Let’s say that you’ve just witnessed or experienced something traumatic in combat like the catastrophic injury of a battle buddy or the detonation of an improvised explosive device.
In one scenario, you go on with life and slowly the symptoms of post-traumatic stress disorder begin to haunt your daily existence. Sudden noises elicit a severe startle response and you no longer feel comfortable in crowds. Something has happened to your brain, and though scientists aren’t exactly sure of the particulars, they think that the amygdala – a portion that plays a key role in the body’s stress response – has become overly sensitive to fear, even when there’s no imminent threat.
To find relief, you might seek out exposure therapy and cognitive behavioral therapy, both of which have shown some success in studies. You might try other treatments that aren’t yet backed by robust scientific evidence, like a service dog or meditation. Either way, the process of recovering could take years.
In another scenario, directly following the trauma, you might receive a dose of a drug that targets a receptor in the brain known to play a role in PTSD. When this receptor is activated, it decreases the brain’s impulse to react to fear and ultimately prevents the onset of PTSD.
This scenario won’t happen next week or next year. But a recent study suggests that it could be possible in the distant future.
In a Science Translational Medicine paper published this month, researchers successfully prevented the onset of PTSD-like symptoms in mice by activating a receptor in the brain that essentially puts a brake on the body’s fear response.
To mimic PTSD in the mice, the scientists immobilized them on a wooden board for two hours. These mice, as well as a control group, were then subjected to a memory test; the traumatized mice acted anxious and froze more often, suggesting that they had difficulty telling the difference between non-threatening and dangerous stimuli.
While these findings are unsurprising, the researchers added a unique element to the study: They dissected the brains of the mice and found a gene in the amygdala, also present in the human brain, that seems to play a significant role in PTSD. It does so by encoding a receptor that regulates how the brain responds to fear. In some traumatized mice, that receptor appeared not to be regulated normally.
To prevent that failure, the researchers traumatized a new group of mice, but then injected them with a drug to activate the key receptor, which blocked the brain’s consolidation of fearful memories. Though the mice had been subjected to terrifying experiences, they exhibited fewer PTSD-like symptoms.
This is not the first time that a drug has shown promise in preventing PTSD. Two studies have found that patients who received morphine within hours of a severe injury were less likely to develop PTSD than those who didn’t. Yet those results were so limited that the federal government’s Agency for Healthcare Research and Quality wrote in a recent report (PDF) that it’s not yet clear how the opiate could prevent PTSD.
That report, which looked at a number of PTSD prevention methods, also found that “for most interventions and outcomes of interest, evidence was either entirely lacking or insufficient to draw conclusions.” The majority of studies reviewed by AHRQ were “fraught with methodological shortcomings and were rated as high risk of bias.”
Dr. Kerry Ressler, a professor and psychiatrist at Emory University and investigator with Howard Hughes Howard Hughes Medical Institute, co-authored the recent study preventing PTSD-like symptoms in mice and says its findings suggest that a drug like morphine is effective not only through typical pain reduction pathways in the brain, but perhaps also through the receptor his group targeted.
If the study’s results are replicated, Ressler believes it may lead to the development of a new drug that stops the brain from becoming overly sensitive to fear following a traumatic experience. Ressler and his team are in talks with the Scripps Institute to develop such a compound for testing in human clinical trials. If those efforts are successful, it will be five to 10 years, Ressler expects, before the drug is used to do what seems impossible now – prevent the crippling response to trauma known as PTSD.
If you think you’re experiencing symptoms of PTSD, visit the National Center for PTSD for more information on treatment.