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

Impaired regulation of emotion: neural correlates of reappraisal and distraction in bipolar disorder and unaffected relatives.
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DOI:
10.1038/tp.2014.137
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发表时间:
2015-01-20
影响因子:
6.8
通讯作者:
Wessa M
Wessa M
中科院分区:
医学1区
文献类型:
--
作者:
Kanske P;Schönfelder S;Forneck J;Wessa M

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情感调节缺陷已被认为是双相情感障碍(BD)的一个重要病理机制。因此,我们调查情绪调节障碍,BD,相关的神经基础和他们的病因相关性的障碍。包括22名患有双极-I障碍的正常胸腺患者和17名BD-I患者的未受影响的一级亲属,以及两组健康的性别、年龄和教育程度匹配的对照组(分别为N=22/17)。参与者接受功能性磁共振成像,同时应用两种不同的情绪调节技术,重新评价和分心,当呈现情绪图像。与对照组相比,BD患者及其亲属在重新评价过程中杏仁核活性下调受损,而在分心过程中则没有。这种缺陷与习惯性使用重新评价有关。在对照组中重新评估时观察到的杏仁核和眶额皮质(OFC)的负连接在BD患者和亲属中被逆转。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,通过重新评价进行情绪调节的缺陷可能代表BD的遗传性神经生物学异常。神经机制包括杏仁核对情绪刺激的反应性控制受损和杏仁核与眶额皮层调节控制区的连接功能障碍。因此,这些是BD脆弱性增加的神经生物学基础的重要方面。
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.
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