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This study tested whether self‐reports of childhood adversity would predict altered error processing under emotional versus non‐emotional task conditions. N = 99 undergraduates completed two selective attention tasks, a traditional color‐word Stroop task and a modified task using emotional words, while EEG was recorded. Participants also completed self‐report measures of adverse and positive childhood experiences, executive functioning, depression, current stress, and emotion regulation. Reports of adversity were robustly correlated with self‐reported challenges in executive functioning, even when controlling for self‐reported depression and stress, but adversity was not correlated with task performance. With regard to neural markers of error processing, adversity predicted an enhanced error‐related negativity and blunted error‐positivity, but only during the emotion‐word blocks of the task. Moreover, error‐related changes in alpha oscillations were predicted by adversity, in a pattern that suggested less error responsiveness in alpha patterns during the emotion block, compared to the color block, among participants with higher adversity. Overall, results indicate alterations in error monitoring associated with adversity, such that in an emotional context, initial error detection is enhanced and sustained error processing is blunted, even in the absence of overt performance changes. This study finds that individual differences in adverse childhood experiences are correlated with altered neural markers of error‐related processing, including enhanced initial error detection and blunted sustained allocation of attention to errors in participants who reported more adversity. However, these results were only evident in a selective attention task condition that included an emotional component, implying that adversity‐related effects on executive control are more likely to emerge under emotional contexts. [ABSTRACT FROM AUTHOR]

A central mechanism of human action control is the prompt binding between actions and the stimuli provoking them. Perceiving the same stimuli again retrieves any bound responses, facilitating their execution. An open question is whether such binding and retrieval only emerges when stimulus–response rules are known upon taking action or also when agents are forced to guess and receive feedback about whether they were successful or not afterward. In two experiments, we tested the hypothesis that knowing rules before responding would boost binding between stimuli and responses during action-taking relative to guessing situations. Second, we assessed whether the content of the feedback matters for binding in that agents might use feedback to build correct stimulus–response bindings even for wrong guesses. We used a sequential prime-probe design to induce stimulus–response binding for prime responses that were either rule-based or guesses, and to measure retrieval of these bindings in response times and errors in the probe. Results indicate that binding and retrieval emerge for successful but not for wrong guesses. Binding effects for correct guesses were consistently small in effect size, suggesting that pre-established stimulus–response bindings from instructed rules might indeed boost binding when taking action. [ABSTRACT FROM AUTHOR]

Accident analyses repeatedly reported the considerable contribution of run-offroad incidents to fatalities in road traffic, and despite considerable advances in assistive technologies to mitigate devastating consequences, little insight into the drivers' brain response during such accident scenarios has been gained. While various literature documents neural correlates to steering motion, the driver's mental state, and the impact of distraction and fatigue on driving performance, the cortical substrate of continuous deviations of a car from the road - i.e., how the brain represents a varying discrepancy between the intended and observed car position and subsequently assigns customized levels of corrective measures - remains unclear. Furthermore, the superposition of multiple subprocesses, such as visual and erroneous feedback processing, performance monitoring, or motor control, complicates a clear interpretation of engaged brain regions within car driving tasks. In the present study, we thus attempted to disentangle these subprocesses, employing passive and active steering conditions within both error-free and error-prone vehicle operation conditions. We recorded EEG signals of 26 participants in 13 sessions, simultaneously measuring pairs of Executors (actively steering) and Observers (strictly observing) during a car driving task. We observed common brain patterns in the Executors regardless of error-free or error-prone vehicle operation, albeit with a shift in spectral activity from motor beta to occipital alpha oscillations within erroneous conditions. Further, significant frontocentral differences between Observers and Executors, tracing back to the caudal anterior cingulate cortex, arose during active steering conditions, indicating increased levels of motor-behavioral cognitive control. Finally, we present regression results of both the steering signal and the car position, indicating that a regression of continuous deviations from the road utilizing the EEG might be feasible. [ABSTRACT FROM AUTHOR]

With the discovery of event‐related potentials elicited by errors more than 30 years ago, a new avenue of research on performance monitoring, cognitive control, and decision making emerged. Since then, the field has developed and expanded fulminantly. After a brief overview on the EEG correlates of performance monitoring, this article reviews recent advancements based on single‐trial analyses using independent component analysis, multiple regression, and multivariate pattern classification. Given the close interconnection between performance monitoring and reinforcement learning, computational modeling and model‐based EEG analyses have made a particularly strong impact. The reviewed findings demonstrate that error‐ and feedback‐related EEG dynamics represent variables reflecting how performance‐monitoring signals are weighted and transformed into an adaptation signal that guides future decisions and actions. The model‐based single‐trial analysis approach goes far beyond conventional peak‐and‐trough analyses of event‐related potentials and enables testing mechanistic theories of performance monitoring, cognitive control, and decision making. Performance monitoring and subsequent adaptations are highly dynamic processes. Here, I review recent advances in single‐trial EEG dynamics analyses that enabled the rigorous testing of predictions based on current theories and mathematically formalized computational models of performance monitoring, cognitive control, and decision making. I show that performance monitoring signals reflecting the transformation of outcome variables to adaptation signals are multiplexed in the EEG. [ABSTRACT FROM AUTHOR]

Abstract It has been demonstrated that during motor responses, the activation of the motor cortical regions emerges in close association with the activation of the medial frontal cortex implicated with performance monitoring and cognitive control. The present study explored the oscillatory neurodynamics of response-related potentials during correct and error responses to test the hypothesis that such continuous communication would modify the characteristics of motor potentials during performance errors. Electroencephalogram (EEG) was recorded at 64 electrodes in a four-choice reaction task and response-related potentials (RRPs) of correct and error responses were analysed. Oscillatory RRP components at extended motor areas were analysed in the theta (3.5–7 Hz) and delta (1–3 Hz) frequency bands with respect to power, temporal synchronization (phase-locking factor, PLF), and spatial synchronization (phase-locking value, PLV). Major results demonstrated that motor oscillations differed between correct and error responses. Error-related changes (1) were frequency-specific, engaging delta and theta frequency bands, (2) emerged already before response production, and (3) had specific regional topographies at posterior sensorimotor and anterior (premotor and medial frontal) areas. Specifically, the connectedness of motor and sensorimotor areas contra-lateral to the response supported by delta networks was substantially reduced during errors. Also, there was an error-related suppression of the phase stability of delta and theta oscillations at these areas. This synchronization reduction was accompanied by increased temporal synchronization of motor theta oscillations at bi-lateral premotor regions and by two distinctive error-related effects at medial frontal regions: (1) a focused fronto-central enhancement of theta power and (2) a separable enhancement of the temporal synchronization of delta oscillations with a localized medial frontal focus. Together, these observations indicate that the electrophysiological signatures of performance errors are not limited to the medial frontal signals, but they also involve the dynamics of oscillatory motor networks at extended cortical regions generating the movement. Also, they provide a more detailed picture of the medial frontal processes activated in relation to error processing.

