Post-traumatic stress disorder (PTSD) is currently defined as a trauma-related or stressor-related disorder in the 5th edition of the “Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association [APA], 2013). It is caused by any traumatic event, but catastrophic events, physical abuse, and combat engagement in war are the most prevalent causes of PTSD (Sullivan, 2012). The symptoms usually start showing three months after an individual experiences a traumatic event, and they need to last for at least one month before an official diagnosis can be made. The most common symptoms include behavioral changes (e.g. avoidance of situations associated with trauma, lack of motivation), mood changes (e.g. higher instances of emotional outbursts and irritability), and detrimental mental states (e.g. re-experiencing traumatic events in dreams or visions, sense of detachment from the self and the environment).
The onset of PTSD is characterized by several physiological changes in the nervous system, which makes treatments difficult. A study on war veterans with PTSD showed that their working memory system, which is responsible for manipulating information input and storing it in long-term memory, undergoes several morphological changes when they experience traumatic combat-related events that are accountable for the onset of PTSD (as cited in Hall et al., 2012). Some of those changes can occur in the amygdala, hippocampus, hypothalamus, and other limbic regions of the brain.
The changes in the working memory affect the affected veteran’s cognitive resources and memory retrieval mechanisms. The working memory in individuals with combat-related PTSD is preoccupied with re-experiencing traumatic events, and because all humans have a limited cognitive capacity, war veterans with PTSD show higher difficulties in performing mental tasks at hand that are not associated with the trauma (Hall et al., 2012). That explains why affected individuals will often suffer from reduced long-term decision-making abilities and problem solving, which can affect their behavioral decisions and mental states.
When the memory retrieval mechanisms are altered in combat PTSD, affected individuals will have no control over their intrusive memories. Intrusive memories are re-lived through highly vivid and sensory-rich episodes that cause strong emotional responses, such as fear or anger, and it is difficult to control their occurrence and outcome because of their unpredictable nature (Brewin, Gregory, Lipton, & Burgess, 2010). Eventually, in order to deal with those memories, individuals will resort to various detrimental coping strategies.
The most common universal coping strategies in war veterans with PTSD are involuntary strategies, which can be considered automatic defensive mechanisms, such as memory intrusion and emotional numbing (van Rooyen & Nqweni, 2012). While those strategies can help individuals avoid confronting with their problems, they will more likely affect their social functions. As they lose motivation to engage in physical and social activities, they will more likely develop other psychological disorders. Around 80 percent of PTSD patients suffer from at least one more disorder, and the most prevalent comorbid disorders are anxiety disorders and depressive disorders (Spinhoven, de Rooij, Heiser, Smit, & Penninx, 2012).
Another common occurrence in war-related PTSD is delayed-onset PTSD. According to APA (2013), delayed-onset PTSD occurs when symptoms show six months after a traumatic event takes place. Horesh, Solomon, Zerach, and Ein-Dor (2011) found that war veterans who reported more pre-war and post-war stressors in their lives were more likely to develop PTSD immediately after combat-related experiences while others could potentially develop delayed-onset PTSD.
Another possible explanation is that time and physical aging can play an important role in delayed-onset PTSD among war veterans. Studies show that suppressing unwanted memories becomes difficult in the later stages of life when brain power reduces because of aging (Anderson, Reinholz, Kuhl, & Mayr, 2011). Horesh et al. (2011) also explain that it is possible for latent memories to resurface several years after war-related stressors when an individual experiences a traumatic event that triggers those memories. However, an alternative explanation suggests that a change in mental state could affect the person’s reaction to new stressors and latent memories, so it is currently impossible to prove whether mental states or external triggers cause traumatic memories to resurface.
In addition, symptoms of PTSD can be enhanced with traumatic brain injuries (TBI), which are a common occurrence in combat-related PTSD. For example, a study on Vietnam War veterans that brain lesions, especially the ones on the frontal lobe, was associated with higher possibilities for engaging in violent behavior (as cited in Williams, 2012). That finding suggests that combat PTSD can have lasting effects because TBI contributes to the reduction of impulse and temperament regulation, so long-term treatment strategies and follow-up sessions need to be included to produce effective treatment results.
Early diagnosis of PTSD in combat veterans is critical for increasing the chances of successful treatments, and there are two possible strategies that can be used to detect the onset of PTSD. First, it is clear that PTSD symptoms usually affect family relationships, but Zerach et al. (2013) found that emotional gaps among family members can also be used to predict PTSD symptoms. Before intrusive memories are expressed, unconscious influences can cause emotional numbing and alter relationships between family members before individuals manifest PTSD symptoms.
Second, using the biopsychosocial model can determine which individuals have a higher predisposition for developing PTSD. The biopsychosocial model divides PTSD-development risk factors into biological (e.g. genetics and abnormal hormonal activity), social (e.g. family history and lack of social support), and psychological (e.g. reactions to stressors, event duration, proximity, and severity) factors. The inability to predict whether physiological changes cause emotional and mental changes or whether they are consequential to those changes is a significant weakness of the model, but it still reveals that treating a single event cannot produce results if other events from different life-development stages contributed to the development of PTSD.
