Neural mediators of behavior therapy for anxiety

描述（由申请人提供）：焦虑症是一种广泛且昂贵的疾病。社交焦虑障碍（SAD）是最常见的焦虑症之一，可导致严重的功能障碍。尽管行为治疗干预焦虑障碍，包括SAD的流行，行为治疗焦虑的神经介质研究不足。在此，我们提出的研究将阐明行为治疗对SAD的神经认知作用。其次，它将允许在神经水平上比较两种不同类型的行为疗法。参与者将被随机分配到认知行为疗法（CBT），等待名单控制（WL），或一种新的行为疗法，接受和承诺疗法（ACT）。主要的比较将在CBT和WL之间进行。次要比较将是CBT和ACT。使用功能性磁共振成像（fMRI）扫描患有SAD的患者在12周CBT/ACT或12周等候名单控制期前后，同时他们完成了一项广泛用于非临床样本的威胁处理任务（情感语言处理任务，或L-PAT），我们期望看到治疗后神经激活的一些变化，相对于等候名单控制期。也就是说，我们预计治疗后杏仁核对负面评价面孔的反应会减少。我们还期望治疗后前额叶激活增加，特别是在右腹外侧前额叶皮层（RVLPFC），这与消极情绪的处理有关。先前对非临床样本的研究表明，RVLPFC可能抑制或抑制杏仁核对威胁的反应；因此，我们预测治疗将会加强这一过程。我们期望看到这两个区域（杏仁核和RVLPFC）的功能连通性在治疗后的差异，这样RVLPFC和杏仁核的激活将在治疗后更强的负相关。我们预测，治疗后症状改善的程度也将与神经激活的预期变化相关，如上所述。我们还提出了一些关于CBT和ACT之间差异的探索性假设，这些差异可能出现在神经水平上。这项工作将是对行为疗法治疗焦虑的神经介质的第一次调查，也是第一次在神经水平上比较两种行为疗法的研究。这项工作将阐明焦虑障碍的特征，并提高对焦虑常用治疗方法的理解。公共卫生相关性：这项工作将是对行为疗法治疗焦虑的神经介质的第一次调查，也是第一次在神经水平上比较两种行为疗法的研究。这项工作将阐明焦虑障碍的特征，并提高对焦虑常用治疗方法的理解。

DESCRIPTION (provided by applicant): Anxiety disorders are widespread and costly. Social anxiety disorder (SAD) is one of the most common anxiety disorders, and can lead to significant functional impairment. Despite the prevalence of behavior therapy interventions for anxiety disorders, including SAD, the neural mediators of behavioral treatment for anxiety are understudied. Here, we propose research that will elucidate the neurocognitive effects of behavior therapy for SAD. Secondarily, it will allow for the comparison of two distinct types of behavior therapy on a neural level. Participants will be randomized to either cognitive-behavioral therapy (CBT), a wait-list control (WL), or a newer form of behavioral therapy, acceptance and commitment therapy (ACT). Primary comparisons will be between CBT and WL. Secondary comparisons will be between CBT and ACT. Using functional magnetic resonance imaging (fMRI) to scan clients with SAD before and after the 12- week CBT/ACT or a 12-week wait-list control period while they complete a threat processing task that has been used extensively with non-clinical samples (the Linguistic Processing of Affect Task, or L-PAT), we expect to see several changes in neural activations after treatment, relative to the wait list control period. Namely, we expect reductions in the amygdala response to negatively-valenced faces after treatment. We also expect a post-treatment increase in prefrontal activation, specifically in the right ventrolateral prefrontal cortex (RVLPFC), which is implicated in the processing of negative affect. Previous work with non-clinical samples has suggested that the RVLPFC may work to inhibit or dampen the amygdala response to threat; therefore, we predict that therapy will work to strengthen this process. We expect to see a post-treatment difference in the functional connectivity of those two regions (the amygdala and RVLPFC), such that activations in the RVLPFC and amygdala will be more strongly negatively correlated after treatment. We predict that the degree of symptom improvement after treatment will also correlate with the expected changes in neural activation, outlined above. We also present some exploratory hypotheses about differences between CBT and ACT that may emerge at a neural level. The proposed work will be one of the first investigations of the neural mediators of behavior therapy treatment for anxiety, and would also be the first study to compare two behavior therapy treatments on a neural level. This work will shed light on the characteristics of anxiety disorders and improve understanding of the treatments commonly used for anxiety. PUBLIC HEALTH RELEVANCE: The proposed work would be one of the first investigations of the neural mediators of behavior therapy treatment for anxiety, and would also be the first study to compare two behavior therapy treatments on a neural level. This work will shed light on the characteristics of anxiety disorders and improve understanding of the treatments commonly used for anxiety.