The ability to detect and subsequently correct errors is important in preventing the detrimental consequences of sleep loss. The Error Related Negativity (ERN), and the error positivity (Pe) are established neural correlates of error processing. Previous work has shown sleep loss reduces ERN and Pe, indicating sleep loss impairs error‐monitoring processes. However, no previous work has examined behavioral error awareness, in conjunction with EEG measures, under sleep loss conditions, and studies of sleep restriction are lacking. Using combined behavioral and EEG measures, we report two studies investigating the impact of total sleep deprivation (TSD) and sleep restriction (SR) on error awareness. Fourteen healthy participants completed the Error Awareness Task under conditions of TSD and 27 completed the same task under conditions of SR. It was found that TSD did not influence behavioral error awareness or ERN or Pe amplitude, however, SR reduced behavioral error awareness, increased the time taken to detect errors, and reduced Pe amplitude. Findings indicate individuals who are chronically sleep restricted are at risk for reduced recognition of errors. Reduced error awareness may be one factor contributing to the increased accidents and injuries seen in contexts where sleep loss is prevalent. This multi‐study report addresses critical gaps in previous literature by combining behavioral and EEG (ERN and Pe) measures to investigate both acute and chronic sleep deprivation effects on error awareness. Our findings provide a new perspective on reduced awareness of errors as a factor contributing to the increased accidents and injuries seen in contexts where sleep loss is prevalent. [ABSTRACT FROM AUTHOR]

Based on previous concepts that a distributed theta network with a central "hub" in the medial frontal cortex is critically involved in movement regulation, monitoring, and control, the present study explored the involvement of this network in error processing with advancing age in humans. For that aim, the oscillatory neurodynamics of motor theta oscillations was analyzed at multiple cortical regions during correct and error responses in a sample of older adults. Response-related potentials (RRPs) of correct and incorrect reactions were recorded in a four-choice reaction task. RRPs were decomposed in the time-frequency domain to extract oscillatory theta activity. Motor theta oscillations at extended motor regions were analyzed with respect to power, temporal synchronization, and functional connectivity. Major results demonstrated that errors had pronounced effects on motor theta oscillations at cortical regions beyond the medial frontal cortex by being associated with (1) theta power increase in the hemisphere contra-lateral to the movement, (2) suppressed spatial and temporal synchronization at pre-motor areas contra-lateral to the responding hand, (2) inhibited connections between the medial frontal cortex and sensorimotor areas, and (3) suppressed connectivity and temporal phase-synchronization of motor theta networks in the posterior left hemisphere, irrespective of the hand, left, or right, with which the error was made. The distributed effects of errors on motor theta oscillations demonstrate that theta networks support performance monitoring. The reorganization of these networks with aging implies that in older individuals, performance monitoring is associated with a disengagement of the medial frontal region and difficulties in controlling the focus of motor attention and response selection. [ABSTRACT FROM AUTHOR]

It has been demonstrated that during motor responses, the activation of the motor cortical regions emerges in close association with the activation of the medial frontal cortex implicated with performance monitoring and cognitive control. The present study explored the oscillatory neurodynamics of response-related potentials during correct and error responses to test the hypothesis that such continuous communication would modify the characteristics of motor potentials during performance errors. Electroencephalogram (EEG) was recorded at 64 electrodes in a four-choice reaction task and response-related potentials (RRPs) of correct and error responses were analysed. Oscillatory RRP components at extended motor areas were analysed in the theta (3.5–7 Hz) and delta (1–3 Hz) frequency bands with respect to power, temporal synchronization (phase-locking factor, PLF), and spatial synchronization (phase-locking value, PLV). Major results demonstrated that motor oscillations differed between correct and error responses. Error-related changes (1) were frequency-specific, engaging delta and theta frequency bands, (2) emerged already before response production, and (3) had specific regional topographies at posterior sensorimotor and anterior (premotor and medial frontal) areas. Specifically, the connectedness of motor and sensorimotor areas contra-lateral to the response supported by delta networks was substantially reduced during errors. Also, there was an error-related suppression of the phase stability of delta and theta oscillations at these areas. This synchronization reduction was accompanied by increased temporal synchronization of motor theta oscillations at bi-lateral premotor regions and by two distinctive error-related effects at medial frontal regions: (1) a focused fronto-central enhancement of theta power and (2) a separable enhancement of the temporal synchronization of delta oscillations with a localized medial frontal focus. Together, these observations indicate that the electrophysiological signatures of performance errors are not limited to the medial frontal signals, but they also involve the dynamics of oscillatory motor networks at extended cortical regions generating the movement. Also, they provide a more detailed picture of the medial frontal processes activated in relation to error processing. [ABSTRACT FROM AUTHOR]

Accident analyses repeatedly reported the considerable contribution of run-off-road incidents to fatalities in road traffic, and despite considerable advances in assistive technologies to mitigate devastating consequences, little insight into the drivers’ brain response during such accident scenarios has been gained. While various literature documents neural correlates to steering motion, the driver’s mental state, and the impact of distraction and fatigue on driving performance, the cortical substrate of continuous deviations of a car from the road – i.e., how the brain represents a varying discrepancy between the intended and observed car position and subsequently assigns customized levels of corrective measures – remains unclear. Furthermore, the superposition of multiple subprocesses, such as visual and erroneous feedback processing, performance monitoring, or motor control, complicates a clear interpretation of engaged brain regions within car driving tasks. In the present study, we thus attempted to disentangle these subprocesses, employing passive and active steering conditions within both error-free and error-prone vehicle operation conditions. We recorded EEG signals of 26 participants in 13 sessions, simultaneously measuring pairs of Executors (actively steering) and Observers (strictly observing) during a car driving task. We observed common brain patterns in the Executors regardless of error-free or error-prone vehicle operation, albeit with a shift in spectral activity from motor beta to occipital alpha oscillations within erroneous conditions. Further, significant frontocentral differences between Observers and Executors, tracing back to the caudal anterior cingulate cortex, arose during active steering conditions, indicating increased levels of motor-behavioral cognitive control. Finally, we present regression results of both the steering signal and the car position, indicating that a regression of continuous deviations from the road utilizing the EEG might be feasible.

For motor learning, the processing of behavioral outcomes is of high significance. The feedback‐related negativity (FRN) is an event‐related potential, which is often described as a correlate of the reward prediction error in reinforcement learning. The number of studies examining the FRN in motor tasks is increasing. This meta‐analysis summarizes the component in the motor domain and compares it to the cognitive domain. Therefore, a data set of a previous meta‐analysis in the cognitive domain that comprised 47 studies was reanalyzed and compared to additional 25 studies of the motor domain. Further, a moderator analysis for the studies in the motor domain was conducted. The FRN amplitude was higher in the motor domain than in the cognitive domain. This might be related to a higher task complexity and a higher feedback ambiguity of motor tasks. The FRN latency was shorter in the motor domain than in the cognitive domain. Given that sensory information can be used as an external feedback predictor prior to the presentation of the final feedback, reward processing in the motor domain may have been faster and reduced the FRN latency. The moderator variable analysis revealed that the feedback modality influenced the FRN latency, with shorter FRN latencies after bimodal than after visual feedback. Processing of outcome feedback seems to share basic principles in both domains; however, differences exist and should be considered in FRN studies. Future research is motivated to scrutinize the effects of bimodal feedback and other moderators within the motor domain. This meta‐analysis highlights the special role of feedback processing in motor learning. It indicates that the feedback‐related negativity (FRN), which is a prominent neural correlate of reinforcement learning, has a higher amplitude and a shorter latency in motor tasks than in cognitive tasks. [ABSTRACT FROM AUTHOR]

Both anxiety and working memory capacity appear to predict increased (more negative) error‐related negativity (ERN) amplitudes, despite being inversely related to one another. Until the interactive effects of these variables on the ERN are clarified, there may be challenges posed to our ability to use the ERN as an endophenotype for anxiety, as some have suggested. The compensatory error monitoring hypothesis suggests that high trait‐anxiety individuals have larger ERN amplitudes because they must employ extra, compensatory efforts to override the working memory demands of their anxiety. Yet, to our knowledge, no ERN study has employed direct manipulation of working memory demands in conjunction with direct manipulations of induced (state) anxiety. Furthermore, little is known about how these manipulations affect other measures of error processing, such as the error‐related pupil dilation response and post‐error behavioral adjustments. Therefore, we manipulate working memory load and anxiety in a 2 × 2 within‐subjects design to examine the interactive effects of working memory load and anxiety on ERN amplitude, error‐related pupil dilation response amplitude, and post‐error behavior. There were no effects of our manipulations on ERN amplitude, suggesting a strong interpretation of compensatory error‐processing theory. However, our worry manipulation affected post‐error behavior, such that worry caused a reduction in post‐error accuracy. Additionally, our working memory manipulation affected error‐related PDR magnitude and the amplitude of the error‐related positivity (Pe), such that increased working memory load decreased the amplitude of these responses. Implications of these results within the context of the compensatory error processing framework are discussed. Working memory load and anxiety appear to influence error‐processing, particularly the error‐related negativity (ERN). However, their interactive effects on error‐processing are still not well understood, particularly in the context of state manipulations. The present study is the first, to our knowledge, to simultaneously manipulate both working memory load and anxiety induction in an ERN paradigm. We also make a novel contribution to the literature by recording simultaneous pupillometry in the same paradigm. [ABSTRACT FROM AUTHOR]

