Posttraumatic Stress Disorders: Psychological Assessment

NB: We do not resell your papers. Upon ordering, we do an original paper exclusively for you.

NB: All your data is kept safe from the public.

Table of Contents

Introduction
Description/Definition of PTSD
Historical Framework of PTSD
Conclusion
References

Introduction

Exposure to traumatic experiences, such as calamities, road crashes, physical attacks, etc., often predisposes victims to distress and anxiety in their aftermath. These symptoms often wane away over time. However, in some cases, the symptoms intensify, leading to posttraumatic stress disorder (PTSD) (Rytwinski, Scur, Feeny, & Youngstrom, 2013). The disorder manifests through flashbacks, nightmarish dreams, alertness, and avoidance symptoms, depending on trauma severity. Related comorbidities, including depression and substance abuse, often affect the at-risk groups, i.e., soldiers and refugees, among others (Bryant et al., 2008). The recommended therapies for PTSD include psychological interventions with limited drug use. In this paper, the description/definition, historical framework, and explanation of the issues associated with PTSD are reported. Scholarly research on PTSD, including evidence for its comorbidities, is presented.

Description/Definition of PTSD

PTSD constitutes a response to an experienced or witnessed traumatic event that posed a threat to the physical wellbeing of an individual or others. In addition, the initial response must be accompanied by severe fright, despair, or horror. The onset of PTSD symptoms occurs within weeks after exposure. However, according to Bryant et al. (2008), the 10^th edition of the International Statistical Classification of Diseases and Related Health Problems caps the onset of PTSD symptoms at six months. Nevertheless, delayed onset has been reported, which explains the low number of people presenting themselves for treatment.

PTSD was adopted by experts in the third revision of the Diagnostic and Statistical Manual for Mental Disorders (DSM-III) to replace terms like “shell shock, nervous shock, and combat fatigue” that described the response to traumatic events (Bryant et al., 2008, p. 659). In the DSM-III, it was defined as a stress disorder resulting from exposure to trauma in war and related events (Bryant et al., 2008). The victims develop intense fear for their safety or that of family/friends. The DSM-IV identifies three categories of PTSD symptoms. The first category comprises re-experiencing symptoms, including regular flashbacks or dreams of the traumatic scenes. The second cluster contains avoidance and numbing symptoms. In this case, the individual displays avoidance behaviors with regard to thoughts or reminders of the traumatic event show disinterest in activities, and appears detached from his/her social world. The third cluster encompasses hyperarousal symptoms. The individual may experience insomnia, irritability, and hyper-alertness due to the trauma.

PTSD diagnosis is made when the aforementioned symptoms persist for four weeks, causing impairment in occupational and psychosocial functioning. The diagnostic assessment of this condition involves the PTSD Checklist (PCL), which is a “self-reported measure” for evaluating the DSM-IV symptoms (Hinton & Lewis-Fernandez, 2011, p. 785). Besides serving as an assessment tool, the PLC is also useful in screening PTSD cases and monitoring symptom changes for individuals receiving treatment. A positive PTSD screen is not a confirmation of the condition; rather, it shows that the severity of the self-reported symptoms calls for further evaluation. A traumatic event may include things like natural calamities, road crashes, rape/sexual assault, or witnessing a homicide/suicide. The aftermath of such experiences is characterized by persistent distress and fear that are symptomatic of PTSD.

Historical Framework of PTSD

History of PTSD Diagnosis

The American Psychiatric Association (APA) first included PTSD in its 1980 DSM-III disease clusters (Hinton & Lewis-Fernandez, 2011). Because of the APA’s nosological classification, it was understood that the disorder had an external etiological agent (exposure to traumatic scenes) and was not symptomatic of psychoneurosis. From a historical perspective, the concept of ‘trauma’ was central to comprehending the causative factors and clinical manifestations of PTSD.

