A Brief History of PTSD

1. “The Reintegration of Veterans with PTSD Back into Their Communities Through the Use of Public Health Initiatives”

2. A Brief History of PTSD 1980 PTSD was codified as a disorder in the (DSM) Diagnostic and Statistical Manual of Mental Disorders. Between 1 & 5 or 1 & 6 people who undergo a traumatic event in there lifetime will develop PTSD. Over the last 60 years great strides have been made in the diagnosis and treatment of PTSD. Past names referring to PTSD are as follows. Nervous Shock Shell Shock Traumatic Neurosis Rape related fear and anxiety PTSD can happen to anyone that is exposed to a traumatic event. Symptoms of chronic PTSD can affect an individual even after 25 years or more after the traumatic event.

3. Of the approximate 1 in 5 veterans that suffer from PTSD only ½ take the steps to seek treatment. Of those that seek help to manage their PTSD, only ½ of those actually receive adequate treatment in managing their PTSD symptoms.

4. Reasoning behind use of Epidemiology and Biostatistics for PTSD tracking. • Over 4 billion dollars are annually spent in compensation and disability claims to veterans with PTSD. • After 13 years of war; an estimated 100,000 – 300,000 OIF/OEF veterans are at significant risk of developing chronic PTSD. • Nearly ½ of the soldiers in the military have experienced multiple deployments & chances of developing PTSD increases with each deployment. • All Americans will bare the cost of treating these veterans through financial or community obligations. • Forming better treatments takes a better understanding of the illnesses and its symptoms. Hence the reasoning behind tracking PTSD to formulate these treatments.

5. Factors of (PTSS) Post Traumatic Stress Symptoms Stressors Classifications of home front stressors No home front stressors before or after the new deployment (No stressors). Home front stressors after but not before the new deployment (New stressors). Home front stressors before but not after the new deployment (Relieved stressors). Home front stressors both before and after the new deployment (Chronic stressors). • Age • Gender • Marital Status • Education Level • Rank • Employment Status • Ethnicity • Parental Status • Pre-disposition to stressors or existing PTSD • Combat Exposure • Other Variables

6. Study Results This study revealed that the occurrence of home front stressors increased the risks of PTSS and that soldiers were more likely to develop precursors to PTSD if PTSS was present before and after the deployment. Overall, the issues that pertain to the lifestyle or family of individuals deployed are relevant to the mental health of the individual.

7. Biological & Molecular effects of PTSD • There are many things that can trigger a traumatic event activating a person’s fight-or-flight response which is the body’s instinctual reflex to possible trauma & works as a survival mechanism normally by increasing the biological output of molecular responses such as the increase of hormones such as adrenaline or body systems such as arterial blood pressure, oxygen exchange in the lungs & many other effects. • This natural response has given man many advantages over the course of evolution. • There are instances though that this natural mechanism displays a dysfunction which happens when a functional impairment causes an individual to become psychologically traumatized creating PTSD within the individual because their normal defense mechanisms against trauma has failed to operate & process the information in a manner that is traditionally in line with the body’s normal functioning. • These individuals are among the population that is biologically susceptible to the pathophysiology that causes PTSD. • These pathological features found in patients with PTSD overlap similarly in patients with traumatic brain injury paralleling the shared signs & symptoms of these syndromes in clinical studies. • The signs & symptoms of PTSD appear to reflect a persistent & abnormal adaptation of neurobiological systems to the stress of a witnessed traumatic event. • The neurobiological systems that regulate stress responses include certain endocrine & neurotransmitter pathways as well the network of brain regions known to regulate fear & behavior at both conscious & unconscious levels.

8. Biological & Molecular Effects of PTSD Changes in the Endocrine system Changes in the Nervous system This is a result of the brain releasing chemicals triggering responses to the chemical stimuli. This can result in phantom sensations or reliving the experiences causing the endocrine system to release hormones as a result of the nervous system thinking it is responding to a crisis. Elevated respiratory output & cardio vascular output are just examples. Flashbacks or mental visions of reliving the experiences are extreme but are seen in severe cases and during therapy & Treatment. • Hormone production levels will either increase or decrease based on the symptoms experienced and the severity of the physiological symptoms. • These endocrine changes will either be protein based or lipid based and can affect cardiovascular output, blood pressure, fluid retention/renal use, sexual arousal and various other systems controlled by the endocrine system. • Changes in the endocrine system can have short term or long lasting effects and prolonged symptoms.