The ability to adapt behavior after erroneous actions is one of the key aspects of cognitive control. Error commission typically causes people to slow down their subsequent actions [post-error slowing (PES)]. Recent work has challenged the notion that PES reflects adaptive, controlled processing and instead suggests that it is a side effect of the surprising nature of errors. Indeed, human neuroimaging suggests that the brain networks involved in processing errors overlap with those processing error-unrelated surprise, calling into question whether there is a specific system for error processing in the brain at all. In the current study, we used EEG decoding and a novel behavioral paradigm to test whether there are indeed unique, errorspecific processes that contribute to PES beyond domain-general surprise. Across two experiments in male and female humans (N = 76), we found that both errors and error-unrelated surprise were followed by slower responses when response-stimulus intervals were short. Furthermore, the early neural processes following error-specific and domain-general surprise showed significant cross-decoding. However, at longer intervals, which provided additional processing time, only errors were still followed by post-trial slowing. Furthermore, this error-specific PES effect was reflected in sustained neural activity that could be decoded from that associated with domain-general surprise, with the strongest contributions found at lateral frontal, occipital, and sensorimotor scalp sites. These findings suggest that errors and surprise initially share common processes, but that after additional processing time, unique, genuinely error-specific processes take over and contribute to behavioral adaptation. [ABSTRACT FROM AUTHOR]

Background: Difficulty in cognitive adjustment after a conflict or error is a hallmark for many psychiatric disorders, yet the underlying neural correlates are not fully understood. We have previously shown that post-success and post-error cognitive controls are associated with distinct mechanisms particularly related to the prefrontal-cerebellar circuit, raising the possibility that altered dynamic interactions in this circuit may underlie mental illness. Methods: This study included 136 patients with three diagnosed disorders [48 schizophrenia (SZ), 49 bipolar disorder (BD), 39 attention deficit hyperactivity disorder (ADHD)] and 89 healthy controls who completed a stop-signal task during fMRI scans. Brain activations for concurrent, post-success, and post-error cognitive controls were analyzed and compared between groups. Dynamic causal modeling was applied to investigate prefrontal-cerebellar effective connectivity patterns during post-success and post-error processing. Results: No significant group differences were observed for brain activations and overall effective connectivity structures during post-success and post-error conditions. However, significant group differences were shown for the modulational effect on top-down connectivity from the prefrontal cortex to the cerebellum during post-error trials (pFWE = 0.02), which was driven by reduced modulations in both SZ and ADHD. During post-success trials, there were significantly decreased modulational effect on bottom-up connectivity from the cerebellum to the prefrontal cortex in ADHD (pFWE = 0.04) and decreased driving input to the cerebellum in SZ (pFWE = 0.04). Conclusions: These findings suggest that patients with SZ and ADHD are associated with insufficient neural modulation on the prefrontal-cerebellar circuit during post-success and post-error cognitive processing, a phenomenon that may underlie cognitive deficits in these disorders. [ABSTRACT FROM AUTHOR]

How parents manifest symptoms of anxiety or depression may affect how children learn to modulate their own distress, thereby influencing the children's risk for developing an anxiety or mood disorder. Conversely, children's mental health symptoms may impact parents' experiences of negative emotions. Therefore, mental health symptoms can have bidirectional effects in parent-child relationships, particularly during moments of distress or frustration (e.g., when a parent or child makes a costly mistake). The present study used simultaneous functional magnetic resonance imaging (fMRI) of parent-adolescent dyads to examine how brain activity when responding to each other's costly errors (i.e., dyadic error processing) may be associated with symptoms of anxiety and depression. While undergoing simultaneous fMRI scans, healthy dyads completed a task involving feigned errors that indicated their family member made a costly mistake. Inter-brain, random-effects multivariate modeling revealed that parents who exhibited decreased medial prefrontal cortex and posterior cingulate cortex activation when viewing their child's costly error response had children with more symptoms of depression and anxiety. Adolescents with increased anterior insula activation when viewing a costly error made by their parent had more anxious parents. These results reveal cross-brain associations between mental health symptomatology and brain activity during parent-child dyadic error processing.

BackgroundError processing and inhibitory control enable the adjustment of behaviors to meet task demands. Functional magnetic resonance imaging studies report brain activation abnormalities in patients with obsessive-compulsive disorder (OCD) during both processes. However, conclusions are limited by inconsistencies in the literature and small sample sizes. Therefore, the aim here was to perform a meta-analysis of the existing literature using unthresholded statistical maps from previous studies.MethodsA voxelwise seed-based d mapping meta-analysis was performed using t-maps from studies comparing patients with OCD and healthy control subjects (HCs) during error processing and inhibitory control. For the error processing analysis, 239 patients with OCD (120 male; 79 medicated) and 229 HCs (129 male) were included, while the inhibitory control analysis included 245 patients with OCD (120 male; 91 medicated) and 239 HCs (135 male).ResultsPatients with OCD, relative to HCs, showed longer inhibitory control reaction time (standardized mean difference = 0.20, p = .03, 95% confidence interval = 0.016, 0.393) and more inhibitory control errors (standardized mean difference = 0.22, p = .02, 95% confidence interval = 0.039, 0.399). In the brain, patients showed hyperactivation in the bilateral dorsal anterior cingulate cortex, supplementary motor area, and pre-supplementary motor area as well as right anterior insula/frontal operculum and anterior lateral prefrontal cortex during error processing but showed hypoactivation during inhibitory control in the rostral and ventral anterior cingulate cortices and bilateral thalamus/caudate, as well as the right anterior insula/frontal operculum, supramarginal gyrus, and medial orbitofrontal cortex (all seed-based d mapping z value >2, p < .001).ConclusionsA hyperactive error processing mechanism in conjunction with impairments in implementing inhibitory control may underlie deficits in stopping unwanted compulsive behaviors in the disorder.

Supplementing an earlier analysis of event‐related potentials in extensive motor learning (Margraf et al., 2022a, 2022b), frontal theta‐band activity (4–8 Hz) was scrutinized. Thirty‐seven participants learned a sequential arm movement with 192 trials in each of five practice sessions. Feedback, based on a performance adaptive bandwidth, was given after every trial. Electroencephalogram (EEG) was recorded in the first and last practice sessions. The degree of motor automatization was tested under dual‐task conditions in a pre‐test–post‐test design. Quantitative error information was transported in both feedback conditions (positive and negative). Frontal theta activity was discussed as a general signal that cognitive control is needed and, therefore, was expected to be higher after negative feedback. Extensive motor practice promotes automatization, and therefore, decreased frontal theta activity was expected in the later practice. Further, it was expected that frontal theta was predictive for subsequent behavioural adaptations and the amount of motor automatization. As the results show, induced frontal theta power was higher after negative feedback and decreased after five sessions of practice. Moreover, induced theta activity was predictive for error correction and, therefore, an indicator of whether the recruited cognitive resources successfully induced behavioural adaptations. It remains to be solved why these effects, which fit well with the theoretical assumptions, were only revealed by the induced part of frontal theta activity. Further, the amount of theta activity during practice was not predictive for the degree of motor automatization. It seems that there might be a dissociation between attentional resources associated with feedback processing and attentional resources associated with motor control. [ABSTRACT FROM AUTHOR]

