Vous êtes sur la page 1sur 6

POST-TRAUMATIC STRESS DISORDER INTRODUCCTION TO PSYCHOLOGY 1010 SALT LAKE CITY COMMUNITY COLLEGE ELIZABET MUNOZ ACEVES

Posttraumatic stress disorder also named PTSD for its initials, is a sever condition that may develop after a person is exposed to one or more traumatic events, such as sexual assault, serious injury or the threat of death, or experiencing or witnessing of a stressor event in which the individual felt intense fear, horror, or powerlessness (Fullerton, CS; Ursano, Wang, 2004). Post-traumatic stress disorder is classified as an anxiety disorder, but, in DSM-5 (Diagnostic and Statistical Manual of Mental Disorders-5) publish in May, 2013, PTSD is classified as a traumaand stress-related disorder (DMS-5, 2013). Typically the individual with PTSD persistently avoids all thoughts, emotions and discussion of the event and sometimes may experience amnesia for it. However the event is commonly relived by the persons though, persistent re-experiencing, flashback, memories, recurring distressing dreams, subjective re-experiencing of the traumatic event or intense negative psychological or physiological response to any objective or subjective reminder of the traumatic event (American Psychiatric Association, 1994). Most people (more than half) will experience at least one traumatic event in there lifetime (Spoont, Michele; Arbisi P, Fu S, Greer N, Kehle-Forbes S, Meis L, Rutks I, 2013). Men are more likely to experience traumatic events, but women are more likely to experience more high impact trauma that can lead to PTSD. Only in the minority of traumatized people will develop PTSD, and more likely it will be women (Royal College of Psychiatrists, 2013), the average risk developing PTSD is around 8% for men, and a little over 20% for women (R.S.P. 2013). Rates of PTSD are higher in combat veterans than other men, with a rate estimate at up to 20% for veterans returning from Iraq and Afghanistan (Spoont, Arbisi, Fu, 2013) our book authors said that many soldiers returning from combat have PTSD symptoms, like flashbacks of battle,

exaggerated anxiety and startle reactions, and even medical conditions that do not arise from physical damage, like paralysis or chronic fatigue (Schacter, Gilbert & Wegner, 2011). In human studies, the amygdala has been shown to be strongly involved in the formation of emotional memories, especially fear-related memories. Neuroimaging studies in humans have revealed both morphological and functional aspects of PTSD (Newport, D Jeffery; Charles B Nemeroff, 2010). However during high stress times the hippocampus, which is associated with the ability to place memories in the correct context of space and time, and with the ability to recall the memory (Gilbert et al., 2011) is suppressed. Now we understand that the hippocampus has a strong influence for PTSD, veterans of the Vietnam War with PTSD showed a 20% reduction in the volume of their hippocampus compared with the veterans who suffered no such symptoms (Carlson, Neil R., 2007). This raises an important question: does the reduce hippocampal volume reflect a preexisting condition that makes the brain sensitive to stress (Gilbert et al., 2011) a preexisting condition that made them susceptible to developing PTSD when they were later exposed to trauma (Gilbert et al., 2011). Well, now we understand what it is, what caused it, and the correlation it has with our prefrontal cortex, amygdala and more important our hippocampus, thus, we need to know more, the DSM says that there are six ways of diagnostic PTSD, A: Exposure to a traumatic event, B: Persistent re-experiencing, C: Persistent avoidance and emotional numbing, D: Persistent symptoms of intense arousal not presented before, E: Duration of symptoms for more than one month, and F: Significant impairment. A variety of medication has shown adjunctive benefits in reducing PTSD symptoms, but, there is no clear drug treatment for PTSD. Positive symptoms (re-expiriencing, hypervigilance, increased arousal) generally respond better to medication than negative symptoms (aoidence,

withdrawal), and it is recommended that any drug trial last for at least 6-8 weeks. With many medications, resuidual symptoms following treatment is the rule rather than the exception, which has led to increase research in aggressive treatment of TSD symptoms (Krystal, John H; Alexander Neurmeister, 2009), but there is some medication that can help. Some medications have shown benefit in preventing PTSD or reducing its incidence, when given in close proximity to a traumatic event. These medications include: clonidine (catapres) to reduce traumatic stress symptoms, beta blockers, propranolol (Inderal) and glucocorticoids. Psychobiological treatments have also found success, especially with cortisol (Feldner MT, Monson CM, Friedman MJ, 2007). Psychological treatments target biological changes that occur after a traumatic event. Many forms of psychotherapy have been advocated for trauma-related problems such as PTSD. Basic counseling practices common to many treatments responses for PTSD include education about the condition and provision of safety and support, the psychotherapy programs with the strongest demonstrated efficacy include cognitive behavioral programs, variants of exposure therapy, stress inoculation training (SIT) variants of cognitive therapy (CT) and many combinations of this procedures ( Cahill, S.P., & Foa, E. B., 2004). Despite these studies there is not significant evidence that medication can prevent PTSD, therefor none routinely administered.

REFERENCE

1. - American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. Pp. 271-280. 2. - American Psychiatric Association (1994). DSM-IV. Washington, DC. 3. - Brom D, Kleber RJ, Delfares PB, (October 1989). Brief psychotherapy for PTSD. J Consult Clin Psychol 57 (5): 607-12. 4. Cahill, S.P., & Foa E.B. (2004). A glass half empty or half full? Where we are and directions for future research in the treatment of PTSD. Advances in the trestment of PTSD: Cognitivebehavioral perspectives (pp.267-3130 5. - Carlson, Neil R. (2007). Physiology of Behavior (9 ed.). Pearson Education, Inc. 6.- Feldner MT, Monson CM, Friedman MJ (2007). "A critical analysis of approaches to targeted PTSD prevention: current status and theoretically derived future directions". Behav Modif 31 (1): 80116. 7. - Fullerton, CS; Ursano, Wang (2004). "Acute Stress Disorder, Posttraumatic Stress Disorder, and Depression in Disaster or Rescue Workers". Am J Psychiatry 161 (8): 13701376. 8. - Krystal, John H; Alexander Neumeister (2009). "Noradrenergic and serotonergic mechansims in the neurobiology of posttraumatic stress disorder and resilience". Brain Research 1293: 1323. 9. - National Collaborating Centre for Mental Health (UK) (2005). "Post-Traumatic Stress Disorder: The Management of PTSD in Adults and Children in Primary and Secondary Care". NICE Clinical Guidelines, No. 26. Gaskell (Royal College of Psychiatrists). Retrieved 1 June 2013.

10. - Newport, D Jeffery; Charles B Nemeroff (2010). "Neurobiology of posttraumatic stress disorder". Current Opinion in Neurobiology 10 (2): 211218. 11. - Spoont, Michele; Arbisi P, Fu S, Greer N, Kehle-Forbes S, Meis L, Rutks I. (January 2013). "Screening for Post-Traumatic Stress Disorder (PTSD) in Primary Care: A Systematic Review". Washington DC: Department of Veterans Affairs. Retrieved 1 June 2013. 12. - Schacter, D. L., Gilbert, D. T, & Wegner, D. M. (2011). Introducing Psychology. New York: Worth Publishers. 13. http://en.wikipedia.org/wiki/post-traumatic_stress_disorder.

Vous aimerez peut-être aussi