A seminal paper published in 2010 argued for the conceptualization of traumatic brain injury (TBI) not as an isolated injury event, but as a disease process that unfolds heterogeneously over many years (Masel & DeWitt, 2010). The purpose of that paper was to summarize the evidence needed to encourage clinicians and, perhaps more importantly, the insurance industry, to recognize TBI as a condition that may require lifelong care. The World Health Organization defines a chronic disease as one that has one or more of the following characteristics: it is permanent, it requires specialized care, and/or it may require a long period of observation, supervision, or care (Pruitt & Epping-Jordan, 2002). The authors summarized scientific evidence that TBI is associated with an increased risk for a broad range of neurological and non-neurological health conditions, which together supported the notion that TBI may initiate and/or accelerate health decline across multiple body systems. Unlike an injury event (such as a broken bone) which has a finite recovery timeline, the sequelae of TBI appear to persist and evolve for years post-injury.
At the time of its publication, this conceptualization was quite novel – and it stimulated a major investment on the part of clinicians, researchers, and the individuals with TBI and their families who have generously participated in research studies, to further investigate whether, and for whom, TBI becomes a chronic disease process. The research conducted in this area over the past decade has led to a better understanding of the heterogeneous long-term outcomes experienced by TBI survivors, and the chronic health burden experienced by some. Here, we will review some of these developments and revisit the ideas first discussed in 2010 in light of new findings, and highlight the pressing questions that remain unanswered.
The role of both comorbid and pre-existing physical health conditions in TBI risk, recovery and long-term outcomes has become more widely recognized. Physical health problems in older adults, such as cerebrovascular diseases and activities of daily living (ADL) limitations, are associated with increased risk for sustaining a TBI in late life (Dams-O’Connor et al., 2016) – which suggests older adults with TBI were already sicker than their uninjured peers. One study reported that among adults over age 50 admitted to inpatient rehabilitation for TBI, 70% had at least one chronic disease diagnosis (Kumar et al., 2018), and the most prevalent conditions were hypertensive disease, musculoskeletal disease, diseases of lipid metabolism, and diabetes. Adults with TBI of all ages have a variety of health problems at 10-year follow-up; the most common are hypertension, fractures, osteoarthritis, high cholesterol, and sleep disorders (Hammond et al., 2019). Not surprisingly, the presence of these conditions influences trajectories of functional outcome and satisfaction with life (Malec et al., 2019).
Additional studies have highlighted particular health conditions, such as post-traumatic headache which affects over 70% of individuals with moderate-to-severe in the first year after injury (Hoffman et al., 2011). Post-traumatic epilepsy is also a major concern for adults with moderate-to-severe TBI, the incidence rate of new-onset seizure disorder (9.2%) is greatest in the first year post-injury (Ritter et al., 2016). A meta-analysis (Mathias & Alvaro, 2012) of 21 studies found 50% of individuals report some form of sleep disturbance after TBI, and between 25-29% have a diagnosed sleep disorder (insomnia, hypersomnia, or apnea). As discussed further below, chronic pain is among the most commonly reported health problems following TBI in both military and civilian settings (Nampiaparampil, 2008). Finally, several studies have reiterated a link between TBI and hypopituitarism, which can result in a number of downstream clinical consequences (Tanriverdi & Kelestimur, 2015). For a TBI to be considered disease causative and/or disease accelerative, one would expect the overall burden of disease to be greater in those with TBI as compared to those without. Very few studies have directly compared those with and without a TBI, though a few studies comparing dementia risk in those with and without TBI report higher rates of diabetes, cerebrovascular and cardiovascular disease in the TBI groups (Barnes et al., 2014; Gardner et al., 2014).
Research over the last decade has extended and expanded upon the associations identified by Masel and DeWitt (2010) between TBI and depression, anxiety, suicide, and substance use disorder. An exhaustive review observed that the incidence of major depressive disorder and post-traumatic stress disorder following TBI exceeded population rates, commonly emerging in the first year, though onset may be delayed with more severe injuries (Ponsford et al., 2018).
