背景:由于高度异质性和合并症,焦虑和重度抑郁障碍的共同和独特的神经机制尚不清楚.使用描述与焦虑和抑郁相关的共同症状和独特症状的维度模型,这项研究调查了症状维度的纵向变化与威胁神经回路的关系。
方法:参与者为18至19岁(N=279,186名女性),他们在基线和10、20和30个月时完成了焦虑和抑郁的自我报告测量。一般不适症状尺寸的线性斜率,恐惧,快感缺失是通过三阶阶乘模型估计的。此外,参与者在基线和30个月时执行巴甫洛夫恐惧调节任务时,获得了功能磁共振成像扫描,包括恐惧获得的三个阶段,灭绝,和灭绝召回。与威胁神经回路相关的感兴趣区域中的神经反应(例如,杏仁核,腹内侧前额叶皮质,并提取下前扣带回皮质)。
结果:用于估计症状维度变化与神经反应之间关系的线性混合模型揭示了两个主要发现:1)在基线恐惧获取过程中对威胁性刺激的更大神经反应与在30个月的预期期内恐惧症状的增加有关;2)在30个月的灭绝回忆过程中,对熄灭刺激的神经反应升高与一般痛苦的变化呈负相关。这表明一般痛苦的更大增加与灭绝记忆的更大缺陷有关。
结论:这些发现提高了我们对焦虑和抑郁发展的病理生理途径的理解,同时将两种疾病之间共享和独特的症状维度分开。
Owing to high heterogeneity and comorbidity, the shared and unique neural mechanisms underlying the development of anxiety and major depressive disorders remain unclear. Using a dimensional model describing shared versus unique symptoms associated with anxiety and depression, this study investigated how longitudinal changes in symptom dimensions relate to threat neurocircuitry.
Participants were 18- to 19-year-olds (N = 279, 186 females) who completed self-report measures of anxiety and depression at baseline and at 10, 20, and 30 months. Linear slopes of symptom dimensions of general distress, fear, and anhedonia-apprehension were estimated through a trilevel factorial model. In addition, functional magnetic resonance imaging scans were obtained while participants performed Pavlovian fear conditioning tasks at baseline and 30 months, including three phases of fear acquisition, extinction, and extinction recall. Neural responses in regions of interest related to threat neural circuitry (e.g., amygdala, ventromedial prefrontal cortex, and subgenual anterior cingulate cortex) were extracted.
Linear mixed models used to estimate relationships between changes of symptom dimensions and neural responses revealed two major findings: 1) greater neural responses to threatening stimuli during fear acquisition at baseline were associated with a greater increase in fear symptoms during the 30-month prospective period; and 2) elevated neural responses to the extinguished stimulus during extinction recall at 30 months were negatively associated with changes in general distress, suggesting that greater increases in general distress are associated with larger deficits in extinction memory.
These findings improve our understanding of pathophysiological pathways underlying the development of anxiety and depression, while separating symptom dimensions that are shared versus unique between the two disorders.