Department of Psychological and Brain Sciences, Texas A&M University, College Station, Texas.
Department of Psychological and Brain Sciences, Texas A&M University, College Station, Texas.
Biol Psychiatry. 2023 Feb 15;93(4):352-361. doi: 10.1016/j.biopsych.2022.08.009. Epub 2022 Aug 18.
Knowledge of the neural mechanisms underlying increased disease burden in anxiety disorders that is unaccounted for by individual categorical diagnoses could lead to improved clinical care. Here, we tested the utility of a joint functional magnetic resonance imaging-electroencephalography neurobiological profile characterized by overvaluation of negative stimuli (amygdala) in combination with blunted elaborated processing of these same stimuli (the late positive potential [LPP], an event-related potential) in predicting increased psychopathology across a 2-year period in people with anxiety disorders.
One hundred ten participants (64 female, 45 male, 1 other) including 78 participants with phobias who varied in the extent of their internalizing comorbidity and 32 participants who were free from psychopathology viewed negative and neutral pictures during separate functional magnetic resonance imaging blood oxygen level-dependent and electroencephalogram recordings. Dysphoria was assessed at baseline and 2 years later.
Participants with both heightened amygdala activation and blunted LPPs to negative pictures showed the greatest increases in dysphoria 2 years later. Cross-sectionally, participants with higher comorbidity load (≥2 additional diagnoses, n = 34) showed increased amygdala activation to negative pictures compared with participants with lower comorbidity load (≤1 additional diagnosis, n = 44) and compared with participants free from psychopathology. In addition, high comorbid participants showed reduced LPPs to negative pictures compared with low comorbid participants.
Heightened amygdala in response to negative stimuli in combination with blunted LPPs could indicate overvaluation of threatening stimuli in the absence of elaborated processing that might otherwise help regulate threat responding. This brain profile could underlie the worsening and maintenance of internalizing psychopathology over time.
焦虑障碍患者的疾病负担增加，而个体的分类诊断并不能解释这一现象，了解其神经机制可能会改善临床护理。在这里，我们测试了一种联合功能磁共振成像-脑电图神经生物学特征的效用，该特征的特点是对负面刺激（杏仁核）的过度评价，以及对这些相同刺激的精细处理（晚期正电位 [LPP]，一种事件相关电位）减弱，以预测焦虑障碍患者在 2 年内的心理病理变化。
110 名参与者（64 名女性，45 名男性，1 名其他），包括 78 名恐惧症患者，他们的内化共病程度不同，以及 32 名没有精神病理学的参与者，在单独的功能磁共振成像血氧水平依赖和脑电图记录期间观看负面和中性图片。在基线和 2 年后评估抑郁。
对负面图片有强烈杏仁核激活和 LPPs 减弱的参与者，2 年后抑郁程度增加最大。在横截面上，共病负荷较高（≥2 个额外诊断，n=34）的参与者对负面图片的杏仁核激活高于共病负荷较低（≤1 个额外诊断，n=44）的参与者，也高于没有精神病理学的参与者。此外，高共病参与者对负面图片的 LPPs 减少，而低共病参与者则相反。
对负面刺激的杏仁核反应增强，LPPs 减弱，可能表明在没有精细处理的情况下对威胁性刺激的过度评价，而精细处理可能有助于调节威胁反应。这种大脑特征可能是导致内化心理病理随时间恶化和维持的原因。
