Multimodal investigation of emotional reactivity as a predictor of later psychopathology in infants at risk for ASD

总结 自闭症谱系障碍（ASD）的特点是社会障碍和限制和重复 行为。具有社交缺陷遗传倾向的人，包括ASD患者及其未受影响的人 亲属也很容易患上内化和外化疾病。存在共病情感 和行为条件损害适应功能，增加家庭压力，并与 精神病住院和住院安置。识别内化和内化的风险因素 外化ASD幼儿及其兄弟姐妹的疾病将改善诊断实践 并促进实施预防和早期干预措施。广泛的研究在一般 人口表明，前两个内在和外在障碍的前兆可以确定 根据情绪反应（eReactivity）水平的升高或降低或 对内部或外部触发的情绪反应。现有的证据虽然有限，但表明， 患有ASD的幼儿和他们未受影响的兄弟姐妹在行为和行为上都表现出非典型的eReactivity特征。 生理水平，虽然证据是不完整的，他们的起源和与后来的联系， 精神病理学基本上是未知的。为了填补这一空白，我们建议前瞻性地研究 150名ASD儿童的弟弟妹妹中4至30个月的eReactivity，由于家庭因素， 有30名患有ASD（HR）的高风险和30名低风险（LR）兄弟姐妹。我们计划检查电子反应到真实的- 世界触发器旨在引起恐惧，愤怒和喜悦，并评估社会和非社会性质的影响 使用最先进的多方法行为和 生理学方法。目的1将前瞻性评估HRASD组（ASD同胞）、HRATP （有发展挑战的兄弟姐妹）和HRTD（没有发展挑战的兄弟姐妹）是 其特征在于对社会与非社会触发的不同的eReactivity模式， 与LRTD组相比，4至30个月的生理指标。目标将阐明， 对社会和非社会触发的情绪反应构成了自闭症的一个新特征， ASD中的表型目标2将研究婴儿期eReactivity发展之间的预测关系 以及30个月时内化和外化症状的严重程度。早期预测因子的识别 内化/外化问题将有助于获得旨在改善 行为和情感上的挑战符合研究领域标准研究框架 建议，该项目（1）采用多层次的分析，（2）调查消极和积极的 效价系统以及唤醒系统，（3）检查ASD风险的长期目标， 提高ASD的诊断精度，并能够发现新的治疗靶点和干预措施， 在疾病的前驱期和早期综合征阶段。

SUMMARY Autism Spectrum Disorder (ASD) is characterized by social impairments and restricted and repetitive behaviors. Those with a genetic liability for social deficits, including individuals with ASD and their unaffected relatives are also at high risk for internalizing and externalizing conditions. The presence of comorbid affective and behavioral conditions impairs adaptive functioning, increases family stress, and is associated with psychiatric hospitalizations and residential placement. Identification of risk factors for internalizing and externalizing disorders amongst young children with ASD and their siblings would improve diagnostic practices and promote implementation of preventative and early interventions. Extensive research in the general population indicates that precursors of internalizing and externalizing disorders can be identified in the first two years of life as indexed by elevated or attenuated levels of Emotional Reactivity (eReactivity), or intensity of emotional reactions in response to internal or external triggers. Extant, albeit limited, evidence suggests that toddlers with ASD and their unaffected siblings exhibit atypical eReactivity profiles both on the behavioral and physiological levels, though the evidence is incomplete and both their origins and the links with later psychopathology are largely unknown. To fill this gap, we propose to prospectively examine the development of eReactivity from 4 to 30 months in 150 younger siblings of children with ASD, who, due to familial factors, are at high risk for developing ASD (HR) and 30 low-risk (LR) siblings. We plan to examine eReactivity to real- world triggers aimed to elicit fear, anger, and joy, and to evaluate the effects of the social and nonsocial nature of the triggers on eReactivity across the three emotions using a state-of-the-art multi-method behavioral and physiological approach. Aim 1 will evaluate prospectively whether the HRASD group (siblings with ASD), HRATP (siblings with developmental challenges), and HRTD (siblings without developmental challenges) are characterized by distinct patterns of eReactivity to social vs nonsocial triggers as measured by behavioral and physiological indices between 4 and 30 months compared to the LRTD group. The aim will clarify if differential emotional reactivity to social and nonsocial triggers constitutes an emerging characteristic of the autism phenotype in ASD. Aim 2 will examine predictive relationships between development of eReactivity in infancy and severity of internalizing and externalizing symptoms at 30 months. Identification of early predictors of internalizing/externalizing problems will facilitate access to early interventions aimed at amelioration of behavioral and emotional challenges. Consistent with the Research Domain Criteria research framework recommendations, the project (1) employs multiple levels of analysis, (2) investigates negative and positive valence systems as well as arousal systems, and (3) examines a spectrum of ASD risk with long-term goals of improving diagnostic precision in ASD and enabling discovery of novel treatment targets and interventions both during prodromal and early syndromal stages of the disorder.