Studies that used the biopsychosocial model to explain the onset of combat-related PTSD found interesting results. For example, it was found that combat-related PTSD was more likely going to develop in war veterans who had previously experienced childhood abuse (as cited in McKeever & Huff, 2003). Therefore, it is possible to suggest that the traumatic event or stressor alone cannot be held exclusively accountable for the onset of PTSD, and treatments based on resolving traumatic events alone cannot be effective if previous contributing factors are not addressed.
Another study found that war-zone events were significant triggers for PTSD development, but the lack of social support at home proved to be a critical determinant of PTSD onset and duration (as cited in McKeever & Huff, 2003). The practical implication of these findings is that the lack of social support, changes in emotional relationships, and personal history can be used to predict which individuals have a higher risk for developing PTSD.
There are several treatment options for treating combat PTSD, but the most effective ones are interpersonal therapy and exposure therapy. Group therapy for PTSD war veterans is often considered ineffective. Although social support from like-minded peers can prove to be beneficial, the unpredictable symptoms, diverse range of comorbidities, and different personal backgrounds can reduce adherence and success rates in group treatments (Sloan, Bovin, & Schnurr, 2012). Pharmacological treatments are also often neglected in PTSD in favor of psychological treatments. Although selective serotonin reuptake inhibitors are currently the first-line treatment for PTSD, studies on PTSD patients show only moderate results and there is a lack of evidence-based guidelines for medication use in PTSD (Forneris et al., 2013).
Interpersonal psychotherapy introduces social support in the treatment process because the therapist needs to develop a trustworthy, emphatic, and transparent relationship with the patient. A study by Bleiberg and Markowitz (2005) found that interpersonal psychotherapy can significantly reduce PTSD-related symptoms. However, it is not applicable in all cases. For example, PTSD patients with comorbid depressive disorders could take a long time to recover. Future studies are required to determine how interpersonal therapy can be adjusted for the needs of different PTSD patients or how patients can be assessed to determine whether they will benefit from this type of treatment.
Exposure therapy is currently listed as the first line of treatment for PTSD by the Department of Defense and Department of Veteran Affairs because it proved effective in treating patients with a variety of comorbid disorders, different symptoms, and different levels of PTSD severity (Rauch, Eftekhari, & Ruzek, 2012). War veterans in exposure therapy showed higher adherence rates than veterans undergoing other treatments, and there were no recorded instances of symptom worsening despite the emotionally challenging nature of exposure therapy (Hembree et al., 2003; Rauch et al., 2012).
While professional combat PTSD treatment is necessary and can be effective, PTSD also needs to be treated as a public health issue because the community needs to participate in creating a positive environment that can lessen the symptoms related to PTSD in affected individuals. It is also clear that post-traumatic stressors, such as inadequate social support upon returning from war, may contribute to the prevalence of PTSD in war veterans more than the actual traumatic memories. Therefore, the affected individuals’ families and communities can significantly decrease PTSD-related symptoms by providing them with proper support.
References
American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.
Anderson, M. C., Reinholz, J., Kuhl, B. A., & Mayr, U. (2011). Intentional suppression of unwanted memories grows more difficult as we age. Psychology and Aging, 26(2), 397-405.
Bleiberg, K. L., Markowitz, J. C. (2005). A pilot study of interpersonal psychotherapy for posttraumatic stress disorder. American Journal of Psychiatry, 162(1), 181–183. doi:10.1176/appi.ajp.162.1.181
Brewin, C. R., Gregory, J. D., Lipton, M., & Burgess, N. (2010). Intrusive images in psychological disorders: Characteristics, neural mechanisms, and treatment implications. Psychological Review, 117(1), 210-232.
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Hall, T., Galletly, C., Clark, C. R., Veltmeyer, M., Metzger, L. J., Gilbertson, M. W., & McFarlane, A. (2012). The relationship between Hippocampal asymmetry and working memory processing in combat-related PTSD–a monozygotic twin study. Biology of Mood & Anxiety Disorders, 2(1), 21-28.
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Spinhoven, P., de Rooij, M., Heiser, W., Smit, J. H., & Penninx, B. W. (2012). Personality and changes in comorbidity patterns among anxiety and depressive disorders. Journal of Abnormal Psychology, 121(4), 874-884. doi:10.1037/a0028234
Sullivan, E. (2012). War-related PTSD, blast injury, and anosognosia. Neuropsychology Review, 22(1), 1-2. doi:10.1007/s11065-012-9188-z
Williams, H. (2012). Repairing shattered lives: Brain injury and its implications for criminal justice. London: Barrow Cadbury Trust. Retrieved from http://www.bctrust.org.uk/wp-content/uploads/2012/10/Repairing-Shattered-Lives_Report.pdf
