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In the past 20 years, research concerning the error-related negativity (ERN), a negative-going deflection in the event-related brain potential (ERP) following an erroneous response, has flourished. Despite a substantial body of research, debate regarding its functional significance persists. In what follows, we selectively review literature on the ERN, and outline several prominent cognitive theories related to the generation and significance of the ERN. Cognitive theories predict that the size of the ERN should relate to variation in behavior, although there is substantial evidence that the ERN and behavioral measures are at least partially dissociable. Moreover, individual difference measures, psychopathology, and motivational factors all appear to impact basic mechanisms that generate the ERN to moderate the magnitude of the ERN, suggesting a need to integrate alternative perspectives into models of ERN amplitude. Insofar as errors prompt the mobilization of defensive responses, we view variation in the ERN in terms of error detection in the service of protecting the organism. Based on data indicating that the ERN is highly stable over time, heritable, and related to broad dimensions of personality, we propose that the ERN is a neural index of a neurobehavioral trait and variation in its amplitude is related in part to individual differences in defensive reactivity. Implications and future directions are considered.

Alterations in frontal and parietal neural activations during working memory task performance have been suggested as a candidate endophenotype of obsessive-compulsive disorder (OCD) in studies involving first-degree relatives. However, the direct link between genetic risk for OCD and neuro-functional alterations during working memory performance has not been investigated to date. Thus, the aim of the current functional magnetic resonance imaging (fMRI) study was to test the direct association between polygenic risk for OCD and neural activity during the performance of a numeric n-back task with four working memory load conditions in 128 participants, including patients with OCD, unaffected first-degree relatives of OCD patients, and healthy controls. Behavioral results show a significant performance deficit at high working memory load in both patients with OCD and first-degree relatives (p < 0.05). A whole-brain analysis of the fMRI data indicated decreased neural activity in bilateral inferior parietal lobule and dorsolateral prefrontal cortex in both patients and relatives. Most importantly, OCD polygenic risk scores predicted neural activity in orbitofrontal cortex. Results indicate that genetic risk for OCD can partly explain alterations in brain response during working memory performance, supporting the notion of a neuro-functional endophenotype for OCD.

Cognitive behavioral therapy (CBT) is an effective treatment for obsessive-compulsive disorder (OCD). However, CBT does not lead to a satisfying symptom reduction in a considerable number of patients with OCD. The identification of variables that predict insufficient treatment response could improve efficient treatment selection and inform the development of specific augmentative treatments. In the current study, we tested whether prediction of treatment response can be improved by including neurobiological markers during working memory (WM) performance. Forty-four patients with a primary OCD diagnosis participated in an n-back WM task with varying WM load while functional Magnetic Resonance Imaging (fMRI) was performed. Subsequently, all patients received CBT in an outpatient clinic. WM load-dependent modulation of the blood-oxygen-level-dependent (BOLD) signal in a bilateral cluster in inferior/superior parietal lobule predicted CBT response over and above clinical and sociodemographic variables (p < 0.05). Higher modulation was associated with larger relative symptom reduction. The results of the current study indicate that the ability of the WM system to flexibly adapt to changing task demands might be a useful indicator of CBT response in OCD. Possibly, this mechanism facilitates relearning processes during exposure-based CBT. However, findings need to be replicated in larger samples.

Studies have shown that people with obsessive–compulsive disorder (OCD) have impairments in spatial working memory (SWM) performance. However, it remains unclear whether this deficit represents a cognitive endophenotype preceding symptoms or a correlate of OCD. We investigated SWM in 69 people with OCD, 77 unaffected first-degree relatives of people with OCD and 106 healthy control participants. Taking age effects into account, SWM performance was best in healthy controls, intermediate in relatives and worst in OCD participants. However, since performance did not differ significantly between healthy controls and relatives, our study does not fully support SWM performance as a core cognitive endophenotype of OCD.

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.

Overactive performance monitoring has been consistently reported in obsessive–compulsive disorder (OCD). OCD is a clinically heterogeneous disorder and is characterized by several symptom dimensions that may have partially distinct neural correlates. We examined whether performance-monitoring alterations are related to symptom severity and symptom dimensions. Electrocortical correlates of performance monitoring were assessed in 72 OCD patients and 72 matched healthy comparison participants during a flanker task. Amplitudes of the error- and correct-related negativity as well as delta and theta power were used to quantify performance-monitoring activity, and a composite measure was derived using factor analysis. Symptom dimension scores were obtained from the Yale-Brown Obsessive Compulsive Scale symptom checklist. OCD patients showed increased electrocortical responses associated with correct and erroneous responses compared to healthy comparison participants. In patients, no correlations were obtained between performance monitoring and global symptom severity as well as lifetime symptom dimension scores. Only a statistical trend was found that higher symmetry/hoarding scores were associated with reduced performance-monitoring activity. For present symptom dimensions scores, an association with rituals/superstitious symptoms was obtained such that higher scores were associated with greater performance-monitoring activity. However, for both dimensions, subjects with low scores or high scores on each dimension were characterized by overactive performance monitoring compared to healthy controls. Overactive brain processes during performance monitoring are a neural correlate of OCD that is independent of global symptom severity and can be observed for all symptom dimensions. This supports the notion of overactive performance monitoring being a candidate endophenotype for OCD.

