Can We Predict Who Is Most at Risk From PTSD?

Allison Inserro

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The field of posttraumatic stress disorder (PTSD) has grown in recent years due to veterans returning from wars in Afghanistan and Iraq, and at the 73rd Annual Scientific Convention of the Society of Biological Psychiatry meeting in New York City, May 10 to 12, one of the nation’s leading experts decided to focus his presentation on the topic on memory consolidation.

Kerry Ressler, MD, PhD, is chief scientific officer and James and Patricia Poitras Chair in Psychiatry at McLean Hospital after having served at Emory University for 18 years. He is also a professor in psychiatry at Harvard Medical School and past president of the Society for Biological Psychiatry. McLean is the psychiatric affiliate of Harvard.

Memory conditioning is 1 element of a neurological framework looking at PTSD, which also includes fear conditioning, dysregulated circuits between the prefrontal cortex and limbic structures, memory reconsolidation, epigenetics, and genetic factors.1

Reactivated, unstable memories combined with epigenetic changes, early-life stress, and genetic factors all affect an individual’s ability to regulate their response to traumatic events.

Moreover, genetic risk factors may account for up to 30% to 40% of the heritability of PTSD.2

PTSD is an intractable disorder, Ressler said, yet it is unique because we know when it starts, which makes it one of the few disorders in psychiatry that could theoretically be prevented.

For instance, if we understand the neurobiology of memory consolidation, emergency departments (EDs) could potentially have the same preventative approach that is used for heart attack and strokes, he said.

There are multiple hard-wired connections that are observed in fear responses. The amygdala, along with hippocampus and prefrontal cortex function, have been consistently shown to be dysregulated in PTSD and are related to fear response. The memory consolidation process starts soon after the event. The response to trauma is a conditioned response, and later trauma cues—whether noises or odors—reactivate fear systems.

Building on previous work, Ressler and his team of researchers are studying trauma patients brought to an ED via ambulance through blood samples and other tests, and are looking for changes that can predict future PTSD.

Some of the work has already shown that increased activity in the hippocampus is a predictor, as are skin conductivity tests. The skin tests were performed as people were recalling the trauma in the ED to researchers.

Ressler also discussed the role that noncoding RNAs (ncRNA) play in PTSD. One of them, GAS5,  expresses differently in some patients who go on to develop PTSD, he said.

1. Ross DA, Arbuckle MR, Travis MJ. An integrated neuroscience perspective on formulation and treatment planning for posttraumatic stress disorder: an educational review. JAMA Psychiatry. 2017;74(4):407-415. doi:10.1001/jamapsychiatry.2016.3325.

2. Banerjee SB, Morrison FG, Ressler KJ. Genetic approaches for the study of PTSD: advances and challenges. Neurosci Lett. 2017;649(10): 139-146. 10.1016/j.neulet.2017.02.058.

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