AJPH PERSPECTIVES
cognitive damage; and mirroring Foley’s argument back to her, the lack of randomized controlled trial evidence supporting longterm treatment.5 The debate created an ongoing and serious fracture within the field. The fracture became a seismic shock in the 2000s when Purdue’s aggressive marketing of its controlled-release opioid Oxycontin as safe for chronic pain intersected with the trafficking of cheap, very pure heroin in smaller cities across the West, Midwest, and Appalachia. Purdue advertised Oxycontin as nonaddictive because the drug was released within the body over 12 hours; recreational users quickly learned to get high by crushing or dissolving the pills, or simply taking very high doses. Overstressed and wellintentioned general practitioners, and a number of unscrupulous “pill mill” operators, wrote liberal prescriptions for the new analgesic. The ready supply of Oxycontin made diversion and sale, particularly by low-income patients on Medicaid or Medicare, attractive and easy; but when pill addicts
found their drug too expensive, they sought an alternative. Traffickers of black-tar heroin had meanwhile arrived in Middle America with a new marketing approach, driving to meet buyers in safe locations and offering inexpensive product, often giving free samples to encourage customer loyalty.6 “When you’re paying 40 dollars a pill and then you hear you can pay 10 dollars for the same effect, of course you’re going to do it.” Hundreds of Oxycontin abusers, many of them middle-class adolescents and young adults, began to see heroin as “a less and less scary and taboo thing.”7 The result has been an alarming increase in heroin use across the country and an epidemic of drug overdose deaths, which increased 137% between 2000 and 2014; overdoses involving prescription opioids and heroin increased 200% in that period. Many who championed liberalized opioid therapy for chronic pain, including Portenoy, have now retreated from that position, acknowledging that their stance led to
unanticipated abuse and tragedy. But as the CDC guidelines demonstrate, patients with severe chronic pain will still need opioids, and physicians will be called on to prescribe it, albeit with more caution and as Foley and Portenoy wrote 30 years ago, the physician’s “intensive involvement.” Prescription under strict guidelines may finally provide the evidence for or against long-term opioid therapy for chronic pain that has been so long lacking. In its absence, the availability and use of opioids, with often deadly results, has been too far governed by other factors: the shrewd targeting of a market niche by a pharmaceutical manufacturer, the costbenefit calculations of insurance carriers, and the creative entrepreneurship of drug traffickers. Marcia L. Meldrum, PhD
ACKNOWLEDGMENTS The author would like to thank Daniel Fox for his help and guidance.
Repeated Concussions: Time to Spur Action Among Vulnerable Veterans The Secretary of the United States Department of Veterans Affairs (VA) Honorable Robert McDonald recently pledged to donate his brain for chronic traumatic encephalopathy (CTE) research. Citing exposures to football, rugby, boxing, and paratrooper escapades as an army ranger, Secretary McDonald suggested that his brain could add to the body of knowledge on the effect of repeated concussions. In the meantime, work is under way to make the connections between the CTE postmortem diagnosis and the clinical findings
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while people are alive. Such knowledge is expected to positively impact medical management for people at risk and inform necessary policies, preventive actions, and health equity issues. Even though recent CTE discussions have focused on the definitive findings among football players and other athletes, the root cause of the pathology— repeated concussion—is prevalent among veterans in the form of traumatic brain injury (TBI). Veterans tend to have a higher incidence of TBI than comparable
counterparts in the general public as a result of military service exposures.1 Since 2000, there
REFERENCES 1. Dowell D, Haegerich TM, Chou R. CDC guideline for prescribing opioids for chronic pain–United States, 2016. MMWR Recomm Rep. 2016;65(1): 1–49. 2. Physicians for Responsible Opioid Prescribing. Letter to the Joint Commission. Available at: http://www.citizen. org/documents/2314b.pdf. Accessed June 13, 2016. 3. Meldrum ML. The property of euphoria: research and the cancer patient. In: Meldrum ML, ed, Opioids and Pain Relief: A Historical Perspective. Seattle, WA: IASP Press; 2002: 196, 198, 200–208. 4. Meldrum ML. The prescription as stigma: opioid pain relievers and the long walk to the pharmacy counter. In: Watkins ES, Greene JA. Prescribed: Writing, Filling, Using and Abusing the Prescription in Modern America. Baltimore, MD: Johns Hopkins University Press; 2012: 195, 201. 5. Katz MH. Long-term opioid treatment of nonmalignant pain: a believer loses his faith. Arch Intern Med. 2010;170(16): 1422–1424. 6. Quinones S. Dreamland: The True Tale of America’s Opiate Epidemic. New York, NY: Bloomsbury Press; 2015. 7. Mars SG, Bourgois P, Karandinos G, Montero F, Ciccarone D. “Every ‘never’ I ever said came true”: Transitions from opioid pills to heroin injecting. Int J Drug Policy. 2014;25: 262–263.