In this preregistered study, we investigated the relationship between neural correlates of performance monitoring and disorders of the anxiety and obsessive–compulsive spectrum. Specifically, we aimed at understanding the role of disorder category, clinical status, family risk, and the transdiagnostic symptom dimensions of anxious apprehension and anxious arousal. To this end, we measured event‐related potentials (ERPs) of performance monitoring (i.e., error‐related negativity, ERN, and correct‐response negativity, CRN) in a large sample of 156 participants, including groups of patients with obsessive–compulsive disorder, social anxiety disorder, and specific phobia, as well as a naturalistic control group. Contrary to our initial expectations, we did not observe significant differences in ERPs among the clinical groups, nor in comparison to the naturalistic control group. However, after creating a more strictly defined healthy control group, we found larger ERN amplitudes in the specific phobia compared with the healthy control group. In addition, when comparing participants with and without a lifetime clinical diagnosis of any internalizing disorder, regardless of their main diagnosis, as well as when comparing those with or without a family risk for internalizing psychopathology, we observed larger amplitudes for both ERN and CRN. Subsequently, we combined data from this study and a previously published subclinical study to examine the role of transdiagnostic symptom dimensions (i.e., anxious apprehension and anxious arousal) across a wider severity spectrum. In this joint sample of 246 participants, gender emerged as a moderator of the link between anxious apprehension and enhanced performance monitoring. Specifically, women with increasing anxious apprehension exhibited elevated ERN and CRN amplitudes. In conclusion, our study challenges the notion of a disorder‐specific link to performance monitoring. Instead, our findings suggest that enhanced performance monitoring is associated with a higher propensity for anxious apprehension and acts as a broad risk marker for internalizing psychopathology, reflecting vulnerability beyond diagnostic borders within the anxiety‐ and obsessive–compulsive spectrum.

A widely shared framework suggests that anxiety maps onto two dimensions: anxious apprehension and anxious arousal. Previous research linked individual differences in these dimensions to differential neural response patterns in neuropsychological, imaging, and physiological studies. Differential effects of the anxiety dimensions might contribute to inconsistencies in prior studies that examined neural processes underlying anxiety, such as hypersensitivity to unpredictable threat. We investigated the association between trait worry (as a key component of anxious apprehension), anxious arousal, and the neural processing of anticipated threat. From a large online community sample ( N = 1,603), we invited 136 participants with converging and diverging worry and anxious arousal profiles into the laboratory. Participants underwent the NPU-threat test with alternating phases of unpredictable threat, predictable threat, and safety, while physiological responses (startle reflex and startle probe locked event-related potential components N1 and P3) were recorded. Worry was associated with increased startle responses to unpredictable threat and increased attentional allocation (P3) to startle probes in predictable threat anticipation. Anxious arousal was associated with increased startle and N1 in unpredictable threat anticipation. These results suggest that trait variations in the anxiety dimensions shape the dynamics of neural processing of threat. Specifically, trait worry seems to simultaneously increase automatic defensive preparation during unpredictable threat and increase attentional responding to threat-irrelevant stimuli during predictable threat anticipation. The current study highlights the utility of anxiety dimensions to understand how physiological responses during threat anticipation are altered in anxiety and supports that worry is associated with hypersensitivity to unpredictable, aversive contexts.

Hyperactive performance monitoring is a robust finding in obsessive–compulsive disorder (OCD). Patients show increased amplitudes of the error-related negativity (ERN) and correct-related negativity (CRN). Recently, two temporo-spatial factors were shown to contribute to both ERPs in healthy individuals. In the present study, it was investigated whether the factor structure underlying ERN and CRN is similar in OCD and which factors differ between groups. A principal component analysis (PCA) was employed to investigate the temporo-spatial factor structure of ERN and CRN. Twenty-six OCD patients and 26 healthy controls conducted a flanker task. EEG data were analyzed as conventional ERP components and as factor scores derived from temporo-spatial PCA. ERP results showed expected increases in ERN and CRN amplitudes in OCD patients. For both groups, the PCA confirmed the assumed factor structure of a central and a fronto-parietal factor contributing to ERN and CRN. Factor scores of both factors were differently affected by response correctness in OCD. Alterations in factor scores indicate increased activity in both an outcome-independent monitoring process and an error-sensitive process, contributing to overactive performance monitoring in OCD.