Military Traumatic Brain Injury: An Examination of Important Differences

Military Traumatic Brain Injury: An Examination of Important Differences

Introduction

Traumatic brain injury (TBI) is likely as old as warfare. In modern military medicine much of the focus has been on the effects of bullets and metallic fragments upon the brain. In World War I, for example, the English neurologist Sir Gordon Holmes detailed his observations on over 2,000 cases of head injury, including a detailed analysis of 23 cases involving penetrating injury to the visual cortex.1 Much of that work was influenced by the work of the Japanese ophthalmologist Tatsuji Inouyewho created the first relatively accurate map of the primary visual cortex; the map was based on his correlational observations of visual field defects following penetrating injuries to the occipital cortex during the Russo-Japanese war of 1904.2 In later years, Teubermade significant contributions to our understanding of the effects of penetrating brain injury in warfare by studying those injured in World War II.3 Alexander Luria, whose work contributed much to the beginnings of what is now known as neuropsychology, also studied injured soldiers during World War II.4,5 His rehabilitation work centered on focal brain injury and how it affected cognition, language, and motor functioning. In addition, the work of Grafman et al.6,7 and Carey et al.8 during the Vietnam era helped increase our understanding of both the acute effects and the late neurobehavioral changes of brain injuries. These contributions have allowed for further developments in modern military medicine and provided a strong foundation for our investigations today.

TBI in Iraq and Afghanistan

In the current conflicts in Iraq and Afghanistan, the focus on severe and penetrating brain injuries has shifted; the attention is now being placed on closed TBI and those brain injuries at the milder end of the spectrum, especially mild TBI (mTBI) or concussion, as it is also known. TBI severity is based on such measures as the Glasgow Coma Scale,9 duration of loss of consciousness or coma, and duration of posttraumatic amnesia. Current United States Department of Defense (DoD) ICD-9 derived diagnoses of TBI in the DoD Health Care System show that for 2009, penetrating brain injury accounted for just 1.4% of the total brain injuries, while severe closed brain injury accounted for less than 1% of the total. Of the of 27,862 TBIs counted in the year 2009, about 78% (21,859) were classified as mild. These percentages are consistent in the period 2003–2009, where a total of 134,476 brain injuries were reported. It should be noted that these numbers are limited to those that presented to the military health care system. There are likely others, largely mTBI, who never sought medical treatment or came to the attention of health care providers. Data suggest that during deployment as many as 20% or more may have suffered a concussion. Those with TBI during deployment are more likely to report postinjury and postdeployment somatic and/or neuropsychiatric symptoms than those without such an injury history.10

In Operation Iraqi Freedom (OIF) and Operation Enduring Freedom (OEF), from October 2001 to January 2005, the Joint Theater Trauma Registry reported that of those with battle injuries, a total of 1,566 combatants sustained 6,609 combat wounds. The wounds were to the head (8%), eyes (6%), ears (3%), face (10%), neck (3%), thorax (6%), abdomen (11%), and extremities (54%). The proportion of head and neck wounds from2001 to 2005 was higher than the proportion suffered in World War II, Korea, and Vietnam wars. Furthermore, while gunshot wounds accounted for 18% of the injuries from 2001 to 2005, those sustained from explosions accounted for 78% of the injuries, the highest proportion seen in any large-scale conflict.11

Blast injury — the “newest” mechanism of injury

As a result of OIF/OEF, injury due to blast has received significant attention,12-15 leading one to believe that this is a “new” injury mechanism. However, the effects of explosions on the brain were described as early as 1916 in the medical literature. 16 Explosions were also a significant source of injury in World War I and World War II, accounting for 35–73% of the injuries, respectively.11 The cluster of symptoms that became known as “shell shock” was originally thought to be related to blast exposure, although the idea was controversial even during World War I and in the years after.17

