Paul Cernasov1, Erin C Walsh2, Jessica L Kinard3, Lisalynn Kelley4, Rachel Phillips1, Angela Pisoni5, Tory A Eisenlohr-Moul6, Macey Arnold4, Sarah C Lowery1, Marcy Ammirato1, Kinh Truong7, Gabriela A Nagy8, Jason A Oliver9, Kevin Haworth4, Moria Smoski10, Gabriel S Dichter11. 1. Department of Psychology and Neuroscience, University of North Carolina-Chapel Hill, Chapel Hill, NC 27514, USA. 2. Department of Psychiatry, University of North Carolina-Chapel Hill, Chapel Hill, NC 57514, USA. 3. Carolina Institute for Developmental Disabilities, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27510, USA; Division of Speech and Hearing Sciences, University of North Carolina-Chapel Hill, Chapel Hill, NC 27514, USA. 4. Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27705, USA. 5. Department of Psychology and Neuroscience, Duke University, Durham, NC 27505, USA. 6. Department of Psychiatry, University of Illinois at Chicago, Neuropsychiatry Institute, Chicago, IL 60612, USA. 7. Department of Biostatistics, University of North Carolina-Chapel Hill, Chapel Hill, NC, 27514, USA. 8. Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27705, USA; Duke University School of Nursing, 307 Trent Drive, Durham, NC 27710, USA. 9. Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27705, USA; Division of Cancer Control and Population Sciences, Duke Cancer Institute, Durham, NC 27705, USA. 10. Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27705, USA; Department of Psychology and Neuroscience, Duke University, Durham, NC 27505, USA. 11. Department of Psychology and Neuroscience, University of North Carolina-Chapel Hill, Chapel Hill, NC 27514, USA; Department of Psychiatry, University of North Carolina-Chapel Hill, Chapel Hill, NC 57514, USA; Carolina Institute for Developmental Disabilities, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27510, USA. Electronic address: dichter@med.unc.edu.
Abstract
BACKGROUND: The neural mechanisms associated with anhedonia treatment response are poorly understood. Additionally, no study has investigated changes in resting-state functional connectivity (rsFC) accompanying psychosocial treatment for anhedonia. METHODS: We evaluated a novel psychotherapy, Behavioral Activation Therapy for Anhedonia (BATA, n = 38) relative to Mindfulness-Based Cognitive Therapy (MBCT, n = 35) in a medication-free, transdiagnostic, anhedonic sample in a parallel randomized controlled trial. Participants completed up to 15 sessions of therapy and up to four 7T MRI scans before, during, and after treatment (n = 185 scans). Growth curve models estimated change over time in anhedonia and in rsFC using average region-of-interest (ROI)-to-ROI connectivity within the default mode network (DMN), frontoparietal network (FPN), salience network, and reward network. Changes in rsFC from pre- to post-treatment were further evaluated using whole-network seed-to-voxel and ROI-to-ROI edgewise analyses. RESULTS: Growth curve models showed significant reductions in anhedonia symptoms and in average rsFC within the DMN and FPN over time, across BATA and MBCT. There were no differences in anhedonia reductions between treatments. Within-person, changes in average rsFC were unrelated to changes in anhedonia. Between-person, higher than average FPN rsFC was related to less anhedonia across timepoints. Seed-to-voxel and edgewise rsFC analyses corroborated reductions within the DMN and between the DMN and FPN over time, across the sample. CONCLUSIONS: Reductions in rsFC within the DMN, FPN, and between these networks co-occurred with anhedonia improvement across two psychosocial treatments for anhedonia. Future anhedonia clinical trials with a waitlist control group should disambiguate treatment versus time-related effects on rsFC.
BACKGROUND: The neural mechanisms associated with anhedonia treatment response are poorly understood. Additionally, no study has investigated changes in resting-state functional connectivity (rsFC) accompanying psychosocial treatment for anhedonia. METHODS: We evaluated a novel psychotherapy, Behavioral Activation Therapy for Anhedonia (BATA, n = 38) relative to Mindfulness-Based Cognitive Therapy (MBCT, n = 35) in a medication-free, transdiagnostic, anhedonic sample in a parallel randomized controlled trial. Participants completed up to 15 sessions of therapy and up to four 7T MRI scans before, during, and after treatment (n = 185 scans). Growth curve models estimated change over time in anhedonia and in rsFC using average region-of-interest (ROI)-to-ROI connectivity within the default mode network (DMN), frontoparietal network (FPN), salience network, and reward network. Changes in rsFC from pre- to post-treatment were further evaluated using whole-network seed-to-voxel and ROI-to-ROI edgewise analyses. RESULTS: Growth curve models showed significant reductions in anhedonia symptoms and in average rsFC within the DMN and FPN over time, across BATA and MBCT. There were no differences in anhedonia reductions between treatments. Within-person, changes in average rsFC were unrelated to changes in anhedonia. Between-person, higher than average FPN rsFC was related to less anhedonia across timepoints. Seed-to-voxel and edgewise rsFC analyses corroborated reductions within the DMN and between the DMN and FPN over time, across the sample. CONCLUSIONS: Reductions in rsFC within the DMN, FPN, and between these networks co-occurred with anhedonia improvement across two psychosocial treatments for anhedonia. Future anhedonia clinical trials with a waitlist control group should disambiguate treatment versus time-related effects on rsFC.
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