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

创伤暴露人群完成振动声学增强呼吸聚焦正念的快感缺失和认知控制缺陷的神经生理机制

基本信息

  • 批准号:
    10752342
  • 负责人:
  • 金额:
    $ 6.87万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2023
  • 资助国家:
    美国
  • 起止时间:
    2023-08-14 至 2026-03-31
  • 项目状态:
    未结题

项目摘要

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.
项目概要/摘要 创伤可能会导致奖励处理减弱(快感缺失)和认知障碍 控制,这是精神健康障碍症状的诱因和延续因素。神经生理学 创伤相关的快感缺乏和认知控制缺陷的基础先前已被研究过 横断面方法,包括脑电图 (EEG) 研究证明 θ 活动 (~4-7 Hz) 和 alpha (~8-14 Hz) 频段在快感缺乏和认知控制的患者中存在异常 赤字。为了以先前的工作为基础并增加这些发现的转化价值,下一步是 检查这些皮质动态在遭受创伤的人的样本中如何变化,以研究个体如何 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 整个基于正念的干预可以揭示对此干预的新反应机制。 因此,theta/alpha 活性的变化可能与针对创伤的新型跨诊断治疗的反应有关。 暴露在外的人被称为振动声学增强呼吸聚焦正念(VABFM)。 VABFM 使用 与呼吸一致振动的独特装置,有望增强刺激敏感性和 有效地参与注意力控制网络,但迄今为止还没有研究检查相关的神经生理学 机制。拟议的研究将利用正在进行的正念机械临床试验的数据 对完成 VABFM 或控制干预的创伤暴露人群 (R01AT011267) 进行基于治疗的治疗。 本研究的 100 名参与者将完成脑电图记录,同时进行 8 次每两周一次的干预 会议,参与者还将完成结构和功能磁共振研究前和研究后 成像(sMRI/fMRI)扫描。每次 sMRI 扫描将用于脑电图源定位分析的联合配准 θ/α 活动。源本地化皮质图将用于实现以下具体目标:(1) 描述遭受创伤的人快感缺乏和认知控制缺陷的神经生理学相关性 (2) 确定与快感缺失相关的 VABFM 治疗反应的神经生理学机制 遭受创伤的人的认知控制。此外,探索性目标将测试之间的一致性 使用功能磁共振成像数据测量创伤暴露人群的快感缺乏和认知控制缺陷 在执行情感认知控制任务期间收集的数据,其中包括与奖励相关的刺激。这 研究将提高我们对快感缺失和认知控制缺陷的神经生理学的理解 患有精神健康障碍的遭受创伤的人,它将展示症状的变化如何相互关联 奖励/注意力网络的潜在神经生理学的变化。总体而言,这些数据提供了独特的 对快感缺失和认知控制缺陷进行全面的神经生理学表型分析的机会 遭受创伤的人并确定新型注意力控制治疗的神经生理学机制。 这将描绘精神健康障碍的大脑机制的个体差异并指导治疗。

项目成果

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Timothy McDermott其他文献

Timothy McDermott的其他文献

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{{ truncateString('Timothy McDermott', 18)}}的其他基金

Self-regulation of Prefrontal Cortex during Emotional Cognitive Control
情绪认知控制过程中前额叶皮层的自我调节
  • 批准号:
    10376765
  • 财政年份:
    2020
  • 资助金额:
    $ 6.87万
  • 项目类别:
Mechanisms of arsenic detoxification by the human microbiome
人体微生物组的砷解毒机制
  • 批准号:
    9750648
  • 财政年份:
    2017
  • 资助金额:
    $ 6.87万
  • 项目类别:
Mechanisms of arsenic detoxification by the human microbiome
人体微生物组的砷解毒机制
  • 批准号:
    9977978
  • 财政年份:
    2017
  • 资助金额:
    $ 6.87万
  • 项目类别:
Mechanisms of arsenic detoxification by the human microbiome
人体微生物组的砷解毒机制
  • 批准号:
    10207533
  • 财政年份:
    2017
  • 资助金额:
    $ 6.87万
  • 项目类别:
Mechanisms of arsenic detoxification by the human microbiome
人体微生物组的砷解毒机制
  • 批准号:
    9290254
  • 财政年份:
    2017
  • 资助金额:
    $ 6.87万
  • 项目类别:
Arsenical production in germ free and humanized mice
无菌小鼠和人源化小鼠中砷的产生
  • 批准号:
    9198224
  • 财政年份:
    2016
  • 资助金额:
    $ 6.87万
  • 项目类别:

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    2022
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