The results of the meta-analysis18 published by the World Health Organization collaborating center task force on mTBI suggest that the vast majority of adults have good outcomes following uncomplicated mTBI, typically recovering in full within months. In terms of cognition, any decrements that are apparent in neuropsychological functioning after mTBI typically resolve in 1–3 months.19 While this suggests that the majority of those sustaining mTBI, even under combat conditions, will have good recovery over the longer term, even transient symptoms may have military operational consequences. Slowed reaction time, headache, dizziness, or inattention may have implications for combat readiness or troop welfare. Even among military personnel that are not injured, there is recognition that combat operations may have cognitive consequences due to stress, sleep deprivation, or other factors.20,21 Troop commanders are increasingly aware of these issues and have been supportive of the military’s effort to screen form TBI on the battlefield, including use of the Military Acute Concussion Evaluation (MACE)22 and standardized DoD clinical practice guidelines around management of mTBI.

Outcome studies in mTBI have typically described civilian populations, but there may be differences in the military population or in mTBI acquired under combat conditions. Even in those without TBI, military deployment can result in increased emotional distress or overt psychiatric disorders. 23,24 In one military sample (prior to the current conflict), increased behavioral problems were shown in a group with TBI, as compared to their uninjured peers.25 In that sample, the relative risk for behavioral discharge was 1.8 times greater for those with mTBI, and discharge for alcoholism or drug use was 2.6 times greater for mTBI. We have very limited knowledge about longer-term outcomes in those diagnosed with TBI in the current conflicts. However, one recent study26 examining psychiatric outcomes of service members with TBI reported lower rates of posttraumatic stress disorder (PTSD) and mood/anxiety disorders among those with both mild and moderate-severe TBI, about 22–27 months following injury. Their study relied on provider diagnosis as opposed to self-report measures, however. This may partly explain the contradictory findings, as not everyone may seek out the help of a health care provider. In service members severely injured enough to require transport to a large military medical center in the United States, even mTBI has been noted to have important implications for the rehabilitation process.27

Blast, as amechanism of injury for TBI,may play a role in symptom presentation and recovery of those injured. In the military injured, blast as a mechanism of injury has been used to guide treatment and structure treatment teams.28 In one sample seen in the Department of Veterans Affairs (VA) polytrauma system, the pattern of injuries was different among those with injuries due to blasts versus other mechanisms. Injuries to the face (including eye, ear, oral, and maxillofacial), penetrating brain injuries, symptoms of posttraumatic stress, and auditory impairments were more common in blast-injured patients than in those with war injuries of other etiologies.29 Another sample in the VA polytrauma system showed that service members injured by blast had a broader spectrum of physical injuries, higher levels of admission and discharge opioid analgesic use, reduced improvement in pain intensity following treatment, and much higher rates of PTSD and other psychiatric diagnoses than those injured in combat via motor vehicle collisions, falls, or other mechanisms.30 This is also consistent with what has been observed in civilian victims of terror attacks, with those injured in blast having more body regions injured than those injured through other mechanisms, and being more severely injured overall.31 In a sample at Walter Reed Army Medical Center (WRAMC), those with TBI related to blast were significantly more likely to have had a skull fracture, seizure, or lower limb amputation than those not injured in a blast. They also were more likely to have acute stress symptoms than those who suffered TBI through other mechanisms.32

Blast-related comorbidities

A polytrauma “triad” has been reported33 with rates of chronic pain, PTSD, and persistent postconcussive symptoms (PPCS) present in 81.5%, 68.2%, and 66.8% of one sample, respectively. From this study, only 3.5% of the individuals seen were without chronic pain, PTSD, or PPCS, and 42.1% of the sample were diagnosed as having all three conditions concurrently. In the polytrauma population this introduces significant challenges for care and requires a multidisciplinary, integrated approach for success to be achieved.34 The prevalence of polytrauma in the blast population may complicate the recovery for those who, under the best of circumstances, would otherwise have an uneventful recovery from their mTBI. Polytrauma patients, even without brain injury, have high rates of neurobehavioral symptoms including memory difficulties, irritability, mood swings, suspiciousness, a motivation, and guilt.35 Some pain conditions, namely headache, also occur frequently in the TBI population.36

In a civilian population, minimal extracranial injuries and low pain have been shown to predict better outcomes for return to work aftermTBI.37 In one group who sustained mTBI and who also suffered extracranial injuries, 44% of the patients with additional injuries were still in treatment at 6 months after injury, compared to just 14% of the patients with isolated mTBI. They also had resumed work less frequently and reported more limitations in their physical functioning. Those that required continued rehabilitative treatments also reported significantly more severe postconcussive symptoms.

