Iverson, Grant L. PhD
Section Editor(s): Caplan, Bruce PhD, ABPP; Issue Editor; Bogner, Jennifer PhD, ABPP; Issue Editor
MILITARY SERVICE MEMBERS are at risk for sustaining a traumatic brain injury (TBI) prior to, during, or following deployment.1 Surveys of recently deployed military personnel have revealed high rates of suspected mild traumatic brain injuries (MTBIs) among service personnel stationed in Iraq or Afghanistan. For example, it has been estimated that 11.2% to 22.8% of service members have sustained a deployment-related MTBI.2–6 As of January 2008, it was estimated that more than 320 000 service members of the 1.64 million who had been deployed screened positive for a “probable traumatic brain injury.”3 These screening estimates of MTBI far exceed the recently published surveillance statistics for TBI in the military. In the third quarter of 2009, the Defense and Veterans Brain Injury Center released official surveillance data representing the number of individual service members who sustained a medically diagnosed TBI of any severity anywhere in the world between 2000 and 2009. The total number of TBIs by year are presented in Figure 1.7 The total number of MTBIs by year are presented in Figure 2.7 Each injured service member was counted only once to represent the total number of injured service members and not the total number of injuries (ie, some service members have sustained multiple injuries). The total number of penetrating and severe TBIs by year are presented in Figure 3.7 The number of TBIs increased significantly between 2006 and 2008 (Figs 1 and 2). The United States Department of Defense (DoD) did not provide an explanation for this increase and multiple factors could have contributed, including possible changes to the methodology by which service members were screened and then clinically diagnosed. Examining trends (not shown in the figures), from 2000 to 2009, 1.3% to 2.5% of all injuries were penetrating and 0.8% to 1.6% of all injuries were severe. Over the years, there has been a gradual linear increase in the percentage of all injuries classified as mild: 2000 (57.8%), 2001 (65.8%), 2002 (72.2%), 2003 (76.0%), 2004 (79.4%), 2005 (81.3%), 2006 (82.9%), 2007 (81.6%), 2008 (77.5%), and 2009 (78.4%).
The published deployment-related injury incidence and prevalence estimates are based on a screening methodology, which undoubtedly will contain false-positive results and some false-negative results. Screening estimates are inflated because the screening questions are designed to identify service members who should be evaluated medically to (i) confirm the diagnosis, and (ii) determine whether they require additional assessment, treatment, or rehabilitation services. It is essential to appreciate that accurate injury surveillance does not reflect the number of service members or veterans with possible or probable residual symptoms, problems, or deficits because of their past injuries. This is because the vast majority of injured service members are expected to recover from 1 or more milder forms of MTBIs (ie, “concussions”). The challenge is to identify service members and veterans who have residual symptoms attributable to the neurobiological effects of an injury to the brain and, if possible, determine whether differential treatment and rehabilitation efforts can reduce symptoms and improve functioning in those individuals so identified.
Iverson and colleagues8 reviewed the literature on MTBI screening in the military, noting that (i) different screening procedures have been used across studies; (ii) for screening programs aimed at maximizing the likelihood of identifying possible MTBIs, a high rate of false-positive results is an inevitable and intended consequence; and (iii) initial screening estimates of the number of service members who sustained an MTBI do not accurately represent either the number of service members who were actually injured (due to false-negative and false-positive results) or the number of service members who remain symptomatic from the injury. A number of concerns relating to the methodology of the screening process were expressed in that article.
This article is a focused follow-up to the review article of Iverson et al.8 Only the current screening program used by the DoD is reviewed, with the goal of carefully delineating the specific steps at which false-positive and false-negative screening results can emerge. Some recommendations for improving the screening methodology are provided.
SCREENING FOR RESIDUAL MTBI
The postdeployment TBI screening questions are reprinted in Table 1 and illustrated in Figure 4. Table 1 was extracted from a larger self-report health questionnaire called the Post-Deployment Health Assessment. Postdeployment health assessments occur at the end of deployment, while in theatre or in transit, or shortly after return to the United States. The vast majority of these assessments occur statewide. A positive screen for a possible brain injury triggers a follow-up interview with a clinician. If the clinician believes the service member has sustained an injury producing ongoing problems, that opinion triggers specialty evaluations, treatment, and rehabilitation services. The DoD and the Department of Veterans Affairs (VA) have made tremendous efforts to harmonize their methodologies for screening and follow-up assessment.