have been 344 030 medical diagnoses of TBIs in the United States Armed Forces and more than 80% of these injuries are considered mild in nature.2 Brain injuries are a major concern in the United States. Annually, an estimated 1.7 million people
ABOUT THE AUTHORS Uchenna S. Uchendu is with the United States Department of Veterans Affairs, Washington, DC. Bennet I. Omalu is with the Department of Pathology, University of California, Davis. David X. Cifu is with the Virginia Commonwealth University School of Medicine, Richmond, and the United States Department of Veterans Affairs Medical Center, Richmond. Leonard E. Egede is with the Medical University of South Carolina, Charleston, and the United States Department of Veterans Affairs Medical Center, Charleston. Correspondence should be sent to Uchenna S. Uchendu, MD Chief Officer, Office of Health Equity, United States Department of Veterans Affairs, 810 Vermont Avenue NW., Washington, DC 20420 (e-mail: [email protected]). Reprints can be ordered at http:// www.ajph.org by clicking the “Reprints” link. This editorial was accepted May 27, 2016. Note. The opinions expressed in this editorial are those of the authors and do not necessarily represent the United States Department of Veterans Affairs or any of the institutions/ organizations affiliated with any of the authors. doi: 10.2105/AJPH.2016.303293
AJPH
August 2016, Vol 106, No. 8
AJPH PERSPECTIVES
Office of Health Equity Traumatic Brain Injury–Chronic Traumatic Encephalopathy (CTE): 2016
experience a TBI. These injuries contribute to a third of all injury deaths.3 Traumatic brain injury is an alteration in brain function or other evidence of brain pathology caused by an external force leading to temporary or permanent impairment of cognitive, physical or psychosocial functions—the polytrauma triad. Mild TBIs (mTBIs) or concussions present with an initial impairment in sensorium (unconscious or altered consciousness) for 30 minutes or less and can result in longstanding deficits in all spheres of functioning in a small percentage of individuals. As a result of an increased use of improvised explosive devices, mTBIs were deemed the “signature injury” of the recent Gulf War occurring in up to 20% of all deployed US service members. Importantly, persistent symptoms and functional difficulties from these combat-associated concussions, which generally last more than three months after injury, have been seen in approximately 40% of these concussed individuals and 8% of all veterans seen in the Veterans Affairs clinics from
August 2016, Vol 106, No. 8
AJPH
the conflicts. The long-term effects of single or multiple mTBIs in later life are poorly understood, but recent research suggests a possible connection between multiple concussions and neurodegeneration. Chronic traumatic encephalopathy is a progressive neurodegenerative syndrome caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration–deceleration forces to the brain. The condition presents clinically after a prolonged latent period as a composite syndrome of mood disorders, and neuropsychiatric and cognitive impairment. It usually presents with a prolonged latency period; however, some patients with CTE may not exhibit the classic prolonged latency period before clinical symptoms begin. Definitive CTE diagnosis remains in direct brain tissue analysis after death; however, a presumptive clinical diagnosis of CTE can be made based on a constellation of pathognomonic symptoms. Chronic traumatic encephalopathy belongs to the spectrum of chronic TBI and is a direct,
long-term, and permanent consequence of TBI. Military veterans who are exposed to all types of TBI, including acceleration–deceleration injuries of the brain from exposure to ordinances, stand a reasonable risk of developing CTE.4,5 Research is beginning to show that some of the posttraumatic stress disorder cases diagnosed in veterans are CTE, which raises concerns for increased rates of CTE in vulnerable Veteran populations. Recent evidence suggests racial/ethnic differences in mortality among veterans with TBI. In a nationally representative study of veterans with TBI, Hispanic veterans had almost twofold increased hazard ratio of death compared with non-Hispanic White veterans (1.6; 95% confidence interval (CI) = 1.0, 2.6) after adjusting for relevant covariates.6 A recent study used nationally representative VA data to examine the association