Individuals with traumatic limb amputations require extensive rehabilitation, and their recovery is influenced by a variety of medical, emotional, and social issues.38,39 In a review of military service members injured in 2001–2006 (87% of these by explosive device), 5.2% of all serious injuries and 7.4% of major limb injuries underwent amputation. This rate is similar to that of previous conflicts (e.g., 8.3% in Vietnam).40 Overall, amputation rates have markedly fallen with less than seven per month for 2009, contrasted to a high of 17 per month in 2007. Blast-induced limb loss with resulting loss of blood, as well as with high numbers of individuals that have sustained penetrating bodily injuries with at least some degree of hemorrhage, have raised concerns around some aspects of the trauma and its potential effects on outcome. Over 80% of the patients treated by one U.S. marine forward resuscitation surgical unit were in hemorrhagic shock.41 With significant loss there is the possibility of hemorrhagic or hypoxemic posttraumatic insults on the central nervous system. It has been shown42 that inadequate cerebral blood flow can contribute to increased morbidity after TBI. It has been reported that hypotension is a significant risk factor for death following trauma, even in the absence of a TBI.43 Following TBI, the brain appears to be especially vulnerable to posttraumatic hypoxemia.42 However, the long-term effects of severe hemorrhage (with or without co-occurring TBI) on cognition, emotion, or other neurobehavioral symptoms are largely unknown.

Sensory difficulties are another concern. Despite excellent protective wear, service members still suffer injuries to the eyes and ears.44,45 In a group of polytrauma patients injured by blast,46 the rates of visual impairment were more than double compared to other causes of polytrauma. Overall, the rate of visual impairment in blast-related injury was 52% compared with 20% for all other sources of injury. In a group of patients with TBI and comorbid combat ocular trauma at WRAMC,47 explosive fragmentary munitions accounted for 79% of TBI-associated combat ocular trauma. Severe TBI was more frequently associated with combat ocular trauma than milder TBI. Overall, TBI occurred in two-thirds of all combat ocular trauma, and ocular trauma was a common finding in all TBI cases. In another sample of Iraq and Afghanistan veterans treated in a VA polytrauma center and injured by blast, 62% complained of hearing loss and 38% reported tinnitus. This compares to rates of 44% with hearing loss and 18% with tinnitus in those injured through some mechanism other than blast.48 For those with impairments in both hearing and vision, the difficulties may be even more significant. Dual sensory impairment has been associated with increased rates of depression,49 and lower overall health-related quality of life.50 Lewet al.51 describe a VA sample in which hearing impairment was identified in 19% of the sample, visual impairment in 34% of the sample, and dual sensory impairment in 32% of the sample. Surprisingly, only 15% of the patients were without sensory impairments in either the auditory or the visual modality. Those with dual sensory impairment had difficulties participating in the rehabilitation process, and showed an overall reduction in both total and motor functional independence measure scores at discharge.

Other difficulties that may hamper recovery following blast injury may include vestibular dysfunction/dizziness and blast effects on cognition. With regards to cognition, severity of injury is more predictive of neuropsychological functioning than is mechanism of injury; analysis of neuropsychological test measures suggest there are no differences in patterns of cognitive test performance in those that suffered TBI related to blast versus other mechanisms.52 Many U.S. military service members who have been exposed to blasts and who are returning from Iraq and Afghanistan also complain of vertigo, gaze instability, motion intolerance, and other symptoms consistent with peripheral vestibular pathology.53 It has been suggested that blast exposure can induce vestibular disorders, and related symptoms are significantly different than those seen in blunt head trauma, with the vestibular characteristics and objective tests of vestibular function significantly worsening in blast exposed patients as a function of time between injury and presentation.54

