Posttraumatic Stress Disorder: Making the Diagnosis

Hani Raoul Khouzam, MD, MPH, FAPA

Ohio State University

Hani Raoul Khouzam, MBBCh, MPH, is the staff psychiatrist at VA Central California Health Care System in Fresno, Calif. He is a health science clinical professor of psychiatry at the University of California, San Francisco and at the Fresno Medical Education Program. He is a consultant psychiatrist in the several counties in New Zealand.

 

 

ABSTRACT: Posttraumatic stress disorder (PTSD) is an anxiety disorder that can develop after a traumatic event is witnessed or experienced. It commonly involves actual or threatened death, serious injury, or threat to a person’s physical integrity, combined with feelings of intense fear, helplessness, or horror. Traumatic events that may cause PTSD include violent personal assaults, natural or man-made disasters, (i.e., terrorist attacks, motor vehicle accidents, rape, physical and sexual abuse, and other crimes), or military combat. Patients with PTSD continue to exhibit symptoms of anxiety, hypervigilance, sleep difficulties, anger, and irritability, in addition to psychological numbness and interpersonal, social, educational, and vocational dysfunctions. They also remember and often relive the traumatic events. The purpose of this article is to introduce primary care clinicians to the history, epidemiology, biological causes, and psychosocial complications of PTSD to review the diagnostic evaluation and the biopsychosocial and spiritual interventions that have been used in treatment. 


Although it was not given a formal name, the psychiatric diagnosis that is now known as posttraumatic stress disorder (PTSD) has been recognized through the centuries by several other monikers including shell shock, battle fatigue, soldier heart, accident neurosis, as well as concentration camp or post-rape syndrome. Exposure to traumatic events has been a part of the human condition since the creation of Adam and Eve1 and symptoms of PTSD have been documented in the lives of heroes and heroines throughout history and literature—examples include Trojan War characters Agamemnon and Achilles in the Odyssey, and Shakespeare's Henry IV and Lady Macbeth.2 

Researchers and clinicians first got involved in studying the plight and sufferings of Vietnam War veterans and set their goal to create a single diagnostic entity to include multiple psychiatric symptoms. As a result, PTSD was formally recognized as a diagnosis in the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), published in 1980.3 

PTSD was originally only referenced as a consequence to a catastrophic traumatic event that was considered outside the range of usual human experience—such as war, torture, rape, manmade disasters (i.e., the Holocaust, the atomic bombings of Hiroshima and Nagasaki, the 9/11 terrorist attacks on the World Trade Center), natural disasters (i.e., earthquakes, hurricanes, flooding and volcano eruptions), and everyday incidents (i.e., factory explosions, airplane crashes and automobile accidents).4 

Over time, the PTSD diagnosis has been revised (Table 1) to include exposure to trauma as a necessary element.The Diagnostic and Statistical Manual of Mental Disorders (DSM-5), published in May of 2013, reclassified PTSD from an anxiety disorder into a new class of "trauma and stressor-related disorders."5As such, a diagnosis of PTSD now requires exposure to a traumatic or stressful event—a decision made based on the clinical recognition of variable expressions of distress as a result of traumatic experience. 

DSMIVTR PTSD

EPIDEMIOLOGY

The lifetime prevalence of PTSD among adults in the US is estimated to be 6.8%.6,7 Furthermore, the lifetime prevalence in men is 3.6% vs. 9.7% in women; the 12-month prevalence is 1.8% in men vs. 5.2% in women.8 The 6-month prevalence of PTSD is estimated to be 3.7% in boys vs. 6.3% in girls, and is associated with high rates of truancy, vandalism, alcohol use, and running away, especially if it occurs before the age of 15.8 

Looking at worldwide estimates, lifetime PTSD prevalence ranges from 0.3% in China to 6.1% in New Zealand.9 However, it is important to note that countries may use differing methodological approaches to collect their data and statistics.9 

The estimated lifetime prevalence of PTSD among Vietnam War veterans was calculated at 30.9% for men vs. 26.9% for women.10 PTSD is estimated in 10.1% of Gulf War veterans.11 Among Operation Enduring Freedom in Afghanistan and Operation Iraqi Freedom veterans, PTSD prevalence is 13.8%.12 

