Heart rate and heart rate variability in obsessive-compulsive disorder: Evidence from patients and unaffected first-degree relatives.

Altered heart rate (HR) and heart rate variability (HRV) are common observations in psychiatric disorders. Yet, few studies have examined these cardiac measures in obsessive-compulsive disorder (OCD). The current study aimed to investigate HR and HRV, indexed by the root mean square of successive differences (RMSSD) and further time domain indices, as putative biological characteristics of OCD. Electrocardiogram was recorded during a five-minute resting state. Group differences between patients with OCD (n = 96), healthy participants (n = 112), and unaffected first-degree relatives of patients with OCD (n = 47) were analyzed. As potential moderators of group differences, we examined the influence of age and medication, respectively. As results indicated, patients with OCD showed higher HR and lower HRV compared to healthy participants. These group differences were not moderated by age. Importantly, subgroup analyses showed that only medicated patients displayed lower HRV compared to healthy individuals, while HR alterations were evident in unmedicated patients. Regarding unaffected first-degree relatives, group differences in HRV remained at trend level. Further, an age-moderated group differentiation showed that higher HRV distinguished relatives from healthy individuals in young adulthood, whereas at higher age lower HRV was indicative of relatives. Both the role of familial risk and medication in HRV alterations need further elucidation. Pending future studies, alterations in HR and potentially HRV might serve as useful indices to characterize the pathophysiology of OCD.

Error-Related Brain Activity in Patients With Obsessive-Compulsive Disorder and Unaffected First-Degree Relatives: Evidence for Protective Patterns.

Background: Indicators of increased error monitoring are associated with obsessive-compulsive disorder (OCD), as shown in electroencephalography and functional magnetic resonance imaging studies. As most studies used strictly controlled samples (excluding comorbidity and medication), it remains open whether these findings extend to naturalistic settings. Thus, we assessed error-related brain activity in a large, naturalistic OCD sample. We also explored which activity patterns might qualify as vulnerability endophenotypes or protective factors for the disorder. To this aim, a sample of unaffected first-degree relatives of patients with OCD was also included. Methods: Participants (84 patients with OCD, 99 healthy control participants, and 37 unaffected first-degree relatives of patients with OCD) completed a flanker task while blood oxygen level-dependent responses were measured with functional magnetic resonance imaging. Aberrant error-related brain activity in patients and relatives was identified. Results: Patients with OCD showed increased error-related activity in the supplementary motor area and within the default mode network, specifically in the precuneus and postcentral gyrus. Unaffected first-degree relatives showed increased error-related activity in the bilateral inferior frontal gyrus. Conclusions: Increased supplementary motor area and default mode network activity in patients with OCD replicates previous studies and might indicate excessive error signals and increased self-referential error processing. Increased activity of the inferior frontal gyrus in relatives may reflect increased inhibition. Impaired response inhibition in OCD has been demonstrated in several studies and might contribute to impairments in suppressing compulsive actions. Thus, increased inferior frontal gyrus activity in the unaffected relatives of patients with OCD may have contributed to protection from symptom development.

Effects of a three-week executive control training on adaptation to task difficulty and emotional interference.

Intact executive functions are characterized by flexible adaptation to task requirements, while these effects are reduced in internalizing disorders. Furthermore, as executive functions play an important role in emotion regulation, deficits in executive functions may contribute to symptom generation in psychological disorders through increased emotional interference. Thus, the present study investigated transfer effects of a three-week executive control training on adaptation to task difficulty and emotional interference in healthy participants (n = 24) to further explore the training's suitability for clinical application. To assess the adaptation to task difficulty, the proportion congruency effect on behavioral data (response times, error rates) and ERP measures (N2, CRN) was assessed in a flanker task with varying frequency of incompatible trials (25%, 75%). To quantify emotional interference, flanker stimuli were superimposed on neutral or negative pictures. Replicating previous results, the training increased interference control as indexed by decreased response times and errors rates, increased N2 amplitude and decreased CRN amplitude in incompatible trials after training. Proportion congruency effects were weaker than expected and not affected by the training intervention. The training lead to a shift in the time-point of emotional interference: before training negative pictures lead to a reduction in CRN amplitude, while after training this reduction was observed for the N2. This pattern illustrates that the training leads to a change in task processing mode from predominant response-related cognitive control to predominant stimulus-related cognitive control (N2), indicating a proactive processing mode.

Error-related activity of the sensorimotor network contributes to the prediction of response to cognitive-behavioral therapy in obsessive-compulsive disorder.