In the deployed combat environment, everyday experience involves exposure to potentially emotionally traumatic situations. A survey of U.S. combat infantry units following combat duty in Iraq or Afghanistan showed high rates of potentially traumatic combat experiences.23 The rate of mental disorders after deployment to Iraq was 27.9%.The rates of PTSD were also significantly associated with having been wounded, with those respondents having a greater than threefold increase. In anyone hospitalized for physical injury there is increased risk of PTSD. One study55 of injured trauma survivors across the United States showed that 22% of the injury survivors had symptoms consistent with the diagnosis of PTSD 12 months after hospitalization. High levels of postinjury emotional distress, as well as physical pain, were associated with an increased risk of PTSD symptoms. In one military survey, the rates of PTSD and depression among soldiers who were seriously injured and required medical evacuation and hospitalization at a tertiary military medical care center was about 4% for PTSD and/or depression at 1 month following injury. These rates increased to 12.2% for PTSD and 8.9% for depression at 4 months, and were roughly the same at 7 months. High levels of self-reported physical problems at the 1-month point were significantly predictive of PTSD and depression at 7 months.56

The relationship between PTSD and physical injury has been previously reported in Israeli war veterans, with odds of developing PTSD following traumatic injury approximately eight times greater than following injury-free emotional trauma.57

The relationship between PTSD and mTBI is complex, and not fully understood. It has been suggested58 that damage to the prefrontal cortex in TBI results in disruption of neural networks involved in the regulation of anxiety, making the affected individual

more vulnerable to the effects of an emotionally traumatic event. In a recent military sample59 of 76 service members with burn injuries, the incidence rate of PTSD was 32% and mTBI was 41%. Eighteen percent screened positive for both conditions. Hoge et al.60 have reported increasing rates of PTSD and depression in a military sample as they experienced an increasingly “threatening” type of injury. The uninjured sample rates of PTSD were about 9%. In those that were injured in a place other than the head, the rates were slightly over 16%. For those with mTBI with alteration of consciousness, the rates were just over 27%. In those with mTBI with loss of consciousness, the rates were over 43%. In a Vietnam era military sample with both TBI and PTSD, mTBI (even in its chronic state) was associated with increased rates of headaches, sleep problems, and memory difficulties. More importantly, TBI has been shown to complicate or prolong recovery from preexisting or comorbid conditions, such as PTSD.61

The frequent co-occurrence of both conditions and potential interactive effects have treatment implications for those injured. Postconcussive symptoms may actually increase the likelihood of developing PTSD, because these symptoms interfere with adequate adjustment to the event.62 In addition, cognitive or neurobehavioral impairments associated with TBI may influence the efficacy of treatments for PTSD or other mental health conditions. Psychotherapeutic or educational strategies may require intact cognition to work maximally. Even subtle attentional ormemory difficulties might affect learning or other aspects of the treatment process. Unfortunately, few psychological treatments for anxiety or PTSD have been studied in people with TBI. There is some evidence for the effectiveness of cognitive behavioral therapy (CBT) for treatment of acute stress following mTBI, and for CBT combined with neurorehabilitation for generalized anxiety in those who sustained TBI of mild to moderate severity. One study63 examined a comprehensive outpatient neuropsychological rehabilitation program that targeted psychological dysfunction, emotional distress, and accompanying functional disabilities. The results suggested that intensive outpatient treatment consisting of both CBT and cognitive remediation was beneficial for the treatment of persistent emotional distress following mTBI and may have had some effect on related cognitive difficulties. There are also few studies of pharmacological treatments of mood and anxiety in TBI patients,64,65 and benefits of medication may be complicated by sensitivity to drug-induced side effects.66

Conclusions

TBI, especially mTBI, is a common consequence of modern warfare. Following TBI, regardless of injury mechanism, there are significant issues that may affect recovery and cause significant distress. These include somatic symptoms, such as headache, sleep disturbance, and dizziness; emotional difficulties, such as irritability and mood change; and cognitive difficulties, such as attentional dysfunction, memory problems, or difficulties in communication. Typically, the frequency and duration of such symptoms is related to injury severity. However, continued expression of symptoms may, in part, be linked to emotional factors.60,67

