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Post-Traumatic Stress Disorder: A Scientific Look

Author: Lukas Byers

Introduction:

Over the past several years there has been increasing criticism of the pathological view on mental health disorders, i.e. fault lies within the client. Some clinicians attribute this to the medical-model approach that Western society has taken in regards to illness and medication. There has been an increased demand for clinicians to view mental health disorders from the biological standpoint, namely for the blame to be placed on outside factors in the client's environment (Makinson & Young, 2012). With this being said, I will do my best to explain PTSD from the biological viewpoint of mental health disorders.

 

The Diagnosis of PTSD:

According to the DSM-5, PTSD is an anxiety disorder that occurs with exposure to one or more traumatic events where actual or perceived death, sexual injury or sexual violation occurs. Symptoms are separated into four different diagnostic clusters: re-experiencing, avoidance, negative cognitions and mood, and arousal. Additionally, symptoms must be present for at least one month in order for the diagnosis to be made. PTSD ultimately causes significant levels of stress to the individual in their social interactions, intimate relationships, ability to work and daily life (American Psychiatric Association, 2013).

When looking at the epidemiology of PTSD in the general public, it is first important to note that traumatic events happen to an estimated 50-70% of the general population. (Qureshi et al., 2011). However, only 6-14% actually develops the symptomatology of PTSD. Why is that the case? Amir, Kaplan, and Kotler (1996) attribute this to the length, duration, and intensity of the traumatic event.

Ozer, Best, Lipsey, and Weiss (2003) conducted a meta-analysis on the predictors of PTSD. They found that social support, peri-traumatic dissociation, prior adjustment to traumatic events, family history of psychopathology, and prior traumatic experiences were all found to be statistically correlated with the development of PTSD. In addition to the risk factors stated above, Flouri (2005) also notes that the appraisal of the traumatic event as a sign of personal weakness by the client increases the risk for developing PTSD.

While there has been no direct correlation found between PTSD and life expectancy in the existing literature, there have been studies noting the long term effects of PTSD on physical health. PTSD has been associated with poor cardiovascular health, gastrointestinal problems, musculoskeletal disorders, dermatological problems, and other comorbid disorders. (Chaudieu et al., 2011)

 

Evidence Based Treatment:

There is one therapeutic modality in particular that has had great success in the treatment of PTSD: Eye Movement Desensitization and Reprocessing (EMDR). In 1987, Dr. Francine Shapiro began to recognize the positive effect eye movement had on memory quality and developed Eye Movement Desensitization (EMD). In 1991 EMD was renamed EMDR and Dr. Shapiro created The EMDR Institute. In 1995 the first randomized clinical trial is published noting the success of EMDR on the treatment of civilian PTSD. A few years later in 2002 randomized clinical trials comparing EMDR with Cognitive Behavior Therapy (CBT) are published with EMDR showing greater success with fewer therapy sessions. In 2004 EMDR is recognized by the American Psychological Association as a recommended effective treatment and is adopted by the VA as the treatment of choice for PTSD (Maxfield, 2009).

EMDR is built on the foundation of adaptive information processing; this foundation addresses factors of personality development and individual pathology. This process of adaptive information processing contributes to what is known as "orienting responses" (ORs). Orienting responses involve retrieving past traumatic memories and changing the negative cognitive schema of the memory into a positive one. (Chen et al., 2014)

The addition of bilateral movement is an important part of the EMDR therapeutic process. Bilateral movement is achieved by the client following the clinician's finger, or alternating repetitive tapping on the knees, chest, or other body part that the client is comfortable with. Bilateral movement is thought to unblock the information processing centers of the brain which allows the client to recall past events that are attributing to a negative coping response to a present stimulus. (Chen et al., 2014)

Ultimately, with both the bilateral movement and ORs, a new set of physiological responses reconnect with the past traumatic event. This results in an integration of positive memories and healthy responses to past adverse events, thereby reducing overall anxiety and reducing the symptoms of PTSD (Chen et al., 2014).

