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BACKGROUND: Performance monitoring entails rapid error detection to maintain task performance. Impaired performance monitoring is a candidate pathophysiological process in psychotic disorders, which may explain the broader deficit in executive function and its known associations with negative symptoms and poor functioning. The current study models cross-sectional pathways bridging neurophysiological measures of performance monitoring with executive function, symptoms, and functioning. METHODS: Data were from the 20-year assessment of the Suffolk County Mental Health Project. Individuals with psychotic disorders (N = 181) were originally recruited from inpatient psychiatric facilities. Data were also collected from a geographically and demographically matched group with no psychosis history (N = 242). Neural measures were the error-related negativity (ERN) and error positivity (Pe). Structural equation modeling tested mediation pathways. RESULTS: Blunted ERN and Pe in the clinical cohort related to impaired executive function (r = 0.26-0.35), negative symptom severity (r = 0.17-0.25), and poor real-world functioning (r = 0.17-0.19). Associations with executive function were consistent across groups. Multiple potential pathways were identified in the clinical cohort: reduced ERN to inexpressivity was mediated by executive function (β = 0.10); reduced Pe to global functioning was mediated by executive function and avolition (β = 0.10). CONCLUSIONS: This supports a transdiagnostic model of psychotic disorders by which poor performance monitoring contributes to impaired executive function, which contributes to negative symptoms and poor real-world functioning. If supported by future longitudinal research, these pathways could inform the development of targeted interventions to address cognitive and functional deficits that are central to psychotic disorders.

Previous research on boredom suggest it function as animportant self-regulatory signal, indicating that the currentstate of the environment carries opportunity-costs andtherefore driving the need to explore alternative activities. Traitboredom proneness is associated with negative consequencesincluding increased risk-taking and impulsivity. Thesefindings often rely on self-reports and not much is known aboutthe role of state and trait boredom in controlled laboratorytasks, or their neural correlates. Sixty-two participantscompleted the Balloon Analogue Risk Task and a go/no-gotask while electrical brain activity was recorded using EEG.Results showed that state boredom leads to impulsivity andpoor performance monitoring, as evident by behavioral,subjective and ERP metrics. Trait boredom was associatedwith increased risk-taking, and modulated the correlationbetween errors and state boredom: high boredom pronenessincreased the sensitivity of trait boredom to errors. Overall,these findings emphasize the involvement of executivefunctions in the interaction between state and trait boredom.

BackgroundAlthough individuals with, or at risk for, psychotic disorders often show difficulties with performance monitoring and feedback processing, findings from studies using event-related potentials (ERPs) to index these processes are not consistent. This meta-analytic review focused on studies of two different indexes of performance monitoring, the early error-related negativity (ERN; n = 25) and the later error positivity (Pe; n = 17), and one index of feedback processing, the feedback negativity (FN; n = 6).MethodsWe evaluated whether individuals (1) with psychotic disorders, or (2) at heightened risk for these disorders differ from healthy controls in available studies of the ERN, Pe, and FN.ResultsThere was a significant, large ERN reduction in those with psychosis (g = -0.96) compared to controls, and a significant, moderate ERN reduction in those at-risk (g = -0.48). In contrast, there were uniformly non-significant, small between-group differences for Pe and FN (gs ≤ |0.16|).ConclusionsThe results reveal a differential pattern of impairment in psychosis. Early performance monitoring (ERN) impairments are substantial among those with psychotic disorders in general and may be a useful vulnerability indicator for these disorders. However, later performance monitoring (Pe) and basic feedback processing (FN) appear to be relatively spared in psychosis.