It is estimated that 80% of patient with PTSD will have co-occurring medical and/or psychiatric disorder.13,14 PTSD is more common among individuals with low socioeconomic status and, particularly in those living in areas in which violence is endemic.9,15 PTSD is more common in women than in men,8,15 and affects people of all ages (younger and elderly persons are the most vulnerable).13-15 Adults who are exposed to psychological trauma are at the highest risk to develop PTSD.15 

CAUSES OF PTSD

PTSD is caused by experiencing, witnessing, or being confronted with an event that involves serious injury, death, or threat to the physical integrity of an individual, along with an emotional response of helplessness and/or intense fear or horror.5 The interaction between a person's biological vulnerability based on genetic (inherited) contributions, psychological characteristics, social or environmental factors, and the exposure to traumatic events could lead or prevent the development of PTSD.12-14 

Biological disturbances. The main biological disturbances in PTSD seems to result from a dysgulation in the naturally occurring stress hormones and an increased sensitivity in the brain anxiety circuits.16 In addition, patients with PTSD were found to have hypersensitivity of the hypothalamic-pituitary-adrenal axis (HPA)16,17 and have increased activation in the brain anatomical fear centers—the amygdala, hypothalamus, locus ceruleus, periaqueductal gray, and parabrachial nucleus.18 Another precursor to PTSD, kindling was first described in patients who experienced seizures, where a sub-threshold electrical or chemical brain stimulation eventually lead to a full-blown seizure and subsequent chronic stimulation led to spontaneous seizures.19 

Traumas that are followed by intrusive thoughts or the reliving of events might kindle the limbic nuclei, which leads to the manifestation of core PTSD symptoms—hypervigilance, avoidance, and increase startling reactions.20 It is still unknown whether these biological changes were present before the traumatic event and predisposed the person to develop PTSD or whether these changes were the result of the PTSD.15-17 

Personal and psychosocial factors. The interaction between various identified psychosocial and environmental factors with personal characteristics can increase an individual’s vulnerability to develop PTSD. These factors include:

• Characteristics of the trauma itself. The trauma’s proximity and severity, as well as the duration of an individual’s exposure to the trauma, should be considered. Examples of severe traumatic events that could lead to PTSD include terrifying violent attacks, war, assault, rape, torture, kidnapping, child abuse, serious accidents, and natural or man-made disasters (Table 2).2

• Characteristics of the individual. These include prior exposure to trauma, family history, childhood adverse events like parental separation and preexisting psychiatric conditions, especially substance abuse, anxiety, or depression.22 There is also evidence of gender specificity; combat exposure, childhood neglect, physical abuse, and molestation are commonly associated with PTSD in men, while women are at a greater risk for PTSD after violent traumatic events (i.e., rape, threat with a weapon, molestation, and physical abuse).22 Clinical observations have consistently shown a correlation between the development of PTSD in adults who were traumatized as children and an association between early trauma exposure and subsequent retraumatization.23The internal and external PTSD vulnerability characteristics are summarized in Table 3.24

• Posttraumatic factors. These include the early emergence of avoidance or numbing, hyperarousal, and re-experiencing symptoms. An accurate PTSD prognosis could significantly improve with the development of posttraumatic growth and resilience (Table 4). Religious and spiritual beliefs, hopefulness, optimistic attitudes, insight, taking initiative, humor, creativity, and independence have all shown to be important factors in enhancing resilience.25,26 The traumatic event is perceived as an opportunity to turn adversity into an opportunity to achieve higher life goals.24-26 

Table 2,3,4

COMPLICATIONS WITH PTSD

Significant disruption of relationships, high unemployment, divorce, and substance abuse are common complications that may result from irritability, isolation, anger, impulsive behaviors, and compromised coping skills.4,12 Patients with PTSD are also at increased risk for the presence of co-occurring psychiatric disorders—such as generalized anxiety disorder, major depressive disorder, panic disorder, panic attacks, agoraphobia, obsessive-compulsive disorder, social phobia, specific phobia, and somatization disorder.13 

Patients with PTSD and any of these disorders may be at a particularly high risk for suicide.12,13 In addition, PTSD patients who are victims of physical and or sexual assault are at high risk for developing mental health complications, homicide, and suicide.27 Studies have shown an association between PTSD and the risk of developing dementia among older US male veterans.28 PTSD has also been linked to an increased risk of cardiovascular disease.29