In the current screening algorithm, a service member or veteran must answer in the affirmative on all 4 screening questions to be identified as “positive” for a possible TBI. The algorithm has strengths and limitations. This algorithm, at face value, appears likely to identify the vast majority of service members and veterans who sustained an injury and who have possible residual symptoms from that injury. The algorithm will, however, fail to identify those who were injured and fully recovered (although these data are likely retrievable).
A problem with the screening program as applied after deployment is that it covers the most recent deployment only; it does not document injuries sustained during previous tours of duty. Because the screening program was implemented after many service personnel had completed 1 or more deployments, injuries during those periods might not be fully documented in the service members' permanent records. Documenting multiple injuries to the brain, even if symptomatic recovery occurs, could have important longer-term career and healthcare implications for service members and veterans. On the basis of the sports literature, athletes with prior concussions are at statistically increased risk for a future concussion9–12 and for slower recovery from any subsequent injuries.9,13 In group studies, researchers have reported that athletes with a history of 3 or more concussions have persisting changes in electrophysiology,14,15 subjective symptoms,14,16 and neuropsychological test performance.16
Another significant concern with the screening algorithm is that it will result in false-positive results. Specifically, at every step in the algorithm, there is the potential for certain factors to increase the likelihood of false-positive results. At step 1 (ie, item 9.a), the individual is asked whether he or she experienced an event involving a blast, motor vehicle accident, fall, or other potential injury mechanism. By using the word “event,” it increases the likelihood that someone could have experienced the event without being physically injured or psychologically affected. The events listed in step 1 could result in a brain injury, psychological injury, physical injury, combination injury, or no significant injury (Fig 4).
In step 2 (ie, item 9.b), the goal is to determine whether the person experienced signs or symptoms indicative of a brain injury. Those are, in fact, classic signs and symptoms discussed in the TBI literature for many decades. The problem, however, is that a combatant who is psychologically traumatized, physically injured, or both, could experience these signs and symptoms—particularly items concerning feeling dazed and confused or having a brief period of amnesia. Thus, although an injury to the brain is sufficient to cause these signs and symptoms, it is not necessary to produce some of them.
Alterations in mental status and poor memory for the event are commonly associated with acute traumatic stress in civilians.17–21 Alterations in mental status, through a range of dissociative experiences, are very common in healthy soldiers who are placed under extreme stress. Morgan and colleagues22 studied general infantry and Special Forces soldiers after the experiential phase of the US Army Survival Course, during which soldiers were confronted with a variety of stressors, including sleep deprivation; semistarvation; lack of control over personal hygiene; and external control over their movement, social contact, and communication. Symptoms of dissociation were extremely common in these soldiers, providing evidence that military stress produces high levels of dissociation in psychologically healthy individuals. The Special Forces soldiers experienced significantly fewer dissociative symptoms than the general infantry soldiers, which could put general infantry soldiers at greater risk for traumatic stress reactions in combat situations.
Therefore, at step 2, combatants who are seriously psychologically traumatized, but who have not sustained an injury to the brain, are very likely to report having been dazed, confused, or briefly amnestic at the time of the trauma. Moreover, it is possible that a service member could endorse feeling “confused” after a blast without being significantly physically or psychologically injured. In a combat situation, coming on to a scene shortly after a blast can be a disorienting, disconcerting and surreal experience in and of itself. Thus, as illustrated in Figure 4, the signs and symptoms in step 2 are exactly the signs and symptoms that are associated with TBI, but they can also occur for other reasons.
