Post-Traumatic Stress Disorder, or PTSD, is a mental health disorder that is associated with people who have witnessed a life-threaten incident or a traumatic and stressful event (Ding, et al.). People who develop PTSD can experience symptoms such as emotional distress, nightmares about the traumatic event, and memory problems. Although PTSD is very common among war veterans, many people regardless of backgrounds can be affected by PTSD. The symptoms of PTSD can last from several days to several years. Scientists have attempted to solve PTSD through different approaches.
Through investigating different approaches toward the treatment of Post- Traumatic Stress Disorder, this research aims to evaluate each approach and finds the effectiveness of each one. The research not only presents a medical perspective toward the possible treatment of PTSD but also a psychological approach to the treatment of PTSD. By first examining the methods used in these experiments, the research provides new ways of approaching mental illness. Then by examining their results, the research provides information about the effectiveness of each method.
Three approaches were evaluated in this research. The first approach stemmed out from a medical perspective toward the treatment of PTSD. It viewed PTSD as a disorder caused by abnormal activities in the amygdala of the brain. To test the hypothesis, scientists used 45 male Wistar rats as the experimentation group, a maze for behavior test, and Co-immunoprecipitation to detect β-arrestin-2 and PDE-4 and Elisa techniques to detect the concentration of cAMP. 45 rats were placed in the facility a week before the experiment for them to acclimate to the new environment. Then, they were divided into 4 groups including one control group and three experimental group.
Three experimental groups experienced the single prolonged stress (SPS) procedure which was a method to prepare PTSD symptoms in animals for 1 day, 7 days, and 14 days, respectively. To measure their behavior, the rats were placed in the center of a maze facing a closed arm. To calculate anxiety, the number of entries into open arms and into closed arms were recorded, and the time spent at open arms and closed arms were recorded. The measurement of anxiety memory are the percentage of open arm entries and the percentage of time spent on the open arms. All rats showed signs of stressed and anxiety. Lastly, the rats were killed, and their brains were removed and examined (Ding, et al.).
Similar to the first approach, the second approach also stemmed out from a medical perspective to the treatment of PTSD. In the second approach, scientists also believed that abnormal brain activities caused PTSD. They conducted an experiment using Sprague-Dawley rats of both sexes to test if the muscarinic receptors of the brain could have an impact on the formation of PTSD. Before the experiment, the rats were housed in the experimental facility for 10 days to acclimate. Then, they were separated into a control group and 5 experimental groups. The 5 experimental groups were injected M1, M2, M3, M4, and M5 receptor respectively. They were exposed to the trauma of dirty cat litter for a week for 10 minutes each day while receiving treatments of fluoxetine, propranolol, or saline to create stressed and anxious emotions. Then, they were placed in a maze to measure the sign intensity of anxiety (Aslı, et. al.).
Different from the first two approaches, the third approach stemmed out of a psychological perspective to PTSD. A team of scientists believed that PTSD was the result of being involved in traumatic events. Therefore, they conducted a survey in 5 counties in Pisco to determine the prevalence of PTSD among adult survivors of the Earthquake. 1012 adults were randomly selected and surveyed to provide a large sample pool (Flores, et. al.).
In the first experiment, the result found that after SPS treatment all rats showed a decrease in β-arrestin-2 and PDE-4. While these two factors decreased, the level of cAMP was increased which lead to an increase PKA and CREB leading to the enhancement of fear memory after traumatic events. In conclusion, β-arrestin-2 was involved in influencing the anxious memory in brain which lead to the development of PTSD (Ding, et al.). If β-arrestin-2 was the main factor in the cause of PTSD, PTSD could be treated simply by controlling the amount of β-arrestin-2.
In the second experiment, female rats showed signs of anxiety more frequently compared to male rats. Lastly, the expression of receptors was measured. The result showed that while the expression of anxiety in rats injected with M2, M3, and M5 increased, it showed a decrease in rats injected with M4 receptor (Aslı, et. al.). The result showed that PTSD could be treated by altering different receptors in different brain regions.
In the third experiment, the result showed a 15.9% of the adults surveyed experienced chronic PTSD. Based on the result, the team investigated the cognitive social capital such as support from families and society and relationships with significant others for 15.9% of the adults, and they found a negative correlation between cognitive social capital and the prevalence of PTSD. While cognitive social capital decreased, the prevalence of PTSD in adults decreased. The result found that social support can help decreasing the rate of PTSD (Flores, et. al.). This research showed by PTSD could be treated simply by giving more emotional support for patients. In this research, most people who suffered from PTSD showed a significance recovery rate when the community was involved in the process of recovery.
This goal of this research is to find the most effective way to the treatment of PTSD. The first and second approach from the medical perspective to the treatment of PTSD show that dysregulated fear process contributed greatly to the formation of PTSD. By altering the chemicals or receptors involved in the process, these two research show a correlation between the amount of chemicals and the different receptors involved in the formation of anxiety and PTSD. A decreasing amount of β-arrestin-2 leads to lesser signs of anxiety (Ding, et al.). Therefore, it is possible to treat PTSD by controlling the chemicals that are involved in fear processing. The first and second experiments have shown that by treating the chemicals and receptors involved in fear processing symptoms of PTSD can be controlled.
However, because medical research is often very costly, the medication is usually expansive when it reaches to retailers. Therefore, it might not be an effective way to treat PTSD because not everyone can afford to purchase expansive medication. The third experiment shows that by giving more emotional support symptoms of PTSD can be soothed. This approach seems like a more cost-effective way to treat patients with PTSD since not everyone has the financial ability to obtain medication. This research is important because it provides new ways for the treatment of PTSD that can have a huge impact on the current treatment of PTSD.
