2
DIAGNOSIS AND ASSESSMENT
Many people are exposed to traumatic events; some of them will experience temporary distress, others acute stress disorder (ASD), and still others will go on to develop posttraumatic stress disorder (PTSD) or other conditions. ASD can be diagnosed only within the first month after a traumatic event (APA 2000). If symptoms persist beyond a month, the person might meet the criteria for PTSD. The criteria for PTSD are listed in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders, Text Revision (DSM-IV-TR, hereafter referred to as the DSM-IV) (Box 2.1) and include symptoms of re-experiencing, intrusive recollections of a traumatic event, as through flashbacks or nightmares; avoidance and numbing, efforts to avoid anything associated with the trauma and numbing of emotions; and hyperarousal as manifested by, for example, difficulty in sleeping or irritability (APA 2000).
PTSD symptoms can vary in severity and frequency and can leave patients with an array of disabilities from mildly distressing to severely incapacitating. Although the onset typically occurs shortly after exposure, the lag between exposure and full manifestation of PTSD is variable and in some cases long (Bremner et al. 1996; Bryant and Harvey 2002; Carty et al. 2006; Gray et al. 2004; Green et al. 1990; Op den Velde et al. 1996; Port et al. 2001; Ruzich et al. 2005); if the onset of symptoms occur more than six months after the trauma it is referred to as delayed onset. PTSD can be chronic or recurrent (Friedman 2003). In some cases, it occurs alone, but most people who have PTSD also have other psychiatric disorders, such as major depressive disorder (Black et al. 2004; Kessler et al. 1995), that occur either at the same time as or after the development of PTSD.
This chapter focuses on the diagnosis and assessment of PTSD beginning with the accepted diagnostic criteria for PTSD (Box 2.1) as described in the American Psychiatric Association’s DSM-IV (APA 2000). The chapter presents additional information that might be useful for a comprehensive assessment of a PTSD patient, such as determining comorbidity, symptom severity, functional status, and neuropsychologic impairments. The chapter concludes with a comment about biomarkers that might be of future use in the diagnosis of PTSD.
CURRENT DIAGNOSTIC CRITERIA
Although there is a long history of descriptions of posttraumatic syndromes, the modern era of diagnosing PTSD began in 1980 with the introduction of PTSD in the third edition of APA DSM (DSM-III). Formal recognition of PTSD led to a large body of systematic research on its features and research findings led to modification and refinement of the diagnostic criteria. But many of the diagnostic criteria in DMS-III are largely unchanged in the latest edition of the diagnostic manual, DSM-IV.
The evidence-based diagnosis of PTSD, according to DSM-IV (see Box 2.1) has several components: exposure to a traumatic event, intrusive re-experiencing of the event, avoidance and numbing, hyperarousal, at least a month of symptoms, and clinically significant distress or impairment that was not present before the trauma.
The World Health Organization disease classification system, the 10th edition of International Classification of Diseases (ICD-10), also includes diagnostic criteria for PTSD. The ICD diagnostic criteria for PTSD are similar to those in DSM-IV but do not include the DSM-IV criterion A2, that a response to a traumatic event involves intense fear, helplessness, or horror.
BOX 2.1 DSM-IV Diagnostic Criteria for Posttraumatic Stress Disorder A. The person has been exposed to a traumatic event in which both of the following were present:
B. The traumatic event is persistently re-experienced in one (or more) of the following ways:
C. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by at least three of the following:
|
D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by at least two of the following:
E. Duration of the disturbance (symptoms in Criteria B, C, and D) is more than one (1) month F. The disturbance causes clinically significant distress and/or impairment in social, occupational, and/or other important areas of functioning SOURCE: Reprinted with permission from APA 2000. |
CLINICAL DIAGNOSIS
After a traumatic event, there is substantial variation among patients with regard to both the timing of the onset of symptoms and the types of symptoms. Furthermore, there might be a delay between the onset of symptoms and when the patient seeks help. Patients also vary in how they present to a health professional. For example, a patient might present at a health facility with a physical or psychiatric complaint unrelated to PTSD, and it is only during the course of evaluating or treating the patient for the presenting complaint that symptoms of PTSD are identified and a diagnosis made. In other cases, a patient might present to a mental health professional who is conversant with the diagnosis of PTSD and is better able to elicit a narrative of exposure and symptoms, or a family member or other person familiar with the veteran might seek advice from a health professional about coping with a veteran who might be suffering from PTSD. The presenting symptoms and initial diagnostic process are variable and will necessitate a brief or long assessment, depending on the veteran’s symptoms, mental and physical health, willingness and capacity to work with the health professional, and the presence of other physical or psychiatric disorders.
