Targeting Attention Orienting to Social Threat to Reduce Social Anxiety in Youth

项目摘要 这个两个站点（佛罗里达国际大学，耶鲁大学）R 01项目提出确认注意偏差 修改治疗（ABMT）作为一种有效的治疗社交焦虑障碍（SAD）在围青春期 青年年龄10至14岁，并检查ABMT的临床疗效的机制。悲伤情绪很普遍， 慢性的，有害的SAD的循证治疗（EBT）应答率明显低于 其他焦虑症，以及有限的见解存在的机制，积极的结果，为那些年轻人， 对现有的EBT做出回应。因此，迫切需要替代治疗方案，特别是 从NIMH的实验治疗方法中产生的转化神经科学方法。 ABMT就是这样一种方法，因为它基于认知神经科学的理论和方法来解决 在极快的时间尺度上运作的干扰注意力。根据NIMH的实验 治疗方法，我们在我们的初步工作中收集了支持ABMT可行性的数据， 可接受性，并确定一个假定的目标机制。我们接下来收集的数据表明， 目标（即，目标接合）和将目标的变化与临床改进相联系（即，目标 验证）。具体而言，我们收集了事件相关电位中目标快速部署过程的数据 (ERP)，并发现与社交威胁刺激相比，患有SAD的青少年表现出更高的P1振幅。 与典型的发展控制，从而表明增强的神经处理过程中的注意力定向， 社会威胁，提供了一个假定的ABMT目标。我们的数据进一步表明ABMT可以降低焦虑的严重程度， (i.e.,临床疗效信号）和P1振幅，这些临床和神经变化一起发生。 这些数据使我们能够提出确证性疗效R 01，以（1）重新证明靶点结合， (2)再次证明ABMT对社交焦虑症状严重程度的影响，（3）证明目标验证， （4）评估结果的维持情况。我们还将（5）探讨注意力控制作为一个主持人， 结果。我们将随机选择260名（每个研究中心N = 130名）年龄在10-14岁之间的门诊转诊青少年， SAD为ABMT或中性控制任务（NCT）。我们假设注意力倾向于社会威胁， 使用点探测任务中的P1 ERP振幅测量，社交焦虑症状严重程度将被 与NCT组相比，ABMT组在治疗后和6个月随访时显著降低。 进一步假设P1振幅将介导社交焦虑症状严重程度的降低。 该项目将提供一个严格的，足够有力的机制测试ABMT青年SAD。 支持性研究结果将使我们能够在社区和实践中进行ABMT的有效性试验 设置.这些发现也将为未来与精确度相关的研究提供关于注意力控制的前景的见解 医学接近。

Project Summary This 2-site (Florida International University, Yale University) R01 project proposes to confirm attention bias modification treatment (ABMT) as an efficacious treatment for social anxiety disorder (SAD) in peripubertal youth ages 10 to 14 years, and examine the mechanisms of ABMT's clinical efficacy. SAD is prevalent, chronic, and impairing. Response rates to evidence-based treatments (EBTs) are markedly lower for SAD than other anxiety disorders, and limited insights exist about mechanisms of positive outcome for those youths who do respond to existing EBTs. Alternative treatment options are therefore critically needed, particularly for translational neuroscience approaches that arise from NIMH's experimental therapeutics approach. ABMT is such an approach, as it is grounded in cognitive neuroscience theory and methods to address perturbed attention that operates on extremely rapid time scales. In accordance with NIMH's experimental therapeutics approach, we collected data in our preliminary work that support ABMT's feasibility and acceptability, and identifies a putative target mechanism. We next collected data demonstrating an effect on the target (i.e., target engagement) and linking changes in the target to clinical improvements (i.e., target validation). Specifically, we collected data on targeted rapidly deployed processes in event related potentials (ERP), and found that youth with SAD show enhanced P1 amplitudes for socially threatening stimuli compared with typically developing controls, thereby indicating enhanced neural processing during attention orienting to social threat, providing a putative ABMT target. Our data further show ABMT to reduce both anxiety severity (i.e., signal of clinical efficacy) and P1 amplitudes, with these clinical and neural changes occurring together. These data position us to propose a confirmatory efficacy R01 to (1) re-demonstrate target engagement, (2) re-demonstrate the effects of ABMT on social anxiety symptom severity, (3) demonstrate target validation, and (4) evaluate the maintenance of outcomes. We also will (5) explore attention control as a moderator of outcomes. We will randomize 260 (N = 130 at each site) clinic referred youths ages 10-14 years who meet for SAD to either ABMT or a Neutral Control Task (NCT). We hypothesize that attention orienting to social threat, measured using P1 ERP amplitudes in the dot-probe task, and social anxiety symptom severity will be significantly lower at post-treatment and 6-month Follow-Up in the ABMT arm compared with the NCT arm. We further hypothesize that P1 amplitudes will mediate reductions in social anxiety symptom severity. This project will provide a rigorous, sufficiently powered mechanistic test of ABMT for SAD in youth. Supportive findings would position us to pursue an effectiveness trial of ABMT in community and practice settings. Findings will also provide insight on attention control's promise for future research relating to precision medicine approaches.