首页> 美国卫生研究院文献>Translational Psychiatry >Impaired regulation of emotion: neural correlates of reappraisal and distraction in bipolar disorder and unaffected relatives
【2h】

Impaired regulation of emotion: neural correlates of reappraisal and distraction in bipolar disorder and unaffected relatives

机译:情绪调节受损:双相情感障碍和未患病亲属的重新评估和分神的神经相关

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Deficient emotion regulation has been proposed as a crucial pathological mechanism in bipolar disorder (BD). We therefore investigated emotion regulation impairments in BD, the related neural underpinnings and their etiological relevance for the disorder. Twenty-two euthymic patients with bipolar-I disorder and 17 unaffected first-degree relatives of BD-I patients, as well as two groups of healthy gender-, age- and education-matched controls (N=22/17, respectively) were included. Participants underwent functional magnetic resonance imaging while applying two different emotion regulation techniques, reappraisal and distraction, when presented with emotional images. BD patients and relatives showed impaired downregulation of amygdala activity during reappraisal, but not during distraction, when compared with controls. This deficit was correlated with the habitual use of reappraisal. The negative connectivity of amygdala and orbitofrontal cortex (OFC) observed during reappraisal in controls was reversed in BD patients and relatives. There were no significant differences between BD patients and relatives. As being observed in BD patients and unaffected relatives, deficits in emotion regulation through reappraisal may represent heritable neurobiological abnormalities underlying BD. The neural mechanisms include impaired control of amygdala reactivity to emotional stimuli and dysfunctional connectivity of the amygdala to regulatory control regions in the OFC. These are, thus, important aspects of the neurobiological basis of increased vulnerability for BD.
机译:情绪低落的调节已被提出为躁郁症(BD)的关键病理机制。因此,我们调查了BD的情绪调节障碍,相关的神经基础及其与疾病的病因相关性。 22名患有双相性I型情感障碍的正常人和17名未受影响的BD-I患者一级亲属,以及两组健康的性别,年龄和文化相匹配的对照组(分别为N = 22/17)包括在内。参加者接受了功能性磁共振成像,同时使用两种不同的情绪调节技术,即重新呈现和分散注意力(当出现情绪图像时)。与对照相比,BD患者和亲属在重新评估期间显示杏仁核活动的下调受损,但在分心期间则没有。这种缺陷与习惯性使用重新评估有关。在BD患者及其亲属中,在重新评估对照过程中观察到的杏仁核和眶额皮质(OFC)的负连通性被逆转。 BD患者与亲属之间无显着差异。正如在BD患者和未受影响的亲属中观察到的那样,通过重新评估而导致的情绪调节不足可能代表了BD背后的可遗传的神经生物学异常。神经机制包括杏仁核对情绪刺激的反应性控制受损,以及杏仁核与OFC中调控区域的功能障碍。因此,这些是BD易损性增加的神经生物学基础的重要方面。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号