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
创伤可能有助于缩减奖励加工(ANHEDONIA)的发展并破坏认知能力
对照,是精神健康障碍症状的降水剂和永恒者。神经生理学
以前已经使用
横截面方法,包括脑电图(EEG)研究,证明了Theta的活性
(〜4-7 Hz)和α(〜8-14 Hz)的频带异常和认知对照的患者异常
缺陷。为了基于这项先前的工作并增加这些发现的翻译价值,下一步是
检查这些皮质动力学在暴露于创伤的人的样本中如何变化以检查个人
症状表现的差异与神经生理学有关。此外,测试这些动态如何改变
在整个基于正念的干预过程中,可以揭示对这种干预措施的新颖机制。
因此,theta/alpha活性的变化可能与对创伤的新经诊断治疗的反应有关
暴露的人称为敏捷的呼吸呼吸集中正念(VABFM)。 VABFM使用
独特的设备,可与呼吸振动,这有望增强刺激灵敏度和
有效地参与注意力控制网络,但迄今为止尚无研究检查相关的神经生理学
机制。拟议的研究将利用正念的持续机械临床试验的数据 -
基于暴露创伤的人(R01AT011267)的基础治疗方法,他们完成了VABFM或控制干预措施。
这项研究的100名参与者将完成脑电图录音,并同时进行八个每两周的干预
会议,参与者还将完成研究前后的结构和功能性磁共振
成像(SMRI/fMRI)扫描。每次SMRI扫描将用于共同注册脑电图源定位分析
theta/alpha活性。源 - 定位的皮质图将用于实现以下特定目的:(1)
表征了暴露于创伤的人的神经生理学相关性和认知控制缺陷
(2)确定VABFM治疗反应的神经生理机制与Anhedonia和
暴露于创伤的人的认知控制。此外,探索目的将测试一致性
通过使用fMRI数据,fMRI/脑电图的痛苦和认知控制缺陷的量度
在进行情感认知控制任务的过程中收集,其中包括与奖励相关的刺激。这
研究将提高我们对Anhedonia的神经生理学和认知控制缺陷的理解
暴露于精神健康障碍的人,它将证明症状的变化如何相关
奖励/注意网络的基础神经生理学的变化。总体而言,这些数据提供了独特的
在抗anthedonia和认知控制缺陷的全面神经生理表型的机会
暴露于创伤的人并确定新型注意力控制治疗的神经生理机制。
这将描述精神疾病的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:
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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:
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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
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9198224 - 财政年份:2016
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