Sleep, Emotional Processing, and Risk for Affective Disorders in Childhood

描述（由申请人提供）：儿童期睡眠不足或睡眠中断是焦虑症和抑郁症后期发展的高度预测因素。这些疾病的综合社会成本估计每年超过1 200亿美元，强调需要早期识别和有效的干预方法。成年人的实验数据表明，睡眠中断和情感障碍之间的关键联系存在于情绪的适应不良处理中。然而，为了描述特定的风险机制，在儿童时期，当睡眠和情绪调节系统正在发育时，理解这些关系是必不可少的。儿童时期对睡眠的需求增加和大脑可塑性增强也表明存在干预的机会“窗口”。本研究将使用一个实验性的睡眠限制范式，以确定50名7至11岁的青春期前儿童的情感风险的认知，行为和生理机制。我们将包括一系列（亚临床）焦虑和抑郁症状的儿童，以确定某些情感特征是否比其他情感特征更容易与睡眠中断相结合。所有儿童都将接受全面的心理社会评估，家庭多导睡眠图和一周的活动记录。一组评估情绪处理（评价、反应和调节）的离散方面的新任务将在一周的正常睡眠后完成，并在两晚的睡眠限制方案后再次完成。此外，本发明还提供了一种方法， 由于高风险轨迹的特点是多个风险和保护因素的存在和相互作用，我们将研究几个理论上相关的认知和生物变量的潜在调节影响。特别是，儿童的认知反应方式，典型的睡眠开始潜伏期，和首选的睡眠模式（即，时间型）将是 作为情绪结果的潜在调节者进行调查。最后，我们将探讨睡眠结构，脑电图频谱功率（在正常和恢复睡眠）和情绪的结果之间的关系，以确定潜在的神经生物学标记的情感反应，在儿童睡眠不足。本研究的长期目标与NIMH的战略计划和研究领域标准（RDoC）一致，是将现有的预防/早期干预方案从非特异性目标推向更明确的风险机制。

DESCRIPTION (provided by applicant): Inadequate or disrupted sleep in childhood is highly predictive for the later development of anxiety disorders and depression. The combined societal cost of these disorders is estimated above $120 billion annually, underscoring a need for early identification and effective intervention methods. Experimental data in adults indicate a critical link between sleep disruption and affective disorders to exist in the maladaptive processing of emotion. In order to delineate specific risk mechanisms however, understanding of these relationships in childhood when sleep and emotion regulatory systems are developing is essential. An increased need for sleep and greater brain plasticity during the childhood years also suggest a 'window' of opportunity for intervention to exist. This study will use an experimental sleep restriction paradigm to identify cognitive, behavioral and physiologic mechanisms of affective risk among 50 pre-adolescent children, ages 7 to 11 years. We will include children with a range of (subclinical) anxious and depressive symptoms in order to determine whether certain affective profiles potentiate greater vulnerability in conjunction with sleep disruption than others. All children will undergo comprehensive psychosocial evaluation, in-home polysomnography and one week of actigraphy. A battery of novel tasks assessing discrete aspects of emotional processing (appraisal, reactivity and regulation) will be completed following a week of normal sleep and again after a 2-night sleep restriction protocol. In addition, because high-risk trajectories are characterized by the presence and interaction of multiple risk and protective factors, we will investigate the potential moderating influence of several theoretically-relevant cognitive and biological variables. In particular, children's cognitive response style, typical sleep onset latency, and preferred sleep pattern (i.e., chronotype) will be investigated as potential moderators of emotional outcomes. Finally, we will explore relationships among sleep architecture, EEG spectral power (during normal and recovery sleep) and emotional outcomes in order to identify potential neurobiological markers of affective response to sleep loss in childhood. The long term goal of this study which aligns with both NIMH's Strategic Plan and Research Domain Criteria (RDoC) is to advance existing prevention/early intervention protocols beyond non- specific targets toward more explicit mechanisms of risk.