In the first DSM-III release, trauma was conceived as a calamitous stressor with an external locus, i.e., not attributable to inherent factors. The authors of the initial PTSD diagnosis were thinking of things like war, sexual assault, torture, and the Holocaust that produced “nervous shock and combat fatigue” in victims (Hinton & Lewis-Fernandez, 2011, p. 786). Other traumatic events that formed the basis for early PTSD diagnosis include the atomic bombs, natural calamities, e.g., severe quakes and cyclones, and man-made disasters like air/train crashes. Therefore, traumatic events were thought to be different from ‘ordinary’ stressors such as debilitating conditions, poverty, social rejection, or heartbreaks.

Logically, negative responses to such stressors would be considered as “adjustment disorders”, not PTSD based on the DSM-III criteria (Rytwinski et al., 2013, p. 301). The duality could be explained by the dominant view that persons with the ability to cope with common stressors would normally crumble when exposed to a traumatic stressor. The uniqueness of PTSD lies in etiology, i.e., responses to an external traumatic stressor. In most cases, meeting the “stressor criterion” is a necessity for PTSD diagnosis (Rytwinski et al., 2013, p. 303). This means that the individual must have prior exposure to a ‘traumatic’ event to be diagnosed with PTSD symptoms. However, research on PTSD diagnosis indicates that the ability to cope with stress differs between persons based on the victim’s socio-demographic profile. This shows that exposure to traumatic events does not always lead to full-blown PTSD.

The aberrant cases that do not conform to the historical formulation of PTSD diagnosis have led to the view that trauma is not entirely an exterior experience. Just like pain, a traumatic event is evaluated as a potential threat by the individual’s “cognitive and emotional processes” (Rytwinski et al., 2013, p. 305). Therefore, because the cognitive/emotional processes differ between individuals, people have different capacities to cope with traumatic stressors. Vulnerable individuals would manifest the DSM-III clinical symptoms, leading to a positive diagnosis. Although the coping capacity differs between individuals, it is recognized that exposure to certain stressors like rape, homicide/suicide, and torture would predispose all people to PTSD.

Revisions to DSM-III Criteria

The 1980 DSM-III formulation for PTSD diagnosis has been reviewed three times to capture symptom duration and severity. The revisions include the “DSM-III-R, DSM-IV, and DSM-IV-TR” made in 1987, 1994, and 2000 (Bryant et al., 2008, p. 663). The key finding in the later revisions was that PTSD is a widespread condition. Its prevalence rate ranges between 3.5% and 9.65% in the U.S. male and female respectively (Bryant et al., 2008). The PTSD prevalence rate is even higher in regions recovering from war or calamities.

The second DSM revision, i.e., DSM-IV criteria, captured the historical exposures to trauma as the first indicator. It also included the symptoms from each of the aforementioned categories, i.e., disturbing flashbacks, avoidance symptoms, and hyper-alertness. The fifth element of the DSM-IV criteria was symptom duration, i.e., how long the symptoms have persisted. The sixth element considered in the criteria was whether the symptoms led to anxiety disorders or functional dysfunction.

DSM-V is the latest version of the diagnostic criteria released in 2013. It contains a range of evidence-based approaches to PTSD diagnosis that are lacking in the earlier editions. According to Friedman, Resick, Bryant, and Brewin (2011), unlike in DSM-III and DSM-IV where PTSD is considered an anxiety-related disorder, in the DSM-V, the definition is extended to include “anhedonic or dysphoric presentations” (p. 753). These generalized feelings of distress are characterized by “mood states and disruptive behavioral symptoms” such as anger, impulsiveness, and self-destructive behavior (Friedman et al., 2011, 756). Therefore, due to the evidence-based revisions in DSM-V, PTSD was excluded from the list of anxiety disorders. The condition presently belongs to the trauma- and stressor-related disorders that involve a pre-exposure to trauma.

Issues Associated with PTSD

A number of questions surround the PTSD etiology and diagnosis. There are questions about the definition of the stressors, the progression of the untreated syndrome (i.e., clinical effects due to recurrent trauma), the cultural context of DSM-V, and effective therapeutic approaches

The Stressor Criterion

As aforementioned, the stressor criterion or ‘A’ cluster is the yardstick for determining the threshold for trauma exposure. The criterion defines direct exposure to scenarios considered traumatic, e.g., catastrophes. Indirect exposure may result from viewing gruesome events in the electronic media, e.g., the 9/11 attack. However, the latter is not considered traumatic in the DSM-V diagnosis. In contrast, recurrent indirect exposure to grim scenes is thought to be traumatic.