between TBI severity and combat by race/ethnicity.7 The study found that 26% of veterans with TBI served in a combat zone between 2004 and 2010; mTBI increased from 12% to 40%, whereas moderate or severe TBI decreased from 89% to 60%. Moderate or severe TBI was higher in non-Hispanic Blacks (80%) and Hispanics (89%) than in non-Hispanic Whites (72%). In the fully adjusted model that included all ethnic groups, non-Hispanic Blacks (odds ratio [OR] = 1.4; 95% CI = 1.4, 1.5) and Hispanics (OR = 1.5; 95% CI = 1.3, 1.7) had higher odds of moderate or severe TBI than did non-Hispanic Whites. However, combat exposure was associated with higher odds of mild TBI in non-Hispanic Blacks (OR = 2.5; 95% CI = 2.2, 2.8) and Hispanics (OR = 3.4; 95% CI = 1.8, 6.4) than in
non-Hispanic Whites (OR = 2.2; 95% CI = 2.1, 2.3). The prevalence of CTE is unknown, and the amount of mTBI or subconcussive trauma exposure necessary to produce CTE is unclear.8 Also, while mTBI has been linked with improvised explosive device blast injuries and mines thus far, veterans from earlier conflicts could have TBI and CTE from exposure to training, boxing, and football in the military. There might even be differences based on the military era or period in which the veterans served. Current Veterans Health Administration TBI screening targets recent Gulf War veterans. Unique exposures from military service add another layer of vulnerability to the usual determinants of health. The VA recognizes this fact in the mission that “seeks to care for those who have borne the battle and for their families and their survivors.” To this end, and in the continuing effort to advance the Veterans Health Administration Health Equity Action Plan—the VA strategic guide for health equity—the VA Office of Health Equity is bringing focus to the topic in a bid to spur action toward addressing health and health care disparities among veterans. For instance, national experts are convening as part of the Focus on Health Equity and Action series to stimulate the conversation through a panel discussion. The moderated cyber seminar session will examine the connection between CTE and TBI, explore the impact on veterans and other vulnerable groups typically impacted by health and health care disparities, address audience questions, and offer suggestions for future actions in policy,
Uchendu et al.
Editorial
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operations, education, and research. Uchenna S. Uchendu, MD Bennet I. Omalu, MD, MBA, MPH, CPE David X. Cifu, MD Leonard E. Egede, MD, MS CONTRIBUTORS All authors contributed equally to this editorial.
ACKNOWLEDGMENTS Many thanks to Kenneth T. Jones, PhD, and Clara E. Dismuke, PhD, for the literature and document review that facilitated our ability to meet the tight timeline for this editorial.
REFERENCES 1. Reid MW, Velez CS. Discriminating military and civilian traumatic brain injuries. Mol Cell Neurosci. 2015;66(pt B): 123–128. 2. Defense and Veterans Brain Injury Center. DoD TBI Worldwide Numbers Since 2000. Available at: http://dvbic.dcoe. mil/sites/default/files/DoD-TBIWorldwide-Totals_2000-2015_Q1Q4_March-30-2016_v1.0_2016-04-14. pdf. Accessed May 19, 2016. 3. Faul M, Xu L, Wald MM, Coronado VG. Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations, and Deaths 2002–2006. Available at: http://www.cdc.gov/traumaticbraininjury/ pdf/blue_book.pdf. Published March 2010. Accessed May 19, 2016. 4. Omalu BI, DeKosky ST, Minster RL, Kamboh MI, Hamilton RL, Wecht CH. Chronic traumatic encephalopathy in a National Football League player. Neurosurgery. 2005;57(1):128–134, discussion 128–134. 5. Omalu BI, Bailes J, Hammers JL, Fitzsimmons RP. Chronic traumatic encephalopathy, suicides and parasuicides in professional American athletes: the role of the forensic pathologist. Am J Forensic Med Pathol. 2010;31(2):130–132. 6. Egede LE, Dismuke C, Echols C. Racial/ethnic disparities in mortality risk among US veterans with traumatic brain injury. Am J Public Health. 2012;102(suppl 2):S266–S271. 7. Dismuke CE, Gebregziabher M, Yeager D, Egede LE. Racial/ethnic differences in combat- and non– combat-associated traumatic brain injury severity in the Veterans Health Administration: 2004–2010. Am J Public Health. 2015;105(8):1696–1702. 8. Gardner RC, Yaffe K. Epidemiology of mild traumatic brain injury and neurodegenerative disease. Mol Cell Neurosci. 2015;66(pt B):75–80.
