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Blast-associated traumatic brain injury in the military as a potential trigger for dementia and chronic traumatic encephalopathy.

TRAUMATIC BRAIN INJURY IN THE UNITED STATES

Traumatic brain injury (TBI) is a disruption in brain function or pathology due to an external force that exceeds the protective capacity of the head and causes neuropsychiatric impairment, either permanent or temporary. Complications of TBI include seizures, spasticity, gait abnormalities, agitation, depression, headaches, insomnia, cognitive decline, dementia, gastrointestinal and urogenital complications, and chronic traumatic encephalopathy. In the United States alone, an estimated 1.7 million people suffer a TBI annually, of which 275,000 require hospitalization. (1) Falls and motor vehicle accidents are the major causes of TBI in the United States.1 Traumatic brain injury is a leading cause of death and disability for individuals between the ages of one and 44 years, and it is estimated that almost 2% of the population currently live with complications and disabilities related to a prior TBI. (2)

TRAUMATIC BRAIN INJURY IN THE US MILITARY

Traumatic brain injury is a major health concern for the US military. With the widespread use by enemy combatants of improvised explosive devices in recent conflicts, there have been a higher proportion of explosive-related head injuries in comparison to previous wars. (3,4) Data from Operation Enduring Freedom, Operation Iraqi Freedom, and Operation New Dawn show that blastrelated injuries are a major cause of TBI for military troops. (5) As illustrated in the Figure, from 2000-2016, there were 357,048 medical diagnoses of traumatic brain injuries in the US military with 82.3% of these injuries classified as mild TBIs. (6) A mild TBI is characterized by the Department of Defense as a confused or disoriented state that lasts less than 24 hours; or loss of consciousness for up to 30 minutes; or memory loss lasting less than 24 hours. Mild TBI is difficult to detect as there is often a lack of any external evidence of damage to the head. A CT scan is generally not indicated for these patients, and if obtained, is often found to be normal. (6) Currently, there are no specific laboratory markers or imaging studies that are routinely performed that can detect any long-lasting damage to these patients. (7) Due to the difficult nature in diagnosing a TBI, there are likely far more mild TBIs that remain undiagnosed in the military.

TRAUMATIC BRAIN INJURY AND A HISTORY OF NEUROPSYCHIATRIC DYSFUNCTION IN WAR: SHELL SHOCK, POSTTRAUMATIC STRESS DISORDER, AND DEMENTIA

The development of neuropsychiatric symptoms in military veterans exposed to high-intensity explosives has been recognized since World War I (WWI). Military troops involved in trench warfare were often barraged with artillery, with many Soldiers developing the neuropsychological impairment known as "shell shock." (8,9) Symptoms of shell shock included fatigue, confusion, nightmares and impaired sight or hearing. Soldiers were often diagnosed once they became unable to function/ perform their duties, usually without any obvious cause that could be identified. Since Soldiers often lacked physical signs of disease, they were often accused of cowardice or malingering. It was later recognized that shell shock shared similar symptoms to posttraumatic stress disorder (PTSD), which would later be recognized during the Vietnam War.

Since the conflicts in Vietnam, Iraq, and Afghanistan, there has been more insight into the neuropsychological dysfunction of military personnel who suffer from PTsD. Similar to the shell shock observed in WWI, PTSD symptoms include disturbing thoughts, flashbacks during trauma-related cues, cognitive and behavioral changes, depression, anxiety, and a higher risk of suicide. Although there is tremendous overlap between PTSD and shell shock in several ways, it is important to acknowledge that patients can also develop PTSD without evidence of TBI or head trauma. Examples include victims of rape, natural disaster survivors, or individuals who have suffered severe psychological stressors. However, evidence shows a TBI alone can be a potential trigger for PTSD as well. A survey of 2,525 US Army Infantry Soldiers deployed to Iraq for one year demonstrated that 44% of Soldiers who suffered a mild TBI with subsequent loss of consciousness met the criteria for PTSD. (10) Another study found blast-related injuries on mice under anesthesia produced PTSD behavioral changes in the absence of psychological stressors. (11) Traumatic brain injury appears to be a very strong risk factor for the development of PTSD. It is also very likely that the majority of Soldiers who suffered from shell shock in WWI would fit the diagnosis of PTSD in modern times.

