Background/Objectives: Obsessive–compulsive disorder (OCD) is associated not only with obsessions and compulsions, but also with cognitive dysfunction involving inhibitory control, cognitive flexibility, working memory, attention, decision-making, feedback learning, and performance monitoring. Electroencephalography (EEG), event-related potentials (ERPs), quantitative EEG, and time–frequency analyses provide temporally
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Background/Objectives: Obsessive–compulsive disorder (OCD) is associated not only with obsessions and compulsions, but also with cognitive dysfunction involving inhibitory control, cognitive flexibility, working memory, attention, decision-making, feedback learning, and performance monitoring. Electroencephalography (EEG), event-related potentials (ERPs), quantitative EEG, and time–frequency analyses provide temporally precise methods for examining how these cognitive abnormalities unfold during information processing. This review aimed to synthesise electrophysiological evidence on the neural correlates of cognitive dysfunction in OCD.
Methods: A systematic literature search was conducted in PubMed/MEDLINE, Scopus, Web of Science Core Collection, Embase, PsycINFO, and Google Scholar from database inception to 30 May 2026. Eligible studies included patients with OCD and used EEG, qEEG, spectral EEG, EEG connectivity, or ERP methods in relation to cognitive performance, cognitive task demands, or cognitive dysfunction. Studies were grouped according to electrophysiological modality and ERP component. Because of methodological heterogeneity, findings were synthesised narratively and mechanistically rather than by meta-analysis. Methodological quality was assessed using ROBINS-I.
Results: The search identified 1321 records, of which 42 studies met the inclusion criteria. Most studies used task-based ERP paradigms, while fewer examined resting-state EEG, qEEG, or oscillatory activity. The most consistent findings concerned altered performance monitoring and cognitive control, especially ERN, N2/N200, Pe, Pc, and P3/P300 abnormalities. ERN findings suggested excessive early error monitoring, whereas N2/N200 and P3/P300 findings indicated task-dependent abnormalities in inhibition, conflict processing, attentional allocation, stimulus evaluation, and context updating. Earlier components, including P50, N1/N100, P2/P200, and N450, suggested abnormalities in sensory gating, early attentional selection, stimulus evaluation, and interference control, particularly under emotionally salient or OCD-relevant conditions. FRN findings indicated altered feedback processing and reinforcement learning, while limited P600 evidence suggested inefficient working-memory preparation. Plain EEG and time–frequency studies further implicated abnormal theta, alpha, beta, and delta activity in monitoring, inhibition, arousal, and network efficiency.
Conclusions: EEG-based evidence suggests that cognitive dysfunction in OCD reflects a dysregulated control system rather than a general reduction in cognitive ability. The disorder appears to involve excessive performance monitoring, abnormal sensory and attentional gating, inefficient inhibition, altered feedback evaluation, and reduced cognitive flexibility. However, the current evidence is limited by heterogeneity in samples, paradigms, EEG methodology, medication status, and statistical approaches. Future studies should use larger, well-characterised samples, standardised EEG/ERP paradigms, direct brain–behaviour analyses, and longitudinal designs to clarify whether electrophysiological abnormalities represent trait markers, state-dependent effects, compensatory mechanisms, or clinically useful predictors of cognitive dysfunction in OCD.
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