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PTSD Essay
What makes people more vulnerable to Post-Traumatic Stress Disorder (PTSD) following a traumatic event, and how can PTSD be prevented?
The Diagnostic and Statistical Manual of Mental Disorders (DSM) IV defines an individual with Post Traumatic Stress Disorder (PTSD) as having been exposed to a traumatic event in which both of the following have occurred; firstly, the person either experienced or witnessed an event that involved “actual or threatened death or serious injury, or a threat to the physical integrity of self or others”. Secondly, the person’s exhibited response had to be one of “intense fear, horror or helplessness”. In addition to these criteria, the individual persistently re-experiences the event. This includes recurrent and intrusive recollections of the event which cause distress, persistent avoidance of stimuli that could be associated with the event, intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event, etc. Some of the symptoms of PTSD bear similarities with those of depression; withdrawal from social circumstances is common as well as a restricted range of affect and problems sleeping.
As with any disorder, not everyone who suffers a traumatic event will develop PTSD, some people are more susceptible to suffering from this after experiencing said traumatic experience; this essay will explore the factors as to why that is, including research from both a biological and social point of view. As an extension of this, this essay will explore ways in which PTSD can possibly be prevented.
From a biological point of view, there is high potential that vulnerability to Post Traumatic Stress Disorder can be genetic. Yehuda’s 1999 research for instance, found that there is an increased prevalence of PTSD in the adult children of Holocaust survivors, despite the fact that they did not experience the trauma themselves nor did they report a greater exposure to life- threatening



References: American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). doi:10.1176/appi.books.9780890423349. Andero, R., Brothers, S. P., Jovanovic, T., Chen, Y. T., Salah-Uddin, H., Cameron, M., ... & Ressler, K. J. (2013). Amygdala-dependent fear is regulated by Oprl1 in mice and humans with PTSD. Science translational medicine,5(188), 188ra73-188ra73. Brady, K., Pearlstein, T., Asnis, G. M., Baker, D., Rothbaum, B., Sikes, C. R., & Farfel, G. M. (2000). Efficacy and safety of sertraline treatment of posttraumatic stress disorder: a randomized controlled trial. Jama, 283(14), 1837-1844. Breslau, N., Peterson, E. L., & Schultz, L. R. (2008). A second look at prior trauma and the posttraumatic stress disorder effects of subsequent trauma: A prospective epidemiologic study. Archives of General Psychiatry, 65, 431-437. Mattocks KM., Skanderson M., Goulet JL. Pregnancy and mental health among women veterans returning from Iraq and Afghanistan. J Womens Health (Larchmt). 2010;19:2159–2166. Meewisse ML., Reitsma JB., de Vries GJ., Gersons BP., Olff M. Cortisol and post-traumatic stress disorder in adults: systematic review and meta-analysis. Br J Psychiatry. 2007;191:387–392. Mowrer, O. H. (1960). Learning theory and behavior. New York: Wiley. Rasmusson, A. M., Hauger, R. L., Morgan, C. A., et al (2000) Biological Psychiatry, 47, 526–539 Rhodes ME., Rubin RT Skinner, B. F. (1938). The behavior of organisms: An experimental analysis. Yehuda R. Advances in understanding neuroendocrine alterations in PTSD and their therapeutic implications. Ann N YAcadSci. 2006 http://www.medicalnewstoday.com/articles/261598.php - published 6/7/2013, retrieved 10/11/2013

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