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Posttraumatic Stress Disorder in Combat Veterans


Over the past three centuries mental outcomes war-related syndromes had various names as shell shock, combat neurosis, combat fatigue, mental conflict, or mechanical impact exhaustion (Shalev and others, 1996). Each name represented a theoretical outlook to the cause of mental trauma (Shalev and others, 1996). The diagnosis of posttraumatic stress disorder describing war related psychological disorders appeared in 1980. This was a turning point, beginning to recognize posttraumatic stress disorders (PTSD) occurring because of long-term reaction to war environment exposure. Stress states resulting from shorter periods of exposure are called combat stress reaction (Friedman and others, 1994). Margoob and others (2004) suggested the study of Charcot in 1890s, was the first study to correlate trauma to psychological symptoms. Charcot suggested that those diagnosed as hysterical patients had the cause of their troubles in their histories. Further, Charcot classified the disorders according to the cause of stress to rape related stress, combat related stress and so forth. The interest in posttraumatic stress disorders has increased over the past 25 years and advances have been made in understanding the nature of the disorder, assessment and treatment (Margoob and others 2004). The aim of this essay is to review briefly yet, comprehensively the recent advances in assessment and treatment of PTSD.

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Understanding the condition

Current wars are characterized by an environment of ambiguity, bewilderment, and the always felt possibility of injury and death if not for the military oneself witnessed in one of the colleagues. This environment often results in a mental distress or a mental disorder for soldiers, the extent of which depends on the type and severity of exposure to trauma, and the time passed from the time of exposure. On individual level, it varies from person to person (Reeves, 2007). PTSD has a tendency to occur in three chronological phases: The immediate phase (during or immediately after exposure) patients display fears, anxiety, confusion, disbelief, substance abuse, unexplained numbness, and adjustment disorder. The second delayed phase (up to two weeks after exposure) is characterized by apathy, grief, social withdrawal, and disturbing thoughts. The third chronic phase (months to years after exposure) is characterized by feeling disappointed, anger, bitterness, sadness, and unrelenting disturbing symptoms. The term PTSD defines cases where the pathological response to trauma persists for more than four weeks (Reeves, 2007).

Epidemiology of PTSD: volume of the problem

Boscarino (2004) analyzed the studies on PTSD and physical disorders and inferred that in the US nearly 5% of men and 10% of women under 55 years have suffered posttraumatic stress disorder (PTSD). Among Vietnam veterans, rates of postwar adjustment and mental health disorders were higher and 25% of PTSD positive veterans reported clinically diagnosed cardiovascular diseases at up to 20 years after service. Kashdan and others (2006) suggested that veterans meeting the criteria of PTSD diagnosis range from 15% to 72%. Reeves (2007) showed that in a survey conducted on 11400 veterans after the first Persian Gulf War (1991) 10% of returning veterans displayed symptoms of PTSD. In 2004, the US Army study showed that more than 3600 veterans returning from Iraq and Afghanistan. That is 9.3% of those served in the two countries, and 17.1% of those who were stationed in Iraq met the screening criteria of PTSD (after Reeves, 2007).

Possible biological mechanisms for the disorder

Boscarino (2004) suggested there is enough evidence in the literature to stand for that severe environmental stressors and subsequent development of PTSD can be correlated to altered neuro endocrine and immune system functions. Because of the decreased cortisol levels often found among PTSD victims, Boscarino (2004) suggested that lowered levels of glucocorticoids may cause elevations in leukocyte and other immune inflammatory activities. Bosacrino (2004) also suggested that besides cytokine-mediated activation of adrenal control, there are cytokine-independent cell-mediated immune-adrenal interactions and that this immune- endocrine side pathology track is responsible for adrenal dysfunction and disease. The physiologic processes involved with the stress-disease pathogenic process are complex; however the hypothalamic-Pituitary-adrenal (HPA) axis in concert with the sympathetic adrenal medulla (SAM) axis are always pointed at in PTSD pathogenesis (Boscarino, 2004). Boscarino (2004) found enough evidence to suggest that physiologic provocation often viewed during recollection of traumatic events by PTSD veterans is associated with alterations in the neuro endocrine functions resulting from changes in the SAM and HPA systems. These neuro endocrine changes point toward the outcomes of an intense status of physio-psychological adjustment (conditioning response) that occurs after exposure to severe stress. Further, this conditioning response starts in the central nervous system; next it is fulfilled by many endocrine mechanisms that have various effects on both the body’s biological systems and nervous system.

