Master of Science / Department of Psychological Sciences / Michael Young / When making decisions, the probability and magnitude of errors can play a major role in changing preferences. Electroencephalography (EEG) research examining the error-related negativity (ERN) and the associated feedback-related negativity (FRN) has indicated that the amplitude of each component may predict subsequent behavioral change. The current study used a version of the Balloon Analogue Risk Task (BART) that involves outcomes that are dynamically changing over time. As the balloon grows, more points are available but the probability of the balloon popping (netting zero points) is higher; the participant decides when to stop the balloon’s expansion to maximize points. The BART was adapted to facilitate the study of the FRN in dynamic environments. The purpose of Experiment 1 was to determine the effect of error magnitude on FRN amplitude during popped (incorrect) trials, whereas Experiment 2 was aimed at determining the effect of error magnitude on FRN amplitude during cashed-in (correct) trials. It was hypothesized that larger errors (i.e., the balloon popping after waiting a long time to cash-in) would result in a larger FRN than smaller errors. In Experiment 1, error magnitude did not contribute to the amplitude of the FRN. In Experiment 2, the masked points possible condition was a replication of Experiment 1. In the unmasked points possible condition, the number of points that could have been earned for each balloon was presented before participants found out how many points were earned. It was expected that there would be a larger FRN magnitude after cashed-in trials in the unmasked points possible condition compared to the masked points possible condition based on the magnitude of the error. In Experiment 2, the amplitude of the FRN was affected by the magnitude of the error on cashed-in trials in the unmasked condition, but not the masked condition. These results are seemingly at odds, and cannot be assimilated into any currently extant model of the FRN. An explanation relying on the motivational importance of errors is discussed.

À ce jour, le rôle des oscillations bêta n’a pas encore été clairement établi. Des travaux récents ont montré que l’activité bêta pendant la préparation du mouvement et celle suivant son exécution sont différemment modulées par les erreurs de mouvements. L’objectif du présent travail a été double : premièrement, déterminer si les modulations de puissance bêta pré- et post-mouvement recrutent des substrats cérébraux différents, deuxièmement, mieux cerner la nature des processus neuronaux reflétés. Grâce à une approche par analyse en composantes indépendantes, nous suggérons fortement que les réponses oscillatoires, aux erreurs cinématiques, observées avant et après le mouvement sont sous-tendues par des structures distinctes, respectivement clairement latéralisées et médiales. De plus, en contrastant différentes tâches motrices, nous montrons que ni l’une ni l’autre des deux activités bêta ne reflètent des mécanismes en lien direct avec les sorties motrices. / The role of beta oscillations has not been clearly established yet. Recent work has shown that the beta activities observed during the preparation phase and after the movement are differently affected by movement errors. The aim of this thesis was twofold: first, to determine whether or not the pre- and post-movement beta power modulations recruit common neural substrates; second, to better understand the nature of the reflected neural processes. Using an independent component analysis approach, we strongly suggest that oscillatory responses to kinematic errors, observed before and after movement, are underpinned by distinct neural structures, respectively clearly lateralized and medial. Moreover, by contrasting different motor tasks, we show that neither of the two beta activities reflects mechanisms directly related to the output of the motor command.

The prevalence and sequelae of moderate-to-severe (M/S) traumatic brain injury (TBI) are significant and pervasive problems, and effective rehabilitation techniques are key. Errorless learning is regarded as a useful tool for memory impairments; however, the efficacy of errorless learning in a M/S TBI population is unclear. The primary goal (aim 1) of this study was to evaluate the efficacy of a single session of errorless vs. errorful learning in a group of M/S TBI survivors and matched controls. A secondary goal (aim 2) was to investigate the neural time course of errorless learning in participants with M/S TBI by analyzing the error-related negativity (ERN) component of the scalp-recorded event-related potential (ERP). The ERN is an electrophysiological measure of error processing that is disrupted in M/S TBI survivors. Measures of neuropsychological performance, self- and informant-report of executive functioning, and affect further informed both study aims. Data from 28 M/S TBI survivors (9 female) and 28 controls (9 female) were analyzed for aim 1, with data from 19 M/S TBI survivors (6 female) and 20 controls (8 female) analyzed for aim 2. There were significant differences between the TBI and control groups with regard to executive, mood, and neuropsychological functioning. Results from aim 1 indicated that TBI participants were slower across learning conditions, while both groups had significantly faster reaction times in the errorless condition. Regarding accuracy, there was not a statistically significant main effect of learning condition (p = .07), group (p = .06), or Group x Condition x Accuracy interaction (p = .33). Indices of memory and executive functioning, and group (TBI, Control) used in regressions predicted accuracy in both learning conditions (ps < .01). The memory composite was a significant independent predictor of errorless accuracy. Results from aim 2 indicated a reliable ERN was present across conditions, although there were no main effects of Condition, Group, or Group x Condition interactions on ERN amplitude or latency (ps > .22). ERN latency was not predictive of accuracy for either condition (ps > .08). Group was a significant independent predictor of accuracy in the errorless condition (p = .05), but not the errorful condition (p = .45). Findings indicate that memory functioning was a better predictor of accuracy than executive functioning or group membership. This suggests that the errorless learning benefit may be specific to memory functioning, rather than other cognitive variables. This conclusion aligns with research reporting that benefits of errorless learning depend upon the severity of memory impairments. Results from ERN analyses are only partially supported by previous research, and further work is needed to clarify the role of neural representations of errorless learning in M/S TBI.

