ADHS ist eine häufig diagnostizierte Erkrankung in der Kinder- und Jugendpsychiatrie; etwa 5 % aller Kinder sind betroffen. Als Kardinalsymptome gelten Hyperaktivität, Aufmerksamkeitsprobleme und erhöhte Impulsivität. Die familiäre Häufung lässt auf eine genetische Prädisposition schließen. In dieser Arbeit werden mittels eines EEGs elektrophysiologische Aktivitäten des Gehirns der teilnehmenden Kinder aufgezeichnet. Dabei bilden die ereignisbezogenen Potentiale (EPs) den Informationsverarbeitungsprozess ab, welcher während der Bearbeitung eines Konfliktparadigmas - in unserer Untersuchung der Eriksen-Flanker Task - entsteht. Es ist bekannt, dass ADHS-Patienten höhere Fehlerraten und längere Reaktionszeiten in derartigen Aufgaben zeigen und Fehler vermehrt in Serien auftreten. Von besonderem Interesse sind Potentiale die direkt nach einem Fehler abgeleitet werden können; die error-related negativitiy (Ne) bzw. positivity (Pe). Die Datenauswertung erfolgte mittels in vorherigen Studien aufgezeichneten Datensätzen. Ziel der Arbeit ist es, den Einfluss der vorangegangenen Antwort, und damit des Primings bzw. der Sequenzeffekte bei ADHS-betroffenen Kindern und einer Kontrollgruppe auf die folgende Antwort und die dabei auftretenden Hirnpotentiale zu untersuchen. Bezüglich der Ne und Pe besteht für ADHS-Patienten eine heterogene Befundlage. Wir konnten feststellen und damit Ergebnisse vorheriger Studien replizieren, dass die Ne- Amplitude bei Kindern mit ADHS – im Gegensatz zur Kontrollgruppe- geringer ausgeprägt ist und keinen Sequenzeffekten (d.h. keinem Priming) unterliegt. Für die Pe-Amplitude konnten wir keine Abweichungen im Vergleich zu der Kontrollgruppe feststellen. Auch unterlag die Pe-Amplitude bei beiden Gruppen keinem Primingeinfluss. Dies lässt den Rückschluss zu, dass nur bei ADHS und nur für die Ne eine neuronale Dysfunktion angenommen werden kann. Dieses Ergebnis weist darauf hin, dass die veränderte Ne-Amplitude möglicherweise störungsspezifisch für ADHS sein könnte und somit die Möglichkeit für den Einsatz als diagnostisches Kriterium besteht.

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.

A substantial amount of behavioural, genetic, and neurophysiological data suggest that Attention Deficit Hyperactivity Disorder (ADHD) is influenced by an underlying abnormality in the midbrain dopamine system. A previous study found that children with ADHD are unusually sensitive to the salience of rewards, mediated in part by the dopamine system (Holroyd, Baker, Kerns & Mueller, 2008). The current study aimed to replicate and expand upon the previous finding using event-related potentials (ERP) recorded from typically developing children and children with ADHD as they navigated a “virtual T-Maze” in two conditions differing on reward saliency. Children also completed a behavioural task designed to measure decision making and sensitivity to reward and punishment. Both groups of children responded to the behavioural task in a way that is indicative of increased sensitivity to reward. Unlike the previous study, the salience of reward as reflected in the ERP did not have an effect on either children with ADHD or typically developing children. However, both groups displayed a larger error-related negativity (ERN) in the condition presented second.