The ability to regulate behaviors and emotions depends in part on the ability to flexibly monitor one's own progress toward a goal. Atypical patterns of response monitoring have been reported in individuals with autism spectrum disorders (ASD). In the current study we examined the error related negativity (ERN), an electrophysiological index of response monitoring, in relation to behavioral, social cognitive, and emotional presentation in higher functioning children (8-16 years) diagnosed with autism (HFA: N = 38) and an age- and IQ-matched sample of children without autism (COM: N = 36). Both HFA and COM participants displayed larger amplitude responses to error compared to correct response trials and these amplitudes did not differ by diagnostic group. For participants with HFA, larger ERN amplitudes were associated with more parent-reported autistic symptoms and more self-reported internalizing problems. However, across the full sample, larger ERN amplitudes were associated with better performance on theory of mind tasks. The results are discussed in terms of the utility of electrophysiological measures for understanding essential moderating processes that contribute to the spectrum of behavioral expression in the development of ASD.

ObjectivesThis study sought to examine the relationship between baseline and on-study apolipoproteins (apo) A-1 and B and lipoprotein(a) [Lp(a)] levels and the development of subsequent cardiovascular (CV) events in the AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglyceride and Impact on Global Health Outcomes) trial.BackgroundNiacin has been reported to lower apoB and Lp(a) and to raise apoA-1.MethodsIndividuals with CV disease and low baseline levels of high-density lipoprotein cholesterol were randomized to simvastatin plus placebo or simvastatin, plus extended-release niacin ([ERN], 1,500 to 2,000 mg/day), with ezetimibe added as needed, in both groups, to maintain an on-treatment low-density lipoprotein cholesterol in the range of 40 to 80 mg/dl. Hazard ratios (HRs) were used to evaluate the relationship between levels of apoA-1, apoB, and Lp(a), and CV events in each treatment group.ResultsBaseline apoB and the apoB/apoA-I ratio were significantly predictive of CV events only for the placebo group (HR: 1.17 [p = 0.018] and HR: 1.19 [p = 0.016]). Baseline and on-study Lp(a) were predictive of CV events in both simvastatin plus placebo (baseline HR: 1.24 [p = 0.002] and on-study HR: 1.21 [p = 0.017]) and the simvastatin plus ERN group (baseline HR: 1.25 [p = 0.001] and on-study HR: 1.18 [p = 0.028]). The ERN modestly increased 1-year apoA-1 (7%), decreased apoB (13%), decreased the ApoB/ApoA-1 ratio (19%), and decreased Lp(a) 21%, but did not reduce CV events.ConclusionsLp(a) was associated with increased CV risk in both treatment groups indicating that it contributes to residual CV risk. However, there was no evidence that ERN reduced CV risk, despite favorable lipoprotein changes.

The current study employed a modified gambling task, in which probabilistic cues were provided to elicit positive or negative expectations. Event-related potentials (ERPs) to ‘‘final outcome’’ and ‘‘probabilistic cues’’ were analyzed. Difference waves between the negative condition and the corresponding positive condition were examined. The results confirm that feedback related negativity (FRN) amplitude is modulated by the interaction of outcome valence and expectancy by showing larger FRN difference waves for unexpected than expected outcomes. More interestingly, the difference wave between ERPs elicited by positive and negative expectations showed a negative deflection, with a frontal midline source density around 280 ms after onset of the predictive cue. Negative expectations were associated with larger FRN amplitudes than positive expectations. This suggests that FRN is elicited by probabilistic cues to pending outcomes.

Optimal behavior in a competitive world requires the flexibility to adapt decision strategies based on recent outcomes. In the present study, we tested the hypothesis that this flexibility emerges through a reinforcement learning process, in which reward prediction errors are used dynamically to adjust representations of decision options. We recorded event-related brain potentials (ERPs) while subjects played a strategic economic game against a computer opponent to evaluate how neural responses to outcomes related to subsequent decision-making. Analyses of ERP data focused on the feedback-related negativity (FRN), an outcome-locked potential thought to reflect a neural prediction error signal. Consistent with predictions of a computational reinforcement learning model, we found that the magnitude of ERPs after losing to the computer opponent predicted whether subjects would change decision behavior on the subsequent trial. Furthermore, FRNs to decision outcomes were disproportionately larger over the motor cortex contralateral to the response hand that was used to make the decision. These findings provide novel evidence that humans engage a reinforcement learning process to adjust representations of competing decision options.