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August 2016, Vol 106, No. 8
cognitive damage; and mirroring Foley’s argument back to her, the lack of randomized controlled trial evidence supporting longterm treatment.5 The debate created an ongoing and serious fracture within the field. The fracture became a seismic shock in the 2000s when Purdue’s aggressive marketing of its controlled-release opioid Oxycontin as safe for chronic pain intersected with the trafficking of cheap, very pure heroin in smaller cities across the West, Midwest, and Appalachia. Purdue advertised Oxycontin as nonaddictive because the drug was released within the body over 12 hours; recreational users quickly learned to get high by crushing or dissolving the pills, or simply taking very high doses. Overstressed and wellintentioned general practitioners, and a number of unscrupulous “pill mill” operators, wrote liberal prescriptions for the new analgesic. The ready supply of Oxycontin made diversion and sale, particularly by low-income patients on Medicaid or Medicare, attractive and easy; but when pill addicts
found their drug too expensive, they sought an alternative. Traffickers of black-tar heroin had meanwhile arrived in Middle America with a new marketing approach, driving to meet buyers in safe locations and offering inexpensive product, often giving free samples to encourage customer loyalty.6 “When you’re paying 40 dollars a pill and then you hear you can pay 10 dollars for the same effect, of course you’re going to do it.” Hundreds of Oxycontin abusers, many of them middle-class adolescents and young adults, began to see heroin as “a less and less scary and taboo thing.”7 The result has been an alarming increase in heroin use across the country and an epidemic of drug overdose deaths, which increased 137% between 2000 and 2014; overdoses involving prescription opioids and heroin increased 200% in that period. Many who championed liberalized opioid therapy for chronic pain, including Portenoy, have now retreated from that position, acknowledging that their stance led to
unanticipated abuse and tragedy. But as the CDC guidelines demonstrate, patients with severe chronic pain will still need opioids, and physicians will be called on to prescribe it, albeit with more caution and as Foley and Portenoy wrote 30 years ago, the physician’s “intensive involvement.” Prescription under strict guidelines may finally provide the evidence for or against long-term opioid therapy for chronic pain that has been so long lacking. In its absence, the availability and use of opioids, with often deadly results, has been too far governed by other factors: the shrewd targeting of a market niche by a pharmaceutical manufacturer, the costbenefit calculations of insurance carriers, and the creative entrepreneurship of drug traffickers. Marcia L. Meldrum, PhD
ACKNOWLEDGMENTS The author would like to thank Daniel Fox for his help and guidance.
Repeated Concussions: Time to Spur Action Among Vulnerable Veterans The Secretary of the United States Department of Veterans Affairs (VA) Honorable Robert McDonald recently pledged to donate his brain for chronic traumatic encephalopathy (CTE) research. Citing exposures to football, rugby, boxing, and paratrooper escapades as an army ranger, Secretary McDonald suggested that his brain could add to the body of knowledge on the effect of repeated concussions. In the meantime, work is under way to make the connections between the CTE postmortem diagnosis and the clinical findings
1366
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Uchendu et al.
while people are alive. Such knowledge is expected to positively impact medical management for people at risk and inform necessary policies, preventive actions, and health equity issues. Even though recent CTE discussions have focused on the definitive findings among football players and other athletes, the root cause of the pathology— repeated concussion—is prevalent among veterans in the form of traumatic brain injury (TBI). Veterans tend to have a higher incidence of TBI than comparable
counterparts in the general public as a result of military service exposures.1 Since 2000, there
REFERENCES 1. Dowell D, Haegerich TM, Chou R. CDC guideline for prescribing opioids for chronic pain–United States, 2016. MMWR Recomm Rep. 2016;65(1): 1–49. 2. Physicians for Responsible Opioid Prescribing. Letter to the Joint Commission. Available at: http://www.citizen. org/documents/2314b.pdf. Accessed June 13, 2016. 3. Meldrum ML. The property of euphoria: research and the cancer patient. In: Meldrum ML, ed, Opioids and Pain Relief: A Historical Perspective. Seattle, WA: IASP Press; 2002: 196, 198, 200–208. 4. Meldrum ML. The prescription as stigma: opioid pain relievers and the long walk to the pharmacy counter. In: Watkins ES, Greene JA. Prescribed: Writing, Filling, Using and Abusing the Prescription in Modern America. Baltimore, MD: Johns Hopkins University Press; 2012: 195, 201. 5. Katz MH. Long-term opioid treatment of nonmalignant pain: a believer loses his faith. Arch Intern Med. 2010;170(16): 1422–1424. 6. Quinones S. Dreamland: The True Tale of America’s Opiate Epidemic. New York, NY: Bloomsbury Press; 2015. 7. Mars SG, Bourgois P, Karandinos G, Montero F, Ciccarone D. “Every ‘never’ I ever said came true”: Transitions from opioid pills to heroin injecting. Int J Drug Policy. 2014;25: 262–263.