La capacité à évaluer les résultats nos actions est fondamentale pour adapter et optimiser notre comportement et dépend d’un système superviseur chargé d’évaluer l’action, détecter les erreurs, déclencher des corrections.Le réseau neuronal sous-jacent la supervision de l’action n’a pas été complètement caractérisé chez l’homme.Dans une première étude nous avons enregistré dans l’Aire Motrice Supplémentaire (AMS) des LFP évoqués par les réponses et modulés par la performance. Des LFP évoqués exclusivement par les erreurs ont été enregistrés plus tardivement dans le cortex préfrontal médian.Dans la deuxième étude, nous avons observé que les activités de hautes-fréquences gamma sont, elles aussi, modulées par la performance des sujets, mais dans un vaste réseau frontal et extra-frontal.Dans une troisième étude, utilisant des enregistrements simultanés électroencéphalographiques (EEG) et magnétoencéphalographiques (MEG), nous observé une activité évoquée par un feedback interne sur l’EEG (mais pas en MEG), alors qu'une activité évoquée par le feedback externe était bien visible sur les enregistrements MEG, indiquant que les générateurs de ces deux activités cérébrales, sont différents. Nos résultats montrent une implication de l’AMSp dans la supervision de l’action chez l’homme, bien plus importante que ce que l’on soupçonnait auparavant. L’AMS évalue précocement, et de façon continue, l’action en cours et elle engage vraisemblablement des structures préfrontales en cas d’erreur seulement. Le traitement de l’erreur d’action, selon qu'il se fonde sur des informations internes ou externes est certainement sous-tendu par des réseaux corticaux différents. / The capacity to evaluate the outcome of our actions is fundamental for adapting and optimizing behaviour. This capability depends on an action monitoring system in charge of assessing ongoing actions, detecting errors, and evaluating outcomes.Electrical brain activity evoked by negative outcomes is thought to originate within the medial part of the frontal cortex. Nonetheless, the underlying neuronal network is incompletely characterised in humans.In the two first studies, we investigated the anatomical substrates of action monitoring in humans using intracerebral local field potential (LFP) recordings of cerebral cortex from epileptic patients. Response evoked LFPs sensitive to outcome were recorded from the Supplementary Motor Area proper (SMA), while LFPs evoked exclusively by errors were recorded later in the medial prefrontal cortex. High-gamma-frequency activity (60-180 Hz) was modulated as a function of action outcome in a vast frontal and extra-frontal network.In a third study using simultaneous recording of electroencephalography (EEG) and magnetoencephalography (MEG), we found that error related activity was detected by EEG (but not by MEG), while feedback-related activity was detected by MEG, indicating that the sources of these two forms of outcome-modulated brain activity are different.To conclude the SMA is much more involved in action monitoring than previously thought. SMA rapidly and continuously assesses ongoing actions and likely engages more rostral prefrontal structures in the case of error. Processing of action errors and of negative externally delivered feedback therefore appears to be supported by distinct cortical networks.

Background. Feelings of doubt and perseverative behaviours are key symptoms of obsessive–compulsive disorder (OCD) and have been linked to hyperactive error and conflict signals in the brain. While enhanced neural correlates of error monitoring have been robustly shown, far less is known about conflict processing and adaptation in OCD. Method. We examined event-related potentials during conflict processing in 70 patients with OCD and 70 matched healthy comparison participants, focusing on the stimulus-locked N2 elicited in a flanker task. Conflict adaptation was evaluated by analysing sequential adjustments in N2 and behaviour, i.e. current conflict effects as a function of preceding conflict. Results. Patients with OCD showed enhanced N2 amplitudes compared with healthy controls. Further, patients showed stronger conflict adaptation effects on reaction times and N2 amplitude. Thus, the effect of previous compatibility was larger in patients than in healthy participants as indicated by greater N2 adjustments in change trials (i.e. iC, cI). As a result of stronger conflict adaptation in patients, N2 amplitudes were comparable between groups in incompatible trials following incompatible trials. Conclusions. Larger N2 amplitudes and greater conflict adaptation in OCD point to enhanced conflict monitoring leading to increased recruitment of cognitive control in patients. This was most pronounced in change trials and was associated with stronger conflict adjustment in N2 and behaviour. Thus, hyperactive conflict monitoring in OCD may be beneficial in situations that require a high amount of control to resolve conflict, but may also reflect an effortful process that is linked to distress and symptoms of OCD.