In the current conflicts in Iraq and Afghanistan much attention has been devoted to explosive blast as an injury mechanism, especially brain injury. While the evidence for primary blast effects (effects of the blast “wave” itself) upon the central nervous system is limited,68 and an area of active investigation,69 there are a number of aspects of blast-induced brain injury that may be different from more “typical” injury mechanisms, such as motor vehicle accidents or falls. These include high rates of sensory impairment, pain issues, and polytrauma. In addition, the emotional context in which the injury occurred must also be considered in understanding the clinical presentation of these patients. Successful treatment of these individuals must use a multidisciplinary approach focused on the varied conditions that occur in those injured. A thorough assessment of all comorbid conditions must be undertaken and addressed. For some individuals this can be accomplished in the primary care setting. For others, especially those suffering polytrauma, a specialized program involving neurology, psychiatry, behavioral health, occupational therapy, physical therapy, pain medicine, and other relevant disciplines should be considered for successful treatment.

References

  1. McDonald, I. 2007. Gordon Holmes Lecture: Gordon Holmes and the neurological heritage. Brain 130: 288–298.
  2. Lanska, D.J. 2009. Historical perspective: neurological advances from studies of war injuries and illnesses. Ann. Neurol.: 444–459.
  3. Semmes, J., S.Weinstein, L. Ghent, et al. 1954. Performance on complex tactual tasks after brain injury in man: analyses by locus of lesion. Am. J. Psychol. 67: 220–240.
  4. Luria, A.R. 1976. The Working Brain: An Introduction to Neuropsychology. Basic Books.New York.
  5. Luria, A.R. 2004. The Man with a Shattered World: The History of a Brain Wound. Harvard Press. Boston.
  6. Grafman, J., B.S. Jonas, A. Martin, et al. 1988. Intellectual function following penetrating head injury in Vietnam veterans. Brain 111: 169–184.
  7. Raymont, V., A. Greathouse, K. Reding, et al. 2008. Demographic, structural and genetic predictors of late cognitive decline after penetrating head injury. Brain 131: 543–558.
  8. Carey, M.E., W. Sacco & J. Merkler. 1982. An analysis of fatal and non-fatal head wounds incurred during combat in Vietnam by U.S. forces. Acta Chir. Scand. 508: 351–356.
  9. Teasdale, G. & B. Jennett. 1974. Assessment of coma and impaired consciousness. A practical scale. Lancet 2: 81– 84.
  10. Terrio, H., L.A. Brenner, B.J. Ivins, et al. 2009. Traumatic brain injury screening: preliminary findings in a US Army Brigade Combat Team. J. Head Trauma Rehabil. 24: 14–23.
  11. Owens, B.D., J.F. Kragh, Jr., J. C. Wenke, et al. 2008. Combat wounds in operation iraqi freedom and operation enduring freedom. J. Trauma 64: 295–299.
  12. Martin, E.M., W.C. Lu, K. Helmick, et al. 2008. Traumatic brain injuries sustained in the Afghanistan and Iraq wars. J. Trauma Nurs. 15: 94–99, quiz 100–101.
  13. Ritenour,A.E.&T.W. Baskin. 2008. Primary blast injury: update on diagnosis and treatment. Crit. Care Med. 36: S311–S317.
  14. Wolf, S.J., V.S. Bebarta, C.J. Bonnett, et al. 2009. Blast injuries. Lancet 374: 405–415.
  15. Okie, S. 2005. Traumatic brain injury in the war zone. N. Engl. J. Med. 352: 2043–2047.
  16. Mott, F.W. 1916. The Lettsomian Lectures: on the effects of high explosives on the central nervous system. Lancet 187: 545–553.
