Obsessive–compulsive disorder (OCD) is a psychiatric condition leading to significant distress and poor quality of life. Successful treatment of OCD is restricted by the limited knowledge about its pathophysiology. This study aimed to investigate the pathophysiology of OCD using electroencephalographic (EEG) event-related potentials (ERPs), elicited from multiple tasks to characterise disorder-related differences in underlying brain activity across multiple neural processes.

ERP data were obtained from 25 OCD patients and 27 age- and sex-matched healthy controls (HCs) by recording EEG during flanker and go/nogo tasks. Error-related negativity (ERN) was elicited by the flanker task, while N200 and P300 were generated using the go/nogo task. Primary comparisons of the neural response amplitudes and the topographical distribution of neural activity were conducted using scalp field differences across all time points and electrodes.

Compared to HCs, the OCD group showed altered ERP distributions. Contrasting with the previous literature on ERN and N200 topographies in OCD where fronto-central negative voltages were reported, we detected positive voltages. Additionally, the P300 was found to be less negative in the frontal regions. None of these ERP findings were associated with OCD symptom severity.

These results indicate that individuals with OCD show altered frontal neural activity across multiple executive function-related processes, supporting the frontal dysfunction theory of OCD. Furthermore, due to the lack of association between altered ERPs and OCD symptom severity, they may be considered potential candidate endophenotypes for OCD.

Social anxiety symptoms are most likely to emerge during adolescence, a developmental window marked by heightened concern over peer evaluation. However, the neurocognitive mechanism(s) underlying adolescent social anxiety remain unclear. Emerging work points to the error-related negativity (ERN) as a potential neural marker of exaggerated self/error-monitoring in social anxiety, particularly for errors committed in front of peers. However, social anxiety symptoms are marked by heterogeneity and it remains unclear exactly what domain(s) of social anxiety symptoms are associated with ERN variation in peer presence, particularly within the adolescent period.

To advance and deepen the mechanistic understanding of the ERN's putative role as a neural marker for social anxiety in adolescence, we leveraged a social manipulation procedure and assessed a developmentally salient domain of social anxiety during adolescence – fear of negative evaluation (FNE). Adolescents residing in Hanzhong, a small city in the southwestern region of mainland China, had EEG recorded while performing a flanker task, twice (peer presence/absence); FNE, as well as global social anxiety symptoms, was assessed.

Overall ERN increases in peer presence. FNE specifically, but not global levels of social anxiety symptoms, predicted ERN in peer presence.

These data are the first demonstration that the ERN relates to a specific domain of social anxiety in adolescents, as well as the first evidence of such relations within a non-WEIRD (Western, Educated, Industrialized, Rich and Democratic) sample. Results have important implications for theory and research into adolescent social anxiety.

Aerobic exercise has demonstrated antidepressant efficacy among adults with major depression. There is a poor understanding of the neural mechanisms associated with these effects. Deficits in reward processing and cognitive control may be two candidate targets and predictors of treatment outcome to exercise in depression.

Sixty-six young adults aged 20.23 years (s.d. = 2.39) with major depression were randomized to 8 weeks of moderate-intensity aerobic exercise (n = 35) or light stretching (n = 31). Depressive symptoms were assessed across the intervention to track symptom reduction. Reward processing [reward positivity (RewP)] and cognitive control [error-related negativity (ERN)] were assessed before and after the intervention using event-related brain potentials.

Compared to stretching, aerobic exercise resulted in greater symptom reduction (gs = 0.66). Aerobic exercise had no impact on the RewP (gav = 0.08) or ERN (gav = 0.21). In the aerobic exercise group, individuals with a larger pre-treatment RewP [odds ratio (OR) = 1.45] and increased baseline depressive symptom severity (OR = 1.18) were more likely to respond to an aerobic exercise program. Pre-treatment ERN did not predict response (OR = 0.74).

Aerobic exercise is effective in alleviating depressive symptoms in adults with major depression, particularly for those with increased depressive symptom severity and a larger RewP at baseline. Although aerobic exercise did not modify the RewP or ERN, there is preliminary support for the utility of the RewP in predicting who is most likely to respond to exercise as a treatment for depression.

Increased neural error-signals have been observed in obsessive-compulsive disorder (OCD), anxiety disorders, and inconsistently in depression. Reduced neural error-signals have been observed in substance use disorders (SUD). Thus, alterations in error-monitoring are proposed as a transdiagnostic endophenotype. To strengthen this notion, data from unaffected individuals with a family history for the respective disorders are needed.

The error-related negativity (ERN) as a neural indicator of error-monitoring was measured during a flanker task from 117 OCD patients, 50 unaffected first-degree relatives of OCD patients, and 130 healthy comparison participants. Family history information indicated, that 76 healthy controls were free of a family history for psychopathology, whereas the remaining had first-degree relatives with depression (n = 28), anxiety (n = 27), and/or SUD (n = 27).

