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.

When researchers began addressing the electrophysiology of conscious error awareness more than a decade ago, the role of the error-related negativity (ERN), alongside the subsequently occurring error positivity (Pe), was an obvious locus of attention given the fact that they are taken as indices of cortical error processing. In contrast to the clear-cut findings that link the amplitude of the Pe to error awareness, the association between the ERN amplitude and error awareness is vastly unclear, with a range of studies reporting significant differences in the ERN amplitude with respect to error awareness, while others observing no modulation of the ERN amplitude. One problem in the studies obtaining null findings is the fact that conclusions are drawn based on small sample sizes, increasing the probability of type II error, especially given the fact that the ERN elicited using various error awareness paradigms tends to be small. The aim of the present study was to therefore address the issue of type II error in order to draw more certain conclusions about the modulation of the ERN amplitude by conscious error awareness. Forty participants performed a manual response inhibition task optimised to examine error awareness. While the early and late Pe amplitudes showed the expected sensitivity to error awareness, the ERN results depicted a more complex picture. The ERN amplitude for unaware errors appeared more negative than that of aware errors, both numerically and on the grand average ERP. The unexpected findings were explained in terms of (a) latency issues in the present data, (b) characteristics of the manual response inhibition task used and the possibility that it elicits variation in neurocognitive processing, and (c), in relation to possible contamination by the contingent negative variation (CNV), an ERP component elicited during response preparation. Suggestions for future research on how to address the issues raised in the present paper are also discussed.

Dans un environnement imprévisible, l'homme n'est pas toujours capable d'adapter son comportement à une situation donnée et commet alors des erreurs. Dans environ 95% des cas, ces erreurs sont commises consciemment. Cependant, le traitement de l'erreur par le cerveau ne s'opère pas de façon binaire. En effet, l'enregistrement de l'activité électromyographique (EMG) des muscles effecteurs des réponses, révèle, dans environ 15% des essais, une amorce de réponse incorrecte, une ébauche d'erreur. Dans ces essais, les sujets ont été capables de détecter, d'inhiber et de corriger leurs ébauches d'erreurs avant de produire la réponse correcte. Ces processus nécessitent-ils l'intervention de la conscience ? Quels en sont les marqueurs ?Nous montrons dans une première étude que les sujets sont capables d'une détection consciente de leurs ébauches d'erreurs dans un faible nombre de cas seulement (environ 30%). Nous mettons en évidence deux prédicteurs d'une telle détection : la taille de la bouffée EMG associée à l'ébauche d'erreur ainsi que le temps mis par les sujets, depuis le début de cette bouffée, pour la corriger et fournir la réponse correcte. Dans une deuxième étude, nous montrons qu'un indice électroencéphalographique (EEG), la Négativité d'erreur (Ne), pourrait servir de stimulus interne pour le cerveau, à la détection consciente des ébauches d'erreurs et des erreurs. Leur accès conscient interviendrait plus tardivement dans les ébauches d'erreurs que dans les erreurs, mais serait reflété dans les deux cas par des activités EEG similaires, la Positivité d'erreur (Pe). Ainsi, la correction des ébauches d'erreurs interfère avec leur accès conscient en le ralentissant. / In an unpredictable environment, man is not always able to adapt its behavior to a given situation and then makes mistakes. In about 95% of cases, these mistakes are made consciously. However, error processing in the brain does not occur in binary mode . Indeed, the recording of the electromyographic (EMG) activity of muscles involved in responses, reveals that, in about 15 % of the trials, there is a subthreshold incorrect EMG activity, called partial error, that precede the correct one. In these trials, the subjects were able to detect, inhibit their partial errors and correct them to produce the correct response.Does these processes require intervention of consciousness? What are the related markers ?We show in a first study that subjects are capable of conscious detection of their partial errors in a small number of cases (about 30 %).We highlight two predictors of such detection : the size of the EMG burst associated with the partial error and the time taken by the subjects, since EMG onset , to correct and to provide the correct response.In a second study , we show that an electroencephalographic (EEG) index, the error negativity (Ne) , could serve as an internal stimulus to the brain, for conscious detection of errors and partial errors. Their conscious access would occur later in partial errors than errors but would be reflected in both cases by similar a similar EEG activity, the error positivity (Pe). Thus, correction of partial errors interfere with their conscious access by slowing it.

