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.
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.
- Aged 21-50
- Medically healthy
- 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
- 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