In step 3, service members or veterans are asked to retrospectively report how they felt, perhaps months ago, after the event or injury event. These acute symptoms are “classic” for concussion and more serious brain injuries. However, the base rates of these symptoms in deployed service members who are not injured are poorly understood. Deployment can be highly stressful, and many service members are sleep deprived. Thus, when asked to retrospectively rate their symptoms, long after an injury event, it is quite possible that some non–injury-related symptoms will be attributed to the injury event and thus intermingled with injury-related symptoms. It is also possible that the service member or veteran will think back and recall experiencing some of the symptoms on a regular basis during deployment, thus failing to appreciate and report them in connection with a real past injury. Finally, and importantly, the acute symptoms in step 3, although considered “classic” concussion symptoms, can also be associated with psychological injuries or orthopedic injuries. In fact, in a prospective civilian study following injured adults from the emergency department to 1 week postinjury, those who had sustained a mild TBI could not be differentiated from those with orthopedic injuries alone on the basis of symptom reporting. Both groups endorsed relatively high levels of postconcussion-like symptoms. In this civilian study, 43% of those with MTBIs and 44% of those with orthopedic injuries endorsed 3 or more postconcussion-like symptoms.23
The most perplexing and challenging step in the algorithm is the final step. A service member or veteran must be currently symptomatic to screen positive for a possible brain injury. The obvious problem with this final step is comorbidity. Comorbidity prevents, in most cases, confident causal inferences regarding the past MTBI. For example, civilians with chronic pain are likely to endorse these symptoms.24–27 Civilians with depression are extremely likely to endorse these symptoms.28 Military personnel and veterans with posttraumatic stress endorse some of these symptoms.2,24,26,27,29–33 Military personnel and veterans who have sustained MTBIs report significantly more postconcussion symptoms than those who have sustained moderate-severe TBIs; however, after controlling for posttraumatic stress disorder (PTSD), there was no difference in symptom reporting between the 2 groups.34 Some researchers have reported that the high rates of symptoms reported by soldiers who have sustained MTBIs are mediated, in large part, by PTSD or depression.2 In contrast, other researchers have reported that MTBI is independently related to symptom reporting in veterans.35
In a large-scale study involving the UK Armed Forces, Fear and colleagues36 screened a cross-sectional cohort of 5869 military personnel. Military personnel were classified as to whether they had (i ) blast exposure; (ii ) exposure to uranium or wounded personnel; (iii ) both blast exposure and exposure to uranium or wounded personnel; or (iv) no exposure to any of these. Approximately 27% of those who had blast exposure reported 3 or more symptoms. However, approximately 21% of those with no exposure to blast, exposure to uranium, or exposure to wounded persons also reported 3 or more symptoms, as did 32% of those who had exposure to uranium or wounded personnel.
Without question, some of the symptoms in items 9.c and 9.d are commonly endorsed by civilians who have no mental health problems, history of brain injury, or neurological problems.37–43 These symptoms are part of the normal human experience. Because the symptoms are nonspecific, the temptation is to simply say that they cannot be due to a past brain injury. This conclusion, of course, is a non sequitur. These symptoms can and are often caused by a brain injury. The problem, again, is related to comorbidity. Symptom endorsement is influenced by any combination of brain injury, preexisting personality characteristics, life stress, psychiatric conditions, substance abuse problems, symptom expectations, misattribution, and response biases, to name only a few.
In the presence of comorbidity, it is extremely difficult to causally connect subjective symptoms to a remote MTBI. Traumatic stress, life stress, depression, insomnia, chronic pain, marital and family distress, and substance abuse, singly or in combination, can be the proximate cause for these symptoms. This fact supports the approach in the DoD and VA to simply aggressively treat what is treatable to try to reduce suffering and improve functioning. There is recognition within the DoD that postdeployment symptoms and problems can have multifactorial causation, and systematically treating specific chief complaints (eg, sleep disturbance and anxiety) can have concomitant benefits in other areas (eg, headaches and cognition) in some military personnel.
RECOMMENDATIONS AND FUTURE DIRECTIONS
The US government is spending hundreds of millions of dollars on healthcare programs for military personnel and veterans and on research relating to TBI and psychological injuries (eg, PTSD and depression). This extraordinary investment will undoubtedly lead to major scientific advances and clear improvements in assessment, treatment, and rehabilitation services for military personnel, veterans, and civilians. To better capitalize on future advances in treatment and rehabilitation services, we must improve the methodology for injury surveillance, symptom documentation, and differential diagnosis. Some recommendations for improving the screening methodology are provided as follows:
1. Researchers, clinicians, government officials, and the media should be cautious and circumspect when interpreting TBI screening data. Screening will result in false-negative and false-positive results. Not all individuals who screen positive for an MTBI will actually have sustained an MTBI during their deployment (ie, false-positive results). More important, the majority of those who sustained an MTBI will likely recover from that injury.