Background: Subclinical obsessive–compulsive symptoms (OCS) are common in children, and increase risk for later onset of obsessive–compulsive disorder (OCD). In pediatric patients with OCD, neuroimaging research implicates altered neural mechanisms for error‐processing, but whether abnormal brain response occurs with subclinical OCS remains poorly understood. Methods: Using functional magnetic resonance imaging (fMRI), 113 youth (8–18 years; 45 female) from a community sample were scanned during an error‐eliciting Go/No‐Go task. OCS were assessed dimensionally using the obsessive–compulsive subscale of the Child Behavior Checklist. The association between OCS scores and error‐related brain activity was examined at the whole‐brain level. Results: Lower OCS scores associated with stronger response to errors in dorsal anterior cingulate cortex (dACC), caudate, putamen, thalamus, and occipital cortex. Additionally, lower OCS related to higher capacity for inhibitory control, as indexed by greater accuracy on No‐Go trials during fMRI scanning. The relationship between lower OCS and better accuracy on No‐Go trials was mediated by greater error‐related dACC activity. Conclusions: The inverse relationship between OCS and error‐related activity in the dACC and extended cortical–striatal–thalamic circuitry may index an adaptive process by which subclinical OCS are minimized in youth. Further, these results identify an observable pattern of brain activity that tracks with subclinical OCS severity. Understanding the link between neural networks for error processing and the normal to abnormal range of OCS may pave the way for brain‐based strategies to identify children who are more likely to develop OCD and enable the targeting of preventive strategies to reduce risk. [ABSTRACT FROM AUTHOR]

• This paper demonstrated an LS-based multipath channel measurement method suitable for the SDR framework. The measurement method focused on signal processing within the SDR software, ensuring compatibility with most USRP devices. • Considering the LS estimation errors stemming from the low-rank correlation matrix within the SDR framework, we proposed employing a scrambled measurement signal to mitigate the correlation among the baseband signals. Furthermore, we illustrated the computational and application feasibility of these scrambled measurement signals through matrix eigenvalue decomposition. • In addition, to enhance the accuracy of channel measurement results, we analyzed and addressed the systematic errors of IQ imbalance and band limitation within the universal SDR framework. Finally, we conducted the proposed measurement method in simulated, semi-physical, and physical channels. Multipath channel measurement is the foundation of multipath channel modeling and analysis. Recently, the software defined radio (SDR) has provided new ideas for the design of multipath channel measurement systems due to universality and reconfigurability. Therefore, this paper introduces a multipath channel measurement method applicable to various SDR platforms. At first, to enhance the resolution of multipath measurements, a signal processing approach combining the least squares (LS) estimation algorithm within the SDR framework is proposed. Furthermore, to mitigate LS estimation errors stemming from high correlation among baseband signals, a scrambled measurement signal is introduced and its effectiveness is demonstrated through eigenvalue decomposition. Next, the systematic errors of In-phase and Quadrature (IQ) imbalance and bandwidth limitation are further analyzed and addressed within the SDR framework. Finally, the proposed measurement method is implemented based on a practical universal software radio peripheral (USRP) device and validated under simulated and real channels. The proposed measurement method mainly focuses on the baseband signal processing within the software component of SDR, making it applicable to most general USRP devices. The experiment results demonstrate that multipath channel measurement results with high accuracy can be obtained. [ABSTRACT FROM AUTHOR]

Adolescence is a developmental period characterized by increased social motivation and a heightened concern of peer evaluation. However, little research has examined social influences on neural functioning in adolescence. One psychophysiological measure of motivation, the error-related negativity (ERN), is an ERP following an error. In adults, the ERN is enhanced by contextual factors that influence motivation, such as social observation and evaluation. The current study examined relations among age and neural responses in social contexts in adolescence. Seventy-six adolescent girls (9-17 years old) completed a flanker task under two different conditions. In the social condition, adolescent girls were informed that two other adolescents would be observing and providing feedback about their performance. In the nonsocial condition, adolescent girls completed a flanker task alone and were told feedback was computer generated. Results revealed that younger adolescents exhibited a larger ERN in social contexts than nonsocial contexts. In contrast, there were no differences in the ERN between contexts among older adolescents. In addition, enhancements of the ERN in social contexts among younger adolescents diminished the relation between the ERN and age. These findings suggest that the ERN is sensitive to social contexts in early adolescence, and developmental changes in the ERN may be partially explained by contextual factors that influence motivation.

The goal of this study was to investigate the neural dynamics of error processing and post-error adjustments in cognitive control and attention to a cognitive task in schizophrenia. We adopted a time-frequency approach in order to examine activity in the theta and alpha frequency bands as indices of cognitive control and attentional engagement. The results showed that error processing was characterized by increases in theta-band activity, accompanied by decreases in alpha-band activity, in both healthy control participants and participants with schizophrenia. However, both the theta and alpha effects were significantly reduced in participants with schizophrenia. Post-error increases in theta activity were associated with improved accuracy on subsequent trials in control participants but not in participants with schizophrenia. In addition, increases in alpha-band activity were found in the prestimulus period before partial attention lapses, but only for control participants and participants with schizophrenia with relatively low positive symptom severity. These results provide evidence for a deficit in cognitive control mechanisms mediated by midfrontal theta activity in schizophrenia, and suggest a particularly pronounced deficit in patients' ability to engage adaptive control mechanisms following errors. Our results also indicate that partial attention lapses can be indexed in both control participants and participants with schizophrenia by increases in alpha activity, but that in schizophrenia this varies as a function of positive symptom severity. We suggest that disrupted theta-band function represents a key deficit of schizophrenia, whereas disruptions in the alpha band may be the byproduct of atypically regulated attention.

Reactive aggression in adolescents is characterized by high levels of impulsivity. This is associated with deficits in response inhibition and error processing and spontaneous emotion-driven responses to a perceived threat. However, the characteristics and cognitive neural mechanisms of response inhibition and error processing to indirect threat in adolescents with high levels of reactive aggression are unclear. This study explored the characteristics and cognitive neural mechanisms of response inhibition and error processing to fearful expressions in adolescents with high levels of reactive aggression using an emotional Go/No-Go paradigm combined with ERP recordings. Adolescents with high levels of reactive aggression (n = 31) and a control group (n = 30) took part in this study. Results showed that when presented with fearful expressions, adolescents with high levels of reactive aggression showed a smaller No-Go P3 effect and smaller ERN amplitudes following commission errors on the No-Go task than the control group. Results suggested that when presented with fearful expressions, adolescents with high levels of reactive aggression have impaired response inhibition in the later stage of actual inhibitory control of the motor system and impaired error processing in the early stage of fast and automatic initial error detection. [ABSTRACT FROM AUTHOR]

The cognitive system readily detects and corrects erroneous actions by establishing episodic bindings between representations of the acted upon stimuli and the intended correct response. If these stimuli are encountered again, they trigger the retrieval of the correct response. Thus, binding and retrieval efficiently pave the way for future success. The current study set out to define the role of the erroneous response itself and explicit feedback for the error during these processes of goal-based binding and retrieval. Two experiments showed robust and similar binding and retrieval effects with and without feedback and pointed towards sustained activation of the unbound, erroneous response. The third experiment confirmed that the erroneous response is more readily available than a neutral alternative. Together, the results demonstrate that episodic binding biases future actions toward success, guided primarily through internal feedback processes, while the erroneous response still leaves detectable traces in human action control. [ABSTRACT FROM AUTHOR]

