Mental disorders present difficulties in the research of their mechanisms, considering the high levels of comorbidity and the lack of specific neuroscience data to evaluate them. Estipulating deficit circuits in the disorders and the best treatment is a complex task, given the limited comprehension of the factors that correlate to the disorders. The utilization of biomarkers has proved an efficient and reliable alternative to provide precise diagnosis. Among the biomarkers, the Error-Related Negativity component, an event-related cortical potential, has presented high indexes of stability and validity in correlating to anxiety, obsessive, and mood-related mental disorders. The present dissertation evaluated irritability traits in a community sample, using a Flanker task, that has consistently elicited Error-Related Negativity according to the literature. Our results corroborate literature and found a frontocentral negativity, that peaked around 100ms after the commission of an error in the Flanker Task. However, our manipulation of negative feedback did not support literature, and ERN amplitudes were less enhanced post negative feedback. The relationship between irritability and ERN remains unclear. Future studies should, therefore, address these questionings.

Over 20 years of research on terror management theory has demonstrated that reminders of death (mortality salience; MS) heighten individuals' investment in prioritized bases of value and meaning. Research in this vein has shown that MS intensifies people's efforts to demonstrate personal value on tasks relevant to their self-esteem ("self-esteem striving"). Though much work illustrates that such responses function to mitigate death-related concerns, to date no work has directly assessed the particular regulatory mechanisms that implement MS-induced self-esteem striving. The present study aimed to do so by measuring neural indices of performance monitoring. During a tasked framed as diagnostic of self-esteem relevant attributes, participants were randomly assigned to receive subliminal primes of the word death or of control terms. Response-locked brain signals were recorded to assess reactivity to correct and incorrect responses during the task. Results showed that death-primed (vs. control) participants exhibited greater neural reactivity following error commission as indexed by larger amplitude of the Error Related Negativity (ERN). Death-primed (vs. control) participants also exhibited intensified behavioral efforts to improve their performance following error commission (i.e., post-error slowing, post-error accuracy), effects that were likely mediated by the activity of neural mechanisms that generate the ERN. Furthermore, among death-primed participants, behavioral improvements on the self-esteem relevant task correlated with attenuations in death thought accessibility. Receiving death primes did not influence neural reactivity to correct responses (Correct Related Negativity; CRN) nor did it heighten a neural index of explicit error awareness (Error Positivity; Pe). Together these findings suggest that MS-induced self-esteem striving is implemented via automatic monitoring and avoidance of errors. The role of avoidance motivation in self-esteem striving is thus discussed.

Current research in stuttering suggests that individuals who stutter (IWS) may have a hyperactive error-monitoring system, leading to the exacerbation and anticipation of verbal dysfluencies. Using a neurophysiological marker of error processing known as the feedback error-related negativity, the current thesis involved three studies. First, a pilot study was conducted to ensure that word feedback cues were usable in the current paradigm. Second, a classic virtual T-maze task was used to assess the generic error processing mechanism of IWS. Third, an adaptation of the T-maze was used to assess the integrity of the reinforcement learning system of IWS and their ability to associate reward and error information of personalized problem words with predictive cues. Results suggest preliminary evidence for functional generic error processing in IWS and disrupted error processing when conditioned predictive cues are needed to predict fluent versus dysfluent outcomes. / Graduate

Mental disorders present difficulties in the research of their mechanisms, considering the high levels of comorbidity and the lack of specific neuroscience data to evaluate them. Estipulating deficit circuits in the disorders and the best treatment is a complex task, given the limited comprehension of the factors that correlate to the disorders. The utilization of biomarkers has proved an efficient and reliable alternative to provide precise diagnosis. Among the biomarkers, the Error-Related Negativity component, an event-related cortical potential, has presented high indexes of stability and validity in correlating to anxiety, obsessive, and mood-related mental disorders. The present dissertation evaluated irritability traits in a community sample, using a Flanker task, that has consistently elicited Error-Related Negativity according to the literature. Our results corroborate literature and found a frontocentral negativity, that peaked around 100ms after the commission of an error in the Flanker Task. However, our manipulation of negative feedback did not support literature, and ERN amplitudes were less enhanced post negative feedback. The relationship between irritability and ERN remains unclear. Future studies should, therefore, address these questionings.