BACKGROUND: Although cognitive behavioral therapy is a highly effective treatment for obsessive-compulsive disorder (OCD), yielding large symptom reductions on the group level, individual treatment response varies considerably. Identification of treatment response predictors may provide important information for maximizing individual treatment response and thus achieving efficient treatment resource allocation. Here, we investigated the predictive value of previously identified biomarkers of OCD, namely the error-related activity of the supplementary motor area (SMA) and the sensorimotor network (SMN, postcentral gyrus/precuneus). METHODS: Seventy-two participants with a primary diagnosis of OCD underwent functional magnetic resonance imaging (fMRI) scanning while performing a flanker task prior to receiving routine-care CBT. RESULTS: Error-related BOLD response of the SMN significantly contributed to the prediction of treatment response beyond the variance accounted for by clinical and sociodemographic variables. Stronger error-related SMN activity at baseline was associated with a higher likelihood of treatment response. CONCLUSIONS: The present results illustrate that the inclusion of error-related SMN activity can significantly increase treatment response prediction quality in OCD. Stronger error-related activity of the SMN may reflect the ability to activate symptom-relevant processing networks and may thus facilitate response to exposure-based CBT interventions.

Cognitive control is quickly adapted to actual task requirements despite misleading context cues-Evidence from the N2, CRN, and ERN.

Cognitive control is flexibly adapted to task requirements in healthy individuals. Medio-frontal negativities in the event-related potential of the electroencephalogram can serve as indicators of cognitive control. With increasing conflict frequency, stimulus-locked control, as indexed by the N2, is increased and response-locked control, as indexed by the correct-related negativity, is reduced. On the behavioral level, this shift is associated with improved conflict resolution as evident in reduced response times and error rates in incompatible trials and a reduced response time congruency effect. Cognitive control adaptation might be implemented through experience-based task sets specifying advantageous processing strategies. Here, we investigated whether the cognitive control task set will be sustained when coupled with a contextual cue, even when the initial task requirements are no longer present. A flanker task with two conflict frequency conditions (25% incompatible and 75% incompatible trials) was presented. In the training phase, the conflict frequency conditions were paired with a distinct context cue (i.e., background color). In the test phase, the previously associated cues were again presented, but conflict frequency was identical in both conditions (50% incompatible trials). Although typical cognitive control adaptation was observed in the training phase on the behavioral and event-related potentials level, this pattern was not sustained in the test phase. Thus, the present study provides further evidence that cognitive control is flexibly adapted to task requirements even in the presence of misleading cues.

Hypermethylation of the oxytocin receptor gene (OXTR) in obsessive-compulsive disorder: further evidence for a biomarker of disease and treatment response.

Obsessive-compulsive disorder (OCD) has recently been linked to increased methylation levels in the oxytocin receptor (OXTR) gene, and OXTR hypermethylation has predicted a worse treatment response to cognitive-behavioural therapy (CBT). Furthermore, OCD is associated with childhood trauma and stressful life events, which have both been shown to affect OXTR methylation. Here, we aimed to replicate findings of increased OXTR methylation as a predictor of disease and worse treatment response in an independent sample that received treatment within the public health care system. In addition, we aimed to extend previous findings by examining associations between OXTR hypermethylation, environmental stressors, OCD diagnosis, and treatment response. Methylation levels at two CpGs within OXTR exon III were compared between n = 181 OCD patients and n = 199 healthy controls using linear regression analysis. In a subsample of OCD patients (n = 98) with documented treatment data, we examined associations between methylation and treatment response to CBT. Childhood adversity and stressful life events were assessed using Childhood Trauma Questionnaire and Life Experience Survey, respectively. OCD patients exhibited significant hypermethylation at CpG site cg04523291 compared to controls, and increased methylation was associated with impaired treatment response. Moreover, hypermethylation at cg04523291 was associated with stressful life events in OCD patients, and with childhood adversity in controls. Yet, there were no significant mediation effects. In conclusion, we replicated the association between OXTR hypermethylation and OCD in the largest sample, so far. Furthermore, our findings support the role of OXTR methylation as a promising biomarker for treatment response in OCD.

Polygenic risk for obsessive-compulsive disorder (OCD) predicts brain response during working memory task in OCD, unaffected relatives, and healthy controls.

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.

Effects of adaptive and non-adaptive three-week executive control training on interference control: Evidence from the N2, CRN, and ERN.