However, they also concluded that the frequency of psychotic spectrum, eating and somatoform disorders did not exceed rates observed in the general population. Substance use disorders were more frequent prior to injury among adults who incur TBIs, but may decline post-injury due to both spontaneous behavior change and more severe injuries limiting safety and/or access (Bogner et al., 2019). There is some suggestion that childhood TBI may predispose individuals to adult substance misuse (Cannella et al., 2019; Weil, et al., 2019).
There has been some progress in identifying efficacious treatments for post-TBI behavioral health challenges. There is evidence that SSRI’s generally, and sertraline specifically, can mitigate depression after TBI (Jorge, et al., 2016). Research examining the nonpharmacological interventions, such as cognitive behavioral therapy (CBT), have demonstrated effectiveness in reducing symptoms of depression (Fann et al., 2015), anxiety (Ponsford et al., 2016), and
emotion dysregulation (Neumann et al., 2017). However, given the heterogeneity among research designs, psychotherapeutic approaches and population characteristics, comprehensive practice recommendations are not yet possible. Emerging areas of concern include the intersection between opioid use disorder and TBI (Corrigan & Adams, 2018). In suicide prevention, there is growing recognition that among persons with brain injury, risk assessment must focus more on opportunity for self-harm and less on emotional distress (Simpson & Brenner, 2019).
The associations between TBI, post-traumatic neurodegeneration and Alzheimer’s Disease and related disorders (ADRDs) has received unprecedented attention in the last decade. Just prior to the publication of the 2010 Masel & Dewitt paper, chronic traumatic encephalopathy (CTE) was discovered post-mortem in the brains of several former professional football players (Omalu et al., 2005), suggesting that this apparently unique pathological disease appears to be associated with repetitive head trauma (McKee et al., 2009). Since then, hundreds more CTE cases have been diagnosed postmortem (McKee et al., 2016), which has resulted in renewed interest in the association between TBI and dementia. Masel and Dewitt (2010) report findings from the Institute of Medicine report (IOM (US), 2008) which concluded that there is sufficient evidence of an association between moderate-severe TBI and Alzheimer’s disease (AD). Research over the past decade, however, has highlighted the complexity of these associations a link between TBI and AD in particular has not been consistently replicated. One review determined that among 11 studies assessing the relationship between TBI and dementia, two studies found no association, and four studies observed an association only in specific subgroups (Dams-O’Connor et al., 2016) . The preponderance of evidence does suggest an association between TBI and neurodegenerative disease, but post-traumatic neurodegeneration may be distinct from AD-like clinical symptoms (Crane et al., 2016; Dams-O’Connor et al., 2013; Nordström & Nordström, 2018; Sayed et al., 2013).
Importantly, several studies have begun to identify potentially modifiable factors that may be associated with increased risk for dementia following TBI, such as sleep fragmentation and intermittent hypoxia (Lim et al., 2013; Osorio et al., 2015), increased immune response and neuroinflammation (Zhu et al., 2012), and overall burden of chronic health conditions that may at least partially mediate the relationship between TBI and dementia (Wilson et al., 2017). This research is promising as increasing physical activity (Blondell et al., 2014), treating disordered sleep (Cedernaes et al., 2017), and managing physical and psychiatric comorbidities (Diniz et al., 2013; Wilson et al., 2017) could potentially stave off cognitive decline and the development of dementia process in late life.