Mental disorders present difficulties in the research of their mechanisms, considering the high levels of comorbidity and the lack of specific neuroscience data to evaluate them. Estipulating deficit circuits in the disorders and the best treatment is a complex task, given the limited comprehension of the factors that correlate to the disorders. The utilization of biomarkers has proved an efficient and reliable alternative to provide precise diagnosis. Among the biomarkers, the Error-Related Negativity component, an event-related cortical potential, has presented high indexes of stability and validity in correlating to anxiety, obsessive, and mood-related mental disorders. The present dissertation evaluated irritability traits in a community sample, using a Flanker task, that has consistently elicited Error-Related Negativity according to the literature. Our results corroborate literature and found a frontocentral negativity, that peaked around 100ms after the commission of an error in the Flanker Task. However, our manipulation of negative feedback did not support literature, and ERN amplitudes were less enhanced post negative feedback. The relationship between irritability and ERN remains unclear. Future studies should, therefore, address these questionings.

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Event-related potentials play a significant role in error processing and attentional processes. Specifically, event-related negativity (ERN), feedback-related negativity (FRN), and the P300 are related to performance monitoring. The current study examined these components in relation to subjective probability, or confidence, regarding response accuracy on a complicated learning task. Results indicated that confidence ratings were not associated with any changes in ERN, FRN, or P300 amplitude. P300 amplitude did not vary according to participants’ subjective probabilities. ERN amplitude and FRN amplitude did not change throughout the task as participants learned. Future studies should consider the relationship between ERN and FRN using a learning task that is less difficult than the one employed in this study.

Rejection sensitivity (RS) can have significant effects on interpersonal relationships. Previous research has shown the negative social effects of RS, but less is known about the cognitive implications of having high levels of RS. The current study examined the effect of RS on various event-related potential (ERP) components associated with performance monitoring (error-related negativity, ERN; feedback-related negativity, FRN) and attention (P300; late positive potential, LPP). Participants completed a social or nonsocial Flanker task and an emotional Stroop task. Results showed an increased ERN on error trials for individuals with higher RS. Although the FRN, P300, and LPP were not influenced by RS, FRN was influenced by an expectancy-valence interaction. FRN amplitude was also sensitive to condition, with correct feedback eliciting significantly more negative FRN in the social condition compared to the nonsocial condition; FRN for unexpected feedback was also greater in the social condition. Overall, the results suggest a relationship between error monitoring and RS, as well as a relationship between social information and feedback processing. Future research should further explore the potential relationship between rejection sensitivity and attention throughout goal-directed tasks.

Performance monitoring is a crucial metacognitive function that allows for adaptive behaviour. Electrophysiological studies on error monitoring specifically, have shown how error trials in different tasks elicit two distinct signatures, the error-related negativity (ERN) and the error positivity (Pe). While studies find a robust relation between error awareness and the Pe, results regarding error awareness and the ERN are more divergent. Also, no agreement has been reached on the mechanisms that elicit these signals. This meta-analysis aims to explore the relation between these electrophysiological signatures and error awareness and how disparities in study design might explain divergent study results. Two meta-analyses were conducted and found a significant effect-size for error awareness on both the ERN and the Pe. Subgroup analyses were conducted to explore how different study-characteristics can influence these outcomes. Although no effects were found, these results remain mainly inconclusive since the number of included studies was very low, and their study designs quite similar.

Autism spectrum disorder (ASD) is a highly heritable neurodevelopmental disorder associated with altered neural connectivity and deficits in self-monitoring, response inhibition, and planning. One promising avenue of research to improve understanding of the symptoms and heritable nature of ASD may be the identification of neural endophenotypes of ASD. The error-related negativity (ERN) and post-error positivity (Pe), scalp-recorded event-related potentials (ERPs), reflect performance monitoring processes and may qualify as candidate endophenotypes of ASD. We collected ERP and behavioral data (error rates, response times) from 18 ASD probands and their families (mother, father, sibling) and 38 control youth and their parents to examine the utility of the ERN and Pe as endophenotypes of ASD. In order to examine differences based on group (ASD vs. control) and kinship (proband, sibling, mother, father), we conducted separate multiple regression analyses on behavioral and ERP data with group and kinship as predictors and families as clusters. We hypothesized that ASD probands would display reduced-amplitude ERN and impaired behavioral performance relative to control youth but no differences in Pe amplitude and that families of ASD probands would display reduced error minus correct (ΔERN) amplitudes and impaired behavioral performance relative to control families but no differences in ΔPe amplitude. We did not observe significant ERN amplitude group differences among ASD probands relative to control youth. Likewise, control youth did not differ from ASD probands on behavioral measures or Pe amplitudes. Analyses by family revealed that group and kinship did not significantly predict ΔERN amplitudes. However, fathers of ASD probands displayed significantly reduced ΔPe amplitudes relative to control fathers and parents displayed significantly larger ΔPe amplitudes and better performance than youth. Together, results do not provide sufficient evidence to support the ERN or Pe as an endophenotype or biomarker of ASD. These findings add to an overall heterogeneous literature on performance monitoring in ASD and point to the need for additional research to understand the state-related or trait-related factors that may contribute to ERN amplitudes in ASD.