Increased ERN amplitudes were found in OCD patients and unaffected first-degree relatives of OCD patients. In addition, unaffected first-degree relatives of individuals with anxiety disorders were also characterized by increased ERN amplitudes, whereas relatives of individuals with SUD showed reduced amplitudes.

Alterations in neural error-signals in unaffected first-degree relatives with a family history of OCD, anxiety, or SUD support the utility of the ERN as a transdiagnostic endophenotype. Reduced neural error-signals may indicate vulnerability for under-controlled behavior and risk for substance use, whereas a harm- or error-avoidant response style and vulnerability for OCD and anxiety appears to be associated with increased ERN. This adds to findings suggesting a common neurobiological substrate across psychiatric disorders involving the anterior cingulate cortex and deficits in cognitive control.

The enhanced error monitoring in patients with obsessive–compulsive disorder (OCD), typically measured with the error-related negativity (ERN), has been found to be temporally stable and independent of symptom expression. Here, we examined whether the error monitoring in patients with OCD could be experimentally modulated by individually tailored symptom provocation.

Twenty patients with OCD and 20 healthy controls performed a flanker task in which OCD-relevant or neutral pictures were presented prior to a flanker stimulus. An individualized stimulus set consisting of the most provoking images in terms of OCD symptoms was selected for each patient with OCD. Response-locked event-related potentials were recorded and used to examine the error-related brain activity.

Patients with OCD showed larger ERN amplitudes than did control subjects in both the OCD-symptom provocation and neutral conditions. Additionally, while patients with OCD exhibited a significant increase in the ERN under the OCD-symptom provocation condition when compared with the neutral condition, control subjects showed no variation in the ERN between the conditions.

Our results strengthen earlier findings of hyperactive error monitoring in OCD, as indexed by higher ERN amplitudes in patients with OCD than in controls. Importantly, we showed that the patients’ overactive error-signals were experimentally enhanced by individually tailored OCD-symptom triggers, thus suggesting convincing evidence between OCD-symptoms and ERN. Such findings imply that therapeutic interventions should target affective regulation in order to alleviate the perceived threatening value of OCD triggers.

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.

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.

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.

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.

Accurate monitoring and integration of both internal and external feedback is crucial for guiding current and future behavior. These aspects of performance monitoring are commonly indexed by two event-related potential (ERP) components: error-related negativity (ERN) and feedback negativity (FN). The ERN indexes internal response monitoring and is sensitive to the commission of erroneous versus correct responses, and the FN indexes external feedback monitoring of positive versus negative outcomes. Although individuals with schizophrenia consistently demonstrate a diminished ERN, the integrity of the FN has received minimal consideration.

The current research sought to clarify the scope of feedback processing impairments in schizophrenia in two studies: study 1 examined the ERN elicited in a flanker task in 16 out-patients and 14 healthy controls; study 2 examined the FN on a simple monetary gambling task in expanded samples of 35 out-patients and 33 healthy controls.

Study 1 replicated prior reports of an impaired ERN in schizophrenia. By contrast, patients and controls demonstrated comparable FN differentiation between reward and non-reward feedback in study 2.

The differential pattern across tasks suggests that basic sensitivity to external feedback indicating reward versus non-reward is intact in schizophrenia, at least under the relatively simple task conditions used in this study. Further efforts to specify intact and impaired reward-processing subcomponents in schizophrenia may help to shed light on the diminished motivation and goal-seeking behavior that are commonly seen in this disorder.

Psychopathy (PP) is associated with a performance deficit in a variety of stimulus–response and stimulus–reinforcement learning paradigms. We tested the hypothesis that failures in error monitoring underlie these learning deficits.

We measured electrophysiological correlates of error monitoring [error-related negativity (ERN)] during a probabilistic learning task in individuals with PP (n=13) and healthy matched control subjects (n=18). The task consisted of three graded learning conditions in which the amount of learning was manipulated by varying the degree to which the response was predictive of the value of the feedback (50, 80 and 100%).

Behaviourally, we found impaired learning and diminished accuracy in the group of individuals with PP. Amplitudes of the response ERN (rERN) were reduced. No differences in the feedback ERN (fERN) were found.

The results are interpreted in terms of a deficit in initial rule learning and subsequent generalization of these rules to new stimuli. Negative feedback is adequately processed at a neural level but this information is not used to improve behaviour on subsequent trials. As learning is degraded, the process of error detection at the moment of the actual response is diminished. Therefore, the current study demonstrates that disturbed error-monitoring processes play a central role in the often reported learning deficits in individuals with PP.