Recently I read press reports from the 69th annual meeting of the American Psychosomatic Society describing a study from Kent State University that found that the immediate use of hydrocortisone in persons who had just experienced a traumatic event reduced the incidence of PTSD symptoms three months after the incident. 1
Having worked with a number of people affected with PTSD, I was excited by these findings, even though they are preliminary in nature. I have seen PTSD ruin patients' lives in spite of their receiving standard treatments.
I can remember a patient named Jeff (not his real name) whom I treated a few years ago. He was a 56-year-old retired career veteran of the Vietnam War, a man whose entire identity was based on his military career. In fact, the first words he said to me were, “I am a warrior.”
Jeff had suffered PTSD symptoms for decades. I recall him describing how, “just the other night, I heard a noise outside of my home, went out in my pajamas and crawled the perimeter to look for the enemy.” PTSD ruined this unfortunate man's life. He was unable to work, to function as a husband and father, and was severely addicted to alcohol.
It is estimated that up to eight percent of the American population suffers from PTSD at any given time. That represents an enormous emotional and financial burden not only those who suffer symptoms, but on those around them-their families, friends, and society. And, those individuals with PTSD are at risk for comorbid somatic disorders that involve immune and inflammatory processes such as such as metabolic syndrome, rheumatoid arthritis, psoriasis and thyroid disease.2
Best practice for PTSD treatment includes the combination of SSRI antidepressants like Paxil and Zoloft with cognitive behavioral therapies designed specifically for PTSD. However, I believe that even this is inadequate to treat people like Jeff.
The study from Kent State suggested to me that there might be a preventive approach to the problem. If true, then the use of a regimen of 20 mg of hydrocortisone twice daily for ten days, initiated within 12 hours of hospital admission following a traumatic event might keep patients from developing the disorder altogether.
I reviewed the literature to put this study into context.
The Neurobiology of PTSD
|ABOUT THE AUTHOR
William M. Glazer, MD, is President of Glazer Medical Solutions of Key West, Fla., and Menemsha, Mass. He is a clinician, researcher, lecturer, and consultant, and has been a member of faculty of the departments of psychiatry at the Yale and Harvard schools of medicine.
Researchers have identified two hormone systems that constitute the primary stress pathways:
The hypothalamic-pituitary-adrenal (HPA) axis is a complex set of interactions between the brain (the hypothalamus and the pituitary gland) and the adrenal glands that results in the release of glucocorticoids, which include hydrocortisone (cortisol). The HPA axis helps regulate things such as your temperature, digestion, immune system, mood, sexuality, energy and, most importantly, stress.
The sympathetic-adrenal-medullary (SAM) system is a part of the body's sympathetic nervous system, which includes a vast network of nerves originating in the spine and communicating to various organ systems throughout the body. The SAM system refers to the part of the sympathetic nervous system that regulates the release of catecholamines (epinephrine and norepinephrine) from the medullary cortex of the adrenal gland. The SAM system is best known for mediating the body's “fight or flight” response to stress.
Normally, when anyone is exposed to significant stress, the “stress hormones” from these two systems kick into gear. It is thought that for certain people, abnormalities in these systems may be associated with risk for PTSD.3 To explore this theory, researchers have intervened in the HPA and SAM systems in the hope of modifying these abnormalities.
Secondary Prevention Strategies
A 2002 study by Pitman et al. targeted the catecholamine response from the SAM system with propranolol, a blocker of norepinephrine in the brain4. Their preliminary work suggested that propranolol treatment might prevent PTSD by altering the memory-enhancing effects of emotional arousal in affected adults.
The study of hydrocortisone was an attempt to intervene on abnormalities in the HPA axis that were thought to lead to PTSD.
In an interview with the lead author of that more recent study, Douglas L. Delahanty, PhD, from the Department of Psychology at Kent State University, I learned more details. In collaboration with emergency room staff from at Summa Health System hospitals in nearby Akron, Ohio, Delahanty's team performed a randomized, double-blind study.