The age-adjusted mortality rates following TBI have not meaningfully changed since 2010 (Brooks et al., 2013). Individuals who survive at least one year following TBI are 2.33X more likely to die then their uninjured counterparts, with a reduced life expectancy of up to 9 years (Brooks et al., 2013; Harrison-Felix et al., 2015). We have learned that the absolute incidence of TBI is increasing in the elderly population due to increased life expectancy and mobility in
The changes in the demographic landscape of TBI have implications for mortality, as older age at TBI is associated with increased risk for acute mortality, greater acute care complications, comorbidities, use of anti-platelet/anti-coagulants, and conservative acute care (McIntyre et al., 2013). Still, relative to general population, individuals with moderate-severe TBI from all age strata are at increased relative risk for mortality, with the exception of adults over 85 (Harrison-Felix et al., 2012). Teenagers and middle-aged adults are at particularly increased relative risk for mortality compared to their counterparts in the general population. The association between mild TBI and mortality is much more tenuous, with little new evidence in the last decade. A study from the European Union counter-intuitively found a lower 6-month all-cause death rate (5%) in the lower income countries than in higher income countries (8%) (De Silva et al., 2009). An American study found an all-cause in-hospital mortality rate of 1.4% in a large sample of patients with mTBI (Selassie et al., 2011). Across both of
these mTBI studies, it was not clear that deaths were directly related to the mTBI, extra-cranial concurrent injuries, or other causes.
The study of TBI as a chronic condition has garnered unprecedented support in the past decade, with findings largely confirming the evidence compiled in the 2010 paper by Masel and Dewitt. Still, there are many more questions than answers. Due to scarcity of studies designed to directly compare the physical and behavioral health of those with and without TBI, it remains unclear whether, when and how a TBI leads to the onset or exacerbation of many of these health challenges relative to uninjured adults. More research is needed to distinguish post-TBI cognitive dysfunction from neurodegenerative disease processes and to elucidate the underlying mechanisms driving post-traumatic neurodegeneration. It will be particularly important to characterize the subgroup(s) of TBI survivors who are at elevated risk for long-term evolving sequelae of TBI so that preventative care efforts can be dispatched accordingly. It will also be important to investigate how the sequelae of TBI interact with one another to alter a person’s health and wellbeing. Post-TBI cognitive impairment, for example, may limit a person’s ability to self-manage his/her health and contribute directly to health decline. It may be the case that certain medical conditions contribute to or exacerbate cognitive impairment and behavioral health disorders. For example, other fields studying trauma suggest that underlying biological abnormalities like persistent autonomic dysregulation (Brod et al., 2014), metabolic function (Brenner et al., 2018) and hyperinflammation (Bollen et al., 2017; Kiecolt-Glaser
et al., 2015) may cause executive dysfunction that increases the likelihood of behavioral health disorders. This information might guide the development of treatments to maximize post-TBI health.
Even as research progresses and knowledge accumulates, current long-term care for TBI survivors can be improved considerably by bringing together leading experts to develop consensus guidelines for treatment of the most common post-TBI conditions and comorbidities. The most valuable clinical practice guidelines will be specific to key subgroups (e.g., older vs younger adults; mild vs severe TBI). The implications of TBI as a chronic disease process on long-term health care needs and health care costs have not yet been fully realized. It is clear that research, advocacy, and policy efforts need to continue at unprecedented levels so that individuals with TBI can more universally gain access to the care they need, when they need it – even decades following the initial event.
