Measuring the brain activity of two key brain regions involved in emotion regulation shortly after acute trauma may help predict whether a person will develop post-traumatic stress disorder (PTSD), according to a new study published in the journal Biological Psychiatry.
The findings show a link between the activity of the amygdala and the anterior cingulate cortex (ACC), a brain region that regulates amygdala function, shortly after trauma and the development of PTSD symptoms within the following year.
For example, trauma victims who show a stronger amygdala response to fearful faces tend to have more severe PTSD symptoms initially and are more likely to maintain these symptoms over the following year. In addition, trauma victims who show a greater drop in ventral ACC activity after seeing repeated fearful images are slower to recover.
The identification of a PTSD biomarker has exciting implications for limiting or preventing symptoms of the disorder, researchers suggested.
“The search for such early biological markers of poor recovery is very important, because it will allow us to find the people who are most at risk right after a trauma, and intervene early, before the onset of disorders such as PTSD or depression,” said first author Dr. Jennifer Stevens from Emory University.
For the study, Stevens and a research team used functional magnetic resonance imaging (fMRI) to measure the brain activity of 31 people approximately one month after a traumatic incident. The trauma was non-military related and involved traumatic events such as a car accident or sexual assault.
As the participants looked at images of fearful faces (an index of threat), the researchers measured how brain activity reacted in the amygdala and ACC, and how the activity changed over time with repeated viewing. Self-reported PTSD symptoms were assessed at one, three, six, and 12 months after the traumatic incident.
The findings show that participants with a greater amygdala response to fearful faces had greater initial symptom severity, and were more likely to maintain PTSD symptoms over the following year. In addition, those with a sharper drop in ventral ACC activity over repeated viewing of fearful images, called habituation, showed a poorer recovery trajectory.
These results suggest that amygdala reactivity and ventral ACC habituation to a threat predict the emergence of PTSD symptoms after trauma.
“The findings also suggest that an over-active amygdala may be one of the causes of PTSD, and that we should try to develop treatments that reduce amygdala reactivity,” said Stevens.
For example, the amygdala could be targeted with interventions such as psychotherapy or pharmacological treatments shortly after trauma occurs.