Early Action Error Processing Is Due to Domain-General Surprise, Whereas Later Processing Is Error Specific.

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, error-specific 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.SIGNIFICANCE STATEMENT Humans typically slow their actions after errors (PES). Some suggest that PES is a side effect of the unexpected, surprising nature of errors, challenging the notion of a genuine error processing system in the human brain. Here, we used multivariate EEG decoding to identify behavioral and neural processes uniquely related to error processing. Action slowing occurred following both action errors and error-unrelated surprise when time to prepare the next response was short. However, when there was more time to react, only errors were followed by slowing, further reflected in sustained neural activity. This suggests that errors and surprise initially share common processing, but that after additional time, error-specific, adaptive processes take over.

Adversity and error-monitoring: Effects of emotional context.

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.

Awareness of errors is reduced by sleep loss.

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.

Beyond peaks and troughs: Multiplexed performance monitoring signals in the EEG.

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.

Young adults who improve performance during dual-task walking show more flexible reallocation of cognitive resources: a mobile brain-body imaging (MoBI) study.

INTRODUCTION: In young adults, pairing a cognitive task with walking can have different effects on gait and cognitive task performance. In some cases, performance clearly declines whereas in others compensatory mechanisms maintain performance. This study investigates the preliminary finding of behavioral improvement in Go/NoGo response inhibition task performance during walking compared with sitting, which was observed at the piloting stage. MATERIALS AND METHODS: Mobile brain/body imaging (MoBI) was used to record electroencephalographic (EEG) activity, 3-dimensional (3D) gait kinematics and behavioral responses in the cognitive task, during sitting or walking on a treadmill. RESULTS: In a cohort of 26 young adults, 14 participants improved in measures of cognitive task performance while walking compared with sitting. These participants exhibited walking-related EEG amplitude reductions over frontal scalp regions during key stages of inhibitory control (conflict monitoring, control implementation, and pre-motor stages), accompanied by reduced stride-to-stride variability and faster responses to stimuli compared with those who did not improve. In contrast, 12 participants who did not improve exhibited no EEG amplitude differences across physical condition. DISCUSSION: The neural activity changes associated with performance improvement during dual tasking hold promise as cognitive flexibility markers that can potentially help assess cognitive decline in aging and neurodegeneration.

The role of left insula mediating impaired error processing in response inhibition in adult heavy drinkers.

Identification of neurobiological mechanisms underlying development of alcohol use disorder is critical to ensuring the appropriate early-phase treatment and prevention of the disorder. To this aim, we tried to elucidate the disturbance of neural functions in heavy drinking, which can lead to alcohol use disorder. Because response inhibition is affected by alcohol use disorder, we examined neural activation and task performance for response inhibition using the Go/No-Go task in an fMRI paradigm in adult non-dependent heavy and light drinkers. We examined the neural activation for error processing and inhibitory control, components of response inhibition. We then investigated the mediating effect of the relevant neural substrate on the relationship between the level of alcohol drinking and task performance using mediation analysis. We found that heavy drinking significantly decreased activation in the left insula during error processing and increased the mean commission error rate for No-Go trials compared with light drinking. Mediation analysis demonstrated full mediation of the left insula activation during error processing for the relationship between drinking level and commission error rate. Our results suggested that left insula activation may be a neural marker pivotal for potential conversion to alcohol use disorder in individuals with high clinical risk such as heavy drinking.

Not all errors are created equal: decoding the error-processing mechanisms using alpha oscillations.

Empirical evidence on error processing comes from the comparison between errors and correct responses in general, but essential differences may exist between different error types. Typically, cognitive control tasks elicit errors without conflicts (congruent errors) and with conflicts (incongruent errors), which may employ different monitoring and adjustment mechanisms. However, the neural indicators that distinguish between both error types remain unclear. To solve this issue, behavioral and electrophysiological data were measured while subjects performed the flanker task. Results showed that a significant post-error improvement in accuracy on incongruent errors, but not on congruent errors. Theta and beta power were comparable between both error types. Importantly, the basic error-related alpha suppression (ERAS) effect was observed on both errors, whereas ERAS evoked by incongruent errors was greater than congruent errors, indicating that post-error attentional adjustments are both source-general and source-specific. And the brain activity in alpha band, but not theta or beta band, successfully decoded congruent and incongruent errors. Furthermore, improved post-incongruent error accuracy was predicted by a measure of post-error attentional adjustments, the alpha power. Together, these findings demonstrate that ERAS is a reliable neural indicator for identifying error types, and directly conduces to the improvement of post-error behavior.

