One of the most commonly encountered weapons in Operation Enduring Freedom and Operation Iraqi Freedom is the improvised explosive device (IED).1-3 From October 2001 until January 2005, explosive devices were responsible for nearly 80% of all casualties reported to the Joint Theater Trauma Registry.4 Compared with casualties in earlier conflicts, military casualties in Afghanistan and Iraq incur a greater percentage of injuries to the face, head, and neck.2
Improvements to personal protective equipment and vehicle armor have reduced death rates, but by improving survival, they may have increased the incidence of traumatic brain injury (TBI) among wartime casualties and perhaps also among veterans who appear physically uninjured. (We use the term “veteran” as an inclusive term for military personnel who served in a combat zone, regardless of the current status as a discharged veteran, active duty service member, or member of the military reserve or National Guard.)
This article addresses the epidemiology, diagnosis, and treatment of mild TBI among combat veterans, with a particular focus on blast injury and the presence of comorbid posttraumatic stress disorder (PTSD).
Causes of TBI
Although current media and scientific attention is focused on TBI from wartime incidents, the causes of TBI among US military service members and veterans include combat, training accidents, and nonmilitary accidents. The incidents are typically associated with blunt head injuries in military service resulting from motor vehicle accidents, military aircraft accidents, accidents during field training exercises or hand-to-hand combat, and combat. Penetrating head trauma occurs but is far less frequent than either blunt injury or injury from blast exposure. Combat experience can lead to blast exposure, but certain military occupational specialists, such as explosive ordnance disposal or military bomb disposal experts, will experience repeated blast exposure in their daily work. Military operations in Afghanistan and Iraq are associated with exposure to the IED, typically a small weapon that contains 20 to 30 pounds of explosive, and the often larger vehicle-borne IED, a device with charge sizes up to several thousand pounds of explosive.
There are 3 mechanisms by which an IED causes injury: blast, blunt impact, and fragment penetration. Of these mechanisms, penetrating injury is uncommon compared with blunt impact and blast injury, and when it does occur, the medical history readily informs the psychiatrist’s diagnostic task.5 The diagnosis of mild TBI often is far more challenging, particularly in the common clinical scenario of comorbid psychiatric illness.
Although the clinical setting of a returning combat veteran suggests an epidemiological setting with elevated risk of TBI, cases of TBI are almost certainly being missed. Moderate or severe TBI is very likely to have resulted in medical care in a military setting, and records of this care should be available to the psychiatrist. Other factors contribute to the possibility of a missed TBI diagnosis, including an incomplete appreciation of TBI sequelae, attributing the clinical presentation to other psychiatric diagnoses, and misperceptions of blast injury biomechanics. On this latter point, we note that a study of blast injuries in civilians showed a missed diagnosis rate of 36% of primary blast–induced TBI cases.6 The complexity of trauma patients with other injuries may contribute to a missed TBI diagnosis, as also may the incorrect belief that loss of consciousness is necessary for TBI.7
? Combat veterans of Afghanistan and Iraq are at elevated risk for TBI and posttraumatic stress disorder (PTSD).
? The pathophysiology of blunt head injury is better understood than that for blast injury.
? Psychiatrists tend to be more comfortable diagnosing and treating mood and anxiety disorders than they are diagnosing and treating TBI.
? Most psychiatric consequences of TBI respond to a symptom-based approach established by the nearest equivalent DSM-IV disorder.
? Body armor is protective against blast injury to the lungs, thus allowing survival from injuries that were previously lethal.
? Stimulant medication can be useful for post-TBI cognitive difficulty, but it should be used with great caution in patients with comorbid anxiety.
? Psychiatrists must consider TBI when evaluating or treating veterans, especially combat veterans.
? The psychiatric signs and symptoms of TBI can be similar to those of PTSD and thus may be easily overlooked.
? TBI is associated with many medical and neurological comorbidities, and an interdisciplinary team approach provides optimal care.
