Neural Mechanisms of Sensory OverResponsivity

感觉过度反应的神经机制

基本信息

批准号：
10394291
负责人：
Elysa Jill Marco
金额：
$ 53.57万
依托单位：
UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
依托单位国家：
美国
项目类别：
财政年份：
2019
资助国家：
美国
起止时间：
2019-07-08 至 2024-04-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10394291
关键词：
3-Dimensional Address Affect Age Anisotropy Anxiety Architecture Attention Deficit Disorder Attentional deficit Auditory Axon Behavior Behavioral Bilateral Biological Markers Biophysics Brain Brain Injuries Categories Child Child Development Child Rearing Clinic Corpus callosum splenium Data Data Set Development Developmental Coordination Disorders Diffusion Magnetic Resonance Imaging Dorsal Educational Intervention Evaluation Failure Functional Imaging Functional disorder Future Goals Hyperactivity Image Impairment Internal Capsule Intervention Studies Knowledge Learning Limb structure Magnetic Resonance Imaging Measures Methods Multicenter Studies Neurites Neurodevelopmental Disorder Neurologic Neuronal Plasticity Pathology Phenotype Play Regression Analysis Research Research Domain Criteria Risk Sensory Sensory Disorders Sleep Stimulus Tactile Testing Work Youth autism spectrum disorder autistic children base cognitive control cognitive training comorbidity connectome density elementary school experience indexing innovation myelination network dysfunction neural network neuroimaging neuromechanism neuropathology novel predictive marker premature preservation relating to nervous system response sensory mechanism sensory processing disorder social thalamocortical tract white matter

项目摘要

Project Summary Sensory over-responsivity (SOR), the unusual negative response to typically non-noxious stimuli, represents a prominent feature of many neurodevelopmental conditions, including Autism Spectrum Disorder (ASD), Anxiety, Attention Deficit/Hyperactivity, and Developmental Coordination Disorders. SOR severely disrupts all aspects of a child's development, including the ability to learn and socially engage. Despite growing recognition of SOR as a core feature in neurodevelopmental conditions, the neural mechanisms of SOR remain unclear. As a result of this gap, SOR has historically been thought to be “behavioral” or due to “bad parenting” or a consequence of “having autism”. This percept has been challenged by data from our lab and others showing white matter microstructural and functional imaging differences in children with sensory processing dysfunction (SPD) and in children with ASD/SOR. Delineating the underlying neural networks that subserve SOR, both auditory and tactile, will not only guide our understanding of this condition, but also shift the conceptualization of SOR to that of a treatable neurologic condition. Obtaining the neural signature of SOR will contribute to finding a biomarker for neural remodeling with cognitive training paradigms similar to what we have piloted in the domain of cognitive control. Our work utilizing in-lab direct assessment of auditory SOR will test the scientific premise that SOR results from the disconnection of a higher-order SOR network: the Posterior Corona Radiata, Superior Longitudinal Fasciculus, and the Cingulate Bundle. We will further determine whether this putative SOR network reflects a general vulnerability in the posterior periventricular regions, which are rich in highly connecting white matter tracts, or is specific to auditory SOR. Furthermore, if this microstructural disconnection is SOR specific, then is it a multi-domain SOR network or does each sensory domain (e.g. auditory and tactile) rely on a unique set of connections-- as is suggested by the non-overlapping sensory domain phenotypes in affected children? A multifaceted phenotype and neuroimaging approach is required to answer these questions. The objective of this proposal is to advance our direct assessment of sensory related behavior and apply novel structural neuroimaging methods to elucidate the neural architecture of SOR using an RDoC approach. To achieve this goal, we will assess auditory and tactile SOR using the Sensory Processing: Three Dimensions Assessment (SP-3D:A) paired with innovative structural imaging, Neurite Orientation Dispersion and Density Imaging, for detailed microstructural assessment, and Edge Density Imaging, for advance connectome assessment, in 170 children, ages 8-12 years, with neurodevelopmental concerns. All phenotype and neuroimaging data will be made available to the field in order to support ongoing understanding of sensory processing in this unique data set.

项目概要感觉过度反应 (SOR)，即对典型无害刺激的异常负面反应，代表许多神经发育疾病的一个显着特征，包括自闭症谱系障碍 (ASD)，焦虑、注意力缺陷/多动和发育协调障碍严重扰乱一切。儿童发展的各个方面，包括学习和社交能力，尽管人们越来越认识到这一点。虽然 SOR 是神经发育状况的核心特征，但 SOR 的神经机制仍不清楚。由于这种差距，SOR 历来被认为是“行为”或“不良养育”或 “患有自闭症”的后果受到了我们实验室和其他实验室数据的挑战。感觉处理功能障碍儿童白质微观结构和功能成像差异 (SPD) 和患有 ASD/SOR 的儿童，描绘了促进 SOR 的潜在神经网络。听觉和触觉不仅会指导我们对这种情况的理解，还会改变概念化获得 SOR 的神经特征将有助于治疗可治疗的神经系统疾病。通过类似于我们试点的认知训练范例来寻找神经重塑的生物标志物我们的工作利用听觉 SOR 的实验室直接评估来测试认知控制领域。 SOR 是由高阶 SOR 网络断开而产生的科学前提：后验放射冠、上纵束和扣带束我们将进一步确定。这个假定的 SOR 网络是否反映了后脑室周围区域的普遍脆弱性，这富含高度连接的白质束，或者是听觉 SOR 所特有的。微观结构断开是SOR特定的，那么它是一个多域SOR网络还是每个感觉领域（例如听觉和触觉）依赖于一组独特的连接——正如非重叠的受影响儿童的感觉域表型？多方面的表型和神经影像学方法是该提案的目的是推进我们对这些问题的直接评估。感觉相关行为并应用新颖的结构神经成像方法来阐明神经结构为了实现这一目标，我们将使用 RDoC 方法评估听觉和触觉 SOR。感觉处理：三维评估 (SP-3D:A) 与创新结构成像相结合，神经突取向色散和密度成像，用于详细的微观结构评估和边缘密度成像，用于高级连接组评估，对 170 名 8-12 岁儿童进行所有表型和神经影像学数据都将提供给该领域。为了支持对这个独特数据集中的感官处理的持续理解。