Little Rock, Arkansas 72205


The purpose of the current study is to develop a better understanding of the brain mechanisms involved in psychological treatments for posttraumatic stress disorder (PTSD). This project will build on past research using script-driven imagery in our lab by investigating brain activity in areas activated during exposure to trauma-related cues. This project will also develop new knowledge concerning volitional control of those areas. The ultimate goal of this study is a better understanding of whether volitional control of these brain areas will improve therapeutic outcomes. This process will first be piloted in a sample of healthy controls. This will allow investigators to refine the methodology prior to recruiting a sample with PTSD.

Study summary:

Post-traumatic stress disorder (PTSD) is characterized by intense emotional distress upon exposure to trauma reminders and avoidance of people and places that can trigger the trauma memory. Neurocircuitry models of PTSD that seek to explain symptoms of heightened emotional reactivity, hypervigilance for threat, and avoidance suggest abnormal activity of neural regions involved in emotional reactivity (e.g., amygdala) and cognitive control of emotional responding (e.g., ventral medial prefrontal cortex, anterior cingulate cortex). While knowledge exists about neurobiological abnormalities associated with PTSD, these data are cross-sectional in nature and ignore individual differences in both neural encoding and subjective aspects of the trauma itself (e.g., whether it elicits fear vs guilt vs disgust). Additionally, the manner by which existing psychological treatments alter these neural mechanisms mediating core PTSD symptoms is unknown. This is problematic, given that state-of-the-art treatment for PTSD is only effective ~60% of the time. Here, the investigator proposes to utilize a novel computational modeling approach combined with state-of-the-art functional magnetic resonance imaging (fMRI)-based neurofeedback to directly identify and modulate the idiosyncratic neural network encoding the trauma memory. Successful pursuit of these aims would 1) provide scientific support for the hypothesis that a distributed network including the amygdala, hippocampus, medial prefrontal cortex (PFC), lateral PFC, and anterior insula mediates emotional responding upon trauma memory recall, and 2) provide proof-of-concept evidence that neurofeedback modulation of this network can boost existing therapy efficacy.


Inclusion Criteria: - Female - Aged 21-50 - Medically healthy Exclusion Criteria: - Claustrophobia, or the inability to lie still in a confined space - Major medical disorders (e.g., HIV, cancer) - Magnetic metallic implants (such as screws, pins, shrapnel remnants, aneurysm clips, artificial heart valves, inner ear (cochlear) implants, artificial joints, and vascular stents) - Electronic or magnetic implants, such as pacemakers - Permanent makeup or tattoos with metallic dyes - Currently pregnant - A self-reported history of loss of consciousness (greater than 10 minutes) - Physical disabilities that prohibit task performance (such as blindness or deafness) - Psychotic disorders (e.g., schizophrenia) - Any other condition that the investigator believes might put the participant at risk



Primary Contact:

Principal Investigator
Keith Bush, PhD.
University of Arkansas

Sonet Smitherman, M.S.
Phone: 501-526-8386

Backup Contact:


Location Contact:

Little Rock, Arkansas 72205
United States

Sonet Smitherman, M.S.
Phone: 501-526-8386

Site Status: Recruiting

Data Source:

Date Processed: March 16, 2018

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