The current pilot study investigated if interference control can be improved by a three-week at-home training comprising a flanker and a n-back task in healthy adults, thus exploring the training's suitability for future clinical application, i.e. as a treatment augmentation for psychological disorders. As training gains are assumed to be modulated by the amount of mismatch between task demands and brain resources, an adaptive and a non-adaptive training were contrasted in separate experiments. In the adaptive training, task difficulty was continuously adapted to participants' performance. In the non-adaptive training procedure, task difficulty remained stable on the lowest difficulty level. As deficits in interference control in psychological disorders often predominantly manifest on the electrophysiological level, the impact of the training procedures on medio-frontal negativities (N2, CRN, ERN) was investigated in addition to behavioral measures. The adaptive training led to significant improvements in interference control, as reflected in reduced response times and error rates in incompatible trials. This was accompanied by specific and complementary changes in medio-frontal negativities: After the adaptive training the N2 in incompatible trials was larger and the CRN in incompatible trials was reduced. The non-adaptive training procedure led to generally faster response times but also an increased error rate, indicating a speed-accuracy trade-off. This was accompanied by global changes to medio-frontal negativities irrespective of compatibility, possibly indicating task disengagement. Taken together, the current studies demonstrate that an adaptive training procedure can improve interference control thereby opening up possible clinical applications.

Emotional interference under low versus high executive control.

Previous research has demonstrated that task-irrelevant emotional distractors interfere with task performance especially under low phasic executive control (i.e., in nonconflict trials). In the present study, we measured medio-frontal ERPs (N2 and correct-related negativity, CRN) to elucidate which aspects of task performance are affected by emotional interference in a flanker task. To create emotional interference, negative and neutral pictures were presented during the flanker stimuli. N2 and CRN were reduced after negative pictures, indicating that conflict processing and performance monitoring are both affected by emotional interference. On the behavioral level, prolonged response times after negative pictures were observed under low phasic executive control (i.e., in compatible trials). Additionally, we explored whether emotional interference is modulated not only by phasic changes in executive control (i.e., conflict vs. nonconflict trials) but also by tonic changes in executive control (i.e., low vs. high overall conflict frequency). To this end, the flanker task consisted of two blocks with 25% versus 75% incompatible trials. Prolonged response times after negative pictures in compatible trials were observed only under low tonic executive control but not under high executive control.

Error-related brain activity as a transdiagnostic endophenotype for obsessive-compulsive disorder, anxiety and substance use disorder.

BACKGROUND: 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. METHODS: 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). RESULTS: 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. CONCLUSIONS: 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.

Schizotypy and smooth pursuit eye movements as potential endophenotypes of obsessive-compulsive disorder.

Patients with obsessive-compulsive disorder (OCD) show dysfunctions of the fronto-striatal circuitry, which imply corresponding oculomotor deficits including smooth pursuit eye movements (SPEM). However, evidence for a deficit in SPEM is inconclusive, with some studies reporting reduced velocity gain while others did not find any SPEM dysfunctions in OCD patients. Interestingly, psychosis-like traits have repeatedly been linked to both OCD and impaired SPEM. Here, we examined a large sample of n = 168 patients with OCD, n = 93 unaffected first-degree relatives and n = 171 healthy control subjects to investigate whether elevated levels of schizotypy and SPEM deficits represent potential endophenotypes of OCD. We applied a SPEM task with high demands on predictive pursuit that is more sensitive to assess executive dysfunctions than a standard task with continuous visual feedback, as episodes of target blanking put increased demands on basal ganglia and prefrontal involvement. Additionally, we examined the relation between schizotypy and SPEM performance in OCD patients and their relatives. Results indicate that OCD patients and unaffected relatives do not show deficient performance in either standard or predictive SPEM. Yet, both patients and relatives exhibited elevated levels of schizotypy, and schizotypy was significantly correlated with velocity gain during standard trials in unmedicated and depression-free OCD patients. These findings highlight the role of schizotypy as a candidate endophenotype of OCD and add to the growing evidence for predisposing personality traits in OCD. Furthermore, intact gain may represent a key characteristic that distinguishes the OCD and schizophrenia patient populations.

Impaired Antisaccades in Obsessive-Compulsive Disorder: Evidence From Meta-Analysis and a Large Empirical Study.

