Neurally targeted group intervention to reduce early childhood anxiety

临床上显著的焦虑影响20%的学龄前儿童，并可能成为慢性，导致抑郁， 滥用药物、辍学甚至自杀。为了减少焦虑并防止其后遗症，临床上 受影响的儿童必须及早得到有效治疗。临床焦虑学龄前儿童的可用干预措施 对一些儿童有效，但不是所有儿童，多达50%的4-7奥尔兹继续符合标准， 治疗后的焦虑症为了解决这个问题，我们利用理论模型和经验 研究表明，努力控制（EC）能力不足可能是焦虑的基础， 阶段EC能力不足反映了额叶脑区的故障（例如，背外侧前额叶 皮层/dlPFC和前扣带皮层/ACC）以自适应地调节威胁回路并维持任务 行为EC的这些神经基质可以使用神经生理学测量来索引，错误相关的神经基质可以被索引。 负性（ERN）和时频通道间相位同步（ICPS）。我们的调查结果 实验室和其他人的工作表明，ERN和ICPS的减少与EC的行为缺陷有关， 增强的威胁反应类似于临床焦虑儿童的记录。作为回应，我们的团队 开发了一个儿童友好型小组EC培训（“营Kidpower”），旨在增加ERN，ICPS和相关 电子商务行为对降低学龄前儿童焦虑症状的作用。我们的初步研究结果表明， 这种简短的认知训练方法涉及预期的EC神经和行为目标， 焦虑症状在这一试点工作的基础上，目前的项目旨在将这些结果复制和推广到 使用随机对照设计的较大样本。这项研究的参与者将是4至6岁的儿童 （n=90）具有临床显著症状的患者，将随机分配至EC培训干预组（n=45）或 游戏组对照（n=45）。在每种情况之前和之后，将使用多水平 方法，包括神经生理学和行为指标的EC，以及临床医生评级和父母， 报告儿童焦虑症状（类型和严重程度）。我们的目标是：1）确认参与我们的 EC培训增加ERN和ICPS并改善EC行为，2）测试这些参与是否 脑行为EC目标对应于焦虑症状的减少，并探索焦虑是否 通过EC培训减少的风险受基线威胁反应措施的影响，以及3）确定 更大剂量的EC训练与更大的神经行为目标参与相关， 减少焦虑症状。通过评估神经科学衍生目标的变化如何与 焦虑症状的变化，这项工作是响应NIMH对实验疗法的呼吁， 解决了设计干预措施以减少幼儿焦虑的迫切需要。

Clinically significant anxiety affects 20% of preschoolers and can become chronic, leading to depression, substance abuse, school-drop out and even suicide. To reduce anxiety and prevent its sequelae, clinically affected children must be effectively treated early. Available interventions for clinically anxious preschoolers are effective for some, but not all children, with as many as 50% of 4-7 year olds continuing to meet criteria for an anxiety disorder after treatment. To address this problem, we leverage theoretical models and empirical research suggesting that insufficient capacity for Effortful Control (EC) may underlie anxiety from its earliest stages. Insufficient capacity for EC reflects failures of frontal brain regions (e.g., dorsolateral prefrontal cortex/dlPFC and anterior cingulate cortex/ACC) to adaptively regulate threat circuits and maintain on-task behavior. These neural substrates for EC can be indexed using neurophysiological measures, the error-related negativity (ERN) and time frequency interchannel phase synchrony (ICPS), respectively. Findings from our labs and the work of others have shown that reduced ERN and ICPS relate to behavioral deficits in EC and enhanced threat reactivity similar to that documented in clinically anxious children. In response, our team developed a child-friendly group EC training (“Camp Kidpower”) designed to increase ERN, ICPS and related EC behaviors in the service of decreasing anxiety symptoms in preschoolers. Results of our pilot study indicate that this brief cognitive training approach engaged the intended EC neural and behavioral targets and reduced anxiety symptoms. Building on this pilot work, the current project aims to replicate and extend these findings in a larger sample using a randomized controlled design. Participants in this study will be 4- to 6-year-old children (n=90) with clinically significant symptoms who will be randomized into the EC training intervention (n=45) or a playgroup control (n=45). Outcomes will be assessed before and after each condition, using a multi-level approach that includes neurophysiological and behavioral indices of EC, as well as clinician-rated and parent- report on child anxiety symptoms (type and severity). Our aims are to: 1) confirm that participation in our EC training increases ERN and ICPS and improves EC behavior, 2) test whether engagement of these brain-behavior EC targets correspond to reductions in anxiety symptoms and explore whether anxiety reduction by EC training is moderated by baseline threat reactivity measures, and 3) identify whether greater dosage of EC training is associated with greater neuro-behavioral target engagement and reduction of anxiety symptoms. By evaluating how changes in neuroscience-derived targets relate to changes in anxiety symptoms, this work is responsive to the NIMH call for experimental therapeutics and addresses an urgent need for the design of interventions to reduce anxiety in young children.