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Updated: Sep 12, 2026

Exploring the Neural Correlates of Cognitive Reappraisal in Obsessive-Compulsive Disorder Using Task-based Functional Magnetic Resonance Imaging
Published on: March 14, 2025
Neural correlates of response inhibition following cognitive behavioral therapy in obsessive-compulsive disorder: a
Metin Çınaroğlu1, Selami Varol Ülker2, Eda Yılmazer3
1Psychology Department, İstanbul Nişantaşı University, Maslak Mahallesi, Taşyoncası Sokak, No: 1V ve No:1Y, Sarıyer/İstanbul, Türkiye. metincinaroglu@gmail.com.
Background:
Cognitive behavioral therapy (CBT) with exposure and response prevention is an established treatment for obsessive-compulsive disorder (OCD), yet the electrophysiological indices through which symptom improvement occurs remain incompletely understood. Response inhibition deficits have been implicated in OCD and may represent a key neurocognitive target of treatment. The present randomized controlled trial (Clinicaltrials.gov registiration no: NCT07000812) examined whether CBT is associated with changes in behavioral and electrophysiological indices of response inhibition.
Methods:
Sixty adults meeting DSM-5 criteria for OCD were randomized to a 12-week CBT program (n = 30) or a waitlist control condition (n = 30). Clinical severity was assessed using the Yale-Brown Obsessive Compulsive Scale (Y-BOCS), alongside measures of obsessive beliefs and intolerance of uncertainty. Response inhibition was evaluated using a Go/No-Go task while electroencephalography was recorded. Mean No-Go P3 amplitude (300-600 ms) at frontocentral regions of interest served as the primary neural outcome. Assessments were conducted at baseline and post-treatment.
Results:
Relative to the waitlist group, participants receiving CBT showed a significant reduction in OCD symptom severity, accompanied by improvements in obsessive beliefs and intolerance of uncertainty. Behavioral performance indicated a reduction in commission errors on No-Go trials following CBT. Electrophysiologically, a significant Group × Time interaction was observed for No-Go P3 amplitude, reflecting an increase from pre- to post-treatment in the CBT group, with no meaningful change in the waitlist group. No baseline differences were observed between groups.
Conclusions:
CBT for OCD was associated with both clinical improvement and enhanced neural indices of response inhibition, as reflected by increased No-Go P3 amplitude. These findings suggest that therapeutic change in OCD may involve increased engagement of electrophysiological indices supporting response inhibition. Integrating electrophysiological measures with clinical outcomes may help clarify the neurocognitive processes underlying effective psychological interventions.
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