have been 344 030 medical diagnoses of TBIs in the United States Armed Forces and more than 80% of these injuries are considered mild in nature.2 Brain injuries are a major concern in the United States. Annually, an estimated 1.7 million people
ABOUT THE AUTHORS Uchenna S. Uchendu is with the United States Department of Veterans Affairs, Washington, DC. Bennet I. Omalu is with the Department of Pathology, University of California, Davis. David X. Cifu is with the Virginia Commonwealth University School of Medicine, Richmond, and the United States Department of Veterans Affairs Medical Center, Richmond. Leonard E. Egede is with the Medical University of South Carolina, Charleston, and the United States Department of Veterans Affairs Medical Center, Charleston. Correspondence should be sent to Uchenna S. Uchendu, MD Chief Officer, Office of Health Equity, United States Department of Veterans Affairs, 810 Vermont Avenue NW., Washington, DC 20420 (e-mail: [email protected]). Reprints can be ordered at http:// www.ajph.org by clicking the “Reprints” link. This editorial was accepted May 27, 2016. Note. The opinions expressed in this editorial are those of the authors and do not necessarily represent the United States Department of Veterans Affairs or any of the institutions/ organizations affiliated with any of the authors. doi: 10.2105/AJPH.2016.303293
AJPH
August 2016, Vol 106, No. 8
AJPH PERSPECTIVES
Office of Health Equity Traumatic Brain Injury–Chronic Traumatic Encephalopathy (CTE): 2016
experience a TBI. These injuries contribute to a third of all injury deaths.3 Traumatic brain injury is an alteration in brain function or other evidence of brain pathology caused by an external force leading to temporary or permanent impairment of cognitive, physical or psychosocial functions—the polytrauma triad. Mild TBIs (mTBIs) or concussions present with an initial impairment in sensorium (unconscious or altered consciousness) for 30 minutes or less and can result in longstanding deficits in all spheres of functioning in a small percentage of individuals. As a result of an increased use of improvised explosive devices, mTBIs were deemed the “signature injury” of the recent Gulf War occurring in up to 20% of all deployed US service members. Importantly, persistent symptoms and functional difficulties from these combat-associated concussions, which generally last more than three months after injury, have been seen in approximately 40% of these concussed individuals and 8% of all veterans seen in the Veterans Affairs clinics from
August 2016, Vol 106, No. 8
AJPH
the conflicts. The long-term effects of single or multiple mTBIs in later life are poorly understood, but recent research suggests a possible connection between multiple concussions and neurodegeneration. Chronic traumatic encephalopathy is a progressive neurodegenerative syndrome caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration–deceleration forces to the brain. The condition presents clinically after a prolonged latent period as a composite syndrome of mood disorders, and neuropsychiatric and cognitive impairment. It usually presents with a prolonged latency period; however, some patients with CTE may not exhibit the classic prolonged latency period before clinical symptoms begin. Definitive CTE diagnosis remains in direct brain tissue analysis after death; however, a presumptive clinical diagnosis of CTE can be made based on a constellation of pathognomonic symptoms. Chronic traumatic encephalopathy belongs to the spectrum of chronic TBI and is a direct,
long-term, and permanent consequence of TBI. Military veterans who are exposed to all types of TBI, including acceleration–deceleration injuries of the brain from exposure to ordinances, stand a reasonable risk of developing CTE.4,5 Research is beginning to show that some of the posttraumatic stress disorder cases diagnosed in veterans are CTE, which raises concerns for increased rates of CTE in vulnerable Veteran populations. Recent evidence suggests racial/ethnic differences in mortality among veterans with TBI. In a nationally representative study of veterans with TBI, Hispanic veterans had almost twofold increased hazard ratio of death compared with non-Hispanic White veterans (1.6; 95% confidence interval (CI) = 1.0, 2.6) after adjusting for relevant covariates.6 A recent study used nationally representative VA data to examine the association between TBI severity