Increasing evidence indicates that patients with obsessive-compulsive disorder (OCD) exhibit alterations in fronto-striatal circuitry. Performance deficits in the antisaccade task would support this model, but results from previous small-scale studies have been inconclusive as either increased error rates, prolonged antisaccade latencies, both or neither have been reported in OCD patients. In order to address this issue, we investigated antisaccade performance in a large sample of OCD patients (n = 169) and matched control subjects (n = 183). As impaired antisaccade performance constitutes a potential endophenotype of OCD, unaffected first-degree relatives of OCD patients (n = 100) were assessed, as well. Furthermore, we conducted a quantitative meta-analysis to integrate our data with previous findings. In the empirical study, OCD patients exhibited significantly increased antisaccade latencies, intra-subject variability (ISV) of antisaccade latencies, and antisaccade error rates. The latter effect was driven by errors with express latency (80-130 ms), as patients did not differ significantly from controls with regards to regular errors (>130 ms). Notably, unaffected relatives of OCD patients showed elevated antisaccade express error rates and increased ISV of antisaccade latencies, as well. Antisaccade performance was not associated with state anxiety within groups. Among relatives, however, we observed a significant correlation between antisaccade error rate and harm avoidance. Medication status of OCD patients, symptom severity, depressive comorbidity, comorbid anxiety disorders and OCD symptom dimensions did not significantly affect antisaccade performance. Meta-analysis of 10 previous and the present empirical study yielded a medium-sized effect (SMD = 0.48, p < 0.001) for higher error rates in OCD patients, while the effect for latencies did not reach significance owing to strong heterogeneity (SMD = 0.51, p = 0.069). Our results support the assumption of impaired antisaccade performance in OCD, although effects sizes were only moderately large. Furthermore, we provide the first evidence that increased antisaccade express error rates and ISV of antisaccade latencies may constitute endophenotypes of OCD. Findings regarding these more detailed antisaccade parameters point to potentially underlying mechanisms, such as early pre-stimulus inhibition of the superior colliculus.

Impaired planning in patients with obsessive-compulsive disorder and unaffected first-degree relatives: Evidence for a cognitive endophenotype.

Patients with obsessive-compulsive disorder (OCD) show deficient planning capacity in the Tower of London (TOL) problem solving task. Preliminary evidence for similar deficits in unaffected first-degree relatives suggests that impaired planning may constitute an endophenotype of OCD. However, results on this issue are inconsistent, possibly owing to small sample sizes and variability in problem structure across TOL tasks. Here, we adopted a computerized version of the TOL task featuring a 2 × 2 factorial design (high/low search depth × full/partial tower goal state) and examined a well-characterized sample of n = 72 OCD patients, n = 76 unaffected first-degree relatives and n = 102 healthy comparison subjects. Both OCD patients and relatives exhibited significantly less accurate problem solving than controls. Search depth, goal hierarchy, or the number of minimum moves did not moderate these group differences. Medication, OCD symptoms, and depressive comorbidity did not affect TOL performance in patients, suggesting a state-independent effect. In conclusion, we found that OCD patients as well as unaffected first-degree relatives show deficient TOL performance across a range of task conditions, strongly supporting the role of impaired planning as an endophenotype of OCD, and contributing to the growing evidence for fronto-striatal dysfunctions in OCD.

Neural correlates of working memory deficits and associations to response inhibition in obsessive compulsive disorder.

Previous research in patients with obsessive-compulsive disorder (OCD) has indicated performance decrements in working memory (WM) and response inhibition. However, underlying neural mechanisms of WM deficits are not well understood to date, and empirical evidence for a proposed conceptual link to inhibition deficits is missing. We investigated WM performance in a numeric n-back task with four WM load conditions during functional Magnetic Resonance Imaging (fMRI) in 51 patients with OCD and 49 healthy control participants who were matched for age, sex, and education. Additionally, a stop signal task was performed outside the MRI scanner in a subsample. On the behavioral level, a significant WM load by group interaction was found for both accuracy (p < 0.02) and reaction time measures (p < 0.03), indicating increased reaction times as well as reduced accuracy specifically at high WM load (3-back) in patients with OCD. Whole-brain analyses of fMRI-data identified neural correlates of a load-dependent WM decrement in OCD in the supplementary motor area (SMA) and the inferior parietal lobule (IPL). Within the OCD sample, SMA-activity as well as n-back performance were correlated with stop signal task performance. Results from behavioral and fMRI-analyses indicate a reduced WM load-dependent modulation of neural activity in OCD and suggest a common neural mechanism for inhibitory dysfunction and WM decrements in OCD.

Volitional saccade performance in a large sample of patients with obsessive-compulsive disorder and unaffected first-degree relatives.