Optimally, a patient is evaluated in a confidential setting with a face-to-face interview by a health professional experienced in the
diagnosis of psychiatric disorders, such as a psychiatrist, psychologist, clinical social worker, or psychiatric nurse. The interview should elicit the patient’s symptoms, assess the history of potentially traumatic events, and determine whether the patient meets the DSM-IV criteria for PTSD or whether the patient has a different psychiatric disorder, such as major depressive disorder or a possible neurologic disorder, such as traumatic brain injury. The health professional should also determine the frequency and severity of symptoms and the associated disability, determine whether there are comorbid psychiatric and medical conditions, and determine whether the patient might be malingering.
In some instances it might be difficult to elicit patient responses regarding each of the DSM-IV criteria, such as avoidance. Many patients do not recognize avoidance, especially once it has become a habit or a “rule.” If a health professional merely asks if the patient avoids anything related to the trauma, the patient may respond negatively. However, if the patient is asked about specifics, such as going out alone at night, driving down deserted highways, or walking past piles of garbage, the patient might respond that they do not engage in those activities, thus providing more detailed information that might assist in the diagnosis. Thus, health professionals might need to ask patients about activities or symptoms in a variety of ways to help determine whether the patient meets the DSM-IV criteria for PTSD.
It is critical that adequate time be allocated for this assessment. Depending on the mental and physical health of the veteran, the veteran’s willingness and capacity to work with the health professional, and the presence of comorbid disorders, the process of diagnosis and assessment will likely take at least an hour or could take many hours to complete.
Unfortunately, many health professionals do not have the time or experience to assess psychiatric disorders adequately or are reluctant to attribute symptoms to a psychiatric disorder. Furthermore, veterans with PTSD might not present to a mental health professional, because they do not attribute their symptoms to a psychiatric disorder, they feel that a stigma is associated with psychiatric illnesses, they have limited access to such professionals, or for other reasons, such as cost. Therefore, health professionals should be aware that veterans, especially those who have
served in war theaters, are at risk for the development of PTSD, but might present with physical or psychiatric complaints that are symptomatic of substance use disorder or other psychiatric conditions. Health professionals should ask all veterans about possible exposure to potentially traumatic events. Additionally, there is evidence that elderly veterans present with more somatic complaints of PTSD (Owens et al. 2005). It has been found that war-related psychiatric disorders are easily missed in the elderly male veteran, further emphasizing the need for direct questioning regarding military service (Macleod 1994).
It should be noted that a person might not meet full criteria for a diagnosis of PTSD and yet still be highly symptomatic and in need of treatment. PTSD symptoms might be mild to severe, and functioning might be influenced by other factors, such as comorbid conditions or social support. Severe symptoms might be disabling even in the absence of a full diagnosis.
A basic component in diagnosing PTSD is determining whether a person has experienced a traumatic event that has led to symptoms indicative of PTSD (see criterion A in Box 2.1). A war environment is rife with opportunities for exposure to traumatic events of many types (for example, see Table 2.1). Types of traumatic stressors related to war include serving in dangerous military roles, such as driving a truck at risk for encountering roadside bombs, patrolling the streets, and searching homes for enemy combatants, suicide attacks, sexual assaults or severe sexual harassment, physical assault, duties involving graves registration, accidents causing serious injuries or death, friendly fire, serving in medical units, killing or injuring someone, seeing someone being killed, injured, or tortured, and being taken hostage. From Vietnam to the present, several self-report questionnaires (discussed in Chapter 3) have been developed and administered to veterans to enhance the ability of well-trained and experienced professionals to assess the veterans’ exposure to traumatic events.
TABLE 2.1 War Experiences Reported by Members of the US Army and Marine Combat Corps after Deployment to Iraq or Afghanistana
Experience |
Percentage Reporting Experience |
||
Army Groups |
Marine Group |
||
|
Afghanistan (N=1,962) |
Iraq (N=894) |
Iraq (N=815) |
Being attacked or ambushed |
58 |
89 |
95 |
Receiving incoming artillery, rocket, or mortar fire |
84 |
86 |
92 |
Being shot at or receiving small-arms fire |
66 |
93 |
97 |
Shooting or directing fire at the enemy |
27 |
77 |
87 |
Being responsible for the death of an enemy combatant |
12 |
48 |
65 |
Being responsible for the death of a noncombatant |
1 |
14 |
28 |
Seeing dead bodies or human remains |
39 |
95 |
94 |
Handling or uncovering human remains |
12 |
50 |
57 |
Seeing dead or seriously injured Americans |
30 |
65 |
75 |
Knowing someone seriously injured or killed |
43 |
86 |
87 |
Participating in demining operations |
16 |
38 |
34 |
ASSESSMENT
In addition to the formal diagnostic process, a more comprehensive assessment of a PTSD patient would include a determination of comorbidity, symptom severity, functional status, neuropsychologic impairments, and malingering.