ASSESSMENT AND EVALUATION

Although the exception to the rule, some patients with PTSD may display altered behavior, agitation, and extreme startle reactions. They may be confused and disoriented. Memory lapse may be observed, though it could be trauma-specific or more widespread.30 Patients have been observed to have poor concentration, lack of impulse control, and altered speech.31 

Mood and affect may change depending on the type and timing of the questions; feelings of anxiety, guilt, and/or fear may be predominant even in the absence of depression. Thoughts and perception may also be altered despite the absence of florid psychosis. Patients may express suicidal or homicidal ideations without a specific plan to act on them, particularly around certain anniversary dates related to the traumatic events.30,31

PTSD diagnosis

To make a diagnosis, primary care providers first need to obtain the relevant history of traumatic stress exposure and posttraumatic stress symptoms to evaluate patients for other psychiatric disorders, including PTSD.4,13,30,31 The DSM-IV-TR diagnostic criteria (Table 5), and the corresponding mnemonic “TRAUMA” (Table 6), can both serve as guides.5 

In addition, there are several important associated features to evaluate: 

• Impaired affect modulation and/or self-destructive and impulsive behavior.

• Dissociative symptoms.

• Depression and/or feelings of ineffectiveness, shame, despair, and hopelessness.

• Obsession with being "permanently damaged," or under constant "threat." 

• Loss of religious and/or spiritual beliefs.

• Hostility, anger, and violence. 

• Personality change, social withdrawal and/or social impairment.

• Interpersonal problems or relationship conflicts. 

• Somatic and sexual dysfunction. 

• Survivor guilt and preoccupation with sins of omission and/or sins of commission.

• Addiction.

Finally, the Short Screening Scale (Table 7)32 can easily be administered in a primary care setting.

Trauma, PTSD

Differentials diagnosis. In the differential diagnosis of PTSD, it is important to consider acute stress disorder, dissociative disorders, depression, generalized anxiety, panic disorder, phobias, substance abuse, psychiatric manifestation of medical conditions, and malingering (Table 8).4 Primary care providers need to be keenly aware that PTSD commonly presents with the psychiatric conditions described in its differential diagnosis and to screen for signs of such co-occurring conditions during a patient’s initial evaluation.34

Physical examination. PTSD patients may have a disheveled appearance and poor personal hygiene. These patients may also present with physical injuries from recent traumatic events, such as bruises from physical abuse, injuries from assault, accidents, natural disasters, or terrorist attacks.35 The physical examination should focus on to alleviate the medical problems that may be causing the most significant distress symptoms, including insomnia, restlessness, fatigue, an exacerbation of medical problems that existed prior to the traumatic experience, and/or newly developed medical and neurological conditions. There is some evidence to indicate a relationship between PTSD and cardiovascular, gastrointestinal, musculoskeletal, and cognitive disorders.28,29 

PTSD diagnosis

After controlling for risk factors such as alcohol consumption, weight, current substance abuse, and smoking, many PTSD patients—especially those in the combat veterans population—have nonspecific ECG abnormalities, atrioventricular conduction defects, infarctions, hypertension, and early onset cognitive decline. 

Additional research is still needed to learn more about these associations before any general conclusion can be reached on the increased co-morbidity of the physical and medical conditions, and how these bodily system dysfunctionsmay be related to PTSD.13,35,36 

Laboratory testing. Although laboratory tests are not absolutely indicated for healthy individuals without physical injuries, it is important to consider screening patients with PTSD for thyroid abnormalities and substance abuse. Research studies have found decreased cortisol levels, elevated norepinephrine and epinephrine levels, and abnormal hypothalamic-pituitary-adrenal axis activity in patients with PTSD.36 Chronic insomnia and or ongoing daytime somnolence may warrant sleep study evaluation. 

