibitory" side of the purported horse-race underlying successful action-stopping. Later studies have lent support to this interpretation by finding that the amplitude and onset of the stop-signal P3 relate to both overt behavior and to movement-related EEG activity in ways predicted by the race model. However, such studies are limited by the ability of EEG to allow direct inferences about the presence (or absence) of true, physiologically inhibitory signaling at the neuronal level. To address this, we here present a cross-modal individual differences investigation of the relationship between the features stop-signal P3 ERP and GABAergic neurotransmission in primary motor cortex (M1, as measured by paired-pulse transcranial magnetic stimulation). Following recent work, we measured short-interval intracortical inhibition (SICI), a marker of inhibitory GABAa activity in M1, in a group of 41 human participants who also performed the stop-signal task while undergoing EEG recordings. In line with the P3-inhibition hypothesis, we found that subjects with stronger inhibitory GABA activity in M1 also showed both faster onsets and larger amplitudes of the stop-signal P3. This provides direct evidence linking the properties of this ERP to a true physiological index of motor system inhibition. We discuss these findings in the context of recent theoretical developments and empirical findings regarding the neural implementation of inhibitory control during action-stopping.

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bioRxiv2020

Unexpected sounds non-selectively inhibit active visual stimulus representations

The brains capacity to process unexpected events is key to cognitive flexibility. The most well-known effect of unexpected events is the interruption of attentional engagement (distraction). We tested whether unexpected events interrupt attentional representations by activating a neural mechanism for inhibitory control. This mechanism is most well-characterized within the motor system. However, recent work showed that it is automatically activated by unexpected events and can explain some of their non-motor effects (e.g., on working memory representations). Here, human participants attended to lateralized flickering visual stimuli, producing steady-state visual evoked potentials (SSVEP) in the scalp-electroencephalogram. After unexpected sounds, the SSVEP was rapidly suppressed. Using a functional localizer (stop-signal) task and independent component analysis, we then identified a fronto-central EEG source whose activity indexes inhibitory motor control. Unexpected sounds in the SSVEP task also activated this source. Using single-trial analyses, we found that sub-components of this source differentially relate to sound-related SSVEP changes: while its N2 component predicted the subsequent suppression of the attended-stimulus SSVEP, the P3 component predicted the suppression of the SSVEP to the unattended stimulus. These results shed new light on the processes underlying fronto-central control signals and have implications for phenomena such as distraction and the attentional blink.

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bioRxiv2020

Non-selective inhibition of the motor system following unexpected and expected infrequent events

Motor inhibition is a key control mechanism that allows humans to rapidly adapt their actions in response to environmental events. One of the hallmark signatures of rapidly exerted, reactive motor inhibition is the non-selective suppression of cortico-spinal excitability (CSE): unexpected sensory stimuli lead to a suppression of CSE across the entire motor system, even in muscles that are inactive. Theories suggest that this reflects a fast, automatic, and broad engagement of inhibitory control, which facilitates behavioral adaptations to unexpected changes in the sensory environment. However, it is an open question whether such non-selective CSE suppression is truly due to the unexpected nature of the sensory event, or whether it is sufficient for an event to be merely infrequent (but not unexpected). Here, we report data from two experiments in which human subjects experienced both unexpected and expected infrequent events during a simple reaction time task while CSE was measured from a task-unrelated muscle. We found that expected infrequent events can indeed produce non-selective CSE suppression - but only when they occur during movement initiation. In contrast, unexpected infrequent events produce non-selective CSE suppression even in the absence of movement initiation. Moreover, CSE suppression due to unexpected events occurs at shorter latencies compared to expected infrequent events. These findings demonstrate that unexpectedness and stimulus infrequency have qualitatively different suppressive effects on the motor system. They also have key implications for studies that seek to disentangle neural and psychological processes related to motor inhibition and stimulus detection.

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