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.

No description available.

Die zugrunde liegenden Prozesse altersbedingter Veränderungen exekutiver Funktionen werden vielfach untersucht. Für eine flexible Anpassung ist die Überwachung von Handlungen und deren Konsequenzen notwendig. Handlungsüberwachung wird mit ereigniskorrelierten Potentialen (EKP) wie der error-related negativity/error negativity (ERN/Ne) und der correct-related negativity/correct negativity (CRN) gemessen. Die Arbeit untersucht die Handlungsüberwachung bei jüngeren und älteren Erwachsenen mit dem Ziel, das Wissen über kompensatorische Strategien bei Älteren und deren Auswirkung auf die EKP Befunde zu erweitern. Ältere zeigten reduzierte ERN/Ne und größere oder vergleichbar große CRN Amplituden im Vergleich zu Jüngeren. Während nur die Jüngeren eine Reduktion der ERN/Ne mit größerer Aufgabenschwierigkeit zeigten, zeigten beide Gruppen eine ERN/Ne Reduktion unter der Instruktion, die Geschwindigkeit anstatt Genauigkeit erforderte. Nur bei Jüngeren variierte die CRN mit der Kompatibilität der Trials, mit der Aufgabenschwierigkeit und Instruktion. Ältere wiesen geringere Fehlerraten und längere Reaktionszeiten als Jüngere auf. Dieses Muster deutet auf eine kompensatorische oder strategische Anpassung in Folge von Defiziten in der Nutzung einer erfolgreichen Kombination von proaktiver und reaktiver Kontrolle hin. Es wird postuliert, dass ERN/Ne und CRN einen gemeinsamen Prozess darstellen, der allgemeine Überwachungsfunktionen reflektiert. Die ERN/Ne beinhaltet zusätzlich einen Prozess, der Fehlerüberwachung signalisiert. Daraus ergibt sich die Vermutung, dass die reduzierte ERN/Ne bei Älteren entweder auf eine Verringerung spezifischer Fehlerprozesse oder auf eine Beeinträchtigung allgemeiner Überwachungsfunktionen zurückzuführen ist. Altersbezogene Veränderungen der EKP Befunde könnten den veränderten Einsatz von kompensatorischer Kontrolle bei Älteren im Vergleich zu Jüngeren reflektieren. Dieser Frage sollte in zukünftigen Studien nachgegangen werden. / Executive functions decline with age and a growing body of research aims at investigating age-related changes of the underlying processes. One important function is to monitor actions and action outcomes, which is necessary for flexible adjustments and learning. This so-called performance monitoring can be measured with event-related potentials (ERP), namely the error-related negativity/error negativity (ERN/Ne) and the correct-related negativity/correct negativity (CRN). This work examined performance monitoring in younger and older adults with the aim to advance knowledge about compensatory strategies in older adults and their implications for ERP results. Findings revealed reduced ERN/Ne and larger or similar-sized CRN in older compared to younger adults. While only younger adults showed a decrease of ERN/Ne with higher task difficulty, both age groups showed a reduction of ERN/Ne in the speed compared to the accuracy condition. Additionally, only younger adults showed variations, in that the CRN was smaller for compatible compared to incompatible trials, in the easy compared to the difficult condition, and in the speed compared to the accuracy condition. Behaviorally, older adults had less errors and longer response latencies than younger adults. This pattern may reflect compensatory or strategic adjustments with age which may be due to deficits in the use of a successful combination of proactive and reactive control. It was further assumed that ERN/Ne and CRN share a common process that reflects general monitoring functions and ERN/Ne includes an additional process that reflects error-specific monitoring. Accordingly, the ERN/Ne attenuation in older adults is either caused by reduced error-specific processing or compromised general monitoring functions. Age-related changes in ERP findings indicate altered engagement of compensatory cognitive control in older compared to younger adults. However, this question has to be further clarified in future studies.