Brain imaging. Although routine brain imaging is not recommended for the diagnosis of PTSD, the presence of prominent cognitive symptoms could warrant brain imaging.37 Computed tomography (CT) may identify traumatic brain injuries; magnetic resonance imaging (MRI) studies of some PTSD patients have shown a decreased hippocampus size and abnormal amygdale. Studies in monozygotic twins show an association between a small hippocampus and the predisposition for the development of PTSD. The suggested laboratory and other studies for PTSD evaluation are summarized in Table 9.13,35-37

PTSD laboratory

The comprehensive treatment of PTSD usually requires an integrated, multidimensional, interdisciplinary approach that combines patient education with pharmacological and psychological treatments and psychosocial and spiritual interventions. Treatment progress is often complicated by the presence of co-occurring psychiatric and medical conditions that need to be well managed. For example, if alcohol or substance abuse problems are present, they should be integrated in the overall treatment and management of patients. The September issue of Consultant will highlight treatment options for PTSD. ■

Acknowledgments:

The author thanks Dr Avak Howsepian for his constructive criticisms; Ms Susan E Shyshka, FACHE, for her administrative and leadership support, Dr Peter Watson for his encouragement; Dr Wessel Meyer for his clinical support; Dr Margaret Aimer for her supervision; Drs Robert Hierholzer, Nestor Manzano, Scott Ahles, and Craig C. Campbell for their academic guidance; and Dr Matthew Battista and Mr Leonard Williams, PA, for their encouragement.

References

1.Book of Genesis: Genesis 39-41. In: Holy Bible, New International Version, (NIV). Biblica, Inc.; 2011.

2.Trimble MD. Post-traumatic stress disorder: history of a concept. In Figley CR (ed). Trauma and its Wake: The Study and Treatment of Post-Traumatic Stress Disorder. New York: Brunner/Mazel; 1985. 

3.The American Psychiatric Association. Diagnostic and statistical manual of mental disorders (3rd ed). Washington, DC; 1980.

4.Khouzam HR, Tan DT, Gill SG. The patient with posttraumatic stress disorder. In: Handbook of Emergency Psychiatry. Philadelphia: Elsevier/Mosby;2007:453-473.

5.The American Psychiatric Association. Diagnostic and statistical manual of mental disorders (5th ed). Washington, DC; 2013. 

6.Kessler RC, Berglund P, Delmer O, et al. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005;62(6):593-602.

7.Kessler RC, Chiu WT, Demler O, et al. Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication.Arch Gen Psychiatry. 2005;62(6):617-627.

8.Kilpatrick DG, Ruggiero KJ, Acierno R, et al. Violence and risk of PTSD, major depression, substance abuse/dependence, and comorbidity: results from the National Survey of Adolescents. J Consult Clin Psychol. 2003;71(4):692-700.

9.Kessler RC, Üstün TB (eds). The WHO World Mental Health Surveys: global perspectives on the epidemiology of mental disorders. New York: Cambridge University Press:1-580.

10.Kulka RA, Schlenger WA, Fairbanks JA, et al. Trauma and the Vietnam War generation: Report of findings from the National Vietnam Veterans Readjustment Study. New York: Brunner/Mazel; 1990.

11.Smith-Osborne A. Mental health risk and social ecological variables associated with educational attainment for gulf war veterans: implications for veterans returning to civilian life. Am J Community Psychol. 2009;44(3-4):327-337.

12.Tanielian T, Jaycox L (eds). Invisible Wounds of War: Psychological and Cognitive Injuries, Their Consequences, and Services to Assist Recovery. Santa Monica, Calif: RAND Corporation; 2008.

13.Khouzam HR, Ghafoori B, Hierholzer R. Progress in the identification,diagnosis and treatment of posttraumatic stress disorder In: Corales TA (ed). Trends in Posttraumatic Stress Disorder Research. New York: Nova Science Publishers, Inc; 2005:1-28.

14.Álvarez MJ, Roura P, Foguet Q, et al. Posttraumatic stress disorder comorbidity and clinical implications in patients with severe mental illness. J Nerv Ment Dis. 2012;200(6):549-552.

15.Norris F, Sloane LB. The epidemiology of trauma and PTSD. In: Friedman MJ, Keane TM, Resick PA (eds). Handbook of PTSD: Science and Practice. New York: Guilford Press; 2007:78-98.

16.Yehuda R, Bierer LM. Transgenerational transmission of cortisol and PTSD risk. Prog Brain Res. 2008;167:121-35. 