The literature on narcissism suggests two contradictory ways how highly narcissistic individuals deal with their failures: They might avoid consciously recognising their failures to protect their ego or they might vigilantly turn towards their failures to process cues that are important for maintaining their grandiosity. We tried to dissolve these contradictory positions by studying event-related potential components of error processing and their variations with narcissism. With a speeded go/no-go task, we examined how the error-related negativity (Ne; reflecting an early, automatic processing stage) and the error positivity (Pe; associated with conscious error detection) vary with Admiration and Rivalry, two narcissism dimensions, under egothreatening conditions. Using multilevel models, we showed that participants with high Rivalry displayed higher Ne amplitudes suggesting a heightened trait of defensive reactivity. We did not find variations of either narcissism dimension with the Pe, which would have pointed to weaker error awareness. Thus, our results only supported the second position: a heightened vigilance to errors in narcissism at early, rather automatic processing stages. [ABSTRACT FROM AUTHOR]

Human research has shown interactions between rewards and cognitive control. In animal models of affective neuroscience, reward administration typically involves administering orosensory sugar signals (OSS) during caloric-deprived states. We adopted this procedure to investigate neurophysiological mechanisms of reward-cognitive control interactions in humans. We predicted that OSS would affect neurophysiological and behavioral indices of error processing oppositely, depending on the relative weight of the OSS-induced 'wanting' and 'liking' components of reward. We, therefore, conducted a double-blind, non-nutritive sweetener-controlled study with a within-subject design. Fasted (16 hr) participants (N = 61) performed a modified Flanker task to assess neurophysiological (error-related negativity [Ne/ERN]) and behavioral (post-error adaptations) measures of error processing. Non-contingent to task performance, we repeatedly administered either a sugar (glucose) or non-nutritive sweetener (aspartame) solution, which had to be expulsed after short oral stimulation to prevent post-oral effects. Consistent with our hypothesis on how 'liking' would affect Ne/ERN amplitude, we found the latter to be decreased for sugar compared to aspartame. Unexpectedly, we found post-error accuracy, instead of post-error slowing, to be reduced by sugar relative to aspartame. Our findings suggest that OSS may interact with error processing through the 'liking' component of rewards. Adopting our reward-induction procedure (i.e. administering OSS in a state of high reward sensitivity [i.e. fasting], non-contingent to task performance) might help future research investigating the neural underpinnings of reward-cognitive control interactions in humans. [ABSTRACT FROM AUTHOR]

Non-suicidal self-injury (NSSI), as a highly prevalent psychiatric symptom in adolescents and young adults, is defined as the deliberate destruction of body tissue without suicidal intent. Impulsivity and dysfunctional response inhibition have been suggested to play a central role in adolescents' vulnerability to self-harm. To investigate the potentially distinct neurobiology of NSSI, we used a well-established Go/No Go task in which activation of the inferior frontal gyrus (IFG) and dorsal anterior cingulate cortex (dACC) is interpreted as a neural correlate of processing failed response inhibition. Task-based functional magnetic resonance imaging data were obtained from 14 adolescents with a diagnosis of major depression and a history of NSSI (MD-NSSI), 13 depressed adolescents without NSSI (MD-only), and 14 healthy controls (HC). In line with hypotheses of dysfunctional response inhibition, we observed increased rates of commission errors in MD-NSSI along with significantly reduced error-related activations of the dACC and IFG. Intact response inhibition, as reflected by low commission error rates not different from HC, was observed in MD-only, along with increased activation of the error-processing network. Our findings support the hypothesis of a distinct neurobiological signature of NSSI. Further research on biomarkers of NSSI could focus on behavioral and neural correlates of failed response inhibition. [ABSTRACT FROM AUTHOR]

The ability to detect and monitor errors enables us to maintain optimal performance across tasks. One neurophysiological index of error monitoring is the error-related negativity (ERN), a fronto-central negative deflection peaking between 0 and 150 ms following an erroneous response. While the developmental literature has illustrated age-related differences in the ERN and its association with anxiety, the literature has mainly focused on the between-person differences of the ERN. Our study examined the within-person variations of the ERN in 115 community-dwelling 9- to 12-year-olds (66 girls; mean age/SD = 11.00/1.16 years). Participants completed an EEG Go/No-Go task and reported their anxiety symptoms. Multilevel growth analyses yielded significant within-person, curvilinear changes in the ERN throughout the task. Youths' trial-level ERN increased (i.e., became more negative) with early errors, but decreased with subsequent errors. This curvilinear pattern was evident in older, but not younger, youths. Age also interacted with anxiety symptoms: younger youths with higher anxiety showed a continuous increase in the ERN throughout the task, whereas older youths with higher anxiety showed an initial increase followed by a decline in the ERN. Our study contributed novel evidence for the development of the ERN and the underlying mechanisms of the ERN-anxiety relationship that cannot be captured by between-person approaches.

Cognitive control deficits and increased intra-subject variability have been well established as core characteristics of attention deficit hyperactivity disorder (ADHD), and there is a growing interest in their expression at the neural level. We aimed to study neural variability in ADHD, as reflected in theta inter-trial phase coherence (ITC) during error processing, a process that involves cognitive control. We examined both traditional event-related potential (ERP) measures of error processing (i.e., error-related negativity [ERN] and error-positivity [Pe]) and theta ITC within a prospective longitudinal study of children at familial risk for ADHD. The participants were 63 male adolescents who were followed since birth. At the age of 17 years old, they performed the stop-signal task (SST) while an electroencephalogram (EEG) recording was continuously carried out. The EEG data from the trials in which the subjects failed to inhibit their response were used to calculate three different neurophysiological measures (i.e., ERN, Pe, and theta ITC). Consistent with our hypotheses, theta ITC during error processing predicted ADHD symptomatology above and beyond the traditional ERP measures. Moreover, we found that ADHD symptoms throughout childhood were uniquely associated with theta ITC, beyond ADHD symptomatology during adolescence. Overall, our findings strengthen the view of increased neural variability (as reflected by theta ITC) as a neurophysiological characteristic of a core neural dysfunction in ADHD., (© 2025 The Author(s). Psychophysiology published by Wiley Periodicals LLC on behalf of Society for Psychophysiological Research.)

The purpose of this study was to investigate the combined effects of random and block practice, with errorless and errorful conditions, on motor learning. One hundred-twenty participants (all male, Mage = 21.19 ± 1.4 years) were randomly assigned to one of eight groups. Participants completed a dart throwing task across the experimental phases. In the retention test, evidence supporting the CI effect was found in the 'errorless' conditions, but not in the 'errorful' conditions. In the transfer tests, the findings indicated that the impact of errorless and errorful conditions on participants' automation levels depends on the structure of practice. Participants in the Random-Errorless group performed better in the transfer tests than those in the Random group and the Random-Errorful group, suggesting greater automation levels following errorless practice. [ABSTRACT FROM AUTHOR]

Adaptive behavior requires the ability to appropriately react to action errors. Post-error slowing (PES) of response times is one of the most reliable phenomena in human behavior. 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 corticospinal excitability (CSE) across four experiments using a Simon task, in which female and male 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 (250 ms), 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-relevant 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 reanalyzed 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 evidence that posterror adaptation is partially achieved through motor inhibition. Moreover, inhibition is engaged in two modes (first nonselective, then selective), aligning with recent multistage theories of error processing. [ABSTRACT FROM AUTHOR]

Errors and their consequences are typically studied by investigating changes in decision speed and accuracy in trials that follow an error, commonly referred to as "post-error adjustments". Many studies have reported that subjects slow down following an error, a phenomenon called "post-error slowing" (PES). However, the functional significance of PES is still a matter of debate as it is not always adaptive. That is, it is not always associated with a gain in performance and can even occur with a decline in accuracy. Here, we hypothesized that the nature of PES is influenced by one's speed-accuracy tradeoff policy, which determines the overall level of choice accuracy in the task at hand. To test this hypothesis, we had subjects performing a task in two distinct contexts (separate days), which either promoted speed (hasty context) or cautiousness (cautious context), allowing us to consider post-error adjustments according to whether subjects performed choices with a low or high accuracy level, respectively. Accordingly, our data indicate that post-error adjustments varied according to the context in which subjects performed the task, with PES being solely significant in the hasty context (low accuracy). In addition, we only observed a gain in performance after errors in a specific trial type, suggesting that post-error adjustments depend on a complex combination of processes that affect the speed of ensuing actions as well as the degree to which such PES comes with a gain in performance. [ABSTRACT FROM AUTHOR]

