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

机译:情绪受损:双相障碍和不受影响亲属中重新遗产和分心的神经相关性

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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:已经提出了缺乏情感调节作为双相障碍(BD)的关键病理机制。因此,我们调查了BD的情感监管障碍,相关神经内衬及其对疾病的病因相关性。二十二次患有双极性障碍和17名未受影响的BD-I患者的一级亲属患者,以及两组健康性别,年龄和教育匹配的对照(分别为22/17次)包括。参与者接受功能磁共振成像,同时应用两种不同的情绪调节技术,重新评估和分心,当呈现情绪图像时。与对照相比,BD患者和亲属在重新评估期间表现出杏仁达拉活动的下调性损害,但在分心期间。这种赤字与习惯性使用的赤字相关。在BD患者和亲属中,在对照中重新评估期间观察到的Amygdala和Orbitofrontal Cortex(OFC)的负连接逆转。 BD患者和亲属之间没有显着差异。在BD患者和未受影响的亲属中观察到,通过重新评估的情感调节缺陷可能代表BD下面的遗传性神经生物学异常。神经机制包括对Amygdala反应性的控制障碍与amygdala对OFC中的调节控制区域的情绪刺激和功能障碍连接。因此,这些是增加BD脆弱性的神经生理学基础的重要方面。

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