Barnes, D. E., Kaup, A., Kirby, K. A., Byers, A. L., Diaz-Arrastia, R., & Yaffe, K. (2014). Traumatic brain injury and risk of dementia in older veterans. Neurology, 83(4), 312–319. https://doi.org/10.1212/WNL.0000000000000616
Blondell, S. J., Hammersley-Mather, R., & Veerman, J. L. (2014). Does physical activity prevent cognitive decline and dementia?: A systematic review and meta-analysis of longitudinal studies. BMC Public Health, 14(1), 510. https://doi.org/10.1186/1471-2458-14-510
Bogner, J., Corrigan, J. D., Yi, H., Singichetti, B., Manchester, K., Huang, L., & Yang, J. (2019). Lifetime History of Traumatic Brain Injury and Behavioral Health Problems in a Population-Based Sample. The Journal of Head Trauma Rehabilitation. https://doi.org/10.1097/HTR.0000000000000488
Bollen, J., Trick, L., Llewellyn, D., & Dickens, C. (2017). The effects of acute inflammation on cognitive functioning and emotional processing in humans: A systematic review of experimental studies. Journal of Psychosomatic Research, 94, 47–55. https://doi.org/10.1016/j.jpsychores.2017.01.002
Brenner, L. A., Hoisington, A. J., Stearns-Yoder, K. A., Stamper, C. E., Heinze, J. D., Postolache, T. T., … Lowry, C. A. (2018). Military-Related Exposures, Social Determinants of Health, and Dysbiosis: The United States- Veteran Microbiome Project (US-VMP). Frontiers in Cellular and Infection Microbiology, 8, 400. https://doi.org/10.3389/fcimb.2018.00400
Brod, S., Rattazzi, L., Piras, G., & D’Acquisto, F. (2014). “As above, so below” examining the interplay between emotion and the immune system. Immunology, 143(3), 311–318. https://doi.org/10.1111/imm.12341
Brooks, J. C., Strauss, D. J., Shavelle, R. M., Paculdo, D. R., Hammond, F. M., & Harrison-Felix, C. L. (2013). Long-term disability and survival in traumatic brain injury: results from the National Institute on Disability and Rehabilitation Research Model Systems. Archives of Physical Medicine and Rehabilitation, 94(11), 2203–2209. https://doi.org/10.1016/j.apmr.2013.07.005
Cannella, L. A., McGary, H., & Ramirez, S. H. (2019). Brain interrupted: Early life traumatic brain injury and addiction vulnerability. Experimental Neurology, 317, 191–201. https://doi.org/10.1016/j.expneurol.2019.03.003
Cedernaes, J., Osorio, R. S., Varga, A. W., Kam, K., Schiöth, H. B., & Benedict, C. (2017). Candidate mechanisms underlying the association between sleep-wake disruptions and Alzheimer’s disease. Sleep Medicine Reviews, 31, 102–111. https://doi.org/10.1016/j.smrv.2016.02.002
Corrigan, J. D., & Adams, R. S. (2018). The intersection of lifetime history of traumatic brain injury and the opioid epidemic. Addictive Behaviors, 90, 143.
Crane, P. K., Gibbons, L. E., Dams-O’Connor, K., Trittschuh, E., Leverenz, J. B., Keene, C. D., … Larson, E. B. (2016). Association of Traumatic Brain Injury With Late-Life Neurodegenerative Conditions and Neuropathologic Findings. JAMA Neurology, 73(9), 1062–1069. https://doi.org/10.1001/jamaneurol.2016.1948
Dams‐O’Connor, K., Gibbons, L. E., Landau, A., Larson, E. B., & Crane, P. K. (2016). Health Problems Precede Traumatic Brain Injury in Older Adults. Journal of the American Geriatrics Society, 64(4), 844–848. https://doi.org/10.1111/jgs.14014
Dams-O’Connor, K., Spielman, L., Hammond, F. M., Sayed, N., Culver, C., & Diaz-Arrastia, R. (2013). An exploration of clinical dementia phenotypes among individuals with and without traumatic brain injury. NeuroRehabilitation, 32(2), 199–209. https://doi.org/10.3233/NRE-130838
Dams-O’Connor, Kristen, Cuthbert, J. P., Whyte, J., Corrigan, J. D., Faul, M., & Harrison-Felix, C. (2013). Traumatic brain injury among older adults at level I and II trauma centers. Journal of Neurotrauma, 30(24), 2001–2013. https://doi.org/10.1089/neu.2013.3047
Dams-O’Connor, Kristen, Guetta, G., Hahn-Ketter, A. E., & Fedor, A. (2016). Traumatic brain injury as a risk factor for Alzheimer’s disease: current knowledge and future directions. Neurodegenerative Disease Management, 6(5), 417–429. https://doi.org/10.2217/nmt-2016-0017
De Silva, M. J., Roberts, I., Perel, P., Edwards, P., Kenward, M. G., Fernandes, J., … CRASH Trial Collaborators. (2009). Patient outcome after traumatic brain injury in high-, middle- and low-income countries: analysis of data on 8927 patients in 46 countries. International Journal of Epidemiology, 38(2), 452–458. https://doi.
