Obsessive-compulsive symptoms predict increased fronto-parahippocampal synchronisation during thought suppression.

Read the full article See related articles

Listed in

This article is not in any list yet, why not save it to one of your lists.
Log in to save this article

Abstract

Background: Thought suppression is suggested as a causal factor in obsessive-compulsive disorder (OCD), as it can lead to an increase in intrusive thoughts. However, the neural mechanisms through which obsessive-compulsive symptoms (OCS) influence thought suppression, particularly in the context of preferential processing of negatively valenced stimuli, remains unclear. We hypothesized that OCS would predict increased inhibitory communication between frontal and parahippocampal neurocircuitry during the suppression of negative words. Additionally, we tested an exploratory analysis to see whether this was mediated by preferential processing of these stimuli. Methods: EEG was recorded from 47 participants tasked with directed forgetting of negative and neutral words. Data from 38 of these participants were analyzed. We examined the influence of OCS on fronto-parahippocampal beta-1 (13-18 Hz) synchronization during a Directed Forgetting task. An exploratory analysis of the mediating role of stimulus processing bias, measured via the late positive potential (LPP) following the word stimulus, was assessed using a mediated moderation model.Results: OCS predicted enhanced fronto-parahippocampal beta-1 synchronisation when instructed to forget negative words. The moderating effect of valence was mediated by preferential processing of negative stimuli, as indicated by increased LPP. Conclusions: Healthy individuals with relatively high OCS exhibit compensatory connectivity between frontal and parahippocampal regions when attempting to suppress negative emotional stimuli. Exploratory analysis showed this compensatory activity is influenced by both preferential processing of negative stimuli and the severity of OCS, providing preliminary evidence of a neural mechanism that may contribute to the persistence of intrusive thoughts in OCD.

Article activity feed