2. Users of screening test results should cautiously interpret the loss of consciousness item. As a rule, it is not possible for individuals to know if or for how long they lost consciousness, unless the event was witnessed and the person was told. Some individuals will mistake dense posttraumatic amnesia for loss of consciousness. It might be of interest to add “witnessed” loss of consciousness to some research relating to injury surveillance.
3. Clinicians and researchers could greatly benefit from having access to in-theatre medical records, such as the Military Acute Concussion Evaluation. As a rule, contemporaneously documented signs and symptoms are more accurate and reliable than retrospective accounts.
4. The most problematic item on the postdeployment health assessment is the “dazed and confused” item. Without question, feeling dazed and confused is a symptom of acute concussion. However, these terms can also be applied to the experience of shock and distress associated with traumatic stress or physical injury. Thus, it is recommended that researchers provide a detailed breakdown of how subjects respond to individual items and combinations of items at step 2 in the screening.
5. It needs to be acknowledged that the 4-step screening process relates, by design, to a single event, and some people experience multiple events. It is also possible that multiple events are recorded at step 1, but it then becomes unclear which of these events is connected to steps 2, 3, and 4. Therefore, follow-up assessments are needed to try to clarify these issues.
6. It would be helpful to collect in-theatre data for the items in step 3 in the following groups: (a) noncombat, well-rested personnel, (b) sleep-deprived service members, (c) personnel who are engaged in multiple stressful operations, (d) individuals who sustained physical injuries not involving the head or brain, and (e) personnel exposed to psychologically traumatic events. This will help clarify the deployment and combat-related base rates of these symptoms.
7. The DoD has a very good clinical practice guideline for identifying and managing concussion in theatre. It would be instructive to identify a cohort of service personnel who have sustained a concussion and have them complete the 4 screening items at 2 weeks postinjury. This concussed group could then be compared with a group of combatants who had experienced a psychologically traumatic event* 2 weeks prior to identify any clear differences in how the groups responded on the screening items.
8. There is a need to improve the process by which the clinician conducts the follow-up evaluation for determining whether (a) there is a history of a probable or definite MTBI, (b) whether the individual is currently symptomatic, and (c) what comorbidities might be causing or contributing to the symptoms. Ideally, there would be an evidence-based standardized approach for gathering this information that could be implemented system-wide.
9. It would be helpful if in-theatre records relating to injury mechanism, severity, and recovery time could be readily accessed during postdeployment and VA follow-up evaluations by clinicians.
Despite our best efforts to address and lessen these clinical and methodological challenges, we will continue to struggle with them for many years to come. Increasingly, it would be helpful to move in the direction of embracing rather than resisting, denying, or ignoring the comorbidity conundrum. The brain is the organ of the mind, and problems with the mind can be caused by TBI, traumatic stress, depression, and other factors, singly or in combination. Classifying service members and veterans into singular diagnostic groups can be administratively parsimonious, but it is not necessarily clinically efficacious. Many treatment and rehabilitation approaches that are effective for traumatic stress, depression, and chronic pain can be adapted for use with individuals who have symptoms and problems that are believed to be partially or largely related to a deployment-related MTBI. If we focus more on symptoms and problems, worry less about the Procrustean process of diagnostic stovepiping, and redouble our efforts to treat what we can treat, we will reduce suffering and improve functioning and quality of life for those who serve and have served.
1. Armed Forces Health Surveillance Center. Frequencies, rates, and trends of use of diagnostic codes indicative of traumatic brain injury (TBI), July 1999-June 2008. Med Surveill Mon Rep. 2008; 10:2–9.
2. Hoge CW, McGurk D, Thomas JL, Cox AL, Engel CC, Castro CA. Mild traumatic brain injury in U.S. Soldiers returning from Iraq. N Engl J Med. 2008; 358:453–463.
