Jones Rhiannon, Leunissen Joost M, Whyte Adrian, Werson Alessa, Bhattacharya Joydeep
University of Winchester, Sparkford Road, Winchester, SO22 4 NR, UK.
University of Southampton, Shackleton Building (44), University Road, Southampton, Hampshire, SO17 1BJ, UK.
Cogn Affect Behav Neurosci. 2025 May 29. doi: 10.3758/s13415-025-01316-x.
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.
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 following the word stimulus, was assessed using a mediated moderation model.
Obsessive-compulsive symptoms 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 late positive potential.
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.
思维抑制被认为是强迫症（OCD）的一个致病因素，因为它会导致侵入性思维增加。然而，强迫症状（OCS）影响思维抑制的神经机制，尤其是在对负性情绪刺激进行优先加工的背景下，仍不清楚。我们假设，在抑制负面词汇时，强迫症状会预示额叶和海马旁神经回路之间抑制性交流的增加。此外，我们进行了一项探索性分析，以观察这是否由这些刺激的优先加工所介导。
记录了47名参与者在定向遗忘负面和中性词汇任务中的脑电图。对其中38名参与者的数据进行了分析。我们在定向遗忘任务中研究了强迫症状对额-海马旁β-1（13 - 18赫兹）同步性的影响。通过单词刺激后的晚期正电位测量的刺激加工偏差的中介作用的探索性分析，使用中介调节模型进行评估。
当被指示遗忘负面词汇时，强迫症状预示着额-海马旁β-1同步性增强。负性情绪的调节作用由对负性刺激的优先加工所介导，晚期正电位增加表明了这一点。
具有相对较高强迫症状的健康个体在试图抑制负面情绪刺激时，额叶和海马旁区域之间表现出代偿性连接。探索性分析表明，这种代偿性活动受负性刺激的优先加工和强迫症状严重程度的影响，为一种可能导致强迫症中侵入性思维持续存在的神经机制提供了初步证据。