  17. Jones, E., N.T. Fear & S.Wessely. 2007. Shell shock andmild traumatic brain injury: a historical review. Am. J. Psychiatry 164: 1641–1645.
  18. Carroll, L.J., J.D. Cassidy, P.M. Peloso, et al. 2004. Prognosis formild traumatic brain injury: results of theWHOCollaborating Centre Task Force on mild traumatic brain injury. J. Rehabil. Med. 43: S84–S105.
  19. Schretlen, D.J. & A.M. Shapiro. 2003. A quantitative review of the effects of traumatic brain injury on cognitive functioning. Int. Rev. Psychiatry 15: 341–349.
  20. Lieberman, H.R., G.P. Bathalon, C.M. Falco, et al. 2005. Severe decrements in cognition function and mood induced by sleep loss, heat, dehydration, and undernutrition during simulated combat. Biol. Psychiatry 57: 422–429.
  21. Lieberman, H.R., G.P. Bathalon, C.M. Falco, et al. 2005. The fog of war: decrements in cognitive performance and mood associated with combat-like stress. Aviat. Space Environ. Med. 76: C7–C14.
  22. French, L.M., M. McCrea & M. Baggett. 2008. The Military Acute Concussion Evaluation (MACE). J. Spec Oper.Med. 8: 77–83.
  23. Hoge, C.W., C.A. Castro, S.C. Messer, et al. 2004. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. N. Engl. J. Med. 351: 13–22.
  24. Polusny, M.A., C.R. Erbes, P.A. Arbisi, et al. 2009. Impact of prior Operation Enduring Freedom/Operation Iraqi Freedom combat duty on mental health in a predeployment cohort of National Guard soldiers. Mil. Med. 174: 353– 357.
  25. Ommaya, A.K., A.M. Salazar, A.L. Dannenberg, et al. 1996. Outcome after traumatic brain injury in the U.S. military medical system. J. Trauma 41: 972–975.
  26. MacGregor, A.J., R.A. Shaffer, A.L. Dougherty, et al. 2010. Prevalence and psychological correlates of traumatic brain injury inOperation Iraqi Freedom. J. Head Trauma Rehabil. 25: 1–8.
  27. French, L.M.&G.W. Parkinson. 2008.Assessing and treating veterans with traumatic brain injury. J. Clin. Psychol. 64: 1004–1013.
  28. Scott, S.G., H.G. Belanger, R.D. Vanderploeg, et al. 2006. Mechanism-of-injury approach to evaluating patients with blast-related polytrauma. J. Am. Osteopath. Assoc. 106: 265–270.
  29. Sayer, N.A., C.E. Chiros, B. Sigford, et al. 2008. Characteristics and rehabilitation outcomes among patients with blast and other injuries sustained during the GlobalWar on Terror. Arch. Phys. Med. Rehabil. 89: 163–170.
  30. Clark, M.E., R.L. Walker, R.J. Gironda, et al. 2009. Comparison of pain and emotional symptoms in soldiers with polytrauma: unique aspects of blast exposure. PainMed. 10: 447–455.
  31. Peleg, K., L. Aharonson-Daniel, M. Michael, et al. 2003. Patterns of injury in hospitalized terrorist victims. Am. J. Emerg. Med. 21: 258–262.
  32. Warden, D. 2006. Military TBI during the Iraq and Afghanistan wars. J. Head Trauma Rehabil. 21: 398–402.
  33. Lew, H.L., J.D.Otis, C. Tun, et al. 2009. Prevalence of chronic pain, posttraumatic stress disorder, and persistent postconcussive symptoms in OIF/OEF veterans: polytrauma clinical triad. J. Rehabil. Res. Dev. 46: 697–702.
  34. Gironda, R.J., M.E. Clark, R.L. Ruff, et al. 2009. Traumatic brain injury, polytrauma, andpain: challenges and treatment strategies for the polytrauma rehabilitation.Rehabil. Psychol. 54: 247–258.
  35. Frenisy, M.-C., H. Benony, K. Chahraoui, et al. 2006. Brain injured patients versusmultiple trauma patients: some neurobehavioral and psychopathological aspects. J. Trauma 60: 1018–1026.
  36. Packard, R.C. 2008. Chronic post-traumatic headache: associations with mild traumatic brain injury, concussion, and post-concussive disorder. Curr. Pain Headache Rep. 12: 67–73.
