Neural Mechanisms of Sensory OverResponsivity

感觉过度反应的神经机制

• 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
• 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

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.

项目摘要 感觉过度反应性（SOR）是对通常无刺激刺激的异常负面反应，代表 许多神经发育状况的重要特征，包括自闭症谱系障碍（ASD）， 焦虑，注意力不足/多动症和发育协调障碍。严重破坏所有人 儿童成长的各个方面，包括学习和社会参与的能力。尽管认可越来越大 在神经发育条件下，SOR作为核心特征，SOR的神经力学仍然不清楚。 由于这一差距，历史上认为SOR是“行为”或“育儿不良”或 “患有自闭症”的结果。我们实验室的数据和其他显示 感觉处理功能障碍儿童的白质微观结构和功能成像差异 （SPD）和患有ASD/SOR的儿童。描绘出对SOR的基础神经网络，两者都 听觉和触觉，不仅会指导我们对这种情况的理解，还将改变概念化 可治疗的神经系统状况。获得SOR的神经签名将有助于 通过认知训练范例找到一种与我们所驾驶的相似的生物标志物进行神经模型的生物标志物 认知控制的领域。我们利用LAB内直接评估听觉SOR的工作将测试 科学前提是SOR是由于高阶SOR网络的断开而导致的： 电晕辐射，上纵向筋膜和扣带束。我们将进一步确定 该假定的SOR网络是否反映了后周期区域中的一般脆弱性， 具有高度连接的白质区域，或者特定于听觉sor。此外，如果这个 微结构断开是特定于SOR的，然后是一个多域SOR网络还是每种感觉 域（例如听觉和触觉）依靠一组唯一的连接 - 正如非重叠所建议的 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 需要回答这些问题。该提议的目的是提高我们对 与感觉相关的行为并应用新颖的结构神经影像学方法来阐明神经结构 使用RDOC方法的SOR。为了实现这一目标，我们将使用 感觉处理：三维评估（SP-3D：A）与创新的结构成像配对， 神经突导向分散和密度成像，用于详细的微观结构评估和边缘 密度成像，用于提前连接的评估，在170名8-12岁的儿童中，有 神经发育问题。所有表型和神经成像数据都将在该领域提供 为了支持在此独特数据集中对感官处理的持续理解。