Reward dysfunction in major depression: multimodal neuroimaging evidence for refining the melancholic phenotype.
Reward dysfunction in major depression: multimodal neuroimaging evidence for refining the melancholic phenotype.
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DOI：
10.1016/j.neuroimage.2014.06.058
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发表时间：
2014-11-01
期刊：
影响因子：
5.7
通讯作者：
Proudfit GH
中科院分区：
文献类型：
--
作者：
Foti D;Carlson JM;Sauder CL;Proudfit GH
奖励功能障碍被认为在重性抑郁症（MDD）的病理生理学中起着核心作用。事件相关电位（ERP）和功能性磁共振成像（fMRI）研究已经确定了MDD的奖励处理缺陷，但这些方法还没有一起应用于一个单一的MDD样本。我们利用多模态神经影像学证据来检查MDD中的奖励功能障碍。此外，我们探讨了神经生物学奖励功能障碍如何映射到MDD亚型。在实验室赌博任务中，记录了34名未服药的抑郁症患者和42名从不抑郁的对照者的反馈负性（FN），反馈负性是奖赏评价的ERP指标。在一个单独的功能磁共振成像会议，使用相同的任务，在一个亚组的24个抑郁症患者和一个对照组的18个非抑郁症对照记录纹状体（VS）激活奖励。MDD时FN振幅变钝。这种效应是由MDD亚组驱动的，其特征是对积极事件的情绪反应受损，这是抑郁性MDD的核心特征。VS激活也观察到类似的模式，这在情绪反应受损的MDD亚组中也是钝化的。FN振幅和VS激活均与完整的、DSM定义的抑郁症或非典型MDD亚型无关。在MDD样本中，FN振幅和VS激活相关，表明方法之间的收敛性。这些结果表明，并不是所有的MDD的特点是奖励功能障碍，并有意义的异质性奖励加工内MDD。目前的研究提供了神经生物学证据，即受损的情绪反应是MDD亚型的关键表型区别，并进一步表明现有的神经元表型可能需要进一步改进。
Reward dysfunction is thought to play a core role in the pathophysiology of major depressive disorder (MDD). Event-related potential (ERP) and functional magnetic resonance imaging (fMRI) studies have identified reward processing deficits in MDD, but these methods have yet to be applied together in a single MDD sample. We utilized multimodal neuroimaging evidence to examine reward dysfunction in MDD. Further, we explored how neurobiological reward dysfunction would map onto subtypes of MDD. The feedback negativity (FN), an ERP index of reward evaluation, was recorded in 34 unmedicated depressed individuals and 42 never-depressed controls during a laboratory gambling task. Ventral striatal (VS) activation to reward was recorded in a separate fMRI session, using an identical task, among a subgroup of 24 depressed individuals and a comparison group of 18 non-depressed controls. FN amplitude was blunted in MDD. This effect was driven by a MDD subgroup characterized by impaired mood reactivity to positive events, a core feature of melancholic MDD. A similar pattern was observed for VS activation, which was also blunted among the MDD subgroup with impaired mood reactivity. Neither FN amplitude nor VS activation were related to the full, DSM-defined melancholic or atypical MDD subtypes. Across the MDD sample, FN amplitude and VS activation were correlated, indicating convergence across methods. These results indicate that not all MDD is characterized by reward dysfunction, and that there is meaningful heterogeneity in reward processing within MDD. The current study offers neurobiological evidence that impaired mood reactivity is a key phenotypic distinction for subtyping MDD, and further suggests that the existing melancholic phenotype may require further refinement.
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