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Moderate-to-severe traumatic brain injury (M/S TBI) is a growing public health concern with significant impact on the cognitive functioning of survivors. Cognitive control and deficits in awareness have been linked to poor recovery and rehabilitation outcomes. One way to research cognitive control is through awareness of errors using electroencephalogram and event-related potentials (ERPs). Both the error-related negativity and the post-error positivity components of the ERP are linked to error awareness and cognitive control processes. Attentional capacity and levels of apathy influence error awareness in those with M/S TBI. There are strong links between awareness, attention, and apathy. However, limited research has examined the role of attention, awareness, and apathy using electrophysiological indices of error awareness to further understand cognitive control in a M/S TBI sample. The current study sought to elucidate the role of apathy in error awareness in those with M/S TBI. Participants included 75 neurologically-healthy controls (divided randomly into two control groups) and 24 individuals with M/S TBI. All participants completed self-report measures of mood, apathy, and executive functioning, as well as a brief neuropsychological battery to measure attention and cognitive ability. To measure awareness, participants completed the error awareness task (EAT), a modified Stroop go/no-go task. Participants signaled awareness of errors committed on the previous trial. The M/S TBI group decreased accuracy while improving or maintaining error awareness compared to controls over time. There were no significant between-group differences for ERN and Pe amplitudes. Levels of apathy in the M/S TBI group were included in three multiple regression analyses predicting proportion of unaware errors, ERN amplitude, and Pe amplitude. Apathy was predictive of error awareness, although not in the predicted direction. Major analyses were replicated using two distinct control groups to determine potential sample effects. Results showed consistent results comparing both control groups to a M/S TBI group. Findings show variable levels of awareness and accuracy over time for those with M/S TBI when compared to controls. Conclusions include varying levels of attention and awareness from the M/S TBI group over time, evidenced by improving awareness of errors when they are happening, but an inability to regulate performance sufficiently to improve accuracy. Levels of apathy are playing a role in error awareness, however, not in predicted directions. The study provides support for the role of attentional impairments in error awareness and encourages future studies to look for varying levels of performance within a given task when using populations linked to elevated levels of apathy and attentional deficits.

[pt] A perda de insight nas próprias habilidades cognitivas pode ser uma característica de uma ampla gama de distúrbios neurológicos e pode ser relevante para os resultados clínicos e a eficácia da reabilitação. Além disso, pesquisas recentes têm mostrado que alterações na metacognição também podem caracterizar o envelhecimento saudável e interferir nas atividades da vida cotidiana, aumentando a incidência de um conjunto de comportamentos que afetam a saúde e a tomada de decisões. Considerando a natureza subjetiva da autoconsciência e a falta de consenso sobre instrumentos de avaliação para medir habilidades metacognitivas, é importante elucidar a neuroarquitetura da consciência metacognitiva e identificar biomarcadores de funções metacognitivas. A presente tese explora este tema através de quatro artigos. De acordo com o Modelo de Consciência Cognitiva (CAM), diferentes tipos de comprometimento da autoconsciência dependem de diferentes perfis de disfunções neurocognitivas, como anosognosia mnemônica e executiva. O primeiro é discutido no Artigo 1, que se concentra nos mecanismos subjacentes à autoconsciência prejudicada na doença de Alzheimer. Especificamente, as evidências sugerem que os pacientes com Alzheimer dependem de informações desatualizadas sobre si mesmos e são incapazes de consolidar novas informações como consequência da amnésia anterógrada e retrógrada. Além disso, achados de neuroimagem mostram que a degeneração fronto-cingulada e temporal estão implicadas em deficiências de autoconsciência. O Artigo 2, por sua vez, concentrou-se nos mecanismos neurais subjacentes à anosognosia executiva. Foi realizada uma revisão sistemática de estudos potenciais relacionados a eventos que investigam o automonitoramento em distúrbios neurológicos foi realizada para entender a contribuição de diferentes estruturas cerebrais para o monitoramento de erros. Especificamente, o estudo concentrou-se na negatividade relacionada ao erro (ERN) e na positividade do erro (Pe), que indexam a detecção de erros e a consciência do erro, respectivamente. Os achados sugerem a presença de processamento de domínio geral de detecção de erros com base em áreas cingulo-operculares e gânglios da base, mas também foi levantada a hipótese de que lesões fora da rede de monitoramento fronto-basal podem levar a déficits específicos de domínio. Para testar a hipótese de especificidade de domínio, foi realizado um estudo de potencial relacionado a eventos (Artigo 3). Um grupo de adultos jovens e idosos completou uma tarefa