Getting off track: Cortical feedback processing network modulated by continuous error signal during target-feedback mismatch.

Performance monitoring and feedback processing - especially in the wake of erroneous outcomes - represent a crucial aspect of everyday life, allowing us to deal with imminent threats in the short term but also promoting necessary behavioral adjustments in the long term to avoid future conflicts. Over the last thirty years, research extensively analyzed the neural correlates of processing discrete error stimuli, unveiling the error-related negativity (ERN) and error positivity (Pe) as two main components of the cognitive response. However, the connection between the ERN/Pe and distinct stages of error processing, ranging from action monitoring to subsequent corrective behavior, remains ambiguous. Furthermore, mundane actions such as steering a vehicle already transgress the scope of discrete erroneous events and demand fine-tuned feedback control, and thus, the processing of continuous error signals - a topic scarcely researched at present. We analyzed two electroencephalography datasets to investigate the processing of continuous erroneous signals during a target tracking task, employing feedback in various levels and modalities. We observed significant differences between correct (slightly delayed) and erroneous feedback conditions in the larger one of the two datasets that we analyzed, both in sensor and source space. Furthermore, we found strong error-induced modulations that appeared consistent across datasets and error conditions, indicating a clear order of engagement of specific brain regions that correspond to individual components of error processing.

Frontal theta reveals further information about neural valence-dependent processing of augmented feedback in extensive motor practice-A secondary analysis.

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.

Prefrontal-cerebellar dynamics during post-success and post-error cognitive controls in major psychiatric disorders.

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.

The performance monitoring system is attuned to others' actions during dyadic motor interactions.

Interpersonal motor interactions require the simultaneous monitoring of one's own and one's partner's actions. To characterize how the action monitoring system tracks self and other behavior during synchronous interactions, we combined electroencephalography recordings and immersive virtual reality in two tasks where participants were asked to synchronize their actions with those of a virtual partner (VP). The two tasks differed in the features to be monitored: the Goal task required participants to predict and monitor the VP's reaching goal; the Spatial task required participants to predict and monitor the VP's reaching trajectory. In both tasks, the VP performed unexpected movement changes to which the participant needed to adapt. By extracting the neural activity locked to the detection of unexpected changes in the VP's action (other-monitoring) or to the participants' action-replanning (self-monitoring), we show that the monitoring system is more attuned to others' than to one's own actions. Additionally, distinctive neural responses to VP's unexpected goals and trajectory corrections were found: goal changes were reflected both in early fronto-central and later posterior neural responses while trajectory deviations were reflected only in later posterior responses. Altogether, our results indicate that the monitoring system adopts an inherent social mode to handle interpersonal motor interactions.

Tasting rewards. Effects of orosensory sweet signals on human error processing.

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.

Effects of trait empathy and expectation on the processing of observed actions.

Recent evidence suggests that the processing of observed actions may reflect an action prediction error, with more pronounced mediofrontal negative event-related potentials (ERPs) for unexpected actions. This evidence comes from an application of a false-belief task, where unexpected correct responses elicited high ERP amplitudes. An alternative interpretation is that the ERP component reflects vicarious error processing, as objectively correct responses were errors from the observed person's perspective. In this study, we aimed to disentangle the two possibilities by adding the factor task difficulty, which varied expectations without affecting the definition of (vicarious) errors, and to explore the role of empathy in action observation. We found that the relationship between empathy and event-related potentials (ERPs) mirrored the relationship between empathy and behavioral expectancy measures. Only in the easy task condition did higher empathy lead to stronger expectancy of correct responses in the true-belief and of errors in the false-belief condition. A compatible pattern was found for an early ERP component (150-200 ms) after the observed response, with a larger negativity for error than correct responses in the true-belief and the reverse pattern in the false-belief condition, but only in highly empathic participants. We conclude that empathy facilitates the formation of expectations regarding the actions of others. These expectations then modulate the processing of observed actions, as indicated by the ERPs in the present study.