Errors and their consequences are typically studied by investigating changes in decision speed and accuracy in trials that follow an error, commonly referred to as “post-error adjustments”. Many studies have reported that subjects slow down following an error, a phenomenon called “post-error slowing” (PES). However, the functional significance of PES is still a matter of debate as it is not always adaptive. That is, it is not always associated with a gain in performance and can even occur with a decline in accuracy. Here, we hypothesized that the nature of PES is influenced by one’s speed-accuracy tradeoff policy, which determines the overall level of choice accuracy in the task at hand. To test this hypothesis, we had subjects performing a task in two distinct contexts (separate days), which either promoted speed (hasty context) or cautiousness (cautious context), allowing us to consider post-error adjustments according to whether subjects performed choices with a low or high accuracy level, respectively. Accordingly, our data indicate that post-error adjustments varied according to the context in which subjects performed the task, with PES being solely significant in the hasty context (low accuracy). In addition, we only observed a gain in performance after errors in a specific trial type, suggesting that post-error adjustments depend on a complex combination of processes that affect the speed of ensuing actions as well as the degree to which such PES comes with a gain in performance.

This study investigated whether detection of a performance mistake is followed by adaptive or detrimental effects on subsequent attention and performance. Using a Stroop task with spatial cueing, along with simultaneous EEG and pupillary measurements, we examined evidence bearing on two alternative hypotheses: maladaptive arousal and adaptive control. Error detection, indexed by the error‐related negativity ERP component, was followed by pupil dilation and suppression of EEG oscillations in the alpha band, two indices of arousal that were associated with one another on a trial‐by‐trial basis. On the trials following errors, there was neural evidence of enhanced spatial cueing, manifested in greater hemispheric activation contralateral to the cued visual field. However, this post‐error enhancement was not followed by changes in Stroop or spatial cueing effects in performance, nor by increased attentional cueing effects in ERP responses to targets. Rather, performance tended to be slower and less accurate following errors compared to correct trials, and higher post‐response arousal, indexed by larger pupils, predicted next‐trial slowing and decreased P2 amplitude to targets. Results favor the maladaptive arousal account of post‐error cognitive control and offer only limited support for adaptive control. This study combines EEG, pupillary, and performance measures to address whether making a mistake leads to arousal, which could either improve or worsen subsequent attention. Results imply that arousal following mistakes is generally disruptive without reliable benefits for attentional focus. The study contributes to understanding of the impact of self‐monitoring on cognition. [ABSTRACT FROM AUTHOR]

• Neural feedback processing is valence-dependent in extensive motor practice. • Feedback-related ERPs are associated to reinforcement and supervised learning. • Increase of the FRN for negative feedback reflects altered error prediction. • A late fronto-central positivity reflects practice-independent supervised learning. • P300 is related to valence-dependent, but practice-independent memory updating. Several event-related potentials (ERPs) are associated with the processing of valence-dependent augmented feedback during the practice of motor tasks. In this study, 38 students learned a sequential arm-movement-task with 192 trials in each of five practice sessions (960 practice trials in total), to examine practice-related changes in neural feedback processing. Electroencephalogram (EEG) was recorded in the first and last practice session. An adaptive bandwidth for movement accuracy led to equal amounts of positive and negative feedback. A frontal located negative deflection in the time window of the feedback-related negativity (FRN) was more negative for negative feedback and might reflect reward prediction errors in reinforcement learning. This negativity increased after extensive practice, which might indicate that smaller errors are harder to identify in the later phase. The late fronto-central positivity (LFCP) was more positive for negative feedback and is assumed to be associated with supervised learning and behavioral adaptations based on feedback with higher complexity. No practice-related changes of the LFCP were observed, which suggests that complex feedback is processed independent from the practice phase. The P300 displayed a more positive activation for positive feedback, which might be interpreted as the higher significance of positive feedback for the updating of internal models in this setting. A valence-independent increase of the P300 amplitude after practice might reflect an improved ability to update the internal representation based on feedback information. These results demonstrate that valence-dependent neural feedback processing changes with extensive practice of a novel motor task. Dissociating changes in latencies of different components support the assumption that they are related to distinct mechanisms of feedback-dependent learning. [ABSTRACT FROM AUTHOR]

• Performance and observation of auditory lexical decisions show similar ERP effects. • Monitoring of response errors under time pressure reveals a Pe-like effect. • Attention to errors in the auditory domain yields a P3b effect. • No typical ERN was observed for neither Performers nor Observers. This study investigates the error processing components in the EEG signal of Performers and Observers using an auditory lexical decision task, in which participants heard spoken items and decided for each item if it was a real word or not. Pairs of participants were tested in both the role of the Performer and the Observer. In the literature, an Error Related Negativity (ERN)-Error Positivity (Pe) complex has been identified for performed (ERN-Pe) and observed (oERN-oPe) errors. While these effects have been widely studied for performance errors in speeded decision tasks relying on visual input, relatively little is known about the performance monitoring signatures in observed language processing based on auditory input. In the lexical decision task, native Dutch speakers listened to real Dutch Words, Non-Words, and crucially, long Pseudowords that resembled words until the final syllable and were shown to be error-prone in a pilot study, because they were responded to too soon. We hypothesised that the errors in the task would result in a response locked ERN-Pe pattern both for the Performer and for the Observer. Our hypothesis regarding the ERN was not supported, however a Pe-like effect, as well as a P300 were present. Analyses to disentangle lexical and error processing similarly indicated a P300 for errors, and the results furthermore pointed to differences between responses before and after word offset. The findings are interpreted as marking attention during error processing during auditory word recognition. [ABSTRACT FROM AUTHOR]

• This is a systematic review on error processing alterations in neurological diseases. • The Error-Related Negativity (ERN) and Theta power are altered in many neurological disorders. • The Positivity Error (Pe) is preserved in most of the neurological disorders. • There are less consistent findings on post-error slowing and other error potentials. Detecting errors in one's own and other's actions is a crucial ability for learning and adapting behavior to everchanging, highly volatile environments. Studies in healthy people demonstrate that monitoring errors in one's own and others' actions are underpinned by specific neural systems that are dysfunctional in a variety of neurological disorders. In this review, we first briefly discuss the main findings concerning error detection and error awareness in healthy subjects, the current theoretical models, and the tasks usually applied to investigate these processes. Then, we report a systematic search for evidence of dysfunctional error monitoring among neurological populations (basal ganglia, neurodegenerative, white-matter diseases and acquired brain injury). In particular, we examine electrophysiological and behavioral evidence for specific alterations of error processing in neurological disorders. Error-related negativity (ERN) amplitude were reduced in most (although not all) neurological patient groups, whereas Positivity Error (Pe) amplitude appeared not to be affected in most patient groups. Also theta activity was reduced in some neurological groups, but consistent evidence on the oscillatory activity has not been provided thus far. Behaviorally, we did not observe relevant patterns of pronounced dysfunctional (post-) error processing. Finally, we discuss limitations of the existing literature, conclusive points, open questions and new possible methodological approaches for clinical studies. [ABSTRACT FROM AUTHOR]

