This proposal for a NIMH Exploratory/Developmental Grant Award (R21) seeks to critically evaluate and expand upon leading neurocircuitry models of trauma and PTSD among assaulted adolescent girls. Existing neurocircuitry models of trauma and PTSD focus almost exclusively on identifying the neural mechanisms that explain observed hypervigilance for threat and deficits in fear extinction learning. While these models have ample empirical support, they do not explain known deficits in risk perceptions of social situations and increased rates of revictimization among assault-exposed and PTSD populations. By contrast, our pilot study demonstrated that assaulted adolescent girls display both worse behavioral performance and decreased activation of anterior cingulate cortex and bilateral anterior insular cortex during a social learning task, which suggests a novel mechanism to explain known social functioning deficits in these populations. Based on these pilot data, we hypothesize that expanding existing neurorcircuitry models to include weakened brain and behavioral correlates of social prediction error encoding increases explanatory power for PTSD symptoms and functional deficits among assaulted adolescent girls. We propose to recruit control, assaulted without PTSD, and assaulted with PTSD adolescent girls and administer both a threat processing task and our previously used social learning task during fMRI. Participants would also complete a standardized risk perception task, in which they are presented with written vignettes depicting increasingly dangerous social situations.
Aim 1 seeks to demonstrate that weakened encoding of social prediction errors among assaulted adolescent girls mediates decreased risk perceptions to the standardized risk social situation vignettes when controlling for variance explained by neural mechanisms on the threat processing task.
Aim 2 seeks to demonstrate that weakened encoding of social prediction errors among assaulted adolescent girls predicts 3-month trajectories of PTSD symptoms when controlling for variance explained by neural mechanisms on the threat detection task. The overarching purpose of the proposed project is to demonstrate increased explanatory power of a neurocircuitry model that includes social processing deficits. Successful completion of the proposed project would stimulate new conceptualizations of the toxic effects of early life trauma and PTSD, and hopefully lead to improved prevention and treatment programs.
This application aims to critically evaluate neurocircuitry models of risk following adolescent assault exposure. Further refinement of our theoretical models would facilitate development of more potent and lasting interventions for this chronically at-risk population.
| Ross, Marisa C; Lenow, Jennifer K; Kilts, Clinton D et al. (2018) Altered neural encoding of prediction errors in assault-related posttraumatic stress disorder. J Psychiatr Res 103:83-90 |
| Cisler, Josh M; Sigel, Benjamin A; Kramer, Teresa L et al. (2015) Amygdala response predicts trajectory of symptom reduction during Trauma-Focused Cognitive-Behavioral Therapy among adolescent girls with PTSD. J Psychiatr Res 71:33-40 |
| Cisler, Josh M; Bush, Keith; James, G Andrew et al. (2015) Decoding the Traumatic Memory among Women with PTSD: Implications for Neurocircuitry Models of PTSD and Real-Time fMRI Neurofeedback. PLoS One 10:e0134717 |
| Cisler, Josh M; Bush, Keith; Scott Steele, J et al. (2015) Brain and behavioral evidence for altered social learning mechanisms among women with assault-related posttraumatic stress disorder. J Psychiatr Res 63:75-83 |