The overall benefit of EMDR is that in comparison with other psychotherapy techniques, the re-exposure to trauma is considerably less due to all work being done in-session with the clinician. Unlike various forms of CBT EMDR does not require outside homework by the client. Studies done by clinicians have shown the success of EMDR in the cessation of chronic pain, and dysfunctional somatic symptoms to past traumatic events. The efficacy of EMDR has been shown not only in PTSD, but Major Depressive Disorder (MDD), and generalized anxiety as well (Shapiro, 2007).

 

Co-Morbid Disorders:

 Lommen and Restifo (2009) cite studies indicating that 29-48% of patients with PTSD will suffer from a severe mental illness. Ozer, Best, Lipsey and Weiss (2003) state that substance abuse (SA) and depression are very often co-morbid because of the ‘numbing effect’ that SA brings. Substance abuse has a 38.5% co-morbidity rate for a current diagnosis, and a 51.9% co-morbidity rate for lifetime PTSD (Reynolds et al., 2005). Leskin, Woodward, Young and Sheikh (2002) state that clients in their sample with a current diagnosis of PTSD report a 96% rate of nightmares, and a 100% rate of insomnia. The nightmares are due to the nature of re-experiencing the event, and insomnia is related to the intense anxiety that presents itself in PTSD.

Morris, Compas and Garber (2012) conducted a meta-analysis on the comorbidity of depression and PTSD. They found rates between 7-19% and as high as 37% in some studies. In regards to suicidal ideations, behavior, and attempts Tarrier and Gregg (2004) reported that in their sample 56.4% of their population reported an aspect of suicidality, 9.6% made suicide attempts, 8.5% reported having plans, and 38.3% reported suicidal ideations. Suicidal behavior is well known to present itself in MDD which is only exaggerated by the PTSD.

Lommen and Restifo (2009) note that PTSD symptomatology may cause psychotic symptoms to present and worsen in clients because of the nature of the psychosocial stressor. Rates of schizophrenia with a co-morbid diagnosis of PTSD ranged from 13-29%. In this particular study, 97% of participants had at least one traumatic event occur, indicating that traumatic events occurred at a higher rate in the schizophrenic/schizoaffective population.

 

History of PTSD:

The history of PTSD can be traced back to accounts from the Civil War, however it was not until World War 1 that it received more attention. Because of trench warfare in WW1, clinicians coined the term “shell shock” to describe the psychological distress that some soldiers were facing. The interest in shell shock receded after WW1 and was brought back to light in World War 2. Like in WW1, the same psychological disturbances were noted but were given different terms such as: “traumatic war neurosis, combat fatigue, battle stress, and gross stress reaction” (Andreasen, 2010, p. 67).

Alexandra Adler, started documenting what is now known as PTSD in the civilian population in the 1940’s and 1950’s. During this time two conceptual frameworks on stress started to be developed: ‘biological’ and ‘psychological’ schools of thought. One focusing on physical factors, and the latter focusing on individual psychopathology (Andreasen, 2010).

The first DSM was printed in 1952 with a diagnosis called “gross stress reaction,” which at the time was a result of ‘exceptional mental and physical stress.’ (Andreasen, 2010, p. 68) The first revision of the DSM came out in 1968 which omitted gross stress reaction, likely due to the lack of warfare at the time. This resulted in no diagnoses for stress disorders between 1968 and 1980 (Andreasen, 2010).

 

In the mid 1980’s the DSM task-force got back together to create the DSM IIV. The task force realized that there was a need for an official stress related diagnosis because of the Vietnam War, and the term post-traumatic stress disorder was introduced. The first diagnosis included three symptoms: re-experiencing, numbing of responsiveness, and cognitive or autonomic symptoms, with the onset being either acute or delayed. Since then, the diagnosis has been changed three separate times from the DSM IIV-R, DSM IV, and now in its current state with the DSM 5 (Andreasen, 2010).

References:

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders: DSM-5. Washington, D.C: American Psychiatric Association.

