Posttraumatic stress disorder (PTSD) is a condition that arises from the failure to recover from a tragic event. It occurs when a person becomes a witness or a victim of such occurrences. PTSD is a psychological disorder that is associated with the flashbacks, memories, or nightmares of the tragic event. These occurrences can be wars, the sudden death of a loved one, terrorist incident, serious accident, violent assault such as rape, and other events that are life-threatening. This research aims to identify the extent of study on PTSD, its methods of research and treatment. It seeks to answer the questions; What is PTSD and how does it affect the brain? How is PTSD treated? Who is exposed to PTSD and what factors lead to the condition?
Annotated Bibliography
Parson, R. G., & Ressler, K. J. (2013). Implications of memory modulation for post-traumatic stress and fear disorders. Nature Neuroscience, 16, 146–153. Retrieved: doi:10.1038/nn.3296
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According to this study, PTSD is a disorder that is based on panic and phobia that is associated with uncontrollable fear that something will repeat itself. The authors affirm that the condition comes as a result of aversive events caused by neural stimuli. It also includes the previous tragic experiences and even the inability to inhibit or extinguish the fear after life-threatening events. The research discusses the recent breakthroughs in the study of PTSD that includes learning of anxiety and memory and also differential susceptibility to panic disorders. The authors cover the interventions that can be included in the extinguishing fear to reconsolidate and enhance recovery. The methods are known to have interference with the development of panic and give an informed designed approach to the regulation of PTSD.
MacNamara, A., Rabinak, C. A., Kennedy, A. E., Fitzgerald, D. A., Liberzon, I., Stein, M. B., & Phan, K. L. (2016). Emotion Regulatory Brain Function and SSRI Treatment in PTSD: Neural Correlates and Predictors of Change. Neuropsychopharmacology, 41, 611–618.
MacNamara et al. define the condition as a chronic and deliberation of circumstances that come as a result of emotional deregulation. The study focuses on military soldiers and suggests that the individuals have the highest prevalence of PTSD. The research includes the veterans from Operation Iraqi Freedom (OIF) and Operations Enduring Freedom (OEF). The study recommends treatment interventions such as Selective Serotonin Reuptake Inhibitors (SSRIs). This therapy is useful as it attempts to remediate neurological emotion regulation activities. The authors offer the variation of SSRIs including paroxetine that increases the activation of both dorsolateral prefrontal cortex (PFC) and supplementary motor areas of the brain to regulate emotions. The treatment reduces the severity of PTSD among the studied subjects as it not only eradicates the symptoms but also restricts episodic PTSD emotions.
Mayo Clinic Staff. ( 2014, April 15). Diseases and Conditions: Post-traumatic stress disorder (PTSD). Retrieved from Mayo Clinic: http://www.mayoclinic.org/diseases-conditions/post-traumatic-stress-disorder/basics/symptoms/con-20022540
This article by Mayo Clinic states that the symptoms of PTSD begin within three months after a tragic incidence, but the condition may not appear until after years following the event. The indicators of PTSD are problematic and cause difficulties in social sectors and also in relationships. According to the article, these symptoms can be divided into intrusive neural changes in emotional reactions, avoidance and negative mood and thinking changes. The former includes unwanted memories that are always recurring about the traumatizing incidence. Avoidance symptoms are characterized by the attempt to avoid thinking about the occurrence and the place that reminds one about the event. Negative mood changes include the difficulties the person has in having positive thoughts. The article also highlights the emotional reactions include intense guilt or shame and even self-destructive behavior.
Grupe, D. W., Wielgosz, J., R. J., & Nitschke, J. B. (2016). Neurobiological correlates of distinct post-traumatic stress disorder symptom profiles during threat anticipation in combat veterans. Psychological Medicine, 46 (09),1885-1895.
This research is an attempt to highlight the psychological effects of combat veterans in different wars. In this article, the researchers explain how the condition affects the brain. This study indicates that PTSD has a disruptive impact on the Ventromedial Prefrontal Cortex (vmPFC) in the subjects without the disorder. It is therefore uncertain to identify the specific areas of the brain that are affected by the condition. It is imperative to note that there is a striking difference between combat veterans with vmPFC dysfunction with and without PTSD regarding various disorders. The study involved 52 male combat veterans who fought in Iraq. The statistics showed that there existed different threat condition and unpredictability in the temporal area. It was from the results that it was evident that there were higher anticipatory responses for safety about the occurrence that was singly driven by deactivation during the anticipation of the threat. The greater prefrontal activation for danger versus safety is what increases PTSD symptoms. Some subjects were seen to be driven by their difference in hyperarousal symptoms. The study concluded that increased PTSD symptoms amongst veterans existed due to the increased anticipatory responses to unpredictable threats. The results were significant in designing an intervention for the control of PTSD.
Fonzo, G. A., Huemer, J., & Etkin, A. (2016). History of childhood maltreatment augments dorsolateral prefrontal processing of emotional valence in PTSD. Journal of Psychiatric Research, (74), 45-54.
This study suggests that PTSD is brought about when there is an increased and decreased reactivity in the amygdala and the prefrontal cortex in response to trauma or threat stimuli. Fonzo and the other researchers bring up a new approach to the description of PTSD which stems from childhood maltreatment. They explain that this maltreatment is a potential risk factor mainly when it is applied in an extended time it influences the neural phenotypes that are responsible for threat process. The study also suggests that CM has effects on both mental valences and conflict which is processed within the stratification of PTSD. The researchers found that the PTSD that is as a result of CM is influenced by negative valence stimuli particularly when the goal of the individual is irrelevant. CM is a historical modifier of the relationship between activation of PTSD and abnormalities amongst children.
