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
- 来源:
- 关键词:AffectiveAftercareAmericanAnhedoniaAttentionBrainCOVID-19 pandemicCaringChronicClinical ResearchClinical TrialsDataData AnalysesDetectionDevelopmentDevicesDiagnosticDiseaseElectroencephalographyFoundationsFrequenciesFunctional Magnetic Resonance ImagingFundingFutureGoalsHumanImpairmentIndividualIndividual DifferencesInterventionLife ExperienceMeasuresMedialMental disordersMentorsMentorshipMindfulness TrainingMotivationNeurosciencesOutcomeParticipantPatientsPerformancePersonsPhenotypePost-Traumatic Stress DisordersPrefrontal CortexReportingResearchRespirationRestRewardsRiskSamplingScanningStimulusSymptomsTestingTrainingTraumaWorkattentional controlbiological adaptation to stresscareercognitive controlcortex mappingdesignearly onsetfunctional MRI scanimprovedmindfulnessmindfulness interventionmultimodalityneurophysiologynovelpediatric traumapost-traumatic symptomsresponseresponse biomarkerreward processingsource localizationspatiotemporalstatisticsstimulus sensitivitytraining projecttrauma exposuretreatment responsevibration
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.
项目摘要/摘要
创伤可导致奖赏加工受阻(快感缺乏)和认知障碍
控制,这是精神健康障碍症状的诱因和永久化。神经生理学
与创伤相关的快感缺乏和认知控制缺陷的基础之前已经被用
横断面方法,包括脑电(EEG)研究表明,theta的活动
快感缺乏和认知控制患者的(~4-7赫兹)和阿尔法(~8-14赫兹)频段异常
赤字。为了在以前工作的基础上,增加这些发现的翻译价值,下一步是
研究这些皮质动力学在创伤暴露人群样本中的变化,以检查个体
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
在整个过程中,基于正念的干预可以揭示出对这种干预做出反应的新机制。
因此,theta/α活性的变化可能与对一种新的创伤跨诊断治疗的反应有关。
暴露在这种环境中的人被称为振音增强呼吸专注正念(VABFM)。VABFM使用
独特的与呼吸同步振动的装置,有望增强刺激敏感度和
有效地利用注意力控制网络,但到目前为止还没有研究检查相关的神经生理学
机制。这项拟议的研究将利用正在进行的正念机械临床试验的数据--
完成VABFM或对照干预的创伤暴露者(R01AT011267)的基础治疗。
这项研究的100名参与者将在8次双周干预的同时完成脑电记录
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。每一次sMRI扫描将用于脑电源定位分析的联合配准
西塔/阿尔法活动。本地化皮质地形图将用于实现以下具体目标:(1)
表征创伤暴露人群快感缺乏和认知控制缺陷的神经生理学相关性
以及(2)确定VABFM治疗反应的神经生理机制与快感缺乏和
创伤暴露人群的认知控制。此外,一个探索性目标将测试
FMRI/EEG测量创伤暴露人群快感缺乏和认知控制缺陷
在执行情感认知控制任务时收集,其中包括与奖励相关的刺激。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
暴露在创伤中的精神健康障碍患者,它将展示症状的变化与
奖赏/注意网络潜在神经生理学的变化。总体而言,这些数据提供了一个独特的
快感缺乏症和认知控制缺陷的综合神经生理表型机会
并确定一种新的注意力控制治疗的神经生理机制。
这将勾勒出精神健康障碍大脑机制的个体差异,并将指导治疗。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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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
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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
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9198224 - 财政年份:2016
- 资助金额:
$ 6.87万 - 项目类别:
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