Diniz, B. S., Butters, M. A., Albert, S. M., Dew, M. A., & Reynolds, C. F. (2013). Late-life depression and risk of vascular dementia and Alzheimer’s disease: systematic review and meta-analysis of community-based cohort studies. The British Journal of Psychiatry: The Journal of Mental Science, 202(5), 329–335. https://doi.org/10.1192/bjp.bp.112.118307
Fann, J. R., Bombardier, C. H., Vannoy, S., Dyer, J., Ludman, E., Dikmen, S., … Temkin, N. (2015). Telephone and in-person cognitive behavioral therapy for major depression after traumatic brain injury: a randomized controlled trial. Journal of Neurotrauma, 32(1), 45–57.
Gardner, R. C., Burke, J. F., Nettiksimmons, J., Kaup, A., Barnes, D. E., & Yaffe, K. (2014). Dementia risk after traumatic brain injury vs nonbrain trauma: the role of age and severity. JAMA Neurology, 71(12), 1490–1497. https://doi.org/10.1001/jamaneurol.2014.2668
Hammond, F. M., Corrigan, J. D., Ketchum, J. M., Malec, J. F., Dams-OʼConnor, K., Hart, T., … Whiteneck, G. G. (2019). Prevalence of Medical and Psychiatric Comorbidities Following Traumatic Brain Injury. The Journal of Head Trauma Rehabilitation. https://doi.org/10.1097/HTR.0000000000000465
Harrison-Felix, C., Kolakowsky-Hayner, S. A., Hammond, F. M., Wang, R., Englander, J., Dams-OʼConnor, K., … Diaz-Arrastia, R. (2012). Mortality after surviving traumatic brain injury: risks based on age groups. The Journal of Head Trauma Rehabilitation, 27(6), E45-56. https://doi.org/10.1097/HTR.0b013e31827340ba
Harrison-Felix, C., Pretz, C., Hammond, F. M., Cuthbert, J. P., Bell, J., Corrigan, J., … Haarbauer-Krupa, J. (2015). Life expectancy after inpatient rehabilitation for traumatic brain injury in the United States. Journal of Neurotrauma, 32(23), 1893–1901.
Hoffman, J. M., Lucas, S., Dikmen, S., Braden, C. A., Brown, A. W., Brunner, R., … Bell, K. R. (2011). Natural history of headache after traumatic brain injury. Journal of Neurotrauma, 28(9), 1719–1725.
Institute of Medicine (US) Committee on Gulf War and Health: Brain Injury in Veterans and Long-Term Health Outcomes. (2008). Gulf War and Health: Volume 7: Long-Term Consequences of Traumatic Brain Injury. Retrieved from http://www.ncbi.nlm.nih.gov/books/NBK214701/
Jorge, R. E., Acion, L., Burin, D. I., & Robinson, R. G. (2016). Sertraline for Preventing Mood Disorders Following Traumatic Brain Injury: A Randomized Clinical Trial. JAMA Psychiatry, 73(10), 1041–1047. https://doi.org/10.1001/jamapsychiatry.2016.2189
Kiecolt-Glaser, J. K., Derry, H. M., & Fagundes, C. P. (2015). Inflammation: depression fans the flames and feasts on the heat. The American Journal of Psychiatry, 172(11), 1075–1091. https://doi.org/10.1176/appi.ajp.2015.15020152
Kumar, R. G., Juengst, S. B., Wang, Z., Dams-O’Connor, K., Dikmen, S. S., O’Neil-Pirozzi, T. M., … Arenth, P. M. (2018). Epidemiology of comorbid conditions among adults 50 years and older with traumatic brain injury. The Journal of Head Trauma Rehabilitation, 33(1), 15–24.
Lim, A. S. P., Kowgier, M., Yu, L., Buchman, A. S., & Bennett, D. A. (2013). Sleep Fragmentation and the Risk of Incident Alzheimer’s Disease and Cognitive Decline in Older Persons. Sleep, 36(7), 1027–1032. https://doi.org/10.5665/sleep.2802
Malec, J. F., Ketchum, J. M., Hammond, F. M., Corrigan, J. D., Dams-Oʼconnor, K., Hart, T., … Bogner, J. (2019). Longitudinal Effects of Medical Comorbidities on Functional Outcome and Life Satisfaction After Traumatic Brain Injury: An Individual Growth Curve Analysis of NIDILRR Traumatic Brain Injury Model System Data. The Journal of Head Trauma Rehabilitation.
