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Distress Intolerance Modulation of Neurophysiological Markers of Cognitive Control during a Complex Go/No-go Task

机译:复杂的去/不去任务期间认知控制的神经生理标志物的遇险不耐性调节。

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摘要

Distress intolerance (DI), a trait-like individual difference reflective of the inability to endure aversive affective states, is relevant to multiple forms of psychopathology, but its relations to theoretically-relevant neurobiological systems has received little attention. Altered response inhibition-related neurobiology has been theorized to underlie individual differences in DI, but little empirical work has been conducted. To test this hypothesis, baseline data from a large clinical sample with elevated risk for affective psychopathology was utilized (N = 254). Participants completed a complex Go/No-go task while EEG was recorded, and No-go N2/P3 amplitudes and latencies were measured. Based upon prior findings on the relations between these components and response inhibition, we hypothesized that DI would predict reduced No-go N2/P3 amplitude and greater No-go N2/P3 latency while controlling for current anxious/depressive symptom severity. Partially consistent with predictions, high DI was independently associated with reduced No-go N2 amplitude but was non-significantly related to latency, though high DI was linked with greater Go N2 latency. Contrary to predictions, no relations between DI and the P3 were found. Further, exploratory analyses revealed positive associations between DI and No-go P2 amplitude/latency. Correlations between components and task performance suggest that observed relations between DI and the P2/N2 may reflect inefficient rather than impaired response inhibition. Overall, results support the theorized relevance of response inhibition-linked neurobiology to individual differences in tolerance of distress over and above distress severity itself, and suggest specific relations between DI and alterations in early selective attention/conflict-monitoring but not evaluative phases of response inhibition.
机译:窘迫不耐症(DI)是一种类似特质的个体差异,反映了无法忍受厌恶的情感状态,与心理病理学的多种形式有关,但其与理论上相关的神经生物学系统的关系很少受到关注。理论上改变反应抑制相关的神经生物学是DI个体差异的基础,但是很少进行经验研究。为了检验该假设,使用了来自大型临床样本的基线数据,这些样本的情感心理病理风险较高(N = 254)。参与者在记录脑电图的同时完成了复杂的Go / No-go任务,并测量了N2 / P3的No-go振幅和延迟。基于这些成分与应答抑制之间关系的先前发现,我们假设DI可以预测No-go N2 / P3振幅的降低和No-go N2 / P3潜伏期的增加,同时控制当前的焦虑/抑郁症状严重程度。部分与预测一致,尽管高DI与更大的Go N2潜伏期相关,但高DI与No-go N2振幅降低独立相关,但与潜伏期无关。与预测相反,没有发现DI和P3之间的关系。此外,探索性分析显示DI与No-go P2振幅/潜伏期之间呈正相关。组件与任务执行之间的相关性表明,DI和P2 / N2之间观察到的关系可能反映了效率低下,而不是削弱了反应抑制能力。总体而言,结果支持与反应抑制相关的神经生物学与个体在其自身的严重程度之上和之上的窘迫耐受性差异之间的理论相关性,并表明DI与早期选择性注意/冲突监测的变化之间的特定关系,但不是反应抑制的评估阶段。

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