Amir, M., Kaplan, Z., & Kotler, M. (1996). Type of trauma, severity of posttraumatic stress disorder core symptoms, and associated features. The Journal of General Psychology, 123(4), 341-351.

Andreasen, N. C. (2010). Posttraumatic stress disorder: A history and a critique. Annals of the New York Academy of Sciences, 1208(1), 67.

Chen, Y., Hung, K., Tsai, J., Chu, H., Chung, M., Chen, S., Chou, K. (2014). Efficacy of eye-movement desensitization and reprocessing for patients with posttraumatic-stress disorder: A meta-analysis of randomized controlled trials. Plos One, 9(8), 1-17.

Chaudieu, I., Norton, J., Ritchie, K., Birmes, P., Vaiva, G., & Ancelin, M. (2011). Late-life health consequences of exposure to trauma in a general elderly population: The mediating role of reexperiencing posttraumatic symptoms. The Journal of Clinical Psychiatry, 72(7), 929.

Dr. Alan Hensley. (n.d.). Retrieved February 19, 2015, from https://therapists.psychologytoday.com/rms/prof_detail.php?profid=106734&sid=1424389978.4229_30893&city=Omaha&county=Douglas&state=NE&spec=19&tr=ResultsName&trow=8&ttot=262

Flouri, E. (2005). Post-traumatic stress disorder (PTSD): What we have learned and what we still have not found out. Journal of Interpersonal Violence: Concerned with the Study and Treatment of Victims and Perpetrators of Physical and Sexual Violence, 20(4), 373-379.

Leskin, G. A., Woodward, S. H., Young, H. E., & Sheikh, J. I. (2002-11-01). Effects of comorbid diagnoses on sleep disturbance in PTSD. Journal of Psychiatric Research,36(6), 449.

Lommen, M. J., J., & Restifo, K. (2009). Trauma and posttraumatic stress disorder (PTSD) in patients with schizophrenia or schizoaffective disorder. Community Mental Health Journal, 45(6), 485-96

Makinson, R. A., & Young, J. S. (2012). Cognitive behavioral therapy and the treatment of posttraumatic stress disorder: Where counseling and neuroscience meet. Journal of Counseling and Development: JCD, 90(2), 131-141.

Maxfield, L. (2009). EMDR milestones: The first 20 years. Journal of EMDR Practice Research, 3(4), 211-216.

Morris, M. C., Compas, B. E., & Garber, J. E. (2012). Relations among posttraumatic stress disorder, comorbid major depression, and HPA function: A systematic review and meta-analysis. Clinical Psychology Review, 32(4), 301.

Nebraska Post Traumatic Stress Disorder Treatment. (n.d.). Retrieved February 19, 2015, from http://dual-diagnosis-drug-rehab.com/post-traumatic-stress-ptsd-State.cfm?State=NE

Ozer, E. J., Best, S. R., Lipsey, T. L., & Weiss, D. S. (2003). Predictors of posttraumatic stress disorder and symptoms in adults: A meta-analysis. Psychological Bulletin, 129(1), 52-73.

Qureshi, S. U., Long, M. E., Bradshaw, M. R., Pyne, J. M., Magruder, K. M., Kimbrell, T., Kunik, M. E. (2011). Does PTSD impair cognition beyond the effect of trauma? Journal of Neuopsychiatry, 23(1), 16-28.

Reynolds, M., Mezey, G. C., Chapman, M., Wheeler, M., Drummond, D. C., & Baldacchino, A. (2005-03-01). Co-morbid post-traumatic stress disorder in a substance misusing clinical population. Drug and Alcohol Dependence, 77(3), 251-258.

Shapiro, F. (2007). EMDR, adaptive information processing, and case conceptualization. Journal of EMDR Practice and Research, 1(2), 68-84.

Tarrier, N., & Gregg, L. (2004). Suicide risk in civilian PTSD patients: Predictors of suicidal ideation, planning and attempts. Social Psychiatry Psychiatric Epidemiology, 39(8), 655.

 

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