9. The hippocampus is a biological component of a portion of the human brain affected by PTSD

10. Biological & Molecular effects of PTSDThe Hippocampus • One of the areas that is affected on a molecular level is the hippocampus. • The hippocampus is a seahorse shaped portion of the brain. Its exact function is unknown but it is believed to be responsible for playing a role in long term memory among other theories. • In studies on animals, exposure to severe stress can damage the hippocampus. • Similar studies in humans suggests a link between the amount of blood volume in the hippocampus correlates with vulnerability to psychological trauma. • Smaller hippocampal volume constitutes a higher risk & susceptibility to PTSD than those with higher volume.

11. Biological and Molecular effects of PTSD A study of the Serotonergic & Noradrenergic markers of PTSD & Depression has shown that research on the biological pathophysiology of PTSD found evidence of the roles of catecholamine & serotonin (5-HT). This finding on the increases of the catecholaminergic or sympathetic nervous system (SNS) activity in PTSD patients is fairly consistent across studies.

12. Biological Pathophysiology of PTSD Serotonergic & Noradrenergic markers of PTSD & Depression effects related to the Sympathetic Nervous System (SNS) PTSD patients also have significantly decreased platelet counts suggesting down-regulation of α2-adrenoceptors (α2-ARs) on platelets within the bloodstream Laboratory trials with yohimbine, a α2-AR antagonist that blocks the presynaptic α2-AR auto-receptor resulted in significantly higher plasma levels of 3-methoxy-4-hydroxyphenylglycol (MHPG), the major NE metabolite. This was more prominent in PTSD veterans than in control groups. These results suggest that central presynaptic α2-ARs are sub-sensitive in PTSD patients • Combat veterans with PTSD have shown significantly higher 24-hour urinary excretion with plasma concentrations of catecholamine, noradrenaline (NE), adrenaline, & dopamine, versus the normal control group, other psychiatric patients, or combat veterans without PTSD. • Combat veterans have shown significantly higher rise in plasma (NE) & peripheral (SNS) activity than normal volunteers following acute stressors within the laboratory with stimuli reminiscent of the trauma linked to their PTSD

13. Biological and Molecular effects of PTSD and Pharmacology • Other studies have tried to identify the implications & relationships between trauma memory for pharmacological treatments which have been proposed for the prevention of PTSD & the idea of reprocessing trauma memories to bring about recovery through treatments such as invasive exposure therapy. • Psychological accounts of PTSD & the biological concept for reconsolidation of active memories suggest that physiological arousal enhances the reprocessing of traumatic memories. • Use of drugs that influence arousal through chemical means may then have effects after the trauma & depend on the psychosocial context that they are used in, thus in theory helping to prevent the development of PTSD in some trauma victims, but impeding recovery in others who would do well without such treatments. • This would mean that you would have to be preemptively treating someone with drug related therapies before they were exposed to the traumatic event in order to use some of these treatments successfully.

14. Psychosocial & Behavioral Health Factors Influenced by PTSD • Public Health is concerned with the psychosocial and behavioral health factors of the community at large. • Public health can gauge these concerns using the ecological model of health behaviors which are identified as the five following factors. • 1) Intrapersonal factors • 2) Interpersonal relations • 3) Institutional factors • 4) Community factors • 5) Public policy • Specific symptom clusters of PTSD are atypical across experiences and are displayed in the following forms in some degree or another. • 1) Hyper-arousal • 2) Re-experiencing • 3) Numbing • 4) Avoidance • These symptom clusters of PTSD cause significant interference in the daily activities related to functioning within the ecological model of health behaviors.

15. Psychosocial Behaviors and PTSD • With over 1.5 million soldiers deployed into the theater of operations and an estimate as high as 10-20% of these veterans experiencing some type or form of PTSD symptoms, it is of particular interest to better understand how PTSD can be displayed or induce other forms of mental health disorders such as OCD or anxiety disorders. • These disorders and the symptoms of PTSD are presenting with different clinical outcomes compared to other instances of PTSD and will thus complicate the treatment process and possibly creates a concern for the public health in how to best address the treatment of this increasing population and return them into active members of the community.

16. Conclusion • The reintegration of veterans with PTSD back into the community through public health initiatives is a lengthy and time consuming process. • It is not something that happens over the course of a night, through 1 meeting, or the application & use of medications. There is no cure all or instant fix solutions. • It is not completed with just a shot in the arm, a pill to pop, or the duration of a course of a prescription drug. It is a life-long process with success being measured in varying degrees. • The public’s health has been sustained in part through the contributions and sacrifices of the veteran community allowing for the continuation of the American lifestyle. • PTSD is perhaps the most painful mental disorder to have treatment for and it can be a life-long process of treatment through either therapy or medication to manage and control the symptoms. • The reintegration of these veterans into being active and participating members of society is paramount to the overall success of the community. • They have valuable skills and experience that contribute to the success of a sustainable economy and in order for the structure of society to remain intact, the public health community needs to accommodate planning and strategies to address how to best help reintegrate these individuals into the home front.