The B-E symptom clusters cover different aspects of PTSD diagnosis. Intrusive recollections that are experienced as vivid reenactments or mental imagery fall under the ‘B’ cluster, while avoidance responses, including agoraphobia, represent the ‘C’ cluster symptoms (Bryant et al., 2008). Negative cognitions or mood alterations characterized by detachment feelings are classified in the ‘D’ cluster. In contrast, the ‘E’ criterion contains symptoms such as angry outbursts and risky behaviors. Other criteria included in DSM-V diagnosis are the illness duration, impact on social/occupational functioning, and exclusion criteria – disproving substance abuse as the cause.

Exposure to Recurrent Trauma

Elhers and Clarke (2000) contend that the PTSD diagnostic criteria, as currently formulated, are less robust in identifying symptoms in individuals exposed to recurrent or prolonged trauma-related experiences such as unnatural torture. For this reason, she suggests different diagnostic criteria for ‘complex PTSD that manifests as “excessive somatization, dissociation, and pathological changes in identity and relationships” (Elhers & Clarke, 2000, p. 322). These alternative criteria resonate with arguments from clinicians working with victims exposed to prolonged trauma. However, there a paucity of research evidence for a ‘complex PTSD’ diagnosis in this group. Therefore, this syndrome is not considered a PTSD subtype in the DSM-V diagnosis. The disorder that manifests similar symptoms as that of the ‘complex PTSD’ is the dissociative subtype.

Cultural Context of DSM-V

The present DSM-V diagnostic criteria have attracted criticisms for being centered on Western cultures, an issue that makes them less effective in non-Western contexts. Friedman et al. (2011) argue that the DSM-V cannot give a valid diagnosis for PTSD in war refugees from non-Western countries. The reason for this bottleneck is that the tool has been applied to diagnose traumatized clients from Western cultures. Therefore, the same diagnosis may not give a correct clinical picture when used in other contexts or societies given the cross-cultural variations in people’s responses to trauma. In this view, meeting the diagnostic criteria does not always mean a positive PTSD diagnosis for non-Western trauma survivors.

Effective Therapeutic Approaches

The clinical efficacy of treatments for PTSD differs, resulting in the simultaneous use of multiple interventions. Further, controversy exists over the most effective rapid intervention for mass survivors in the aftermath of trauma. The available interventions show variable levels of efficacy. The approaches that yield a significant success include cognitive-behavioral therapy (CBT) used with antidepressants. The CBT interventions, such as CPT, have been shown to be highly effective, especially when applied to war veterans and women sexual assault survivors (Raskind et al., 2013). Other interventions with variable levels of efficacy include Stress Inoculation therapy and FDA-approved drugs such as Sertraline and prazosin.

Research on PTSD

Since the 1980s, research on PTSD has focused on developing robust tools for PTSD assessment/diagnosis, related neurobiological disorders, disease progression, and comorbidities.

PTSD Assessment

Researchers have sought to develop effective psychometric assessment tools for PTSD diagnosis in war veterans. Keane, Wolfe, and Taylor (1987) were the first researchers to formulate psychometric evaluation protocols for evaluating PTSD symptoms in Vietnam War survivors. The instruments proved to be highly reliable and effective. Adaptations of the evaluation instruments have been applied in assessing PTSD in victims of rape and natural calamities as well as in epidemiological studies.

Neurobiological Research

Scholarly evidence indicates that PTSD is linked to neurobiological or CNS abnormalities. According to Resick, Nishith, and Griffin (2003), the psychophysiological symptoms of the syndrome that have a neurobiological basis include “hyper-arousal of the sympathetic nervous system, startle eyeblink reflex, and insomnia” (p. 346). Further, certain neuroendocrine malfunctions related to coping mechanisms are associated with PTSD. A good example is a hypothalamic-pituitary-adrenocortical system that influences adaptation to drastic stimuli changes. Other related neurobiological alterations include elevated amygdala activity and suppressed hippocampus activity (Resick et al., 2003).

