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

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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.