Recent evidence indicates that patients with obsessive-compulsive disorder (OCD) as well as their unaffected first-degree relatives show deficits in the volitional control of saccades, suggesting that volitional saccade performance may constitute an endophenotype of OCD. Here, we aimed to replicate and extend these findings in a large, independent sample. One hundred and fifteen patients with OCD, 103 healthy comparison subjects without a family history of OCD, and 31 unaffected first-degree relatives of OCD patients were examined using structured clinical interviews and performed a volitional saccade task as well as a prosaccade task. In contrast to previous reports, neither patients nor relatives showed impairments in the performance of volitional saccades compared to healthy controls. Notably, medicated patients did not differ from nonmedicated patients, and there was no effect of depressive comorbidity. Additional analyses investigating correlations between saccade performance and OCD symptom dimensions yielded no significant associations. In conclusion, the present results do not support the notion that volitional saccade execution constitutes an endophenotype of OCD. Possible explanations for inconsistencies with previous studies are discussed.

Frontal alpha asymmetry in OCD patients and unaffected first-degree relatives.

Frontal electroencephalographic alpha asymmetry as an indicator of trait approach and trait inhibition systems has previously been studied in individuals with obsessive-compulsive disorder (OCD) with mixed results. We explored frontal alpha asymmetry as a possible risk factor in OCD by investigating a large sample of OCD patients (n = 113), healthy control participants (n = 113), and unaffected 1st-degree relatives of OCD patients (n = 37). Additionally, the relationship between OCD symptom dimensions and frontal alpha asymmetry was explored. OCD patients and healthy control participants did not differ in alpha asymmetry scores. Hence, the current results do not support the notion that OCD as a diagnostic entity is associated with a shift in frontal cortical activity. Furthermore, alpha asymmetry scores were not statistically related to specific OCD symptom dimensions. Reasons for inconsistent results in OCD are discussed and should be explored in future studies. Compared to OCD patients and healthy control participants, unaffected 1st-degree relatives of OCD patients showed increased left frontal activity. Such asymmetry has previously been found to be associated with positive affect and adaptive emotion regulation under stress. Because stressful life events play an important role in the onset and exacerbation of OCD, increased left frontal activity might serve as a resilience factor in unaffected 1st-degree relatives. Future studies should follow up on these results with longitudinal risk studies and pre- and posttherapy assessments to further explore causality of this putative factor. (PsycINFO Database Record

Presupplementary Motor Area Contributes to Altered Error Monitoring in Obsessive-Compulsive Disorder.

BACKGROUND: Hyperactive performance monitoring, as measured by the error-related negativity (ERN) in the event-related potential, is a reliable finding in obsessive-compulsive disorder (OCD) research and may be an endophenotype of the disorder. Imaging studies revealed inconsistent results as to which brain regions are involved in altered performance monitoring in OCD. We investigated performance monitoring in OCD with simultaneous recording of electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) signals to determine the neural source of the enhanced ERN. METHODS: Concurrent EEG and fMRI data were collected from 20 patients with OCD and 22 healthy control subjects during a flanker task. Independent component analysis was used separately on EEG and fMRI to segment the data functionally and focus on processes of interest. The ERN, hemodynamic responses following errors, and intraindividual correlation of the ERN and blood oxygen level-dependent activity were compared between groups. RESULTS: Patients with OCD showed significantly increased ERN amplitudes. Blood oxygen level-dependent activity in midcingulate cortex was not significantly different between groups. Increased activation of the right amygdala and the subgenual anterior cingulate cortex following errors was observed in patients with OCD. Increased intraindividual correlation of the ERN and activity of the presupplementary motor area was found in patients with OCD compared with healthy controls. CONCLUSIONS: Higher error-related activity was found in the amygdala and subgenual anterior cingulate cortex, suggesting a stronger affective response toward errors in patients with OCD. Additionally, increased correlation of the ERN and presupplementary motor area may indicate stronger recruitment of proactive control in OCD.

Complementary modulation of N2 and CRN by conflict frequency.

The present study investigated the modulation of the N2 and the correct-related negativity (CRN) by conflict frequency. Conflict costs, as measured by reaction times and error rate, were reduced with increasing conflict frequency, indicating improved conflict resolution. N2 amplitudes in incompatible trials increased with higher conflict frequency, while postresponse CRN amplitudes decreased. In concert with behavioral findings of reduced conflict costs and greater interference suppression, the increase of N2 might reflect enhanced conflict resolution during stimulus processing. The CRN, however, might reflect postresponse implementation of cognitive control, which is reduced when conflict is already adequately resolved during stimulus processing. Furthermore, N2 and CRN in incompatible trials were inversely related on the between- and within-subject level, implying that the two modes of implementing cognitive control are applied complementarily.

Performance monitoring in obsessive-compulsive disorder: a temporo-spatial principal component analysis.

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.