When the sister of Vishnu Murty began showing signs of post-traumatic stress disorder after a complicated surgical procedure, the Temple University neurobiologist raised concerns with her sister’s doctor.
“I was like, ‘Hey, I’m really worried about my sister. Is there anything one can do?’” she recalls to Reverse.
She told him to take a deep breath and offered him some statistical reassurance: About 75 percent of people two weeks after a traumatic event will show some signs of PTSD because that’s the body’s natural response to trauma. But six months later, that number drops to between 10 and 15 percent.
But if almost everyone starts showing traits of PTSD after a traumatic event, why do some people develop PTSD and others don’t? To answer this question, Murty, who studies how threat influences memory formation, turned to an old friend: the hippocampus.
The hippocampus is a deep region of the brain involved in learning and memory. In an article published on July 26 in The Journal of NeuroscienceMurty and his team found that a heightened emotional state after threatening or traumatic events can short-circuit the hippocampus’ ability to process information as expected and form memories. This, in turn, could put some people at risk of developing PTSD.
What’s new – This research is one of several articles to emerge from a national research initiative to better understand what happens in the brain after trauma at the behavioral, physiological, and genetic levels. Launched in September 2016 by the National Institutes of Health, the Advancing Understanding of Recovery after Trauma, or AURORA, study has compiled a vast amount of data collected over the years from thousands of participants across the US. who reported experiencing recent trauma.
Of this group of participants, Murty and his colleagues involved 116 people in their experiment. All participants reported experiencing trauma in the past two weeks. The researchers asked them to do a series of activities to observe their reaction to fear stimuli, such as hearing a startling noise. Participants were then made to lie down in an MRI scanner and look at a series of fearful or expressionless faces.
“The reason we used fear faces is that we wanted this trustworthy biothreat provocateur,” says Murty.
“If you think from an evolutionary perspective, if you see me making a face of fear, then you know there is a threat. It is a communicative signal that there is a threat in the environment.”
Individuals who showed less activity in their hippocampi and were more reactive to alarming stimuli also tended to report more severe PTSD symptoms.
Why does it matter? Fear reactions to seemingly harmless stimuli or situations are a cardinal feature of PTSD, says Murty. Neuroscientists know that the generation of fear in the brain is governed by an extensive brain network called the limbic system, which includes not only the hippocampus, but also the amygdala and the almond-shaped hypothalamus, a diamond-shaped structure that controls emotion. production of norepinephrine, a hormone that influences fear.
Several studies suggest that people with severe PTSD have a smaller hippocampus, and this characteristic may make them more likely to develop PTSD. But how trauma is related to hippocampal function or how it determines PTSD risk is not well understood.
“What’s so exciting about this study?” says Noah Philip, a PTSD researcher and professor of psychiatry and human behavior at Brown University. Reverse, “It’s that you’re looking at a group of people who’ve just been through trauma and asking what’s going on in their brains that makes them more likely to develop PTSD or, in this case, PTSD symptoms.”
Murty and colleagues’ findings could provide a means of determining early who is at risk of developing PTSD and perhaps even preventing the condition from developing. Currently, identifying these individuals is a challenge.
“There are a lot of factors that go into risk, there are a lot of factors that go into resilience, and all of that is very hard to predict in real time,” says Philip.
Whats Next – Murty theorizes that because the hippocampus is involved in providing context to memories, the disconnect between an exaggerated fear response and PTSD may have to do with missing the proper context for a memory.
“The more you can include the traumatic event in your own life narrative, the less likely you are to suffer from symptoms.”
“If you go through the world and you don’t have the boundary conditions of where your fear should go… without the hippocampus, you basically lose this flexible, high-resolution memory of the event,” says Murty.
This study did not involve participants taking memory tests, so Murty and colleagues were unable to assess whether the connection between reduced hippocampal activity and severe PTSD symptoms involved memory in any way. That’s something he hopes to discover with further study, and one that may lead to novel approaches to PTSD treatments, such as finding ways to stimulate the hippocampus through storytelling.
“There are these therapeutic techniques in PTSD that the more you can include the traumatic event in your own life narrative, the less likely you are to suffer from symptoms,” he says.
“The one thing we’ve been thinking about is whether we can get people to take emotional memories and form narratives that really engage their hippocampus more. Could that be a possible therapeutic approach?”
Murty says any treatment approach remains a distant ideal, but ultimately his research could provide insights that help prevent and treat the millions of people around the world living with PTSD.