  37. Stulemeijer, M., S.P. Van Der Werf, B. Jacobs, et al. 2006. Impact of additional extracranial injuries on outcome after mild traumatic brain injury. J. Neurotrauma 23: 1561– 1569.
  38. Pasquina, P.F., J.W. Tsao, D.M. Collins, et al. 2008. Quality of medical care provided to service members with combatrelated limb amputations: report of patient satisfaction. J. Rehabil. Res. Dev. 45: 953–960.
  39. Messinger, S.D. 2009. Incorporating the prosthetic: traumatic, limb-loss, rehabilitation and refigured military bodies. Disabil. Rehabil. 31: 2130–2134.
  40. Stansbury, L.G., S.J. Lalliss, J.G. Branstetter, et al. 2008. Amputations in U.S. military personnel in the current conflicts in Afghanistan and Iraq. J. Orthop. Trauma 22: 43–46.
  41. Chambers, L.W., P. Rhee, B.C. Baker, et al. 2005. Initial experience of US Marine Corps forward resuscitative surgical system during Operation Iraqi Freedom. Arch. Surg. 140: 26–32.
  42. DeWitt, D.S. & D.S. Prough. 2009. Blast-induced brain injury and posttraumatic hypotension and hypoxemia. J.Neurotrauma 26: 877–887.
  43. Shafi, S.&L. Gentilello. 2005.Hypotension does not increase mortality in brain-injured patients more than it does in nonbrain- injured patients. J. Trauma 59: 830–835.
  44. Helfer, T.M., M. Canham-Chervak, S. Canada, et al. 2010. Epidemiology of hearing impairment and noise-induced hearing injury among U.S. military personnel, 2003–2005. Am. J. Prev.Med. 38: S71–S77.
  45. Hilber, D., T.A. Mitchener, J. Stout, et al. 2009. Eye injury surveillance in the U.S. Department of Defense, 1996–2005. Am. J. Prev.Med. 38: S78–S85.
  46. Goodrich, G.L., J. Kirby, G. Cockerham, et al. 2007. Visual function in patients of a polytrauma rehabilitation center: a descriptive study. J. Rehabil. Res. Dev. 44: 929–936.
  47. Weichel, E.D., M.H. Colyer, C. Bautista, et al. 2009. Traumatic brain injury associated with combat ocular trauma. J. Head Trauma Rehabil. 24: 41–50.
  48. Lew, H.L., J.F. Jerger, S.B. Guillory, et al. 2007. Auditory dysfunction in traumatic brain injury. J. Rehabil. Res. Dev. 44: 921–928.
  49. Capella-McDonnall, M.E. 2005. The effects of single and dual sensory loss on symptoms of depression in the elderly. Int. J. Geriatr. Psychiatry 20: 855–861.
  50. Chia, E.M., P. Mitchell, E. Rochtchina, et al. 2006. Association between vision and hearing impairments and their combined effects on quality of life. Arch. Ophthalmol. 124: 1465–1470.
  51. Lew, H.L., D.W. Garvert, T.K. Pogoda, et al. 2009. Auditory and visual impairments in patients with blast-related traumatic brain injury: effect of dual sensory impairment on functional independence measure. J. Rehabil. Res. Dev. 46: 819–826.
  52. Belanger, H.G., T. Kretzmer, R. Yoash-Gantz, et al. 2009. Cognitive sequelae of blast-related versus othermechanisms of brain trauma. J. Int. Neuropsychol. Soc. 15: 1–8.
  53. Scherer, M.R. & M.C. Schubert. 2009. Traumatic brain injury and vestibular pathology as a comorbidity after blast exposure. Phys. Ther. 89: 980–992.
  54. Hoffer,M.E., C. Balaban,K.Gottshall, et al. 2010. Blast exposure: vestibular consequences and associated characteristics. Otol. Neurotol 31: 232–236.
  55. Zatzick,D.F., F.P. Rivara, A.B.Nathens, et al. 2007. A nationwide US study of post-traumatic stress after hospitalization for physical injury. Psychol. Med. 37: 1469–1480.
  56. Grieger, T.A., S.J. Cozza, R.J. Ursano, et al. 2006. Posttraumatic stress disorder and depression in battle-injured soldiers. Am. J. Psychiatry 163: 1777–1783, quiz 860.