Determination of comorbidity is an essential component of the optimal assessment of a patient with PTSD. Comorbidity refers to the presence of at least one disorder in addition to the presenting diagnosis (for example, PTSD and major depressive disorder in the same person, or PTSD and substance abuse in the same person). PTSD is marked by high rates of comorbidity; some studies indicate that more than 80% of people who have a diagnosis of PTSD also have major depressive or another psychiatric disorder (Black et al. 2004; Kessler et al. 1995). For example,
Kulka et al. (1990) found that 22% of Vietnam veterans with PTSD also had alcohol abuse or dependence. Hyer et al. (1993) found comorbidity rates of 68 to 82% for PTSD and lifetime prevalence of alcohol abuse. While a thorough clinical interview is likely to uncover existing comorbidities, some diagnostic instruments, such as the Structured Clinical Interview for DSM-IV, might also be used.
A comprehensive evaluation also will assess symptom severity (frequency and intensity), especially as related to following the course of the illness and the response to treatment. Symptom severity might be measured with a self-report questionnaire (for example, the PTSD Checklist); however, such questionnaires should not be used as a standalone measure but as an adjunct to a diagnostic interview. Chapter 3 provides a discussion of some of the instruments that are available to assess the severity of PTSD symptoms.
PTSD might impair a veteran’s ability to work or to engage successfully in other socially defined roles, such as functioning as a parent or spouse or being able to support a family. Functional ability should be assessed independently of symptom severity in a comprehensive assessment. A diagnostic instrument, such as the Clinician-Administered PTSD Scale (see Chapter 3) can be used to query the patient about perceived impairment in his or her social and occupational functioning. The topic of functional ability is being considered by a separate Institute of Medicine committee, the Committee on Veterans’ Compensation for Post Traumatic Stress Disorder, which has been established to conduct a study on compensation for PTSD.
Once a patient has been diagnosed with PTSD, testing might be useful in characterizing neurobehavioral and neurocognitive impairments. Although neuropsychologic testing might be used to validate the subjective reports of some patients, such tests might be diagnostically confusing, as impairments in attention, working memory, speed of information processing, delayed recall, and a number of other impairments might characterize not only PTSD, but also other psychiatric disorders, such as generalized anxiety disorder, major depressive disorder, most severe sleep disorders, chronic pain syndromes, postconcussive syndrome, and substance abuse. Some
studies show that the domains for which the most evidence of PTSD-related impairment exists are attention and memory (Vasterling et al. 2005), and executive functioning and global intellectual functioning (Wilson and Keane 2004). There are numerous neuropsychologic tests that might be used to determine the presence and level of those impairments (for example, the California Verbal Learning Test, Rey Auditory Verbal Learning Test, the continuous Visual Memory Test, the Verbal and Non Verbal Tests of the Wechsler Memory Scale, and the Recognition Memory Test). It should be noted, however, that those tests are seldom used in clinical settings but are employed primarily in research.
Some people who present with PTSD symptoms might be suspected of malingering, that is, suspected of faking PTSD or intentionally exaggerating their symptoms (APA 2000; Wilson and Keane 2004). The DSM acknowledges the potential for malingering in the presentation of PTSD and recommends that health professionals keep several factors in mind when assessing a patient, particularly in a medicolegal context; these include any significant discrepancies between a patient’s reports of his or her symptoms and the clinical findings, a lack of cooperation on the patient’s part in the diagnostic process or in following prescribed treatment, and the presence of antisocial personality disorder (APA 2000).
Malingering in connection with PTSD might be suggested by several psychometric instruments, such as MMPI-2 and the Impact of Event Scale-Revised. Resnick (1995) provides a checklist of eight indicators, the presence of two or more of which suggests malingering. Those indicators, some of which are similar to items described in the DSM are poor work record; prior incapacitating injuries; discrepant capacity for work and recreation; unvarying, repetitive dreams; antisocial personality traits; overidealized functioning before the trauma; evasiveness; and inconsistency in symptoms. Building on the indicators, Wilson and Keane (2004) suggest that clinicians also consider whether the patient demonstrates falsification of documentation, an overemphasis on “flashback” experiences relative to other PTSD symptoms, a tendency to focus blame for all problems on symptoms of PTSD, and psychometric testing that shows a pattern of malingering and does not
indicate probable PTSD. This topic will be considered by the Institute of Medicine Committee on Veterans’ Compensation for Post Traumatic Stress Disorder.
