Post-Traumatic Stress Disorder (PTSD) is a severe and debilitating condition in which sufferers frequently relive a traumatic event via nightmares and flashbacks. This can lead to irritability, insomnia and anxiety. Commonly associated with military personnel following combat experiences, PTSD can also affect individuals following difficult events such as crime or childbirth. While PTSD is estimated to affect around one in three people who have experienced a traumatic event, it has not been clear why some people develop the disorder whilst others do not. It has, however been identified that for those who experience a concussion (a traumatic brain injury from the brain bouncing within the skull) during a distressing event, PTSD may be more likely to later develop. In exciting new research from the University of California Los Angeles, the mystery of why a concussion renders the brain more vulnerable to PTSD may have been revealed.

To establish how concussion affects the functioning of the brain, fear conditioning was performed on rats who either had concussion-like or non-injuring brain surgery. Both groups of rats were exposed to white noise before being administered foot shocks which are known to cause rats to freeze in fear. The pairing of benign noise with the frightening shocks was repeated until the noise alone was sufficient to elicit the shock’s fearful freezing response- an indication that the pair of stimuli had become associated. The presentation of a fear response following an otherwise benign stimulus in these circumstances can be seen as comparable to an individual with PTSD experiencing anxiety when later exposed to sensory elements that were present during their traumatic event despite there being no current threat.

In revealing results, rats who had been concussed showed longer freezing times when exposed to the noise compared to the rats who had not been concussed, as well as increased heart rates and blood pressure levels. These increased responses indicate that the rats who experienced a concussion formed stronger fear memories during their traumatic experience. Furthermore, study of the brains of the concussed rats highlighted that in their amygdalae – the region of the brain linked to fear – five times more neurons were active during noise exposure than in the non-concussed rats. This indicates that after a concussion the brain may become more sensitive to fear, generating heightened and prolonged responses to stimuli associated with threat. This may explain why sufferers of PTSD show such severe symptoms of anxiety when presented with their personal fear triggers.

For soldiers and other individuals suffering with PTSD, this research may suggest that returning the amygdala’s activity to a more normal rate may be the key to reducing their challenging symptoms and improving quality of life. Suggestions have been made regarding pharmaceutical and behavioural means of achieving this, including the idea of reconditioning to remove the unwanted fear response and reduce the sensitivity of the amygdala. However, it is likely that brain studies involving human participants and sufferers of PTSD itself may be required before new treatments can be confidently recommended.