Longitudinal Manifestation

Longitudinal studies have shown that persistent PTSD can progress to a full-blown psychiatric problem if not treated. The course of severe PTSD is characterized by relapses. There is a delayed onset type of the syndrome, whereby the individual does not develop any of the symptoms in the aftermath of exposure to trauma (Friedman et al., 2011). The individual begins to show PTSD symptoms six months to one year after exposure. Nevertheless, the manifestation of some of the symptoms may be prompted at any time by repeated exposure to the trauma scenes.

PTSD Comorbidities

A positive PTSD diagnosis based on the DSM-V criteria signifies the possibility of multiple comorbid diagnoses. According to De Jong et al. (2001), the co-occurring conditions include dysthymic depression, drug/alcohol abuse, and anxiety disorders, among others. The high rate of comorbidity points to the frail nature of the DSM-V criteria in PTSD diagnosis. It shows that a positive diagnosis can result from any of the comorbid conditions, as the technique is not fully exclusionary. Further, comorbid disorders affect the efficacy of interventions. It requires a clinician to use interventions for PTSD and comorbid conditions at the same time to achieve success.

Additional Information

A number of diagnosable PTSD subtypes exist. In the latest edition of DSM-V, the syndrome was placed in a new cluster – the trauma and stressor-related disorder. There are two PTSD subtypes that have been identified, namely, the dissociative and preschool types. The former is diagnosed in people who meet the DSM-V criteria and show severe depersonalization, while the latter occurs in children aged below six years (De Jong et al., 2001, 556). Unlike the dissociative type, the preschool one does not meet the DSM-V criteria for PTSD diagnosis.

Conclusion

PTSD is a multifactorial stress disorder that results from exposure to trauma. The DMS-V criteria identify three major symptom clusters that define a positive PTSD diagnosis. The symptoms cause severe social and emotional impairment. Effective therapies differ depending on the socio-demographic profiles of the victims. However, CBT coupled with medications (antidepressants) is fronted as an effective intervention for PTSD symptom management.

References

Bryant, R., Mastrodomenico, J., Felmingham, L., Hopwood, S., Kenny, L., Kandris,

E.,…Creamer, M. (2008). Treatment of acute stress disorder: A randomized controlled trial. Archives of General Psychiatry, 65, 659-667.

De Jong, J., Komproe, M., Ivan, H., von Ommeren, M., El Masri, M., Araya, M.,…Somasundarem, D. (2001). Lifetime events and posttraumatic stress disorder in 4 post-conflict settings. Journal of the American Medical Association, 286, 555-562.

Elhers, A., & Clarke, M. (2000). A cognitive model of posttraumatic stress disorder. Behaviour Research and Therapy, 38, 319–345.

Friedman, M., Resick, P., Bryant, R., & Brewin, C. (2011). Considering PTSD for DSM-5. Depression and Anxiety, 28, 750-769.

Hinton, E., & Lewis-Fernandez, R. (2011). The cross-cultural validity of posttraumatic stress disorder: Implications for DSM-5. Depression and Anxiety, 28, 783-801.

Keane, M., Wolfe, J., & Taylor, K. (1987). Post-traumatic stress disorder: Evidence for diagnostic validity and methods of psychological assessment. Journal of Clinical Psychology, 43, 32-43.

Raskind, M., Peterson, K., Williams, T., Hoff, D., Hart, K., Holmes, H.,…Peskind, E. (2013). A trail of prazosin for combat trauma PTSD with nightmares in active-duty soldiers returned from Iraq and Afghanistan. American Journal of Psychiatry, 6(1), 113-122.

Resick, P., Nishith, P., & Griffin, M. (2003). How well does cognitive-behavioral therapy treat symptoms of complex PTSD? An examination of child sexual abuse survivors within a clinical trial. CNS Spectrums, 8, 340-355.

Rytwinski, N., Scur, M., Feeny, N., & Youngstrom, E. (2013). The co-occurrence of major depressive disorder among individuals with posttraumatic stress disorder: A meta-analysis. Journal of Traumatic Stress, 26, 299–309.

Click Here To Order Now!