Neural signature of error processing in major depression.

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.

Error-related modulations of the sensorimotor post-movement and foreperiod beta-band activities arise from distinct neural substrates and do not reflect efferent signal processing.

While beta activity has been extensively studied in relation to voluntary movement, its role in sensorimotor adaptation remains largely uncertain. Recently, it has been shown that the post-movement beta rebound as well as beta activity during movement-preparation are modulated by movement errors. However, there are critical functional differences between pre- and post-movement beta activities. Here, we addressed two related open questions. Do the pre- and post-movement error-related modulations arise from distinct neural substrates? Do these modulations relate to efferent signals shaping muscle-activation patterns or do they reflect integration of sensory information, intervening upstream of the motor output? For this purpose, first we exploited independent component analysis (ICA) which revealed a double dissociation suggesting that distinct neural substrates are recruited in error-related beta-power modulations observed before and after movement. Second, we compared error-related beta oscillation responses observed in two bimanual reaching tasks involving similar movements but different interlimb coordination, and in which the same mechanical perturbations induced different behavioral adaptive responses. While the task difference was not reflected in the post-movement beta rebound, the pre-movement beta activity was differently modulated according to the interlimb coordination. Critically, we show an uncoupling between the behavioral and the electrophysiological responses during the movement preparation phase, which demonstrates that the error-related modulation of the foreperiod beta activity does not reflect changes in the motor output from primary motor cortex. It seems instead to relate to higher level processing of sensory afferents, essential for sensorimotor adaptation.

The dynamics of error processing in the human brain as reflected by high-gamma activity in noninvasive and intracranial EEG.

Error detection in motor behavior is a fundamental cognitive function heavily relying on local cortical information processing. Neural activity in the high-gamma frequency band (HGB) closely reflects such local cortical processing, but little is known about its role in error processing, particularly in the healthy human brain. Here we characterize the error-related response of the human brain based on data obtained with noninvasive EEG optimized for HGB mapping in 31 healthy subjects (15 females, 16 males), and additional intracranial EEG data from 9 epilepsy patients (4 females, 5 males). Our findings reveal a multiscale picture of the global and local dynamics of error-related HGB activity in the human brain. On the global level as reflected in the noninvasive EEG, the error-related response started with an early component dominated by anterior brain regions, followed by a shift to parietal regions, and a subsequent phase characterized by sustained parietal HGB activity. This phase lasted for more than 1 s after the error onset. On the local level reflected in the intracranial EEG, a cascade of both transient and sustained error-related responses involved an even more extended network, spanning beyond frontal and parietal regions to the insula and the hippocampus. HGB mapping appeared especially well suited to investigate late, sustained components of the error response, possibly linked to downstream functional stages such as error-related learning and behavioral adaptation. Our findings establish the basic spatio-temporal properties of HGB activity as a neural correlate of error processing, complementing traditional error-related potential studies.

Evidence for a general performance-monitoring system in the human brain.

Adaptive behavior relies on the ability of the brain to form predictions and monitor action outcomes. In the human brain, the same system is thought to monitor action outcomes regardless of whether the information originates from internal (e.g., proprioceptive) and external (e.g., visual) sensory channels. Neural signatures of processing motor errors and action outcomes communicated by external feedback have been studied extensively; however, the existence of such a general action-monitoring system has not been tested directly. Here, we use concurrent EEG-MEG measurements and a probabilistic learning task to demonstrate that event-related responses measured by electroencephalography and magnetoencephalography display spatiotemporal patterns that allow an effective transfer of a multivariate statistical model discriminating the outcomes across the following conditions: (a) erroneous versus correct motor output, (b) negative versus positive feedback, (c) high- versus low-surprise negative feedback, and (d) erroneous versus correct brain-computer-interface output. We further show that these patterns originate from highly-overlapping neural sources in the medial frontal and the medial parietal cortices. We conclude that information about action outcomes arriving from internal or external sensory channels converges to the same neural system in the human brain, that matches this information to the internal predictions.

