Anxiety, sleep disruption and emotional brain dysregulation

焦虑、睡眠中断和情绪大脑失调

• 批准号: 8609072
• 负责人: Matthew P Walker
• 金额: $ 30.7万
• 依托单位: UNIVERSITY OF CALIFORNIA BERKELEY
• 依托单位国家: 美国
• 财政年份: 2012
• 资助国家: 美国
• 起止时间: 2012-02-15 至 2017-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8609072
• 关键词: Affect; Amygdaloid structure; Anxiety; Anxiety Disorders; Aversive Stimulus; Brain; Clinical; Comorbidity; Development; Electroencephalography; Emotional; Emotions; Etiology; Evaluation; Event; Frequencies; Functional Magnetic Resonance Imaging; High Prevalence; Impairment; Individual; Investigation; Limbic System; MRI Scans; Maintenance; Measures; Medial; Mediating; Medical; Methods; Neural Pathways; Participant; Physiological; Population; Prefrontal Cortex; Process; Psychopathology; Public Health; Recovery; Regulation; Relative (related person); Severities; Sleep; Sleep Deprivation; Societies; Symptoms; Testing; Time; cost; density; deprivation; design; effective therapy; experience; improved; insight; neurobehavioral; neurophysiology; palliative; prevent; relating to nervous system; research study; restoration; sleep abnormalities; trait

DESCRIPTION (provided by applicant): Sleep disruption is a recognized and problematic symptom across the anxiety disorders spectrum. Individuals suffering anxiety additionally display a hallmark signature of enhanced amygdala reactivity to aversive stimuli. Independently, sleep loss in healthy participants results in amplified amygdala reactivity, together with raised levels of anxiety, while the beneficial presence of sleep conversely offers a palliative reduction in next-day aversive reactivity and anxiety. Despite these parallel lines of evidence, the relationship between sleep, anxiety and emotional brain reactivity remains uncharacterized. The need to explore this potentially causal interaction is not only imperative for gaining a deeper understanding of the pathophysiological etiology underlying anxiety, but also for the development of improved preventative strategies and effective treatments for amelioration of anxiety. Across separate experiments combining functional MRI (fMRI), sleep EEG recordings and neurobehavioral assessments, this proposal will test the hypothesis that high anxiety status (1) prevents the normal physiological benefit of sleep in regulating next-day amygdala reactivity, (2) imposes greater vulnerability of the amygdala to the aggravating effects of sleep loss, and (3) negates the benefit of recovery sleep in restoring normative amygdala reactivity, following sleep loss. As such, this proposal represents a systematic evaluation of how anxiety status alters the sleep-dependent regulation of optimal emotional brain function, and how a lack of sleep contributes to the amplified neural signature associated with high anxiety status. Understanding the causal associations between anxiety, sleep impairment, and emotional brain reactivity has considerable clinical and public health ramifications, as well as direct translational treatment applicability. Moreover, considering the continued erosion of sleep time across society, particularly in young populations susceptible to anxiety-related emotion difficulties, the applicability of these studies further increases in relevance.

描述（由申请人提供）：睡眠中断是焦虑症谱系中公认的问题症状。患有焦虑症的人还表现出杏仁核对厌恶刺激的反应增强的标志性特征。独立而言，健康参与者的睡眠不足会导致杏仁核反应增强，同时焦虑水平升高，而有益的睡眠反过来可以缓解第二天的厌恶反应和焦虑。尽管有这些相似的证据，但睡眠、焦虑和情绪性大脑反应之间的关系仍未被明确。探索这种潜在的因果相互作用的必要性不仅是为了更深入地了解焦虑的病理生理病因，而且也是为了开发改进的预防策略和有效的治疗方法来改善焦虑。通过功能磁共振成像（fMRI）、睡眠脑电图记录和神经行为评估相结合的独立实验，本提案将验证以下假设：高焦虑状态(1)阻止睡眠在调节第二天杏仁核反应中的正常生理益处，(2)使杏仁核更容易受到睡眠不足的加重影响，以及(3)在睡眠不足后恢复正常杏仁核反应的恢复性睡眠的益处。因此，这一建议代表了对焦虑状态如何改变最佳情绪大脑功能的睡眠依赖调节的系统评估，以及睡眠不足如何导致与高焦虑状态相关的神经信号放大。了解焦虑、睡眠障碍和情绪性大脑反应之间的因果关系具有相当大的临床和公共卫生影响，以及直接转化治疗的适用性。此外，考虑到整个社会睡眠时间的持续减少，特别是在易受焦虑相关情绪困难影响的年轻人中，这些研究的适用性进一步增加了相关性。