Attention-deficit/hyperactivity disorder (ADHD), characterized by symptoms of inattention and/or hyperactivity and impulsivity, is a neurodevelopmental disorder associated with executive dysfunctions, including response inhibition and error processing. Research has documented a common co-occurrence between ADHD and pediatric irritability. The latter is more characterized by affective symptoms, specifically frequent temper outbursts and low frustration tolerance relative to typically developing peers. Shared and non-shared neural correlates of youths with varied profiles of ADHD and irritability symptoms during childhood remain largely unknown. This study first classified a large sample of youths in the Adolescent Brain Cognitive Development (ABCD) study at baseline into distinct phenotypic groups based on ADHD and irritability symptoms (N = 11,748), and then examined shared and non-shared neural correlates of response inhibition and error processing during the Stop Signal Task in a subset of sample with quality neuroimaging data (N = 5,948). Latent class analysis (LCA) revealed four phenotypic groups, i.e., high ADHD with co-occurring irritability symptoms (n = 787, 6.7%), moderate ADHD with low irritability symptoms (n = 901, 7.7%), high irritability with no ADHD symptoms (n = 279, 2.4%), and typically developing peers with low ADHD and low irritability symptoms (n = 9,781, 83.3%). Latent variable modeling revealed group differences in the neural coactivation network supporting response inhibition in the fronto-parietal regions, but limited differences in error processing across frontal and posterior regions. These neural differences were marked by decreased coactivation in the irritability only group relative to youths with ADHD and co-occurring irritability symptoms and typically developing peers during response inhibition. Together, this study provided initial evidence for differential neural mechanisms of response inhibition associated with ADHD, irritability, and their co-occurrence. Precision medicine attending to individual differences in ADHD and irritability symptoms and the underlying mechanisms are warranted when treating affected children and families. [ABSTRACT FROM AUTHOR]

Binding and retrieval of stimulus features, response features, and their attentional weighting tune cognitive processing to situational demands. The two mechanisms promote successful actions, especially in situations in which such actions depend on controlled processing. Here we explored binding and retrieval of attentional control states that follow from erroneous actions. By definition, such errors are characterized by insufficient cognitive control but at the same time, error detection has been shown to trigger corresponding adjustments to prevent future failures. We reanalyzed existing datasets and conducted a novel experiment to investigate whether error-induced control states become bound to task-relevant stimuli. Results point towards a binding and retrieval of error-induced control states; however, the effect appears to be less reliable than for binding and retrieval of specific stimulus and response features. We discuss potential implications and alternative interpretations in terms of a mediating impact of error-induced control.

Attention-deficit/hyperactivity disorder (ADHD), characterized by symptoms of inattention and/or hyperactivity and impulsivity, is a neurodevelopmental disorder associated with executive dysfunctions, including response inhibition and error processing. Research has documented a common co-occurrence between ADHD and pediatric irritability. The latter is more characterized by affective symptoms, specifically frequent temper outbursts and low frustration tolerance relative to typically developing peers. Shared and non-shared neural correlates of youths with varied profiles of ADHD and irritability symptoms during childhood remain largely unknown. This study first classified a large sample of youths in the Adolescent Brain Cognitive Development (ABCD) study at baseline into distinct phenotypic groups based on ADHD and irritability symptoms (N = 11,748), and then examined shared and non-shared neural correlates of response inhibition and error processing during the Stop Signal Task in a subset of sample with quality neuroimaging data (N = 5,948). Latent class analysis (LCA) revealed four phenotypic groups, i.e., high ADHD with co-occurring irritability symptoms (n = 787, 6.7%), moderate ADHD with low irritability symptoms (n = 901, 7.7%), high irritability with no ADHD symptoms (n = 279, 2.4%), and typically developing peers with low ADHD and low irritability symptoms (n = 9,781, 83.3%). Latent variable modeling revealed group differences in the neural coactivation network supporting response inhibition in the fronto-parietal regions, but limited differences in error processing across frontal and posterior regions. These neural differences were marked by decreased coactivation in the irritability only group relative to youths with ADHD and co-occurring irritability symptoms and typically developing peers during response inhibition. Together, this study provided initial evidence for differential neural mechanisms of response inhibition associated with ADHD, irritability, and their co-occurrence. Precision medicine attending to individual differences in ADHD and irritability symptoms and the underlying mechanisms are warranted when treating affected children and families.

The human cognitive system houses efficient mechanisms to monitor ongoing actions. Upon detecting an erroneous course of action, these mechanisms are commonly assumed to adjust cognitive processing to mitigate the error's consequences and to prevent future action slips. Here, we demonstrate that error detection has far earlier consequences by feeding back directly onto ongoing motor activity, thus cancelling erroneous movements immediately. We tested this prediction of immediate auto-correction by analysing how the force of correct and erroneous keypress actions evolves over time while controlling for cognitive and biomechanical constraints relating to response time and the peak force of a movement. We conclude that the force profiles are indicative of active cancellation by showing indications of shorter response durations for errors already within the first 100 ms, i.e. between the onset and the peak of the response, a timescale that has previously been related solely to error detection. This effect increased in a late phase of responding, i.e. after response force peaked until its offset, further corroborating that it indeed reflects cancellation efforts instead of consequences of planning or initiating the error.

Objective . Over the last decades, error-related potentials (ErrPs) have repeatedly proven especially useful as corrective mechanisms in invasive and non-invasive brain-computer interfaces (BCIs). However, research in this context exclusively investigated the distinction of discrete events into correct or erroneous to the present day. Due to this predominant formulation as a binary classification problem, classical ErrP-based BCIs fail to monitor tasks demanding quantitative information on error severity rather than mere qualitative decisions on error occurrence. As a result, fine-tuned and natural feedback control based on continuously perceived deviations from an intended target remains beyond the capabilities of previously used BCI setups. Approach. To address this issue for future BCI designs, we investigated the feasibility of regressing rather than classifying error-related activity non-invasively from the brain. Main results. Using pre-recorded data from ten able-bodied participants in three sessions each and a multi-output convolutional neural network, we demonstrated the above-chance regression of ongoing target-feedback discrepancies from brain signals in a pseudo-online fashion. In a second step, we used this inferred information about the target deviation to correct the initially displayed feedback accordingly, reporting significant improvements in correlations between corrected feedback and target trajectories across feedback conditions. Significance. Our results indicate that continuous information on target-feedback discrepancies can be successfully regressed from cortical activity, paving the way to increasingly naturalistic, fine-tuned correction mechanisms for future BCI applications., (Creative Commons Attribution license.)

Previous studies demonstrated binding and retrieval of stimuli and correct responses even for those episodes in which the actual response was wrong (goal-based binding and retrieval). In the current study, we tested whether binding based on a co-activation of stimuli and erroneous responses occurred simultaneously with goal-based binding, which could have been masked by a more efficient retrieval of goal-based bindings in previous studies. In a pre-registered experiment (n = 62), we employed a sequential prime-probe design with a three-choice colour categorisation task. Including three different responses in the task allowed us to conduct separate tests for stimulus-based episodic retrieval of either the correct response (goal-based) or of the actual erroneous response (coactivation-based) after committing an error. Replicating previous findings, our study provides support for goal-based binding of stimuli and correct responses after errors, while showing that there is no independent coactivation-based binding of the erroneous response itself. [ABSTRACT FROM AUTHOR]

Binding and retrieval of stimulus features, response features, and their attentional weighting tune cognitive processing to situational demands. The two mechanisms promote successful actions, especially in situations in which such actions depend on controlled processing. Here we explored binding and retrieval of attentional control states that follow from erroneous actions. By definition, such errors are characterized by insufficient cognitive control but at the same time, error detection has been shown to trigger corresponding adjustments to prevent future failures. We reanalyzed existing datasets and conducted a novel experiment to investigate whether error-induced control states become bound to task-relevant stimuli. Results point towards a binding and retrieval of error-induced control states; however, the effect appears to be less reliable than for binding and retrieval of specific stimulus and response features. We discuss potential implications and alternative interpretations in terms of a mediating impact of error-induced control. [ABSTRACT FROM AUTHOR]

