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A Novel Framework for Impaired Imitation in ASD

自闭症谱系障碍模仿障碍的新框架

基本信息

批准号：
10222491
负责人：
Joshua B Ewen
金额：
$ 61.8万
依托单位：
HUGO W. MOSER RES INST KENNEDY KRIEGER
依托单位国家：
美国
项目类别：
财政年份：
2017
资助国家：
美国
起止时间：
2017-09-01 至 2024-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10222491
关键词：
Attention Basic Science Behavior Biological Markers Child Clinical Development Disease Effectiveness Electroencephalography Elements Event Eye Future Gestures Goals Heterogeneity Human Impairment Individual Investigation Laboratories Learning Skill Measures Motor Motor output Movement Neuropsychology Pattern Perception Performance Phenotype Physiological Physiology Process Psychophysics Publishing Research Research Personnel Role Sampling Signal Transduction Social Functioning Social Interaction Symptoms System Techniques Testing Visual Work autism spectrum disorder autistic children base clinically relevant communication behavior cost course development indexing individualized medicine individuals with autism spectrum disorder novel peer preservation repetitive behavior response secondary analysis social communication social skills targeted treatment visual motor

项目摘要

Project Summary There is long-standing recognition that people with autism spectrum disorders (ASD) have difficulty imitating others’ actions; some investigators have highlighted impaired imitation as being a core contributor to the development of autism. What is yet unknown is precisely how imitation in children with ASD differs from that of typically developing peers. Following an in-depth review of videos of children imitating, we have identified a task parameter that separates preserved from impaired gesture imitation in ASD: children with ASD have difficulty imitating when the task requires two separate movement elements be coordinated simultaneously. By contrast, imitation is relatively preserved when movement elements are performed serially. The coordination of simultaneous movements is a hallmark of actions performed in the real world. With an eye to optimizing common therapies that depend heavily on imitation, the next step is to tease apart where, in the chain from perception to action, the capacity limitation in simultaneous processing lies. To do this, we propose a rigorous research plan that encompasses three complementary experimental techniques. The first is psychophysical task manipulation: In Aim 1, we will control for a potential confound (total number of gestures). In Aim 2, we will specifically examine the perceptual contribution to simultaneity limitations in ASD, by minimizing the required motor output. The second technique is correlation with relevant clinical neuropsychological measures: In Aim 1, we will examine, within the ASD group, the association between the performance cost of simultaneous (vs. serial) imitation and a clinical measure of praxis/imitative function. We will also assess the relationship between simultaneity cost and certain aspects of social function in ASD that may depend on the simultaneous processing of multiple perceptual items and response plans. In Aim 2, we will examine the relationship between attentional demands in simultaneous imitation and clinical measures of divided attention. The third experimental technique is EEG: Based on published results from our laboratory and others, we hypothesize that simultaneous processing demands will be characterized by an increased magnitude of task-related modulation of EEG activity (event-related synchronization/desynchronization: ERS/ERD) in controls. By examining for limitations of this effect in ASD, in either motor or visual networks, or both, we can assess the locus of capacity limitation. By better understanding the relative contributions of perceptual and motor processes, we can optimize the critical therapies in ASD that depend on imitation. Further, by better characterizing the underlying physiology, we open a path to neuro-stimulatory therapies. If, as Rogers and Pennington (1991) suggest, imitation is key to successful vs. aberrant development in children prone to ASD, the application of such therapies in a developmental context could alter the course of the development of ASD symptoms.

项目概要人们长期以来都认识到患有自闭症谱系障碍 (ASD) 的人难以模仿他人的行为；一些研究人员强调，模仿受损是造成这种现象的一个核心因素。自闭症的发展。目前尚不清楚的是自闭症儿童的模仿与正常儿童的模仿有何不同。通常是发展中的同伴。经过对儿童模仿视频的深入审查，我们发现了一个区分 ASD 中保留的手势模仿和受损的手势模仿的任务参数：患有 ASD 的儿童有当任务需要同时协调两个独立的运动元素时，模仿会很困难。经过相比之下，当动作元素连续执行时，模仿相对保留。的协调同时运动是在现实世界中执行的动作的标志。着眼于优化严重依赖模仿的常见疗法，下一步是梳理出链条中的哪些地方感知到行动，同时处理的能力是有限的。为此，我们提出了严格的研究计划包含三种互补的实验技术。第一个是心理物理任务操作：在目标 1 中，我们将控制潜在的混淆（手势总数）。在目标 2 中，我们将通过最小化所需的电机输出。第二种技术是与相关临床神经心理学测量的相关性：In Aim 1，我们将在 ASD 组内检查同时（与同步）性能成本之间的关联。系列）模仿和实践/模仿功能的临床测量。我们还将评估之间的关系同时性成本和 ASD 社会功能的某些方面可能取决于同时性处理多个感知项目和响应计划。在目标 2 中，我们将检查关系同时模仿中的注意力需求与分散注意力的临床测量之间的关系。第三个实验技术是脑电图：根据我们实验室和其他实验室发表的结果，我们假设同时处理需求的特点是与任务相关的数量级增加控制中脑电图活动的调节（事件相关的同步/去同步：ERS/ERD）。经过检查自闭症谱系障碍（ASD）中这种效应的局限性，无论是在运动网络还是视觉网络，或两者中，我们可以评估容量限制点。通过更好地理解知觉和运动的相对贡献过程中，我们可以优化依赖于模仿的 ASD 关键疗法。进一步，通过更好通过表征潜在的生理学特征，我们开辟了一条神经刺激疗法的道路。如果像罗杰斯和 Pennington (1991) 认为，对于容易患自闭症谱系障碍的儿童来说，模仿是成功与异常发展的关键，在发育环境中应用此类疗法可能会改变 ASD 的发展过程症状。