Dr Capehart reports that he is listed as the sole inventor on a patent application describing tizanidine for the treatment of certain psychiatric disorders. This patent is owned by the federal government and there are no current licensing agreements with this patent. Dr Bass reports that he has no conflicts of interest concerning the subject matter of this article.
1. Brethauer S, Chao A, Chambers L, et al. Invasion vs insurgency: US Navy/Marine Corps forward surgical care during Operation Iraqi Freedom. Arch Surg. 2008;143:564-569.
2. Wade AL, Dye JL, Mohrle CR, Galarneau MR. Head, face, and neck injuries during Operation Iraqi Freedom II: results from the US Navy-Marine Corps Combat Trauma Registry. J Trauma. 2007;63:836-840.
3. Bird SM, Fairweather CB. Military fatality rates (by cause) in Afghanistan and Iraq: a measure of hostilities. Int J Epidemiol. 2007;36:841-846.
4. Owens BD, Kragh JF Jr, Wenke JC, et al. Combat wounds in operation Iraqi Freedom and operation Enduring Freedom. J Trauma. 2008;64:295-299.
5. Martin EM, Lu WC, Helmick K, et al. Traumatic brain injuries sustained in the Afghanistan and Iraq wars. Am J Nurs. 2008;108:40-47; quiz 47-48.
6. Bochicchio GV, Lumpkins K, O’Connor J, et al. Blast injury in a civilian trauma setting is associated with a delay in diagnosis of traumatic brain injury. Am Surg. 2008;74:267-270.
7. Rutland-Brown W, Langlois JA, Nicaj L, et al. Traumatic brain injuries after mass-casualty incidents: lessons from the 11 September 2001 World Trade Center attacks. Prehosp Disaster Med. 2007;22:157-164.
8. Hooker DR. Physiological effects of air concussion. Am J Physiol. 1924;67:219-274.
9. Bowen IG, Fletcher ER, Richmond DR. Estimate of Man’s Tolerance to the Direct Effects of Air Blast. 1968. http://www.dtic.mil/cgi-bin/GetTRDoc?AD=AD693105&Location=U2&doc=GetTRDoc.pdf. Accessed June 3, 2011.
10. Bass CR, Rafaels KA, Salzar RS. Pulmonary injury risk assessment for short-duration blasts. J Trauma. 2008;65:604-615.
11. Rafaels K, Bass CR, Panzer M, et al. Primary brain blast tolerance. PEO Soldier Conference on TBI and Helmet Design. Springfield, VA; 2011.
12. Gaber TA. Evaluation of the Addenbrooke’s Cognitive Examination’s validity in a brain injury rehabilitation setting. Brain Inj. 2008;22:589-593.
13. Coldren RL, Kelly MP, Parish RV, et al. Evaluation of the Military Acute Concussion Evaluation for use in combat operations more than 12 hours after injury. Mil Med. 2010;175:477-481.
14. Lane-Brown A, Tate R. Interventions for apathy after traumatic brain injury. Cochrane Database Syst Rev. 2009;(2):CD006341.
15. Kraus MF, Little DM, Donnell AJ, et al. Oculomotor function in chronic traumatic brain injury. Cogn Behav Neurol. 2007;20:170-178.
16. Mehlenbacher A, Capehart BP, Bass CR, Burke JR. Sound induced vertigo: superior canal dehiscence resulting from blast exposure. Arch PMR. In press.
17. Nampiaparampil DE. Prevalence of chronic pain after traumatic brain injury: a systematic review. JAMA. 2008;300:711-719.
18. Silver JM, McAllister TW, Arciniegas DB. Depression and cognitive complaints following mild traumatic brain injury. Am J Psychiatry. 2009;166:653-661.
19. Brenner LA, Terrio H, Homaifar BY, et al. Neuropsychological test performance in soldiers with blast-related mild TBI. Neuropsychology. 2010;24:160-167.