Thursday, April 3, 2025
4/3/2025
The effects of trauma-focused psychotherapy on reward circuitry function and information encoding - Project Summary/Abstract The objective of this study is to identify how a trauma-focused psychotherapy for PTSD, cognitive processing therapy (CPT), alters the function and information processing of the brain during reward learning. Preliminary data indicate abnormal function of the brain’s reward circuit (ventromedial prefrontal cortex, ventral striatum) during reward learning in PTSD. Changes in this circuitry may serve as one mechanism of therapeutic improvement in diminished positive affect symptoms. This is an important area of study, as PTSD diminished positive affect symptoms (e.g., difficulty experiencing positive emotions, diminished interest) are poorly understood neurobiologically and consistently associated with poorer quality of life and worse clinical outcomes. We will assess neural circuitry function and neural encoding (representation in brain signal) of reward-related information parameters with functional magnetic resonance imaging (fMRI). Parameters will be derived from reinforcement learning (RL) computational models of reward task behavior before and after CPT treatment. Preliminary data indicate CPT alters the function and neural encoding of RL information parameters in PTSD, and that changes vary by whether imminent threat is embedded in the reward processing context. This is an ecologically valid approach to studying this construct, as: a) PTSD is characterized by hypervigilance for threat; b) individuals with PTSD often perceive threat in the absence of explicit threat; and c) trauma-focused psychotherapies utilize techniques that may impact both threat and reward-based processes. The rationale is that improved understanding of therapeutic mechanisms may lead to identification of novel treatment targets, which can be utilized to improve treatment outcomes. The central hypothesis is that CPT will alter neural encoding of RL parameters during reward learning variably as a function of threat context. We will recruit 120 individuals with chronic PTSD. Individuals will undergo clinical and fMRI assessment to measure brain function during reward learning with a contextual threat manipulation. RL computational models will facilitate examination of neural encoding under contexts where threat is present or absent. Participants will then be randomized (stratified on presence of comorbid major depressive disorder to ensure equal representation across arms) to receive either immediate, individual CPT treatment or to a delayed treatment condition (N=60 each). Individuals will then repeat clinical and fMRI assessments, and those in delayed treatment will then commence with CPT treatment. It is predicted that CPT will: a) in the absence of threat, enhance neural RL encoding in the ventral striatum and ventromedial prefrontal cortex and decrease neural encoding in the amygdala; and b) under threat (of shock), promote a reduction in ventral striatal/ventromedial prefrontal RL neural encoding and an adaptive, treatment-facilitated increase in dorsolateral prefrontal cortex RL encoding. Outcomes will enhance understanding of trauma-focused psychotherapy mechanisms and may provide novel future treatment targets.
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