Traumatic brain injury has also been recognized as a potential risk factor for the development of dementia and neurodegeneration. (12) Individuals who suffer from dementia typically demonstrate a decline in cognitive ability that is often severe enough to interfere with daily life. These individuals may demonstrate memory loss, cognitive decline, and behavioral or psychological changes. A study of US Navy and Marine Corps veterans hospitalized during WWII demonstrated an association between TBI in early to midlife with the development of dementia later in life. (13) Veterans who sustained a TBI that resulted in loss of consciousness or posttraumatic amnesia longer than 30 minutes but less than 24 hours were more than twice as likely to develop dementia. (13) Veterans who sustained a TBI severe enough to cause loss of consciousness or posttraumatic amnesia greater than 24 hours were more than 4 times likely to develop dementia compared to the control counterparts. (13) These findings demonstrate that TBI-related complications may manifest much later in life, and our veterans may actually have a higher risk of developing dementia compared to the civilian population.

TRAUMATIC BRAIN INJURY AND CHRONIC TRAUMATIC ENCEPHALOPATHY

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that is thought to develop secondary to repetitive head trauma, including concussive and subconcussive injuries. The clinical presentation of CTE varies, and often overlaps with other neuropsychological disorders including Alzheimer's, Parkinson's, and PTSD. Patients with CTE often exhibit both cognitive and behavioral impairment including chronic headaches, memory difficultly, poor impulse control, aggression, depression, suicidal tendencies, and also dementia. (14,15) Behavioral changes are typically seen earlier in the disease, and these patients may often be diagnosed with PTSD. Later in the disease process, patients show symptoms such as memory loss and cognitive decline consistent with dementia.

Chronic traumatic encephalopathy is a newly recognized disease with few confirmed diagnoses. The disease is a clinical diagnosis that can only be confirmed postmortem. It is often regarded as a disease that develops from repetitive head trauma in athletes, such as football players and wrestlers, who suffer multiple concussive injuries. However, new data suggests military personnel may be at risk for developing CTE, and a single blast-related TBI may be sufficient to trigger the neuropathologic changes seen in CTE. (16) Brain pathology of postmortem athletes who have suffered repetitive concussive injuries have demonstrated distinct neuropathologic changes that differentiate CTE from other known forms of dementia. (15-17) Comparison of brains from postmortem military veterans exposed to blast injuries demonstrated neuropathology that was indistinguishable from the neuropathology of young athletes with CTE. (16) Furthermore, experiments on rodents exposed to an isolated blast-related injury demonstrated neuropathology similar to that of patients found to have CTE from repetitive head trauma. (16) This study in rodents also showed that TBI from blast-related head injuries resulted in progressive neurodegeneration that continued for more than one year after the initial injury. These studies demonstrate that isolated blast-associated TBIs could trigger the development of CTE-like symptoms and neuropathology. (16)

COMMENT

Traumatic brain injury is a serious public health concern in both civilian life and in the US military. Today, our military troops have a greater risk of TBIs due to the increased use of improvised explosive devices and subsequent blast-related injuries. Evidence shows that a mild TBI is a risk factor for developing long-term neuro-psychiatric conditions such as PTSD, dementia, and even CTE. Since CTE is a newly discovered disease that can currently only be confirmed postmortem, CTE may be overlooked as a differential diagnosis and mistaken for other neuro-psychiatric diseases. Chronic traumatic encephalopathy should be considered in patients that have a previous history of a TBI and are being evaluated for a neuropsychiatric disorder. Furthermore, the diagnosis of CTE may better explain the development of symptoms in veterans found to have shell shock, PTSD, or other forms of dementia. Any patient with a history of TBI should be counseled and closely followed to ensure appropriate care and social support. With increasing awareness that military service members are at risk for TBI-related neurodegenerative diseases, further research into diagnostic studies, preventive strategies, and eventually therapeutic interventions is essential for the wellbeing of our veterans.

REFERENCES

(1.) Faul M, Xu L, Wald MW, Coronado VG. Taumatic Brain Injury in the United States: Emergency Department Visits, Hospitalization, and Deaths 20022006. Atlanta, GA: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 2010. Available at: https://www. cdc.gov/traumaticbraininjury/pdf/blue_book.pdf. Accessed April 14, 2017.

(2.) Cicerone KD, Kalmar K. Persistent post-concussive syndrome: structure of subjective complaints after mild traumatic brain injury. The Journal of Head Trauma Rehabilitation. 1995; 10(3):1-18.

