Neurophysiological mechanisms of anhedonia and cognitive control deficits in trauma-exposed people completing vibroacoustically augmented breath focused mindfulness

项目总结/摘要 创伤可能导致奖励处理（快感缺失）和认知障碍的发展。 控制，这是在心理健康障碍的症状的沉淀和永久化。神经生理 创伤相关的快感缺失和认知控制缺陷的基础先前已经使用 横截面的方法，包括脑电图（EEG）研究表明，在theta的活动， （~4-7 Hz）和α（~8-14 Hz）频段在快感缺乏和认知控制患者中异常 赤字为了建立在这一先前的工作和增加这些发现的转化价值，下一步是 研究这些皮质动力学如何在创伤暴露人群中变化，以研究个体 症状表现的差异与神经生理学有关。此外，测试这些动态如何变化 在基于正念的干预中，可以揭示对这种干预的反应的新机制。 因此，theta/alpha活性的变化可能与对创伤的新型转诊断治疗的反应有关- 振动声学增强呼吸专注正念（VABFM）。VABFM使用 与呼吸同步振动的独特装置，预期可增强刺激敏感度， 有效地参与注意力控制网络，但迄今为止还没有研究检查过相关的神经生理学 机制等这项拟议中的研究将利用正在进行的正念机制临床试验的数据， 完成VABFM或对照干预的创伤暴露人群（R 01 AT 011267）的基础治疗。 本研究的100名参与者将完成EEG记录，同时进行8次每两周一次的干预 会议，参与者还将完成研究前和研究后的结构和功能磁共振 成像（sMRI/fMRI）扫描。每次sMRI扫描将用于EEG源定位分析的配准 theta/alpha活动。源定位皮层地图将用于实现以下特定目标：（1） 描述创伤暴露人群中快感缺乏和认知控制缺陷的神经生理学相关性 和（2）确定与快感缺乏相关的VABFM治疗反应的神经生理学机制， 认知控制的能力。此外，探索性目标将测试以下方面的一致性： 创伤暴露者快感缺乏和认知控制缺陷的fMRI/EEG研究 在情感认知控制任务的执行过程中收集，其中包括奖励相关的刺激。这 研究将提高我们对快感缺乏和认知控制缺陷的神经生理学的理解， 创伤暴露的人与心理健康障碍，它将展示如何变化的症状， 奖励/注意力网络的潜在神经生理学变化。总的来说，这些数据提供了一个独特的 对儿童快感缺乏和认知控制缺陷进行综合神经生理学表型分析的机会 创伤暴露的人，并确定一种新的注意力控制治疗的神经生理机制。 这将描绘心理健康障碍的大脑机制的个体差异，并将指导治疗。

PROJECT SUMMARY/ABSTRACT Trauma can contribute to the development of dampened reward processing (anhedonia) and disrupted cognitive control, which are precipitants and perpetuators of symptoms in mental health disorders. The neurophysiological underpinnings of trauma-related anhedonia and cognitive control deficits has previously been examined using cross-sectional approaches, including electroencephalography (EEG) studies demonstrating that activity in theta (~4-7 Hz) and alpha (~8-14 Hz) frequency bands are aberrant in patients with anhedonia and cognitive control deficits. To build upon this prior work and increase the translational value of these findings, one next step is to examine how these cortical dynamics vary within a sample of trauma-exposed people to examine how individual differences in symptom presentation relate to neurophysiology. Further, testing how these dynamics change throughout a mindfulness-based intervention could reveal novel mechanisms of response to this intervention. Thus, changes in theta/alpha activity could relate to response to a novel transdiagnostic treatment for trauma- exposed people called vibroacoustically-augmented breath focused mindfulness (VABFM). VABFM uses a unique device that vibrates in concert with respiration, which is expected to enhance stimulus sensitivity and efficiently engage attentional control networks, but no studies to date have examined relevant neurophysiological mechanisms. The proposed study will leverage data from an ongoing mechanistic clinical trial of mindfulness- based treatment for trauma-exposed people (R01AT011267) who complete VABFM or a control intervention. 100 participants from this study will complete EEG recordings concurrent with eight bi-weekly intervention sessions, and participants will also complete pre- and post-study structural and functional magnetic resonance imaging (sMRI/fMRI) scans. Each sMRI scan will be used for co-registration for EEG source localization analyses of theta/alpha activity. Source-localized cortical maps will be used to accomplish the following specific aims: (1) characterize neurophysiological correlates of anhedonia and cognitive control deficits in trauma-exposed people and (2) Identify neurophysiological mechanisms of VABFM treatment response relevant to anhedonia and cognitive control in trauma-exposed people. Additionally, an exploratory aim will test congruence between fMRI/EEG measures of anhedonia and cognitive control deficits in trauma-exposed people by using fMRI data collected during performance of an affective cognitive control task, which includes reward-related stimuli. This research will improve our understanding of the neurophysiology of anhedonia and cognitive control deficits in trauma-exposed people with mental health disorders, and it will demonstrate how changes in symptoms relate to changes in the underlying neurophysiology of reward/attention networks. Overall, these data provide a unique opportunity for comprehensive neurophysiological phenotyping of anhedonia and cognitive control deficits in trauma-exposed people and to identify neurophysiological mechanisms of a novel attentional control treatment. This will delineate individual differences in brain mechanisms of mental health disorders and will guide treatment.