PTSD development

PTSD is a severe condition that occurs after experiencing traumatic events. Although many people go through trauma, only a small percentage of them, around 25% to 35%, develop PTSD. Identifying the factors that make some individuals more vulnerable is essential for preventing and treating this disorder.

A recent research conducted by Carmen Sandi and Simone Astori at EPFL, published in Biological Psychiatry, highlights the impact of glucocorticoids on the development of PTSD. These hormones are released by our body in response to stress, such as cortisol. The study offers valuable information on the behavioural and biological characteristics linked to PTSD susceptibility.

Sandi explains that there are significant variations in the glucocorticoid levels released into the bloodstream during times of stress. It has been observed that individuals with PTSD often have lower levels of glucocorticoids after experiencing trauma, which was initially believed to be a result of the trauma itself.

Investigating whether this trait is a preexisting risk factor for PTSD has been a long-standing question. However, the challenge lies in collecting biological measures before trauma and accessing animal models to study the causal role of these traits.

The researchers utilized a rat model that imitates individuals with reduced cortisol responses to investigate the connection between PTSD symptoms and a diminished hormonal response to stress. They measured the size of various brain regions using MRI scans, trained the rats to associate a cue with fear, monitored their sleep patterns, and recorded their brain activity.

By utilizing a combination of techniques, the scientists found that a decreased sensitivity to glucocorticoids resulted in a linked response involving multiple traits, such as hindered fear extinction in males, decreased size of the hippocampus, and disruptions in rapid-eye-movement sleep. It is important to note that difficulties with fear extinction are a common symptom of PTSD and disturbances in rapid-eye-movement sleep have been linked to memory consolidation issues in individuals with PTSD.

The researchers continued their study by administering human cognitive and behavioural therapy to the rats to decrease their learned fears. Following this, the rats were given corticosterone, resulting in a decrease in excessive fear and disturbances in rapid-eye-movement sleep. Additionally, the levels of the stress-related neurotransmitter norepinephrine in the brain returned to normal.

Sandi's study establishes a causal link between low glucocorticoid responsiveness and the development of PTSD symptoms after traumatic experiences, specifically impaired fear extinction. Furthermore, the study reveals that low glucocorticoids are also causally involved in determining other risk factors and symptoms previously thought to be unrelated to PTSD.

The study's lead author, Silvia Monari, explains that their research provides new mechanistic evidence that low levels of glucocorticoids, such as cortisol, in humans can lead to a predisposition for developing PTSD and difficulties in extinguishing traumatic memories. This evidence was previously missing and highlights the importance of addressing cortisol levels in individuals at risk for PTSD.

The timing of PTSD-related differences has yet to be fully understood. To address this, a study was conducted where brain scans were taken from 104 trauma survivors, typically involved in car accidents, at 1, 6, and 14 months post-incident. The researchers aimed to identify early predictors of chronic PTSD development by analyzing brain activity shortly after the trauma.

Dr. Liberzon's study found that heightened activity in the right inferior frontal gyrus, a region linked to cognitive control and emotional reappraisal, suggests better recovery from early PTSD symptoms in survivors of trauma. The study highlights the crucial role of cortical and cognitive areas in fear regulation and development.