BIOMARKERS OF POSTTRAUMATIC STRESS DISORDER
A biomarker is a measurable biologic change that occurs in association with a disease before, simultaneously with, or as a consequence of the disease. A biomarker is not a diagnostic marker. In the case of PTSD, it does not imply causation, because the necessary cause of PTSD is by definition a traumatic event. Biomarkers might represent pre-existing characteristics of people prone to PTSD, rather than effects of PTSD or even effects of the traumatic event. Many potential biomarkers are under study and they support a biologic basis of PTSD.
Examples of potential biomarkers being studied are increased concentrations of corticotrophin-releasing factor (e.g., Charney 2004; Yehuda 2002); measures of hyperarousal in response to stimuli and of delayed habituation to loud noises (e.g., Orr et al. 2003); measures of physiologic changes in noradrenergic brain systems and the hypothalamic-pituitary-adrenal axis (e.g., Southwick et al. 1994); alterations of brain structures, such as hyperactivation of the amygdala and hypoactivation of the prefrontal cortex (e.g., Pissiota et al. 2002; Shin et al. 2004; Vermetten and Bremner 2002); sleep disturbances (e.g., Breslau et al. 2004); and reduced volume of the hippocampus (e.g., Bremner et al. 1995; Gilbertson et al. 2002; Smith 2005). Currently, no biomarkers are useful in diagnosing PTSD, assessing the risk of developing it, or charting its progression.
New and future biomarker studies might help elucidate the way in which genetic, developmental, biologic, psychologic, experiential, and environmental factors interact to influence risk of, vulnerability to, and resistance to PTSD. Such studies will inform pathophysiologic models that might bring further breakthroughs in diagnosis and assessment.
CONCLUSION
As noted in this chapter, the core clinical features and diagnostic criteria of PTSD are well-established, and are efficacious in guiding the diagnosis and assessment of patients. The committee concluded that an optimal assessment of a patient consists of a face-to-face interview in a confidential setting with a health professional experienced in the diagnosis of psychiatric disorders. It is critical that adequate time be allocated for that assessment. Depending on the mental and physical health of the veteran, the veteran’s willingness and capacity to work with the health professional, and the presence of comorbid disorders, the process of diagnosis and assessment will likely take at least an hour or could take many hours to complete.
REFERENCES
American Psychiatric Association. 2000. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC: American Psychiatric Association.
Black DW, Carney CP, Peloso PM, Woolson RF, Schwartz DA, Voelker MD, Barrett DH, Doebbeling BN. 2004. Gulf War veterans with anxiety: Prevalence, comorbidity, and risk factors. Epidemiology 15(2):135–142.
Bremner JD, Randall P, Scott TM, Bronen RA, Seibyl JP, Southwick SM, Delaney RC, McCarthy G, Charney DS, Innis RB. 1995. MRI-based measurement of hippocampal volume in patients with combat-related posttraumatic stress disorder. American Journal of Psychiatry 152(7):973–981.
Bremner JD, Southwick SM, Darnell A, Charney DS. 1996. Chronic PTSD in Vietnam combat veterans: Course of illness and substance abuse. American Journal of Psychiatry 153(3):369–375.
Breslau N, Lucia VC, Davis GC. 2004. Partial PTSD versus full PTSD: An empirical examination of associated impairment. Psychological Medicine 34(7): 1205–1214.
Bryant RA, Harvey AG. 2002. Delayed-onset posttraumatic stress disorder: A prospective evaluation. Australian and New Zealand Journal of Psychiatry 36(2):205–209.
Carty J, O’Donnell ML, Creamer M. 2006. Delayed-onset PTSD: A prospective study of injury survivors. Journal of Affective Disorders 90(2–3):257–261.
Charney DS. 2004. Psychobiological mechanisms of resilience and vulnerability: Implications for successful adaptation to extreme stress. American Journal of Psychiatry 161(2):195–216.
Friedman MJ. 2003. Post Traumatic Stress Disorder: The Latest Assessment and Treatment Strategies. Kansas City, MO: Compact Clinicals.
Gilbertson MW, Shenton ME, Ciszewski A, Kasai K, Lasko NB, Orr SP, Pitman RK. 2002. Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Nature Neuroscience 5(11):1242–1247.