  57. Koren, D., D. Norman, A. Cohen, et al. 2005. Increased PTSD risk with combat-related injury: a matched comparison study of injured and uninjured soldiers experiencing the same combat events. Am. J. Psychiatry 162: 276–282.
  58. Kennedy, J.E., M.S. Jaffee, G.A. Leskin, et al. 2007. Posttraumatic stress disorder and posttraumatic stress disorder-like symptoms and mild traumatic brain injury. J. Rehabil. Res. Dev. 44: 895–920.
  59. Gaylord, K.M., D.B. Cooper, J.M. Mercado, et al. 2008. Incidence of posttraumatic stress disorder and mild traumatic brain injury in burned service members: preliminary report. J. Trauma 64: S200–S206.
  60. Hoge, C.W., D.McGurk, J.L. Thomas, et al. 2008.Mild traumatic brain injury in U.S. soldiers returning from Iraq. N. Engl. J. Med. 358: 453–463.
  61. Vanderploeg, R.D., H.B. Belanger & G. Curtiss. 2009. Mild traumatic brain injury and posttraumatic stress disorder and their associations with health symptoms. Arch. Phys. Med. Rehabil. 90: 1084–1093.
  62. Meares, S., E.A. Shores, A.J. Taylor, et al. 2008. Mild traumatic brain injury does not predict acute postconcussion syndrome. J. Neurol. Neurosurg. Psychiatry 79: 300–306.
  63. Tiersky, L.A., V. Anselmi, M.V. Johnston, et al. 2005. A trial of neuropsychologic rehabilitation in mild-spectrum traumatic brain injury. Arch. Phys.Med. Rehabil. 86: 1565–1574.
  64. Warden,D.L., B. Gordon,T.W.McAllister, et al. 2006.Guidelines for the pharmacologic treatment of neurobehavioral sequelae of traumatic brain injury. J.Neurotrauma 23: 1468–1501.
  65. Lee, H.B., C.G. Lyketsos & V. Rao. 2003. Pharmacological management of the psychiatric aspects of traumatic brain injury. Int. Rev. Psychiatry 15: 359–370.
  66. Warden, D.L. & L.A. Labbate. 2005. Posttraumatic stress disorder and other anxiety disorders. In Textbook of Traumatic Brain Injury. J.M. Silver, T.W. McAllister & S.C. Yudofsky, Eds.: 231–243. American Psychiatric Publishing, Inc. Arlington.
  67. Belanger, H.G., T. Kretzmer, R.D. Vanderploeg, et al. 2009. Symptom complaints following combat-related traumatic brain injury: relationship to traumatic brain injury severity and posttraumatic stress disorder. J. Int. Neuropsychol. Soc. 16: 194–199.
  68. Warden,D.L.,L.M.French, L. Shupenko, et al. 2009. Case report of a soldier with primary blast brain injury. Neuroimage 47: T152–T153.
  69. Champion, H.R., J.B. Holcomb & L.A. Young. 2009. Injuries from explosions: physics, biophysics, pathology, and required research focus. J. Trauma 66: 1468–1477.
Posted on BrainLine January 10, 2011

Comments

From 1980 when i fell off a hydraulic stand used to work on big aircraft! First it was a long time ago and the safety issues were null and void compared to today's standards!! 3 decades worth of anxieties, headaches, insomnia,and chronic pain that goes with TBI. Still the military has not taken responsibility  for what happened. They have never giving me any compensation. Only the doctors help me out!!  I feel so sorry to my fellow troops that have to deal with TBI!  It only gets worse in severe cases. I urge all vet's that have TBI to get proper care for this injury. Because like i said it only gets worse over time. 

WW II and Vietnam War veterans would have reported a multitude of cranial shock-wave injuries had they even know they were injured!  To say that fewer injuries were reported doesn't reflect that fewer injuries were sustained.  Today, those very veterans are experiencing PTSD and Parkinson symptoms due to untreated TBI.

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