Department of Psychiatry and Behavioral Sciences, Stanford School of Medicine, Stanford, California; Department of Psychology, Palo Alto University, Palo Alto, California.
Department of Psychiatry and Behavioral Sciences, Stanford School of Medicine, Stanford, California.
Biol Psychiatry. 2020 Oct 1;88(7):576-586. doi: 10.1016/j.biopsych.2020.02.011. Epub 2020 Feb 21.
Anxiety and stress reactivity are risk factors for the development of affective disorders. However, the behavioral and neurocircuit mechanisms that potentiate maladaptive emotion regulation are poorly understood. Neuroimaging studies have implicated the amygdala and dorsolateral prefrontal cortex (DLPFC) in emotion regulation, but how anxiety and stress alter their context-specific causal circuit interactions is not known. Here, we use computational modeling to inform affective pathophysiology, etiology, and neurocircuit targets for early intervention.
Forty-five children (10-11 years of age; 25 boys) reappraised aversive stimuli during functional magnetic resonance imaging scanning. Clinical measures of anxiety and stress were acquired for each child. Drift-diffusion modeling of behavioral data and causal circuit analysis of functional magnetic resonance imaging data, with a National Institute of Mental Health Research Domain Criteria approach, were used to characterize latent behavioral and neurocircuit decision-making dynamics driving emotion regulation.
Children successfully reappraised negative responses to aversive stimuli. Drift-diffusion modeling revealed that emotion regulation was characterized by increased initial bias toward positive reactivity during viewing of aversive stimuli and increased drift rate, which captured evidence accumulation during emotion evaluation. Crucially, anxiety and stress reactivity impaired latent behavioral dynamics associated with reappraisal and decision making. Anxiety and stress increased dynamic casual influences from the right amygdala to DLPFC. In contrast, DLPFC, but not amygdala, reactivity was correlated with evidence accumulation and decision making during emotion reappraisal.
Our findings provide new insights into how anxiety and stress in children impact decision making and amygdala-DLPFC signaling during emotion regulation, and uncover latent behavioral and neurocircuit mechanisms of early risk for psychopathology.
焦虑和应激反应是情感障碍发展的风险因素。然而,增强适应不良情绪调节的行为和神经回路机制仍知之甚少。神经影像学研究表明杏仁核和背外侧前额叶皮层(DLPFC)在情绪调节中起作用,但焦虑和应激如何改变它们的特定情境因果回路相互作用尚不清楚。在这里,我们使用计算模型为情感病理生理学、病因学和神经回路的早期干预提供信息。
45 名儿童(10-11 岁;25 名男孩)在功能磁共振成像扫描期间重新评估了厌恶刺激。为每个孩子获取了焦虑和应激的临床测量值。使用行为数据的漂移扩散建模和功能磁共振成像数据的因果回路分析,以及国家心理健康研究所研究领域标准方法,用于描述潜在的行为和神经回路决策动力学,这些动力学驱动情绪调节。
儿童成功地重新评估了对厌恶刺激的负面反应。漂移扩散建模表明,情绪调节的特点是在观看厌恶刺激时初始偏向积极反应性增加,并且漂移率增加,这捕获了情绪评估过程中的证据积累。至关重要的是,焦虑和应激反应会损害与再评价和决策相关的潜在行为动态。焦虑和应激增加了右侧杏仁核到 DLPFC 的动态因果影响。相比之下,DLPFC 的反应性,而不是杏仁核的反应性,与情绪再评价期间的证据积累和决策相关。
我们的研究结果提供了新的见解,说明儿童的焦虑和应激如何影响情绪调节期间的决策和杏仁核-DLPFC 信号传递,并揭示了潜在的行为和神经回路机制,这些机制是精神病早期风险的原因。