de flanker perceptual e de memória, e os resultados demonstraram que é possível diferenciar processos de automonitoramento em domínios cognitivos. Além disso, os achados de Pe demonstraram um declínio global da consciência de erro no envelhecimento. Curiosamente, apenas em adultos mais velhos, o aumento de Pe dentro da tarefa foi específico para o domínio da memória, sugerindo a presença de efeitos de aprendizagem para a memória, mas não para as decisões perceptivas. Foi levantada a hipótese de que as deficiências na percepção do erro podem estar associadas ao declínio sensorial no envelhecimento. Assim, o Artigo 4 investigou a associação entre Pe e potenciais bloqueados por estímulo em adultos jovens e idosos durante o desempenho da tarefa flanker de memória, a fim de entender a contribuição dos processos sensoriais ou de memória para mudanças relacionadas à idade na consciência de erro. Os resultados mostraram que a lembrança eficiente de estímulos foi associada a uma maior consciência de erro em adultos jovens e mais velhos e que a redução da consciência de erro em adultos mais velhos foi associada a deficiências no processamento perceptivo de estímulos. No geral, este trabalho contribui para nossa compreensão dos processos neurocognitivos subjacentes à consciência metacognitiva e correlatos neurais de diferentes tipos de anosognosia e apóia a conceituação multidimensional da consciência metacognitiva delineada pelo CAM. Os resultados do estudo oferecem novos insights sobre marcadores neurais de processos metacognitivos que podem servir para avaliação clínica e desenvolvimento de treinamento e reabilitação cognitiva. / [en] Loss of insight in own s cognitive abilities can be a feature of a wide range of neurological disorders and can be relevant for clinical outcomes and rehabilitation effectiveness. Furthermore, recent research has shown that changes in metacognition can also characterize healthy aging and interfere with everyday life activity, increasing the incidence of a set of behaviours affecting health and decision making. Considering the subjective nature of self-awareness and the lack of consensus on assessment instruments to measure metacognitive abilities, it is important to elucidate the neuroarchitecture of metacognitive awareness and identify biomarkers of metacognitive functions. The current thesis explores this topic through four articles. According to the Cognitive Awareness Model (CAM), different type of self-awareness impairments depends on different profiles of neurocognitive dysfunctions, such as mnemonic and executive anosognosia. The former is discussed in Article 1, which focuses on mechanisms underlying impaired self-awareness in Alzheimer s disease. Specifically, the evidence suggests that Alzheimer s patients rely on outdated information about the self and are unable to consolidate new information as consequence of anterograde and retrograde amnesia. Moreover, neuroimaging findings show that fronto-cingulate and temporal degeneration are implicated in self-awareness impairments. Article 2 focused instead on neural mechanisms underlying executive anosognosia. A systematic review of event-related potential studies investigating self-monitoring in neurological disorders was conducted to understand the contribution of different brain structures to error monitoring. Specifically, the study focused on the error-related negativity (ERN) and the error positivity (Pe), which index error detection and error awareness, respectively. The findings suggest the presence of domain-general processing of error detection relying on cingulo-opercular areas and basal ganglia, but it was also hypothesized that lesions outside the fronto-basal monitoring network may lead to domain-specific deficits. To test the domain- specificity hypothesis, an event-related potential study was conducted (Article 3). A group of young and older adults completed a perceptual and a memory flanker task and the findings demonstrated that it is possible to differentiate self-monitoring processes across cognitive domains. Moreover, Pe findings demonstrated a global decline of error awareness in aging. Interestingly, in older adults only, within-task increase in Pe was specific to the memory domain, suggesting the presence of learning effects for memory but not for perceptual decisions. It was hypothesized that error awareness impairments may be associated with sensory decline in aging. Thus, Article 4 investigated the association between Pe and stimulus-locked potentials in young and older adults during memory flanker task performance, in order to understand the contribution of sensory or memory processes to age-related changes in error awareness. The findings showed that efficient stimulus recollection was associated with higher error awareness in both young and older adults and that reduced error awareness in older adults was associated with impairments in perceptual processing of stimuli. Overall, this work contributes to our understanding of neurocognitive processes underlying metacognitive awareness and neural correlates of different types of anosognosia and supports the multidimensional conceptualization of metacognitive awareness delineated by the CAM. The study s results offer novel insights into neural markers of metacognitive processes that can serve clinical assessment and the development of cognitive training and rehabilitation.