Molecular Psychiatry ( IF 9.6 ) Pub Date : 2024-01-26 , DOI: 10.1038/s41380-024-02429-4 Melissa Klug 1 , Verena Enneking 1 , Tiana Borgers 1 , Charlotte M Jacobs 1 , Katharina Dohm 1 , Anna Kraus 1 , Dominik Grotegerd 1 , Nils Opel 1, 2, 3, 4 , Jonathan Repple 1, 5 , Thomas Suslow 6 , Susanne Meinert 1, 7 , Hannah Lemke 1 , Elisabeth J Leehr 1 , Jochen Bauer 8 , Udo Dannlowski 1 , Ronny Redlich 1, 3, 4, 9
Biased emotion processing has been suggested to underlie the etiology and maintenance of depression. Neuroimaging studies have shown mood-congruent alterations in amygdala activity in patients with acute depression, even during early, automatic stages of emotion processing. However, due to a lack of prospective studies over periods longer than 8 weeks, it is unclear whether these neurofunctional abnormalities represent a persistent correlate of depression even in remission. In this prospective case-control study, we aimed to examine brain functional correlates of automatic emotion processing in the long-term course of depression. In a naturalistic design, n = 57 patients with acute major depressive disorder (MDD) and n = 37 healthy controls (HC) were assessed with functional magnetic resonance imaging (fMRI) at baseline and after 2 years. Patients were divided into two subgroups according to their course of illness during the study period (n = 37 relapse, n = 20 no-relapse). During fMRI, participants underwent an affective priming task that assessed emotion processing of subliminally presented sad and happy compared to neutral face stimuli. A group × time × condition (3 × 2 × 2) ANOVA was performed for the amygdala as region-of-interest (ROI). At baseline, there was a significant group × condition interaction, resulting from amygdala hyperactivity to sad primes in patients with MDD compared to HC, whereas no difference between groups emerged for happy primes. In both patient subgroups, amygdala hyperactivity to sad primes persisted after 2 years, regardless of relapse or remission at follow-up. The results suggest that amygdala hyperactivity during automatic processing of negative stimuli persists during remission and represents a trait rather than a state marker of depression. Enduring neurofunctional abnormalities may reflect a consequence of or a vulnerability to depression.
中文翻译:
抑郁症长期病程中杏仁核过度活跃对潜意识负面情绪处理的持续存在
有人认为,有偏见的情绪处理是抑郁症的病因和维持的基础。神经影像学研究表明,即使在情绪处理的早期、自动阶段,急性抑郁症患者的杏仁核活动也会发生与情绪一致的变化。然而,由于缺乏超过 8 周的前瞻性研究,目前尚不清楚这些神经功能异常是否代表抑郁症的持续相关性,即使在缓解期也是如此。在这项前瞻性病例对照研究中,我们的目的是检查抑郁症长期病程中自动情绪处理的大脑功能相关性。在自然设计中, n = 57 名急性重度抑郁症 (MDD) 患者和n = 37 名健康对照 (HC) 在基线时和 2 年后接受功能磁共振成像 (fMRI) 评估。根据研究期间的病程,患者被分为两个亚组( n = 37 例复发, n = 20 例未复发)。在功能磁共振成像期间,参与者接受了情感启动任务,该任务评估了与中性面部刺激相比,潜意识中呈现的悲伤和快乐的情绪处理。对作为感兴趣区域 (ROI) 的杏仁核进行组 × 时间 × 条件 (3 × 2 × 2) 方差分析。在基线时,与 HC 患者相比,MDD 患者的杏仁核过度活跃导致悲伤高峰期存在显着的组 × 条件交互作用,而组间的快乐高峰期没有差异。在这两个患者亚组中,无论随访时是否复发或缓解,杏仁核对悲伤素的过度活跃在 2 年后仍然持续存在。 结果表明,杏仁核在自动处理负面刺激过程中过度活跃在缓解期间持续存在,并且代表了抑郁症的一种特征而不是状态标志。持久的神经功能异常可能反映了抑郁症的后果或脆弱性。