Masel, B. E., & DeWitt, D. S. (2010). Traumatic Brain Injury: A Disease Process, Not an Event. Journal of Neurotrauma, 27(8), 1529–1540. https://doi.org/10.1089/neu.2010.1358
Mathias, J. L., & Alvaro, P. K. (2012). Prevalence of sleep disturbances, disorders, and problems following traumatic brain injury: a meta-analysis. Sleep Medicine, 13(7), 898–905.
McIntyre, A., Mehta, S., Aubut, J., Dijkers, M., & Teasell, R. W. (2013). Mortality among older adults after a traumatic brain injury: a meta-analysis. Brain Injury, 27(1), 31–40. https://doi.org/10.3109/02699052.2012.700086
McKee, A. C., Cairns, N. J., Dickson, D. W., Folkerth, R. D., Keene, C. D., Litvan, I., … TBI/CTE group. (2016). The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy. Acta Neuropathologica, 131(1), 75–86. https://doi.org/10.1007/s00401-015-
McKee, A. C., Cantu, R. C., Nowinski, C. J., Hedley-Whyte, E. T., Gavett, B. E., Budson, A. E., … Stern, R. A. (2009). Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. Journal of Neuropathology and Experimental Neurology, 68(7), 709–735. https://doi.org/10.1097/NEN.0b013e3181a9d503
Nampiaparampil, D. E. (2008). Prevalence of chronic pain after traumatic brain injury: a systematic review. Jama, 300(6), 711–719.
Neumann, D., Tsaousides, T., Spielman, L., Kajankova, M., Guetta, G., Gordon, W., & Dams-O’Connor, K. (2017). Improving emotion regulation following web-based group intervention for individuals with traumatic brain injury. Journal of Head Trauma Rehabilitation, 32(5), 354–365.
Nordström, A., & Nordström, P. (2018). Traumatic brain injury and the risk of dementia diagnosis: A nationwide cohort study. PLoS Medicine, 15(1), e1002496. https://doi.org/10.1371/journal.pmed.1002496
Omalu, B. I., DeKosky, S. T., Minster, R. L., Kamboh, M. I., Hamilton, R. L., & Wecht, C. H. (2005). Chronic Traumatic Encephalopathy in a National Football League Player. Neurosurgery, 57(1), 128–134. https://doi.org/10.1227/01.NEU.0000163407.92769.ED
Osorio, R. S., Gumb, T., Pirraglia, E., Varga, A. W., Lu, S.-E., Lim, J., … Alzheimer’s Disease Neuroimaging Initiative. (2015). Sleep-disordered breathing advances cognitive decline in the elderly. Neurology, 84(19), 1964–1971. https://doi.org/10.1212/WNL.0000000000001566
Ponsford, J., Alway, Y., & Gould, K. R. (2018). Epidemiology and Natural History of Psychiatric Disorders After TBI. The Journal of Neuropsychiatry and Clinical Neurosciences, 30(4), 262–270. https://doi.org/10.1176/appi.neuropsych.18040093
Ponsford, J., Lee, N. K., Wong, D., McKay, A., Haines, K., Alway, Y., … O’donnell, M. L. (2016). Efficacy of motivational interviewing and cognitive behavioral therapy for anxiety and depression symptoms following traumatic brain injury. Psychological Medicine, 46(5), 1079–1090.