When unexpected events occur during goal‐directed behavior, they automatically trigger an orienting‐related cascade of psychological and neural processes through which they influence behavior and cognition. If the unexpected event was caused by an action error, additional error‐specific, strategic‐related processes have been proposed to follow the initial orienting period. Little is known about the neural interactions between action errors and unexpected perceptual events, two instantiations of unexpected events, in these two putative stages of post‐error processing. Here, we aimed to address this by investigating the electrophysiological dynamics associated with action errors and unexpected perceptual events using scalp EEG with a focus on the frontal midline (FM) delta‐to‐theta oscillations (1–8 Hz) indicative of the performance‐monitoring system. Specifically, we examined how the timing of unexpected sounds would influence behavior and neural oscillations after action errors, depending on the length of the intertrial interval (ITI). Our data showed that unexpected sounds aggravated post‐error decreases in accuracy when they occurred (1) immediately after errors (i.e., post‐error orienting period), regardless of ITI and (2) immediately after the post‐error stimulus (i.e., post‐error strategic period), at short ITIs. Meanwhile, action errors and unexpected sounds independently produced increased FM delta‐to‐theta power during the post‐error orienting period, regardless of ITIs. However, when unexpected sounds occurred during the post‐error strategic period, action errors produced lower FM delta‐to‐theta power than correct responses, at short ITIs. These differential effects of unexpected events on behavior and FM delta‐to‐theta dynamics support the notion of the two post‐error periods during which different processes are implemented. We provide evidence from behavior and frontal midline delta‐to‐theta oscillations in support of the notion of the two post‐error periods (immediately following an error or following the subsequent stimulus). Error processing is differentially affected by the occurrence of other unexpected events during the two post‐error periods. These findings are in line with the adaptive orienting theory of error processing. [ABSTRACT FROM AUTHOR]

When we make errors, we tend to experience a negative emotional state. In addition, if our errors are witnessed by other people, we might expect those observers to respond negatively. However, little is known about how implicit social feedback like facial expressions influences error processing. We explored this using the cognitive control phenomenon of post-error slowing: the tendency to slow the response immediately following an error. Adult participants performed a difficult perceptual task: estimating which of two lines (horizontal or vertical) was longer. The background showed an irrelevant distractor face with a happy, sad, or neutral expression. Participants slowed after errors only when the subsequent distractor face was happy, but not when the subsequent distractor was sad or neutral nor when a happy face followed a correct response. This suggests that information about others' affect, even non-interactive, task-irrelevant information, has performance- and valence-dependent effects on adaptive cognitive control.

Non-suicidal self-injury (NSSI), as a highly prevalent psychiatric symptom in adolescents and young adults, is defined as the deliberate destruction of body tissue without suicidal intent. Impulsivity and dysfunctional response inhibition have been suggested to play a central role in adolescents’ vulnerability to self-harm. To investigate the potentially distinct neurobiology of NSSI, we used a well-established Go/No Go task in which activation of the inferior frontal gyrus (IFG) and dorsal anterior cingulate cortex (dACC) is interpreted as a neural correlate of processing failed response inhibition. Task-based functional magnetic resonance imaging data were obtained from 14 adolescents with a diagnosis of major depression and a history of NSSI (MD-NSSI), 13 depressed adolescents without NSSI (MD-only), and 14 healthy controls (HC). In line with hypotheses of dysfunctional response inhibition, we observed increased rates of commission errors in MD-NSSI along with significantly reduced error-related activations of the dACC and IFG. Intact response inhibition, as reflected by low commission error rates not different from HC, was observed in MD-only, along with increased activation of the error-processing network. Our findings support the hypothesis of a distinct neurobiological signature of NSSI. Further research on biomarkers of NSSI could focus on behavioral and neural correlates of failed response inhibition.

The clinical presentation of major depression (MD) is heterogenous and comprises various affective and cognitive symptoms including an increased sensitivity to errors. Various electrophysiological but only few functional magnetic resonance imaging (fMRI) studies investigated neural error processing in MD with inconsistent findings. Thus, reliable evidence regarding neural signatures of error processing in patients with current MD is limited despite its potential relevance as viable neurobiological marker of psychopathology. We therefore investigated a sample of 16 young adult female patients with current MD and 17 healthy controls (HC). During fMRI, we used an established Erikson-flanker Go/NoGo-paradigm and focused on neural alterations during errors of commission. In the absence of significant differences in rates of errors of commission in MD compared to HC, we observed significantly (p < 0.05, FWE-corrected on cluster level) enhanced neural activations of the dorsal anterior cingulate cortex (dACC) and the pre-supplementary motor area (pre-SMA) in MD relative to HC and thus, in brain regions consistently associated to neural error processing and corresponding behavioral adjustments. Considering comparable task performance, in particular similar commission error rates in MD and HC, our results support the evidence regarding an enhanced responsivity of neural error detection mechanisms in MD as a potential neural signature of increased negative feedback sensitivity as one of the core psychopathological features of this disorder. [ABSTRACT FROM AUTHOR]

A number of studies suggest that event‐related potential (ERP) components previously associated with error processing might represent expectation violation instead of valence. When observing others, these processes might further be modulated by trait empathy. We suggest that trait empathy modulates expectancy formation and that these expectancies then influence observed response processing as reflected in a frontocentral negative ERP component resembling the previously described observer error‐related negativity. We acquired single trial ERPs of participants who observed another person in a true‐ or false‐belief condition answering correctly or erroneously. Additionally, we prompted participants' expectancy in some trials. Using linear mixed model analyses, we found that for low empathy participants, expectations for the false‐belief condition decreased throughout the experiment, so that expectations were more pronounced in participants with higher empathy toward the end of the experiment. We also found that single trial expectancy measures derived from regression models of the measured expectancies predicted the amplitude of the frontocentral negative ERP component, and that neither the addition of empathy nor accuracy or trial type (true‐ or false‐belief) led to the explanation of significantly more variance compared with the model just containing expectancy as predictor. These results suggest that empathy modulates the processing of observed responses indirectly via its effect on expectancy of the response. Inconclusive results regarding empathy in action observation could be explained by an interaction with expectancy. We applied a novel method combining single trial electroencephalography measures and linear mixed model analysis to investigate this theory. We were able to show an indirect influence of empathy on event‐related potential amplitudes via expectancy formation. [ABSTRACT FROM AUTHOR]

Error‐related negativity (ERN), an electroencephalogram (EEG) component following an erroneous response, has been associated with the subjective motivational relevance of error commission. A smaller EEG event, the correct response negativity (CRN), occurs after a correct response. It is unclear why correct behavior evokes a neural response similar to error commission. CRN might reflect suboptimal performance: in tasks where speed is motivationally relevant (i.e., incentivized), a correct but slow response may be experienced as a minor error. The literature is mixed on the relationship between CRN and response time (RT), possibly due to different motivational structures, tasks, or individual traits. We examined ERN and CRN in a go/no‐go task where correctness and speed were encouraged using a points‐based feedback system. A key individual trait, regulatory focus, describes a person's tendency to seek gains (promotion focus) and avoid losses (prevention focus). Trait regulatory focus was measured, and participants were randomly assigned to one of three conditions: points gain, points loss, and informative‐only feedback. Participants committed too few errors to reliably model ERN effects. CRN amplitude related to RT in all feedback conditions, with slower responses having larger CRN. Participants with stronger promotion focus had a more exaggerated RT/CRN relationship in the point gain condition, suggesting that regulatory fit influences the motivational relevance of speed and thus the negative subjective experience and CRN for slower responses. These findings are consistent with the claim that CRN reflects RT when RT is motivationally relevant and that the CRN/RT relationship reflects the degree of subjective motivational relevance. Our findings show that larger correct response negativities are associated with slower responses in a task with explicit response time feedback. Using regulatory fit theory, we further show that the correct response negativity reflects subjective motivational value from regulatory fit between promotion orientation strength and feedback framed as point gains. These findings suggest that correct response negativity reflects response time when response time is motivationally relevant. [ABSTRACT FROM AUTHOR]