and combat by race/ethnicity.7 The study found that 26% of veterans with TBI served in a combat zone between 2004 and 2010; mTBI increased from 12% to 40%, whereas moderate or severe TBI decreased from 89% to 60%. Moderate or severe TBI was higher in non-Hispanic Blacks (80%) and Hispanics (89%) than in non-Hispanic Whites (72%). In the fully adjusted model that included all ethnic groups, non-Hispanic Blacks (odds ratio [OR] = 1.4; 95% CI = 1.4, 1.5) and Hispanics (OR = 1.5; 95% CI = 1.3, 1.7) had higher odds of moderate or severe TBI than did non-Hispanic Whites. However, combat exposure was associated with higher odds of mild TBI in non-Hispanic Blacks (OR = 2.5; 95% CI = 2.2, 2.8) and Hispanics (OR = 3.4; 95% CI = 1.8, 6.4) than in
non-Hispanic Whites (OR = 2.2; 95% CI = 2.1, 2.3). The prevalence of CTE is unknown, and the amount of mTBI or subconcussive trauma exposure necessary to produce CTE is unclear.8 Also, while mTBI has been linked with improvised explosive device blast injuries and mines thus far, veterans from earlier conflicts could have TBI and CTE from exposure to training, boxing, and football in the military. There might even be differences based on the military era or period in which the veterans served. Current Veterans Health Administration TBI screening targets recent Gulf War veterans. Unique exposures from military service add another layer of vulnerability to the usual determinants of health. The VA recognizes this fact in the mission that “seeks to care for those who have borne the battle and for their families and their survivors.” To this end, and in the continuing effort to advance the Veterans Health Administration Health Equity Action Plan—the VA strategic guide for health equity—the VA Office of Health Equity is bringing focus to the topic in a bid to spur action toward addressing health and health care disparities among veterans. For instance, national experts are convening as part of the Focus on Health Equity and Action series to stimulate the conversation through a panel discussion. The moderated cyber seminar session will examine the connection between CTE and TBI, explore the impact on veterans and other vulnerable groups typically impacted by health and health care disparities, address audience questions, and offer suggestions for future actions in policy,
Uchendu et al.
Editorial
1367
AJPH PERSPECTIVES
operations, education, and research. Uchenna S. Uchendu, MD Bennet I. Omalu, MD, MBA, MPH, CPE David X. Cifu, MD Leonard E. Egede, MD, MS CONTRIBUTORS All authors contributed equally to this editorial.
ACKNOWLEDGMENTS Many thanks to Kenneth T. Jones, PhD, and Clara E. Dismuke, PhD, for the literature and document review that facilitated our ability to meet the tight timeline for this editorial.
REFERENCES 1. Reid MW, Velez CS. Discriminating military and civilian traumatic brain injuries. Mol Cell Neurosci. 2015;66(pt B): 123–128. 2. Defense and Veterans Brain Injury Center. DoD TBI Worldwide Numbers Since 2000. Available at: http://dvbic.dcoe. mil/sites/default/files/DoD-TBIWorldwide-Totals_2000-2015_Q1Q4_March-30-2016_v1.0_2016-04-14. pdf. Accessed May 19, 2016. 3. Faul M, Xu L, Wald MM, Coronado VG. Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations, and Deaths 2002–2006. Available at: http://www.cdc.gov/traumaticbraininjury/ pdf/blue_book.pdf. Published March 2010. Accessed May 19, 2016. 4. Omalu BI, DeKosky ST, Minster RL, Kamboh MI, Hamilton RL, Wecht CH. Chronic traumatic encephalopathy in a National Football League player. Neurosurgery. 2005;57(1):128–134, discussion 128–134. 5. Omalu BI, Bailes J, Hammers JL, Fitzsimmons RP. Chronic traumatic encephalopathy, suicides and parasuicides in professional American athletes: the role of the forensic pathologist. Am J Forensic Med Pathol. 2010;31(2):130–132. 6. Egede LE, Dismuke C, Echols C. Racial/ethnic disparities in mortality risk among US veterans with traumatic brain injury. Am J Public Health. 2012;102(suppl 2):S266–S271. 7. Dismuke CE, Gebregziabher M, Yeager D, Egede LE. Racial/ethnic differences in combat- and non– combat-associated traumatic brain injury severity in the Veterans Health Administration: 2004–2010. Am J Public Health. 2015;105(8):1696–1702. 8. Gardner RC, Yaffe K. Epidemiology of mild traumatic brain injury and neurodegenerative disease. Mol Cell Neurosci. 2015;66(pt B):75–80.
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August 2016, Vol 106, No. 8