Genetics of PTSD

From genetic research stand point, PTSD is a complex polygenetic disorder and there is likely no identified PTSD gene. Alternatively, there are many possible different genes, each of which has an interchangeable and additive role to the inherited likelihood for PTSD, in a probability mode. The published studies highlight that possible genes are involved in the dopaminergic system; however, there are conflicts between studies thus, it is difficult to draw conclusions (Koenen, 2003).

Behavioral and cognitive factors in PTSD

Interpretation of PTSD observation at a behavioral concept and generalization depends on the two factors theory suggested by Mowrer in 1960 (after Herman, J., 1997). These two factors are linking the emotion experienced during a traumatic event to sights, sounds, or other sensations. The second factor is avoidance that is signals (cues) reminding the individual with the traumatic event stir up the psychological disturbances, so the patient tries to avoid these cues (Herman, J. 1997). The range of signals or cues increases over time because of generalization (similar cues to the original one stir up emotional disturbances). High order conditioning (where an originally neutral cue stirs up anxiety) also increases the range of cues (Herman, J. 1997). Behavioral interpretation explains reexperiencing of anxiety and symptoms of avoidance seen in PTSD cases. However it fails to explain the recurring flutter between reexperiencing and avoidance and the changing sense of meaning. Therefore, a cognitive model (fear structure) is suggested to explain these phenomena, it consists of: 1- visual, audible, and other senses stimuli accompanied the trauma. 2- The physiological, and emotional responses to the trauma, and 3- the meaning associated with both 1, and 2 (McNally and others, 2003).

Diagnosis and assessment of PTSD

The first question to ask is what qualifies a combat traumatic event to be a stressor. The response to the following questions should provide the answer: 1- Did the veteran suffer a severe (or a life threatening) injury resulting from a traumatic event. 2- Did the veteran suffer an injury that would affect future employment, 3- did the veteran witness a death or a severe injury in combat. 4- Did the veteran have a true fear that life was in danger despite the absence of a traumatic injury, and 5- did the veteran suffer an abuse to his or her person (Kaplan consulting and counseling, 2006).

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The second question to ask should be what are the criteria for diagnosis? According to Kaplan consulting and counseling (2006), criteria for diagnosis are: 1- Criteria A (gateway criteria, all required). These are: a- The veteran has witnessed a trauma that caused or threatened a serious injury, death, or personal abuse. b- The traumatic event should have caused great fear, horror, or deep feeling of helplessness. 2- Criteria B (reexperiencing symptoms, at least one of the following should be present). a-recurring disturbing interfering recalling of the event. b- Nightmares involving the traumatic incident, c- experience as if living the incident once again. d- Fear, anxiety on exposure to similar conditions of the trauma cues, and f- increased symptoms of arousal on exposure to similar cues. 3- Criteria C (symptoms of avoidance, at least three of the following should be present): a- efforts to avoid cues, feelings, people, or places associated with the trauma. b- gaps in remembering the time order of the traumatic events, c- reduced interest in previously enjoyable activities. d- Feelings of being detached or being strange from others, e- feeling that the course of life will be short or changed. f- Emotional freezing, with the affected veteran appears emotionally cold and unresponsive. 4- Criteria D (hyperarousal manifestations, at least three should be present): a- sleep disturbances, b- outbreaks of anger, c- difficult to focus, d-being constantly on guard, and e- abnormally increased alarming frightened response to unexpected stimuli (noises, flashes of light…etc). To diagnose PTSD, the duration of symptoms should be at least 1 month (Kaplan consulting and counseling, 2006).

Watson, and others (2008) prepared the best practices manual for posttraumatic stress disorder (PTSD) compensation and pension examinations. The assessment protocol in this manual included two instruments for assessment, namely, the trauma exposure assessment protocol, and assessment of PTSD. The objective of the trauma exposure assessment tool is to document whether the veteran was exposed to a traumatic event, during military service, severe enough to meet the DSM-IV (Diagnostic and Statistical Manual for Mental Disorders-IV) stressor criterion. The DSM-IV stressor criterion is the gateway criterion (Criteria A) mentioned previously. Watson and others (2008) suggested the following guidelines for interview assessment of trauma exposure: 1- To familiarize the veteran to the trauma assessment, as it may help to alert the veteran that although brief, trauma assessment interview may cause some distress. It is important also to inform the veteran that trauma assessment interview is a mutual collaborative process and unnecessarily detailed answers are not needed. 2- Documentation of trauma related information including a tale description of the traumatic episode. Such description should include features of the event; date and place, names of witnessed other individuals, what healthcare facilities provided treatment, what decorations or medal received, and the veteran’s view of supposed results and subjective emotional reaction and behavioral response. Watson and other suggested the following protocol for assessment of PTSD. The PTSD assessment protocol has four objectives, first is to establish or deny the diagnosis of PTSD. In this pursuit, various methods can be used as questionnaires, interviews. Many clinicians recommend the Minnesota multiphasic personality inventory (MMPI) as a helpful tool. In addition, the infrequency psychopathology scale is a useful validity measure. Establishing the diagnosis may need some biological measure as heart rate, measuring blood pressure, measuring skin conductance, EKG, and measuring muscle tension. The second step in assessment is to determine the symptoms’ severity, next is to establish the logical relationship between trauma and resulting symptoms. Finally is to describe how PTSD symptoms change social, occupational performance and quality of life of the veteran.