3. Tanielian T, Jaycox LH, eds. Invisible Wounds of War: Psychological and Cognitive Injuries, Their Consequences, and Services to Assist Recovery. Santa Monica, CA: Rand Corporation; 2008.
4. Schwab KA, Ivins B, Cramer G, et al. Screening for traumatic brain injury in troops returning from deployment in Afghanistan and Iraq: initial investigation of the usefulness of a short screening tool for traumatic brain injury. J Head Trauma Rehabil. 2007; 22:377–389.
5. Mental Health Advisory Team (MHAT-V). Operation Iraqi Freedom 06-08: Iraq. Operation Enduring Freedom 8: Afghanistan, chartered by the Office of the Surgeon Multi-National Force-Iraq, the Office of the Command Surgeon, and the Office of the Surgeon General United States Army Medical Command. http://www.armymedicine.army.mil
. Accessed February 14, 2008.
6. Terrio H, Brenner LA, Ivins B, et al. Traumatic brain injury screening: preliminary findings in a US army brigade combat team. J Head Trauma Rehabil. 2009; 24:14–23.
8. Iverson GL, Langlois JA, McCrea MA, Kelly JP. Challenges associated with post-deployment screening for mild traumatic brain injury in military personnel. Clin Neuropsychol. 2009; 23:1299–1314.
9. Guskiewicz KM, McCrea M, Marshall SW, et al. Cumulative effects associated with recurrent concussion in collegiate football players: the NCAA Concussion Study. JAMA. 2003; 290:2549–2555.
10. Gerberich SG, Priest JD, Boen JR, Straub CP, Maxwell RE. Concussion incidences and severity in secondary school varsity football players. Am J Public Health. 1983; 73:1370–1375.
11. Zemper ED. Two-year prospective study of relative risk of a second cerebral concussion. Am J Phys Med Rehabil. 2003; 82:653–659.
12. Delaney JS, Lacroix VJ, Leclerc S, Johnston KM. Concussions during the 1997 Canadian Football League season. Clin J Sport Med. 2000; 10:9–14.
13. Covassin T, Stearne D, Elbin R. Concussion history and postconcussion neurocognitive performance and symptoms in collegiate athletes. J Athl Train. 2008; 43:119–124.
14. Gaetz M, Goodman D, Weinberg H. Electrophysiological evidence for the cumulative effects of concussion. Brain Inj. 2000; 14:1077–1088.
15. De Beaumont L, Brisson B, Lassonde M, Jolicoeur P. Long-term electrophysiological changes in athletes with a history of multiple concussions. Brain Inj. 2007; 21:631–644.
16. Iverson GL, Gaetz M, Lovell MR, Collins MW. Cumulative effects of concussion in amateur athletes. Brain Inj. 2004; 18:433–443.
17. Birmes P, Brunet A, Carreras D, et al. The predictive power of peritraumatic dissociation and acute stress symptoms for posttraumatic stress symptoms: a three-month prospective study. Am J Psychiatry. 2003; 160:1337–1339.
18. Cardena E, Spiegel D. Dissociative reactions to the San Francisco Bay Area earthquake of 1989. Am J Psychiatry. 1993; 150:474–478.
19. Harvey AG, Bryant RA. Dissociative symptoms in acute stress disorder. J Trauma Stress. 1999; 12:673–680.
20. Freinkel A, Koopman C, Spiegel D. Dissociative symptoms in media eyewitnesses of an execution. Am J Psychiatry. 1994; 151:1335–1339.
21. Madakasira S, O'Brien KF. Acute posttraumatic stress disorder in victims of a natural disaster. J Nerv Ment Dis. 1987; 175:286–290.
22. Morgan CA III, Hazlett G, Wang S, Richardson EG Jr, Schnurr P, Southwick SM. Symptoms of dissociation in humans experiencing acute, uncontrollable stress: a prospective investigation. Am J Psychiatry. 2001; 158:1239–1247.
23. Meares S, Shores EA, Taylor AJ, et al. Mild traumatic brain injury does not predict acute postconcussion syndrome. J Neurol Neurosurg Psychiatry. 2008; 79:300–306.
