Dimensional Sleep Disturbance in Relation to Positive/Negative Affect Systems

描述(由申请人提供)：失眠是情绪和焦虑症的一贯危险因素。然而，这种风险关系背后的神经机制却知之甚少。在这项探索性研究中，我们将收集初步数据来测试一个新的假说，该假说解决了这些机制：失眠与积极和消极情感系统的调节失调有关，类似于抑郁症。更具体地说，我们假设失眠与皮层下结构激活增加有关，皮质下结构服从消极情绪，皮层下结构服从奖赏和积极情绪，前额叶控制积极和消极情绪改变。为了更好地消除与失眠相关的调节失调，我们将使用经过充分验证的和更具探索性的任务情感任务，旨在从多个层面评估情感处理，从情感处理到对情感的自愿调节，再到与个人相关的持续情感。认识到失眠等睡眠障碍与正常睡眠形成一个连续体，我们将使用Promis睡眠障碍(PSD)量表作为自变量，这是一种具有既定人口常模的维度衡量标准。我们将进行临床评估，包括睡眠和情绪的维度和分类测量，从所有PSD(n=60，每PSD三分之20)的参与者中抽样。我们将进行功能磁共振成像(FMRI)研究，以检查积极和消极情绪背后的神经机制，这两个因素构成因变量。我们将解决以下具体目标：具体目标1。检查作为失眠严重程度函数的积极情绪的神经机制。我们假设，更严重的失眠与以下因素有关：在预期和接受金钱奖励的过程中，腹侧纹状体的激活减少，内侧前额叶皮质的激活增加；对自愿情绪调节任务(增加积极情绪)的反应；以及对与个人相关的持续积极情绪(品尝)任务的反应。具体目的2。研究失眠严重程度对负性情绪起作用的神经机制。我们假设，更严重的失眠将与杏仁核激活的增加和背外侧和腹内侧额叶皮质对急性威胁任务中愤怒面部表情的反应减少有关；作为回应，自愿情绪调节任务(减少负面情绪)；以及在与个人相关的持续负面情绪(冥想)任务中。我们还将解决专注于激活其他大脑区域、关键大脑结构之间的连通性以及分类参与者群体之间的反应的探索性目标。我们研究的创新特征包括使用连续的失眠测量作为自变量，以及使用与失眠和抑郁现象相关的新的激活任务。这项研究解决了将失眠与情感障碍联系起来的合理机制，并将支持随后的R01，重点关注失眠的神经影响机制及其通过行为治疗的调节。

DESCRIPTION (provided by applicant): Insomnia is a consistent risk factor for mood and anxiety disorders. However, the neural mechanisms underlying this risk relationship are poorly understood. In this exploratory study, we will collect preliminary data to test a novel hypothesis addressing these mechanisms: That insomnia is associated with dysregulation of positive and negative affect systems, similar to that seen in depression. More specifically, we hypothesize that insomnia is associated with increased activation of subcortical structures subserving negative affect, reduced activation of subcortical structures subserving reward and positive affect, and altered prefrontal control of both positive and negative affect. In order to better defne the dysregulation associated with insomnia, we will use both well-validated and more exploratory tasks affective tasks designed to evaluate affective processing at multiple levels, from affective processing, to voluntary regulation of affect, to personally-relevant sustained affect. Recognizing that sleep disturbances such as insomnia form a continuum with normal sleep, we will use the PROMIS Sleep Disturbance (PSD) scale, a dimensional measure with established population norms, as the independent variable. We will conduct clinical assessments, including dimensional and categorical measures of sleep and mood, in participants sampled from the full range of the PSD (n=60, 20 per PSD tertile). We will conduct functional magnetic resonance imaging (fMRI) studies to examine the neural mechanisms underlying positive and negative affect, which constitute the dependent variables. We will address the following Specific Aims: Specific Aim 1. To examine neural mechanisms subserving positive affect as a function of insomnia severity. We hypothesize that greater insomnia severity will be associated with reduced activation of ventral striatum and increased activation of medial prefrontal cortex during anticipation and receipt of monetary reward; in response to a voluntary affect regulation task (increase positive affect); and in response to a personally-relevant sustained positive affect (savoring) task. Specific Aim 2. To examine neural mechanisms subserving negative affective as a function of insomnia severity. We hypothesize that greater insomnia severity will be associated with increased activation of amygdala and reduced activation of dorsolateral and ventromedial prefrontal cortex in response to angry facial expressions during an acute threat task; in response a voluntary emotion regulation task (decrease negative affect); and during a personally-relevant sustained negative affect (rumination) task. We will also address exploratory aims focused on activation of other brain regions, connectivity between key brain structures, and responses among categorical participant groups. Innovative features of our study include the use of a continuous insomnia measure as the independent variable, and the use of novel activation tasks relevant to the phenomenology of insomnia and depression. This study addresses a plausible mechanism linking insomnia to affective disorders, and will support a subsequent R01 focusing on neural mechanisms of affect in insomnia and their modulation by behavioral treatment.