17. Works Cited: http://www.ptsd.va.gov/professional/newsletters/research-quarterly/V20N1.pdf Litz, B., & Schlenger, W. (2009). PTSD in service members and new veterans of the Iraq and Afghanistan wars: A bibliography and critique. PTSD Research Quarterly, 20(1), 1-8. Retrieved from http://www.ptsd.va.gov/professional/newsletters/research-quarterly/V20N1.pdf (Litz & Schlenger, 2009) http://www.veteransandptsd.com/PTSD-statistics.html Veterans & PTSD. (2013). Veterans statistics: PTSD, depression, TBI, suicide. Retrieved from http://www.veteransandptsd.com/PTSD-statistics.html (Veterans & PTSD, 2013) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2891773/ Aust, N. (2010). Prevalence estimates of combat-related PTSD: A critical review. NIHPA Author Manuscripts, 44(1), 4-19. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2891773/ (Aust, 2010) http://epirev.oxfordjournals.org/content/27/1/78.full Galea, S., Nandi, A., & Vlahov, D. (2004). The epidemiology of post-traumatic stress disorder after disasters. Oxford Journals, 27(1), 78-91. Retrieved from http://epirev.oxfordjournals.org/content/27/1/78.full (Galea, Nandi & Vlahov, 2004) Interian, A., Kline, A., & Janal, M. (2014). Multiple deployments and combat trauma: Do homefront stressors increase the risk for posttraumatic stress symptoms?. Journal of traumatic stress, 27(1), 90-97. doi: 10.1002/jts.21885 (Interian, Kline & Janal, 2014) Thomas, B. (2012, September 19). Strong star: South Texas research organizational network guiding studies on trauma and resilience. Retrieved from http://psychiatry.uthscsa.edu/Research/STRONG_STAR_A.asp (Thomas, 2012) For more information on STRONG STAR and its research projects, visit www.strongstar.org Sherin, J., & Nemeroff, C. (2011). Post-traumatic stress disorder: the neurobiological impact of psychological trauma. Dialogues in clinical neuroscience, 13(3), 263-278. doi: PMC3182008 (Sherin & Nemeroff, 2011) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182008/ Yehuda, R., Koenen, K., & Galea, S. (2011). The role of genes in defining a molecular biology of PTSD. Disease Markers, 30(2-3), 67-76. doi: 10.3233/DMA-2011-0794 (Yehuda, Koenen & Galea, 2011) http://iospress.metapress.com/content/w77t770111456543/ McCleery, J., & Harvey, A. (2005). Integration of psychological & biological approaches to trauma memory: Implications for pharmacological prevention of PTSD. Journal of traumatic stress, 17(6), 485-496. doi: 10.1007/s10960-004-5797-5 (McCleery & Harvey, 2005) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182008/ Maes, M., Lin, A., & Verkerk, R. (1999). Serotonergic & noradrenergic markers of post-traumatic stress disorder with & without major depression. Neuropsychopharmacology, (20), 188-197. doi: 10.1016/S0893-133X(98)00058-X (Maes, Lin & Verkerk, 1999) http://www.nature.com/npp/journal/v20/n2/full/1395241a.html Schneider, M. (2012). Introduction to public health. (4th ed., pp. 221-236). Burlington, MA: Jones & Bartlett Learning. (Schneider, 2012) Beckham, J. (1999). Smoking and anxiety in combat veterans with chronic posttraumatic stress disorder: A review. Journal of Psychoactive Drugs, 31(2), 103-110. doi: 10.1080/02791072.1999.10471731 (Beckham, 1999) http://www.tandfonline.com/doi/abs/10.1080/02791072.1999.10471731#.U0Su7jjD_ip Tuerk, P., Grubaugh, A., & Hamner, M. (2009). Diagnosis and treatment of PTSD-related compulsive checking behaviors in veterans of the Iraq war: The influence of military context on the expression of PTSD symptoms. The American Journal of Psychiarty, 166(7), 762-767. doi: 10.1176/appi.ajp.2009.08091315 (Tuerk, Grubaugh & Hamner, 2009) http://journals.psychiatryonline.org/article.aspx?articleid=100938 Krause, E., Kaltman, S., & Goodman, L. (2006). Role of distinct PTSD symptoms in intimate partner reabuse: A prospective study. Journal of traumatic stress, 19(4), 507-516. doi: 10.1002/jts.20136 (Krause, Kaltman & Goodman, 2006) http://onlinelibrary.wiley.com/doi/10.1002/jts.20136/abstract