24. Smith-Seemiller L, Fow NR, Kant R, Franzen MD. Presence of post-concussion syndrome symptoms in patients with chronic pain vs mild traumatic brain injury. Brain Inj. 2003; 17:199–206.
25. Radanov BP, Dvorak J, Valach L. Cognitive deficits in patients after soft tissue injury of the cervical spine. Spine. 1992; 17:127–131.
26. Iverson GL, McCracken LM. “Postconcussive” symptoms in persons with chronic pain. Brain Inj. 1997; 11:783–790.
27. Gasquoine PG. Postconcussional symptoms in chronic back pain. Appl Neuropsychol. 2000; 7:83–89.
28. Iverson GL. Misdiagnosis of persistent postconcussion syndrome in patients with depression. Arch Clin Neuropsychol. 2006; 21:303–310.
29. McCauley SR, Boake C, Levin HS, Contant CF, Song JX. Postconcussional disorder following mild to moderate traumatic brain injury: anxiety, depression, and social support as risk factors and comorbidities. J Clin Exp Neuropsychol. 2001; 23:792–808.
30. Karzmark P, Hall K, Englander J. Late-onset post-concussion symptoms after mild brain injury: the role of premorbid, injury-related, environmental, and personality factors. Brain Inj. 1995; 9:21–26.
31. Gunstad J, Suhr JA. Cognitive factors in postconcussion syndrome symptom report. Arch Clin Neuropsychol. 2004; 19:391–405.
32. Wilde EA, Bigler ED, Gandhi PV, et al. Alcohol abuse and traumatic brain injury: quantitative magnetic resonance imaging and neuropsychological outcome. J Neurotrauma. 2004; 21:137–147.
33. Schneiderman AI, Braver ER, Kang HK. Understanding sequelae of injury mechanisms and mild traumatic brain injury incurred during the conflicts in Iraq and Afghanistan: persistent postconcussive symptoms and posttraumatic stress disorder. Am J Epidemiol. 2008; 167:1446–1452.
34. Belanger HG, Kretzmer T, Vanderploeg RD, French LM. Symptom complaints following combat-related traumatic brain injury: relationship to traumatic brain injury severity and posttraumatic stress disorder. J Int Neuropsychol Soc. 2010; 16(1):194–199.
35. Vanderploeg RD, Belanger HG, Curtiss G. Mild traumatic brain injury and posttraumatic stress disorder and their associations with health symptoms. Arch Phys Med Rehabil. 2009; 90:1084–1093.
36. Fear NT, Jones E, Groom M, et al. Symptoms of post-concussional syndrome are non-specifically related to mild traumatic brain injury in UK Armed Forces personnel on return from deployment in Iraq: an analysis of self-reported data. Psychol Med. 2009; 39(8):1379–1387.
37. Gouvier WD, Uddo-Crane M, Brown LM. Base rates of post-concussional symptoms. Arch Clin Neuropsychol. 1988; 3:273–278.
38. Machulda MM, Bergquist TF, Ito V, Chew S. Relationship between stress, coping, and post concussion symptoms in a healthy adult population. Arch Clin Neuropsychol. 1998; 13:415–424.
39. Iverson GL, Lange RT. Examination of “postconcussion-like” symptoms in a healthy sample. Appl Neuropsychol. 2003; 10:137–144.
40. Mittenberg W, DiGiulio DV, Perrin S, Bass AE. Symptoms following mild head injury: expectation as aetiology. J Neurol Neurosurg Psychiatry. 1992; 55:200–204.
41. Trahan DE, Ross CE, Trahan SL. Relationships among postconcussional-type symptoms, depression, and anxiety in neurologically normal young adults and victims of brain injury. Arch Clin Neuropsychol. 2001; 16:435–445.
42. Sawchyn JM, Brulot MM, Strauss E. Note on the use of the postconcussion syndrome checklist. Arch Clin Neuropsychol. 2000; 15:1–8.
43. Wong JL, Regennitter RP, Barrios F. Base rate and simulated symptoms of mild head injury among normals. Arch Clin Neuropsychol. 1994; 9:411–425.
Without injuries involving the head or brain. Cited Here...
brain injury; concussion; epidemiology; screening; surveillance
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