17.Phillips ML, Drevets WC, Rauch SL, Lane R. Neurobiology of emotion perception I: The neural basis of normal emotion perception. Biol Psychiatry.2003;54:504-514.

18.Laurent V, Westbrook RF. Distinct contributions of the basolateral amygdala and the medial prefrontal cortex to learning and relearning extinction of context conditioned fear. Learn Mem. 2008;15(9):657-66.

19.Post RM, Weiss N, Smith MA. Sensitization and kindling: implications for the evolving neural substrates of posttraumatic stress disorder. In: Friedman MJ, Charney DS, Deutch AY (eds). Neurobiological and Clinical Consequences of Stress: From Normal Adaptation to PTSD. Philadelphia: Lippincott-Raven; 1995:203-224.

20.Liberzon I, Britton JC, Phan KL. Neural correlates of traumatic recall in posttraumatic stress disorder. Stress. 2003;6:151-156.

21.Wolff N, Frueh BC, Shi J, et al. Trauma exposure and mental health characteristics of incarcerated females self-referred to specialty PTSD treatment.Psychiatr Serv. 2011;62(8):954-958.

22.Karunakara UK, Neuner F, Schauer M, et al. Traumatic events and symptoms of post-traumatic stress disorder amongst Sudanese nationals, refugees and Ugandans in the West Nile. Afr Health Sci. 2004;4(2):83-93.

23.Barlow J, Birch L. Midwifery practice and sexual abuse. Br J Midwifery. 2004;12(2):72-75.

24.Ahmed AS. Post-traumatic stress disorder, resilience and vulnerability. Adv Psychiatry Treat. 2007;13:369-375.

25.Bonanno GA. Loss, trauma, and human resilience: have we underestimated the human capacity to thrive after extremely aversive events? Am Psychol.2004;59(1):20-28. 

26.Charney DS. Psychobiological mechanisms of resilience and vulnerability: implications for successful adaptation to extreme stress. Am Psychiatry. 2004;161(2):195-216.

27.Nakajima S, Masaya I, Akemi S, Takako K. Complicated grief in those bereaved by violent death: the effects of post-traumatic stress disorder on complicated grief. Dialogues Clin Neurosci. 2012;14(2):210-214.

28.Yaffe K, Vittinghoff E, Lindquist K, et al. Posttraumatic Stress Disorder and Risk of Dementia Among US Veterans Arch Gen Psychiatry. 2010;67(6):608-613.

29.Boscarino JA. A prospective study of PTSD and early-age heart disease mortality among Vietnam veterans: implications for surveillance and prevention.Psychosom Med. 2008;70:668-676.

30.Samuelson KW, Neylan TC, Lenoci M, et al. Longitudinal effects of PTSD on memory functioning. J Int Neuropsychol Soc. 2009;15(6):853-861.

31.Vasterling JJ, Duke LM, Brailey K, et al. Attention, learning, and memory performances and intellectual resources in Vietnam veterans: PTSD and no disorder comparisons. Neuropsychology. 2002;16(1):5-14.

32.Breslau N, Peterson EL, Kessler RC, Schultz LR. Short screening scale for DSM-IV posttraumatic stress disorder. Am Psychiatry. 1999;156:908-911.

33.Khouzam HR. A simple mnemonic for the diagnostic criteria for post-traumatic stress disorder. West J Med. 2001;174(6):424.

34.Khouzam HR, Donnelly NJ. Posttraumatic stress disorder. Safe, effective management in the primary care setting. Postgrad Med. 2001;110(5):60-2, 67-70, 77-78.

35.Gilbertson MW, Orr SP, Rauch SL, Pitman RK. Trauma and posttraumatic stress disorder. In: Stern TA, Rosenbaum JF, Fava M, et al (eds). Massachusetts General Hospital Comprehensive Clinical Psychiatry (1st ed). Philadelphia: Mosby Elsevier; 2008.

36.Boscarino JA. Posttraumatic stress disorder and physical illness: results from clinical and epidemiologic studies. Ann N Y Acad Sci. 2004;1032:141-153. 

37.Dickie EW, Brunet A, Akerib V, Armony JL. An fMRI investigation of memory encoding in PTSD: influence of symptom severity. Neuropsychologia.2008;46(5):1522-1531.