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.

Moderate-to-severe traumatic brain injury (M/S TBI) can affect an individual's ability to perform daily tasks. For example, individuals with M/S TBI are more likely to commit errors on tasks such as making a meal or wrapping a present. The neural processes involved in such errors are poorly understood. Studies suggest that neurophysiologic markers of cognitive control and error processing may be helpful in gaining additional insight into errors on naturalistic action tasks. Unfortunately, previous experimental methods left a methodological gap which limited the use of neurophysiological markers in the study of naturalistic action. Several recent studies in healthy adults have suggested one method of bridging the gap by having individuals observe another person's errors. The current study was the first study to employ the method in a TBI population as a possible means of gaining additional insight into the detrimental effects of M/S TBI on the performance of naturalistic actions. In order to gain additional insight into the effects of M/S TBI on the completion of naturalistic tasks I used two neurophysiologic markers of cognitive control and error processing. They were the observer error related negativity (oERN) and the P300 components of the scalp-recorded event-related potential (ERP). I hypothesized that individuals with M/S TBI would demonstrate error-specific changes in the two oERN and P300 that would correlate with self-reported difficulties in daily functioning. The study consisted of two experiments. One compared 15 individuals with M/S TBI to 17 demographically similar healthy controls on an error related naturalistic action based picture task. The second compared an overlapping sample of 16 individuals with M/S TBI to 16 demographically similar controls as they watched a confederate complete the Erikson flanker task, a commonly used task in the study of electrophysiological markers. Accuracy (error vs. correct) and group (M/S TBI vs. control) effects were analyzed using 2 x 2 repeated measures ANOVAs on ERP amplitude and latency. Pearson product-moment correlations were calculated to evaluate the relationship between the P300 and oERN and measures of self-reported executive functioning (Frontal Systems Behavior Scale, FrSBe) and neuropsychological measures. Findings supported a difference between the control and M/S TBI groups in how errors were processed during the naturalistic actions based picture task. There was an interaction between group membership and response accuracy (error vs. correct) on P300 amplitude and P300 latency. Controls demonstrated reduced P300 amplitude and latency on error trials compared to correct trials. Individuals with M/S TBI did not demonstrate a significant difference between correct trials and error trials on P300 amplitude and latency. The amplitude and latency of the P300 were correlated with self-reported functional difficulties in individuals with M/S TBI but not control participants. A Fisher's r -- z analysis indicated that correlations differed significantly between groups; however, an outlier was identified in the correlational data. Removal of the outlier data led to non-significant results in the Fisher's r -- z analysis. Taken together, results of the picture task supplied evidence that for individuals with M/S TBI differences in neurophysiologic markers between groups could be explained by reduced adaptation to complexity or by possible deficits in a secondary error processing pathway for complex errors. Future research could focus on better defining the functional relationship between P300 amplitude and latency and increased errors in naturalistic actions following M/S TBI. Observation of the flanker task did not elicit oERN waveforms from either healthy controls or from individuals with M/S TBI. The results could be due to problems with the current task, but also raised some concerns about previous studies using the flanker task which employed a slightly different methodology requiring participants to count errors. The current study did not require participant to count errors. As a whole, the study supplied partial support for using electrophysiological markers of error processing to gain additional understanding increased errors in the performance of naturalistic actions following M/S TBI.

No description available.

The successful execution of goal-directed movement requires the evaluation of many levels of errors. On one hand, the motor system needs to be able to evaluate ‘high-level’ errors indicating the success or failure of a given movement. On the other hand, as a movement is executed the motor system also has to be able to correct for ‘low-level’ errors - an error in the initial motor command or change in the motor command necessary to compensate for an unexpected change in the movement environment. The goal of the present research was to provide electroencephalographic evidence that error processing during motor control is evaluated hierarchically. The present research demonstrated that high-level motor errors indicating the failure of a system goal elicited the error-related negativity, a component of the event-related brain potential (ERP) evoked by incorrect responses and error feedback. The present research also demonstrated that low-level motor errors are associated with parietally distributed ERP component related to the focusing of visuo-spatial attention and context-updating. Finally, the present research includes a viable neural model for hierarchical error processing during motor control.

The successful execution of goal-directed movement requires the evaluation of many levels of errors. On one hand, the motor system needs to be able to evaluate ‘high-level’ errors indicating the success or failure of a given movement. On the other hand, as a movement is executed the motor system also has to be able to correct for ‘low-level’ errors - an error in the initial motor command or change in the motor command necessary to compensate for an unexpected change in the movement environment. The goal of the present research was to provide electroencephalographic evidence that error processing during motor control is evaluated hierarchically. The present research demonstrated that high-level motor errors indicating the failure of a system goal elicited the error-related negativity, a component of the event-related brain potential (ERP) evoked by incorrect responses and error feedback. The present research also demonstrated that low-level motor errors are associated with parietally distributed ERP component related to the focusing of visuo-spatial attention and context-updating. Finally, the present research includes a viable neural model for hierarchical error processing during motor control.