Executive functioning and psychological symptoms in food addiction: a study among individuals with severe obesity.

Food addiction (FA) has recently emerged as a new field in the study of obesity. Previous studies have contributed to identifying psychological correlates of FA. However, few researchers have examined the cognitive profile related to this condition; up until now, attentional biases related to food cues and a poorer performance monitoring have been observed. The present study aimed to examine the psychological profile and executive functioning related to FA in individuals with severe obesity and awaiting bariatric surgery. Participants (N = 86) were split into two groups, according to their level of FA symptoms (low FA vs high FA). Groups were compared on questionnaires measuring binge eating, depression and anxiety symptoms, and impulsivity as well as on measures reflecting executive functioning (D-KEFS and BRIEF-A). The relationship between FA groups and patterns of errors during the D-KEFS' Color-Word Interference Test was further analyzed. Individuals within the high FA group reported significantly more binge eating, depressive and anxiety symptoms, and more metacognitive difficulties. They also tended to show a poorer inhibition/cognitive flexibility score and a typical pattern of errors, characterized by an increased number of errors as the tasks' difficulty rose as opposed to a decreased number of errors, which characterizes an atypical pattern of errors. The present results show that the inability to learn from errors or past experiences is related to the severity of FA and overall impairments.Level of evidence Level V, descriptive study.

Conscious and unconscious performance monitoring: Evidence from patients with schizophrenia.

The ability to detect our own errors is an essential component of action monitoring. Using a masking paradigm in normal adults, we recently discovered that some error-detection processes can proceed without awareness, while other markers of performance monitoring such as the Error-Related Negativity (ERN) are tightly linked to conscious perception. Interestingly, research on cognitive deficit in schizophrenia has shown that the ERN is altered in these patients. In the present study, we therefore tested if the error detection impairment in schizophrenia is specific to conscious perception or is also found under non-conscious conditions, probing whether these performance monitoring processes are truly distinct. Thirteen patients with schizophrenia and thirteen age-matched healthy control subjects performed a speeded number comparison task on masked stimuli while EEG and MEG signals were recorded. Conscious perception and error-detection were assessed on a trial-by-trial basis using subjective reports of visibility and confidence. We found that patients with schizophrenia presented altered cingulate error-detection responses in conscious trials, as reflected by a decreased ERN. By contrast, on unconscious trials, both controls and schizophrenia patients performed above chance in evaluating the likelihood of having made an error. This dissociation confirms the existence of two distinct performance monitoring systems, and suggests that conscious metacognition in schizophrenia is specifically altered while non-conscious performance monitoring remains preserved.

Error-related brain activity and internalizing disorder symptom dimensions in depression and anxiety.

BACKGROUND: Research suggests that enhanced neural reactivity to errors, measured via the error-related negativity (ERN), is relatively unique to internalizing psychopathologies (IPs) and symptom clusters characterized by excessive worry and apprehension. However, no prior study has tested the association between the ERN and IP symptom dimensions in a heterogeneous, clinically representative patient population. The current study was designed to address this gap in the literature and clarify the role of the ERN in an adult IP treatment-seeking patient sample. METHOD: Eighty-five participants completed a well-validated flanker task known to robustly elicit the ERN and a battery of questionnaires assessing a range of IP symptoms. All participants had at least one IP diagnosis and over 75% had co-occurring IPs. A principal components analysis (PCA) was performed on the questionnaire data indicating two distinct factors that characterized the IP sample: affective distress/misery and fear-based anxiety. RESULTS: Analyses indicated that within this sample, an enhanced ERN, but not CRN, was associated with greater fear-based anxiety symptoms but had no relation with distress/misery symptoms. CONCLUSIONS: Together, these findings indicate that an enhanced ERN may not be specific to worry/apprehension and may extend to the IP fear dimension. The results also converge with a broader literature suggesting that fear-based psychopathology is characterized by an exaggerated reactivity to threat and this objective, psychophysiological response tendency may distinguish fear disorders from distress.