Gray MJ, Bolton EE, Litz BT. 2004. A longitudinal analysis of PTSD symptom course: Delayed-onset PTSD in Somalia peacekeepers. Journal of Consulting and Clinical Psychology 72(5):909–913.
Green BL, Lindy JD, Grace MC, Gleser GC, Leonard AC, Korol M, Winget C. 1990. Buffalo Creek survivors in the second decade: Stability of stress symptoms. American Journal of Orthopsychiatry 60(1):43–54.
Hoge CW, Castro CA, Messer SC, McGurk D, Cotting DI, Koffman RL. 2004. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. New England Journal of Medicine 351(1):13–22.
Hyer L, McCranie E, Peralme L. 1993. Dual diagnosis: PTSD and alcohol abuse. NCP Clinical Newsletter 3(3–4).
Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB. 1995. Posttraumatic stress disorder in the National Comorbidity Survey. Archives of General Psychiatry 52(12):1048–1060.
Kulka RA, Schlenger WE, Fairbank JA, Hough RL, Jordan BK, Marmar CR, Weiss DS. 1990. Trauma and the Vietnam War Generation: Report of Findings From the National Vietnam Veterans Readjustment Study. New York: Brunner/Mazel.
Macleod AD. 1994. The reactivation of post-traumatic stress disorder in later life. Australian and New Zealand Journal of Psychiatry 28(4):625–634.
Op den Velde W, Hovens JE, Aarts PG, Frey-Wouters E, Falger PR, Van Duijn H, De Groen JH. 1996. Prevalence and course of posttraumatic stress disorder in Dutch veterans of the civilian resistance during World War II: An overview. Psychological Reports 78(2):519–529.
Orr SP, Metzger LJ, Lasko NB, Macklin ML, Hu FB, Shalev AY, Pitman RK, Harvard/Veterans Affairs Posttraumatic Stress Disorder Twin Study Investigators. 2003. Physiologic responses to sudden, loud tones in monozygotic twins discordant for combat exposure: Association with posttraumatic stress disorder. Archives of General Psychiatry 60(3):283–288.
Owens GP, Baker DG, Kasckow J, Ciesla JA, Mohamed S. 2005. Review of assessment and treatment of PTSD among elderly American armed forces veterans. International Journal of Geriatric Psychiatry 20(12):1118–1130.
Pissiota A, Frans O, Fernandez M, von Knorring L, Fischer H, Fredrikson M. 2002. Neurofunctional correlates of posttraumatic stress disorder: A PET symptom provocation study. European Archives of Psychiatry & Clinical Neuroscience 252(2):68–75.
Port CL, Engdahl B, Frazier P. 2001. A longitudinal and retrospective study of PTSD among older prisoners of war. American Journal of Psychiatry 158(9):1474–1479.
Resnick PJ. 1995. Guidelines for the evaluation of malingering in posttraumatic stress disorder. In: Simon RI, Editor. Posttraumatic Stress Disorder in Litigation: Guidelines for Forensic Assessment. Washington, DC: American Psychiatric Press. Pp. 117–134.
Ruzich MJ, Looi JCL, Robertson MD. 2005. Delayed onset of posttraumatic stress disorder among male combat veterans: A case series. American Journal of Geriatric Psychiatry 13(5):424–427.
Shin LM, Orr SP, Carson MA, Rauch SL, Macklin ML, Lasko NB, Peters PM, Metzger LJ, Dougherty DD, Cannistraro PA, Alpert NM, Fischman AJ, Pitman RK. 2004. Regional cerebral blood flow in the amygdala and medial prefrontal cortex during traumatic imagery in male and female Vietnam veterans with PTSD. Archives of General Psychiatry 61(2):168–176.
Smith ME. 2005. Bilateral hippocampal volume reduction in adults with post-traumatic stress disorder: A meta-analysis of structural MRI studies. Hippocampus 15(6):798–807.
Southwick SM, Bremner D, Krystal JH, Charney DS. 1994. Psychobiologic research in post-traumatic stress disorder. Psychiatric Clinics of North America 17(2):251–264.
Vasterling JJ, Brewin CR. 2005. Neuropsychology of PTSD: Biological, Cognitive, and Clinical Perspectives. New York: Guilford Press.
Vermetten E, Bremner JD. 2002. Circuits and systems in stress. II. Applications to neurobiology and treatment in posttraumatic stress disorder. Depression and Anxiety 16(1):14–38.
Wilson JP, Keane TM. 2004. Assessing Psychological Trauma and PTSD (2nd Ed.). New York: Guilford Press.
Yehuda R. 2002. Post-traumatic stress disorder. New England Journal of Medicine 346(2):108–114.