Kognitive Kontrolle bezieht sich auf eine Vielzahl mentaler Fähigkeiten, die es uns erlauben im täglichen Leben zielgerichtete Entscheidungen zu treffen und sich flexibel an sich ständig ändernde Umweltanforderungen anzupassen. Das Ziel der vorliegenden Dissertation war es heraus zu finden, ob Kernfunktionen im Bereich der Konfliktüberwachung, Konfliktkontrolle, Fehlerverarbeitung und die daraus resultierenden Verhaltensanpassungen durch ein einheitliches Kontrollnetzwerk geleistet werden, oder ob spezifische Mechanismen die möglicherweise durch unabhängige neuronale Kontrollschleifen realisiert sind, die Flexibilität unserer Anpassungsfähigkeit steuern. Studie 1 und Studie 2 untersuchen sowohl generelle aus auch spezifische Aspekte der Konflikt- und Fehlerverarbeitung mit Hilfe klassischer Konfliktparadigmen und dem Einsatz von Zeit-Frequenz-analytischen Auswertungsmethoden. Studie 1 untersucht anhand 3 verschiedener Konfliktparadigmen (Simon, Flanker, NoGo) die Modulation der Theta Aktivität (4-8 Hz) und verortet diese grob innerhalb des medial frontalen Cortex (MFC), einer Struktur die durch eine Vielzahl von Studien als entscheidend bei der Konfliktverarbeitung angesehen wird. Die gefundene Theta Aktivität wurde in Studie 2 genutzt, um auch dynamische Netzwerkaktivierungen bei der Bearbeitung von Reiz- und Reaktionskonflikten zu beobachten. Es konnte gezeigt werden, dass ein vermutetes Netzwerk bestehend aus MFC, lateralen präfrontalen Cortices und motorischen Arealen bei der Lösung von Reaktionskonflikten beteiligt ist. In Studie 3 wird eine Simon-Aufgabe, die innerhalb von belohnenden oder bestrafenden Kontexten durchgeführt wurde, genutzt um zu zeigen, dass Konflikt- und Fehlerverarbeitung differentiell durch die Kontextmanipulation beeinflusst werden. Entgegen voriger Annahmen scheinen mehrere neuronale Kontrollsysteme an der Lösung von Konflikten und daraus resultierenden Verhaltensanpassungen beteiligt zu sein. / Cognitive control refers to a set of mental abilities that allow us goal-directed behavior in everyday life and to flexibly adapt to permanently changing environmental demands. The goal of the present dissertation was to investigate whether core functions in the area of conflict monitoring, conflict control, error processing and behavioral adjustments caused by these processes are enabled via a unitary control network or whether specific mechanisms that are possibly realized via independent control loops are responsible for the flexibility of our adaptability. Study 1 and 2 investigate general as well as specific aspects of conflict and error processing by using classic conflict paradigms and time-frequency-analytic methods. Study 1 compares the modulation of theta activity (4-8 Hz) across 3 conflict paradigms (Simon, Flanker, NoGo) and roughly situates it within medial frontal cortex (MFC), a structure which has been characterized as crucial for conflict processing in manifold studies. The found theta activity has been used in study 2, to observe dynamic network activations during processing of stimulus and response conflicts. Data confirmed that a hypothesized network consisting of MFC, lateral prefrontal cortices and motor areas is involved in conflict resolution. In study 3 we used a Simon task which was executed either during a rewarding or a punishing context assessing the influence of motivational contexts on conflict adaptation revealing that conflict and error processing were influenced differentially by the context manipulation. Against previous assumptions, several neuronal control systems seem to be engaged during conflict resolution and resulting behavioral adjustments.

Behavioral adaptation and cognitive control are crucial for goal-reaching behaviors. Every creature is ubiquitously faced with choices between behavioral alternatives. Common sense suggests that errors are an important source of information in the regulation of such processes. Several theories exist regarding cognitive control and the processing of undesired outcomes. However, most of these models focus on the consequences of an error, and less attention has been paid to the mechanisms that underlie the commissioning of an error. In this article, we present an integrative review of neuro-cognitive models that detail the determinants of the occurrence of response errors. The factors that may determine the likelihood of committing errors are likely related to the stability of task-representations in prefrontal networks, attentional selection mechanisms and mechanisms of action selection in basal ganglia circuits. An important conclusion is that the likelihood of committing an error is not stable over time but rather changes depending on the interplay of different functional neuro-anatomical and neuro-biological systems. We describe factors that might determine the time-course of cognitive control and the need to adapt behavior following response errors. Finally, we outline the mechanisms that may proof useful for predicting the outcomes of cognitive control and the emergence of response errors in future research.