Hannah Carl1, Erin Walsh2, Tory Eisenlohr-Moul3, Jared Minkel4, Andrew Crowther5, Tyler Moore3, Devin Gibbs3, Chris Petty6, Josh Bizzell7, Gabriel S Dichter8, Moria J Smoski9. 1. Department of Psychology & Neuroscience, Duke University, Durham, NC 27710, USA. 2. Program on Integrative Medicine, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA. 3. Department of Psychiatry, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA. 4. Department of Psychiatry, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA; Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham NC 27710, USA. 5. UNC Neurobiology Curriculum, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA. 6. Duke-UNC Brain Imaging and Analysis Center, Duke University Medical Center, Durham, NC 27710, USA. 7. Department of Psychiatry, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA; Duke-UNC Brain Imaging and Analysis Center, Duke University Medical Center, Durham, NC 27710, USA; Carolina Institute for Developmental Disabilities, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA. 8. Department of Psychiatry, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA; Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham NC 27710, USA; UNC Neurobiology Curriculum, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA; Duke-UNC Brain Imaging and Analysis Center, Duke University Medical Center, Durham, NC 27710, USA; Carolina Institute for Developmental Disabilities, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA. Electronic address: dichter@med.unc.edu. 9. Department of Psychology & Neuroscience, Duke University, Durham, NC 27710, USA; Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham NC 27710, USA.
Abstract
BACKGROUND: The purpose of the present investigation was to evaluate whether pre-treatment neural activation in response to rewards is a predictor of clinical response to Behavioral Activation Therapy for Depression (BATD), an empirically validated psychotherapy that decreases depressive symptoms by increasing engagement with rewarding stimuli and reducing avoidance behaviors. METHODS: Participants were 33 outpatients with major depressive disorder (MDD) and 20 matched controls. We examined group differences in activation, and the capacity to sustain activation, across task runs using functional magnetic resonance imaging (fMRI) and the monetary incentive delay (MID) task. Hierarchical linear modeling was used to investigate whether pre-treatment neural responses predicted change in depressive symptoms over the course of BATD treatment. RESULT: MDD and Control groups differed in sustained activation during reward outcomes in the right nucleus accumbens, such that the MDD group experienced a significant decrease in activation in this region from the first to second task run relative to controls. Pretreatment anhedonia severity and pretreatment task-related reaction times were predictive of response to treatment. Furthermore, sustained activation in the anterior cingulate cortex during reward outcomes predicted response to psychotherapy; patients with greater sustained activation in this region were more responsive to BATD treatment. LIMITATION: The current study only included a single treatment condition, thus it unknown whether these predictors of treatment response are specific to BATD or psychotherapy in general. CONCLUSION: Findings add to the growing body of literature suggesting that the capacity to sustain neural responses to rewards may be a critical endophenotype of MDD.
BACKGROUND: The purpose of the present investigation was to evaluate whether pre-treatment neural activation in response to rewards is a predictor of clinical response to Behavioral Activation Therapy for Depression (BATD), an empirically validated psychotherapy that decreases depressive symptoms by increasing engagement with rewarding stimuli and reducing avoidance behaviors. METHODS:Participants were 33 outpatients with major depressive disorder (MDD) and 20 matched controls. We examined group differences in activation, and the capacity to sustain activation, across task runs using functional magnetic resonance imaging (fMRI) and the monetary incentive delay (MID) task. Hierarchical linear modeling was used to investigate whether pre-treatment neural responses predicted change in depressive symptoms over the course of BATD treatment. RESULT: MDD and Control groups differed in sustained activation during reward outcomes in the right nucleus accumbens, such that the MDD group experienced a significant decrease in activation in this region from the first to second task run relative to controls. Pretreatment anhedonia severity and pretreatment task-related reaction times were predictive of response to treatment. Furthermore, sustained activation in the anterior cingulate cortex during reward outcomes predicted response to psychotherapy; patients with greater sustained activation in this region were more responsive to BATD treatment. LIMITATION: The current study only included a single treatment condition, thus it unknown whether these predictors of treatment response are specific to BATD or psychotherapy in general. CONCLUSION: Findings add to the growing body of literature suggesting that the capacity to sustain neural responses to rewards may be a critical endophenotype of MDD.
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