Pruitt, S., & Epping-Jordan, J. (2002). Innovative care for chronic conditions: building blocks for action: global report (Vol. 2). Retrieved from http://books.google.com/books?l=en&lr=&id=eCRKMEg8W6UC&oi=fnd&pg=PA1&dq=world+health+organization+chronic+conditions:+building+blocks+for+action&ots=7B_9WPRFiW&si
Ritter, A. C., Wagner, A. K., Fabio, A., Pugh, M. J., Walker, W. C., Szaflarski, J. P., … Dreer, L. E. (2016). Incidence and risk factors of posttraumatic seizures following traumatic brain injury: A Traumatic Brain Injury Model Systems Study. Epilepsia, 57(12), 1968–1977. https://doi.org/10.1111/epi.13582
Roozenbeek, B., Maas, A. I. R., & Menon, D. K. (2013). Changing patterns in the epidemiology of traumatic brain injury. Nature Reviews Neurology, 9(4), 231–236. https://doi.org/10.1038/nrneurol.2013.22
Sayed, N., Culver, C., Dams-O’Connor, K., Hammond, F., & Diaz-Arrastia, R. (2013). Clinical phenotype of dementia after traumatic brain injury. Journal of Neurotrauma, 30(13), 1117–1122. https://doi.org/10.1089/neu.2012.2638
Selassie, A. W., Fakhry, S. M., & Ford, D. W. (2011). Population-based study of the risk of in-hospital death after traumatic brain injury: the role of sepsis. The Journal of Trauma, 71(5), 1226–1234. https://doi.org/10.1097/TA.0b013e318226ecfc
Simpson, G. K., & Brenner, L. A. (2019). Suicide Prevention after Neurodisability: An Evidence-Informed Approach. Oxford University Press.
Tanriverdi, F., & Kelestimur, F. (2015). Pituitary dysfunction following traumatic brain injury: clinical perspectives. Neuropsychiatric Disease and Treatment, 11, 1835–1843. https://doi.org/10.2147/NDT.S65814
Weil, Z. M., Karelina, K., & Corrigan, J. D. (2019). Does pediatric traumatic brain injury cause adult alcohol misuse: Combining preclinical and epidemiological approaches. Experimental Neurology, 317, 284–290. https://doi.org/10.1016/j.expneurol.2019.03.012
Wilson, L., Stewart, W., Dams-O’Connor, K., Diaz-Arrastia, R., Horton, L., Menon, D. K., & Polinder, S. (2017). The chronic and evolving neurological consequences of traumatic brain injury. The Lancet Neurology, 16(10), 813–825. https://doi.org/10.1016/S1474-4422(17)30279-X
Zhu, B., Dong, Y., Xu, Z., Gompf, H. S., Ward, S. A. P., Xue, Z., … Xie, Z. (2012). Sleep disturbance induces neuroinflammation and impairment of learning and memory. Neurobiology of Disease, 48(3), 348–355. https://doi.org/10.1016/j.nbd.2012.06.022
Raj Kumar, PhD MPH, is a neuroepidemiologist and currently a post-doctoral fellow at the Brain Injury Research Center at Mount Sinai where he is studying the effects of physical and mental health comorbidities on recovery from TBI.
Eric Watson, PhD, is a post-doctoral fellow in Clinical Neuropsychology and Rehabilitation Research at the Brain Injury Research Center within the Department of Rehabilitation and Human Performance at Mount Sinai.
Brent Masel, MD, is a Clinical Professor of Neurology at the University of Texas Medical Branch, and serves as the Medical Director of the Brain Injury Association of America.
John D. Corrigan, PhD, is a Professor in the Department of Physical Medicine and Rehabilitation at Ohio State University and Director of
the Ohio Valley Center for Brain Injury Prevention and Rehabilitation, which, among other activities, is the designated lead agency in the state of Ohio for TBI policy and planning.
Kristen Dams-O’Connor, PhD, is Director of the Brain Injury Research Center of Mount Sinai and Associate Professor in the Departments of Rehabilitation Medicine and Neurology at Icahn School of Medicine at Mount Sinai in New York, NY. She leads the Late Effects of TBI (LETBI) Project, a TBI brain donor program focused on characterizing the clinical and pathological signatures of post-traumatic neurodegeneration. She is also Project Director of the New York
the aging population (Roozenbeek, et al., 2013), and the rate of TBI hospitalization in adults over 75 is exceeding population growth in this age group Traumatic Brain Injury Model System of care at Mount Sinai.