Post Traumatic Stress Syndrome

Post Traumatic Stress Syndrome

The stories are familiar, “I was serving in the 1st-3rd Marine Battalion in Baghdad, constantly facing danger in the guise of Saddam’s National guard and then suicide bombers and insurgents,” or “I was a first responder at the World Trade Center on September 11th, and I was there when the tower collapsed, which not only hurt me but caused the deaths of many fellow firefighters and friends, including members of my own fire company and while I am thankful to be alive I keep seeing that day or those events over and over again.” Sometimes, what a person feels may not even be a flashback, but an increase in heartbeat or other symptoms brought on by stimuli that may remind the person of the horrific events they faced in the past. The circumstances of Post Traumatic Stress Disorder are clear as it is necessary for a person to have experienced a traumatic event that directly put in harms way either the patient or the people around him when it occurred. What is not clear however, is what causes some to experience this disorder while others seem to manage just fine. This paper will attempt to review various articles to examine what neurobiological factors and structures may be behind the chemical causation of Post Traumatic Stress Disorder.

Post-traumatic stress disorder (PTSD) is a term for the psychological consequences of exposure to stressful experiences that involve actual or threatened death, serious physical injury or the threat to bodily harm which a person finds highly traumatic. The diagnostic criteria for PTSD according to Diagnostic and Statistical Manual of Mental Disorders -IV has six categories from A to F. The "A” category says that a person has been exposed to a horrific event involving actual or threatened death or harm to a person or others. The "B" category includes the most recognizable symptoms of PTSD such as daytime fantasies, traumatic nightmares, and flashbacks. Also, trauma-related stimuli that trigger recollections of the original event have the power to evoke mental images, emotional responses, and psychological reactions associated with the trauma. The "C” category consists of symptoms that PTSD patients use as an attempt to reduce the likelihood that they will expose themselves to trauma-related stimulus. PTSD patients also use these strategies in an attempt to lessen the intensity of their psychological response if they are exposed to such stimuli. Behavioral strategies include avoiding any situation in which they perceive a risk of confronting trauma-related stimuli. Category "D", symptoms resemble panic and generalized anxiety disorders. While symptoms such as insomnia and irritability are generic anxiety symptoms, hyper-vigilance and startle are more characteristic of PTSD. The "E", category specifies how long symptoms must persist in order to qualify for the (chronic or delayed) PTSD diagnosis. The "F", category specifies that the survivor must experience significant social, occupational, or other distress as a result of these symptoms.

While it is accepted that an outside traumatic event of a notable magnitude must occur for PTSD to take place, what is still up for debate is the internal workings that cause some people to experience this disorder while others manage to function normally. Mason and his colleagues have found a link between PTSD and hypothyroidism. They discovered there is an elevation of serum free triiodothyronine, total riiodothyronine and total thryoxine levels in combat related stress disorder (Mason 629). However, Dennis Chamey believe that PTSD is related to a dysfunction of several brain structures, particularly the amygdale, locus coerulus and hippocampus as well as the noradrenergic, dopamine, opiate and corticotrophin-releasing factor neurochemical systems.(Chamey 294). Matthew Friedman found that there is a connection between PTSD and SSRI and believes that targeting the 5-HT neurons may relieve a patient of there PTSD symptoms (Friedman 44) whereas Douglas Bremmer believes that PTSD is related to the prefrontal cortex. While studying War Veterans, he found that sufferers of PTSD had decreased Benzodiazepine Receptor Binding in the prefrontal cortex, causing soldiers to feel a greater anxiety and he believes that it’s this part of the brain and this specific binding that may cause the symptoms of PTSD (Bremmer 1120). Rachel Yehuda found a connection between PTSD and lower 24-hour urinary cortisol excretion, lower basal plasma cortisol levels and a greater number of lymphocyte cytosolic glucocorticoid receptors than nonpyschiatric normal subjects and depressed patients (Yehuda 982).

While all of these researchers have different conclusions to what causes PTSD, they did all study the same group of people, namely war veterans. Moreover, the veterans of these wars were all from western nations, mostly America though the Yehuda study did look at