What Causes PTSD?
Currently, many scientists are focusing on genes that play a role in creating fear memories. Understanding how fear memories are created may help to refine or find new interventions for reducing the symptoms of PTSD. For example, PTSD researchers have pinpointed genes that make stathmin, a protein needed to form fear memories. In one study, mice that did not make stathmin were less likely than normal mice to “freeze,” a natural, protective response to danger, after being exposed to a fearful experience. They also showed less innate fear by exploring open spaces more willingly than normal mice.
GRP (gastrin-releasing peptide), a signaling chemical in the brain released during emotional events, GRP seems to help control the fear response, and lack of GRP may lead to the creation of greater and more lasting memories of fear. Researchers have also found a version of the 5-HTTLPR gene, which controls levels of serotonin — a brain chemical related to mood that appears to fuel the fear response. Like other mental disorders, it is likely that many genes with small effects are at work in PTSD.
Studying parts of the brain involved in dealing with fear and stress also helps researchers to understand possible causes of PTSD better. One such brain structure is the amygdala, known for its role in emotion, learning, and memory. The amygdala appears to be active in fear acquisition, or learning to fear an event (such as touching a hot stove), as well as in the early stages of fear extinction, or learning not to fear.
Storing extinction memories and dampening the original fear response appears to involve the prefrontal cortex (PFC) area of the brain, which is involved in tasks such as decision-making, problem-solving, and judgment. Certain areas of the PFC play slightly different roles. For example, when it deems a source of stress controllable, the medial PFC suppresses the amygdala, an alarm center deep in the brainstem, and controls the stress response. The ventromedial PFC helps sustain the long-term extinction of fearful memories, and the size of this brain area may affect its ability to do so.
Individual differences in these genes or brain areas may only set the stage for PTSD without actually causing symptoms. Environmental factors, such as childhood trauma, head injury, or a history of mental illness, may further increase a person's risk by affecting the early growth of the brain. Also, personality and cognitive factors, such as optimism and the tendency to view challenges in a positive or negative way, as well as social factors, such as the availability and use of social support, appear to influence how people adjust to trauma. More research may show what combinations of these or perhaps other factors could be used someday to predict who will develop PTSD following a traumatic event.
In the last decade, rapid progress in research on the mental and biological foundations of PTSD has led scientists to focus on prevention as a realistic and important goal. For example, NIMH-funded researchers are exploring new and orphan medications thought to target underlying causes of PTSD in an effort to prevent the disorder. Other research is attempting to enhance cognitive, personality, and social protective factors and to minimize risk factors to ward off full-blown PTSD after trauma. Still, other research is attempting to identify what factors determine whether someone with PTSD will respond well to one type of intervention or another, aiming to develop more personalized, effective, and efficient treatments.
As gene research and brain imaging technologies continue to improve, scientists are more likely to be able to pinpoint when and where in the brain PTSD begins. This understanding may then lead to better-targeted treatments to suit each person's own needs or even prevent the disorder before it causes harm.
At Cognitive Behavioral Therapy Los Angeles, we are experts in the field of evidence-based treatment for PTSD. Call or email today to schedule an appointment.