Soldiers' Amygdalae Show Scars

A year and a half after soldiers have returned from war, impairments in the regulatory circuitry of the amygdala remain.

Aug 30, 2011
Kerry Grens

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A chronically overactive amygdala, the brain region involved in fear, is a hallmark of an unhealthy response to traumatic events. New research, published today (August 30) in Molecular Psychiatry, shows that some soldiers—who have no mental health deficits after a return from deployment—also harbor signs of trauma within the regulatory network of this brain region.

The findings could help researchers determine “what changes [in the brain] help us predict who becomes sick and who recovers and leads a normal life,” said Ahmad Hariri, a professor at Duke University who was not involved in this study.

The amygdala mediates humans' fear response, and researchers have found that its overreaction is related to psychological disorders such as posttraumatic stress disorder (PTSD), anxiety and depression. People with PTSD, for example, have heightened activity in the amygdala when they are exposed to potential stressors, such as images of threatening faces.

In the new study, the researchers compared 23 Dutch combat soldiers who had been deployed to Afghanistan with 16 soldiers who stayed home. They measured brain activity using fMRI as the soldiers were exposed to angry or fearful faces.

The findings revealed different neural responses to the faces depending on how much fear the soldiers experienced—and not necessarily how much combat they were in. Immediately after returning from Afghanistan, those soldiers who reported feeling the greatest threat abroad displayed the most activity in the amygdala when they viewed the faces. Soldiers who didn't feel as threatened had a less sensitive amygdala.

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Over time, this reactivity returned to the levels seen before the soldiers went to war. Hariri told The Scientist that this short term sensitivity in the amygdala is what he would predict to occur in healthy people.

The amygdala's activity in relation to a part of the brain involved in decision-making and emotion, however, remained altered in these soldiers a year and a half after they returned from Afghanistan. Normally, the activity of the amygdala and the dorsal anterior cingulate cortex (ACC) oppose one another—high activity in the amygdala corresponds to low activity in the dorsal ACC, and vice versa. But in those soldiers returning from war, and who experienced the most fear, this coupling was less strong, and it stayed that way.

“The amygdala normalized, but the cognitive control processes remained impaired,” said Guillén Fernández, a professor at Radboud University Nijmegen and the senior author of the study. “So there is a functional scar” that could possibly make people more vulnerable to the stressful effects of re-deployment or other potentially traumatic events.

The long term changes Fernández's group found appeared to be stable and did not worsen, which might explain why the soldiers did not develop any mental illnesses. “I think what this shows is that all these brain changes are essentially healthy adaptations to a dangerous environment,” said Guido van Wingen, the lead author of the study and a postdoctoral researcher at Radboud University Nijmegen.

The group did not compare these soldiers to those who did develop a mental illness, such as PTSD. But the patterns they found appear similar to those found among people with PTSD in other studies, Fernández said, causing him to question what compensatory mechanisms might help these soldiers ward off the disorder.

“The current research would suggest that alterations in circuitry related to the amygdala could predict who goes on to experience depression or anxiety and who goes on to return to normal,” Hariri said. “The biggest missing piece of the puzzle is, how do these persistent changes affect the behavior of these soldiers?” There are larger studies ongoing in the United States to help answer that question.

G.A. van Wingen, et al., “The neural consequences of combat stress: long-term follow-up,” Molecular Psychiatry, doi:10.1038/mp.2011.110, 2011.