(3.) Owens BD, Kragh JF Jr, Wenke JC, Macaitis J, Wade CE, Holcomb JB. Combat wounds in Operation Iraqi Freedom and Operation Enduring Freedom. J Trauma. 2008; 64:295-299.

(4.) United States Government Accountability Office. Mild traumatic brain injury screening and evaluation implemented for OEF/OIF Veterans, but challenges remain. February 2008 [internet]. Available at: https://digital.library.unt.edu/ark:/67531/ metadc302992/m1/1/. Accessed April 14, 2017.

(5.) Wojcik BE, Stein CR, Bagg K, Humphrey RJ, Orosco J. Traumatic brain injury hospitalizations of U.S. Army soldiers deployed to Afghanistan and Iraq. Am JPrev Med. 2010; 38(suppl):S108-S116.

(6.) Defense and Veterans Brain Injury Center. DoD Worldwide Numbers for TBI [internet]. 2016. Available at: http://dvbic.dcoe.mil/dod-worldwidenumbers-tbi. Accessed April 14, 2017.

(7.) Mac Donald CL, Johnson AM, Cooper D, et al. Detection of blast-related traumatic brain injury in U.S. military personnel. N Engl J Med. 2011; 364(22):2091-2100.

(8.) Mott FW. The effects of high explosives upon the central nervous system, II. Lancet. 1916; 4826:441-449.

(9.) Mott FW. The effects of high explosives upon the central nervous system, III. Lancet. 1916; 4828:545-553.

(10.) Hoge CW, McGurk D, Thomas JL, Cox AL, Engel CC, Castro CA. Mild traumatic brain injury in US Soldiers returning from Iraq. N Engl J Med. 2008; 358:453-463.

(11.) Elder GA, Dorr NP, De Gasperi R, et al. Blast exposure induces post-traumatic stress disorder-related traits in a rat model of mild traumatic brain injury. JNeurotrauma. 2012; 29:2564-2575.

(12.) Fleminger S, Oliver DL, Lovestone S, Rabe-Hesketh S, Giora A. Head injury as a risk factor for Alzheimer's disease: the evidence 10 years on; a partial replication. J Neurol Neurosurg Psychiatry. 2003; 74:857-862.

(13.) Plassman BL, Havlik RJ, Steffens DC, et al. Documented head injury in early adulthood and risk of Alzheimer's disease and other dementias. Neurology. 2000; 55:1158-1166.

(14.) Stern RA, Daneshvar DH, Baugh CM, et al. Clinical presentation of neuropathologically-confirmed chronic traumatic encephalopathy in athletes. Neurology. 2013; 81:1122-1129.

(15.) Baugh CM, Stamm JM, Riley DO, et al. Chronic traumatic encephalopathy: neurodegenera tion following repetitive concussive and subconcussive brain trauma. Brain Imaging Behav. 2012; 6:244-254.

(16.) Goldstein LE, Fisher AM, Tagge CA, et al. Chron ic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model. Sci Transl Med. 2012; 4(134):134ra60. Available at: https://doi.org/10.1126/scitransl med.3003716. Accessed April 14, 2017. DOI: 10.1126/scitranslmed.3003716.

(17.) Gavett BE, Stern RA, McKee AC. Chronic traumatic encephalopathy: a potential late effect of sport-related concussive and subconcussive head trauma. Clin Sports Med. 2011; 30(1):179-188.

Jamal Hasoon, MD

AUTHOR

Dr Hasoon is a resident physician in the Department of Anesthesiology at the Baylor College of Medicine, Houston, Texas.
DoD Numbers for Traumatic Brain Injury
Worldwide--Totals

2000-2016 (Q1-Q3)

Penet rating        5,045      1.4%
Severe              3,733      1.0%
Moderate           32,434      9.1%
Mild               294,010    82.3%
Not Classifiable   21,826      6.1%

Iotal-All          357048    357.048
Seventies

Source: Defense Medical Surveillance System
(DMSS)
Theater Medical Data Store (TMDS) provide by the
Armed Forces Health Surveillance Center(AFHSB)

Prepared by the Defense and Veterans Brains Injury
Center(DVBIC)

Note: Table made from pie chart.
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Author:Hasoon, Jamal
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Date:Jan 1, 2017
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