Aupperle, R. L., Stillman, A. N., Simmons, A. N., Flagan, T., Allard, C. B., Thorp, S. R., Stein, M. B. (2016). Intimate Partner Violence PTSD and Neural Correlates of Inhibition. Journal of Traumatic Stress, 29 (2), 33-40.
Aupperle et al. link PTSD to the deficits of neuroimaging and response inhibition. The other cause is also attributed to the prefrontal cortex recruitment differences. The study assesses the relationship between the neural responses and the condition in intimate partner violence (IPV). It was conducted on ten women with PTSD from IPV and twelve others without a history of trauma and exposed to magnetic resonance. The study links PTSD to the difficulties that come from disengagement standard mode in the brain in which cognitive duties require low cognitive power. Accordingly, the snags affect the region of the brain that is responsible for salience processing as they have high cognitive requirements. The results also show that prevalence of violence among intimate partners is a cause of PTSD.
Hien, D. A., Jiang, H., Campbell, A. N., Hu, M., Miele, G. M., Cohen, L. R., Brigham, G. S., et al. (2010). Do treatment improvements in PTSD severity affect substance use outcomes? A secondary analysis from a randomized clinical trial in NIDA’s clinical trials network. American Journal of Psychiatry, 95-101.
Some evidence of cross sectional epidemiological studies has made conclusions of high rates of PTSD among subjects using substances. Other longitudinal studies also support the hypothesis of self-medication and conclude that the individuals who have PTSD have high risks of developing drug use disorder. Hien et al. examine the interventions for the reduction of PTSD symptoms and substance use among females in the treatment of outpatient substance abuse disorder. The results from this research pointed out that change in PTSD influences substance abuse outcomes. However, there is minimal evidence on whether the reduction in the latter improves PTSD symptoms. This study supports the self-medication model and gives empirical evidence for focusing on PTSD on improving the outcomes of substance abuse in subjects with severe PTSD symptoms.
Ehlers, A., Bisson, J., Clark, D. M., Creamer, M., Pilling, S., Richards, D. et al. (2010). Do all psychological treatments really work the same in posttraumatic stress disorder? Clinical Psychology Review, 30, 269-276.
Ehlers at al. reviews the previous articles that purport that all bona fide interventions are equally helpful in PTSD. The study contracts the findings with others that suggest that the psychological treatments that are focused on PTSD such as cognitive behavioral therapy (CBT) and eye movement desensitization and reprocessing (EMDR). This study concludes that the above interventions are more effective than the ones that are not focused on trauma. The recommendations of the review are five. First, the procedures for selection that are biased should not be included in future meta-analyses. Secondly, the studies should be such that there are controls that demonstrate how trauma-focused treatments are more effective than natural recovery solely. Thirdly, effective mechanisms for therapeutic interventions should be examined in future studies. The exclusion criteria in the meta-analysis should be transparent in reporting. Finally, the bona fide treatments should be based on theoretical and empirical grounds instead of the intent of the investigator's judgment.
References
Aupperle, R. L., Stillman, A. N., Simmons, A. N., Flagan, T., Allard, C. B., Thorp, S. R., Stein, M. B. (2016). Intimate Partner Violence PTSD and Neural Correlates of Inhibition. Journal of Traumatic Stress, 29 (2), 33-40.
Ehlers, A., Bisson, J., Clark, D. M., Creamer, M., Pilling, S., Richards, D. et al. (2010). Do all psychological treatments really work the same in posttraumatic stress disorder? Clinical Psychology Review, 30, 269-276.
Fonzo, G. A., Huemer, J., & Etkin, A. (2016). History of childhood maltreatment augments dorsolateral prefrontal processing of emotional valence in PTSD. Journal of Psychiatric Research, (74), 45-54.
Grupe, D. W., Wielgosz, J., R. J., & Nitschke, J. B. (2016). Neurobiological correlates of distinct post-traumatic stress disorder symptom profiles during threat anticipation in combat veterans. Psychological Medicine, 46 (09),1885-1895.
Hien, D. A., Jiang, H., Campbell, A. N., Hu, M., Miele, G. M., Cohen, L. R., Brigham, G. S., et al. (2010). Do treatment improvements in PTSD severity affect substance use outcomes? A secondary analysis from a randomized clinical trial in NIDA’s clinical trials network. American Journal of Psychiatry, 95-101.
MacNamara, A., Rabinak, C. A., Kennedy, A. E., Fitzgerald, D. A., Liberzon, I., Stein, M. B., & Phan, K. L. (2016). Emotion Regulatory Brain Function and SSRI Treatment in PTSD: Neural Correlates and Predictors of Change. Neuropsychopharmacology, 41, 611–618.
Mayo Clinic Staff. ( 2014, April 15). Diseases and Conditions: Post-traumatic stress disorder (PTSD). Retrieved from Mayo Clinic: http://www.mayoclinic.org/diseases-conditions/post-traumatic-stress-disorder/basics/symptoms/con-20022540
Parson, R. G., & Ressler, K. J. (2013). Implications of memory modulation for post-traumatic stress and fear disorders. Nature Neuroscience, 16, 146–153. Retrieved: doi:10.1038/nn.3296
