Research
Post-traumatic stress disorder New approach may help prevent, as well as treat, this devastating disorder. By William H. Frey II, PhD
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ost-traumatic stress disorder (PTSD) is a severe anxiety disorder that can develop after an individual is exposed to one or more traumatic events, such as sexual assault, serious injury, or the threat of death. PTSD is characterized by a group of symptoms that may include high levels of anxiety; disturbing, recurring flashbacks; and avoidance or numbing of memories of the event. Symptoms can last a lifetime.
Who is at risk? Approximately 7.7 million American adults and many more millions worldwide have PTSD. But it isn’t just adults who are affected. Children and adolescents exposed to war, physical or sexual assault, abuse, accidents, disasters, or other life-threatening or frightening events are also at
risk for PTSD. Some individuals may experience PTSD after a friend or family member is exposed to danger or is severely harmed. The sudden, unexpected death of a loved one can also precipitate the disorder. Not everyone is equally susceptible to PTSD. Many individuals who are exposed to a traumatic event do not develop this condition. There is some evidence that a susceptibility to it may run in families. Women are more likely to develop PTSD than men because they are more likely to experience high-impact trauma.
Delayed onset increases hope Intrusive memories of the precipitating event, including flashbacks and nightmares, have been reported to contribute more to the biological and psychological dimensions of PTSD than the event itself. These symptoms may not begin until years after the initial trauma. Delayed onset may indicate that there is a significant window of opportunity during which people who have experienced a traumatic event could be treated to prevent the onset of PTSD’s devastating symptoms.
The brain and stress
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Minnesota Health care news January/February 2014
Research in the 1980s showed that glucocorticoids (compounds that the body produces in response to stress) can damage nerve cells in the hippocampus, an area of the brain that is key to both memory and emotional response. One way this damage may occur is by glucocorticoids’ inhibition of glucose uptake and use in the hippocampus. This is critical since glucose is the only source of energy used by brain cells under normal conditions. Cortisol, a major glucocorticoid released in response to stress, has been reported to reduce glucose use in the hippocampus of healthy elderly adults. Glucocorticoids also decrease the capacity of the hippocampus to survive neurological damage by inhibiting glucose transport by up to 30 percent. Nor are these adverse effects on glucose restricted to the hippocampus. Glucocorticoids released in response to major stress inhibit glucose use throughout the brain, as well as inhibiting glucose transport in nerve cells studied in test tubes.
PTSD and glucocorticoids Subsequent research revealed that cortisol concentrations in combat veterans with PTSD were significantly higher than in healthy people. Patients with PTSD related to childhood abuse had cortisol levels that were an average 61 percent higher during the time leading up to a cognitive stress challenge. In addition, the abuse survivors’ cortisol levels were 46 percent higher during the actual cognitive challenge, compared with people without PTSD. Animal models demonstrate that glucocorticoids