Treatment of PTSD

The Institute of Medicine (IOM) Committee on treatment of PTSD (2007) conducted a systematic review of the relevant published literature on treatment of PTSD (a total of 2771 studies). The Committee suggested there are two classes for treatment of PTSD. First are pharmacotherapy protocols, and second are psychotherapy protocols. Pharmacotherapy modalities include alpha-adrenergic blockers, anticonvulsants, antipsychotic medications as olanzapine and risperidone. Medications acting on brain chemical transmitters as serotonin reuptake inhibitors and monoamine oxidase inhibitors (MAOIs) were also used. However, the committee inferred there is lacking evidence as to the efficacy of treatment using the following pharmacotherapy modalities: alpha adrenergic blockers, anticonvulsants, new antipsychotics, benzodiazepines, MAOIs, and serotonin reuptake inhibitors. Psychotherapy treatment included many modalities as cognitive behavioral therapy, cognitive restructuring, coping skills training, eye movement desensitization and reprocessing therapy, and group format therapy. The committee found enough evidence to infer the efficacy of exposure therapy, while evidence is not enough for cognitive restructuring, coping skills training, eye movement desensitization and reprocessing, and group format therapy.


Exposure to trauma during combat targets veterans’ memory of the trauma as they rethink to understand what happened during the time of trauma. This results in a stress disorder that includes sleep disorders, anxiety and unproportional anger, anxiety, and a sense of being on guard. The main characteristics of PSTD are reexperiencing the trauma on exposure to similar cues, and avoidance of similar situations, places or people who bring up the trauma memory. The magnitude of the problem varies from one person to another, and according to the magnitude of trauma. Assessment is not only important for the veteran’s physical and psychological health, but also important for estimating suitable compensation and pension. Treatment of the disorder can be pharmacological or psychotherapy, however in either cases, there are lacking evidence as to the benefits of either modality.


Boscarino, J. A. (2004). Posttraumatic Stress Disorder and Physical Illness Results from Clinical and Epidemiologic Studies. Ann. N.Y. Acad. Sci., 1032, 141-153.

Friedman, M. J., Schnurr, P. P., and Coyle, M. A. (1994). Post-Traumatic Stress Disorder In The Military Veteran. Psychiatric Clinic Of North America, 17 (2), 265-277.

Herman, J. (1997). Trauma and Recovery: The Aftermath of Violence from Domestic Abuse to Political terror. New York: Basic Books.

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Institute of Medicine (IOM). (2007). Treatment of Posttraumatic Stress Disorder: An Assessment of the Evidence. Washington, D.C.: The National Academies Press.

Kaplan Consulting and Counseling. (2006). Insights on Trauma and PTSD, volume 1, issue 3. Cleveland.

Kashdan, T. B., Julian, T., Merritt, K., and Uswatte, G. (2006). Social anxiety and posttraumatic stress in combat veterans: Relations to well-being and character strengths. Behaviour research and Therapy, 44, 561-583.

Koenen, K., C. (2003). A Brief Introduction to Genetic research in PTSD. PTSD Research Quarterly, from The National Center for Post-Traumatic Stress Disorder, 14 (3), 1-8.

Margoob, M., A., Wani, Z. A., Murtaza, I., Hussein, A., Majid, A., Khan, A., Y., and Shafie, M. (2004). Post Traumatic Stress Disorder: An Overview. JK-Practitioner, 11 (2), 88-94.

McNally, R. J., Bryant, R. A., and Ehlers, A. (2003). Does Early Psychological Intervention Promote Recovery From Posttraumatic Stress? Psychological Science In The Public Interest, 4 (2), 49-53.

Reeves, R. R. (2007). Diagnosis and Management of Posttraumatic Stress Disorder. JAOA, 107 (5), 181-189.

Shalev, A., Y., Bonne, O., and Eth, S. (1996). Treatment of Posttraumatic Stress Disorder. A Review. Psychosomatic Medicine, 58, 165-182.

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Watson, P. et al: US Department of Veterans Affairs. (2008). Best Practice Manual for Posttraumatic Stress Disorder (PTSD) Compensation and Pension Examination. Washington, D.C.: National government publications.

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