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Concussion (mTBI) and, more broadly, Traumatic Brain Injury (TBI) affect millions of people globally each year, with indirect impacts reaching an even larger population. While the issue has gained significant attention in the context of sports—especially in the NFL in the US and increasingly across various sports worldwide—TBI is, in reality, a daily concern in Emergency Departments (EDs) around the world.
At present, the diagnosis of TBI relies largely on subjective assessments of physical symptoms and patient-reported experiences. Clinicians typically use a combination of the Glasgow Coma Scale (GCS), clinical indicators such as pupillary response, and CT scan results. However, these methods are estimated to be accurate in diagnosing TBI only about 37% of the time. 1, 2.
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Researchers are exploring alternative, less invasive methods for diagnosing TBI, with biological biomarkers emerging as a promising avenue.
Glia, for example, is focusing on nucleic acid-based markers that have demonstrated exceptional sensitivity and specificity. These biomarkers offer significant potential, particularly for predicting outcomes such as Return to Play, Work, School, or Duty—the “holy grail” in TBI research.
Medicine, more broadly, is increasingly focusing on the brain. Growing recognition of psychological conditions like depression and anxiety, coupled with concerted efforts to tackle neurodegenerative diseases such as Alzheimer’s and Parkinson’s, is laying a strong foundation for the development of advanced TBI diagnostics.
From a practical standpoint, a blood-based pathology test is critical to addressing the social and financial burdens of TBI. However, it is equally important to develop Point of Care (PoC) tests at the "front line"—such as in emergency departments—to aid in rapid diagnosis and triage, helping to mitigate long-term effects and optimise recovery outcomes.
An internal injury with marked internal effects and external outcomes.
Globally, TBI is the leading cause of death and disability in children and adults and is involved in nearly half of all trauma deaths. In Australia, Europe and the United States, the estimated annual incidence of TBI requiring hospitalisation is 100 per 100 000 population, with 80%–90% of cases categorised as mild TBI (mTBI). In the US it affects more than 3.5 million people each year alone.3.
Annual hospital presentations for sport related concussions between the ages of 0-19 in the US are reported to be 175,000.4. Of these, up to 15% most likely continue to be asymptomatic resulting in performance decline for a prolonged period of time (2 years) following their last concussion, a finding which is highly important for future discussion about current RTP guidelines and reducing the risk of re-injury in this and indeed all age groups. Evidence also suggests that TBI may be a risk factor for the later development of neurodegenerative disorders, including Alzheimer's disease.5-11.
The impact of TBI is significant, and includes the personal burden endured by survivors and their families, as well as the substantial economic toll on society.12.
We and others argue that the use of biomarkers is a useful and important approach to comprehensively assess brain function following concussion.13.
Globally, traumatic brain injury (TBI) is the leading cause of death and disability in children and adults and is involved in nearly half of all trauma deaths. For some young adults in the US, the annual incidence of emergency department presentations for TBI is reportedly as high as 760 per 100 000 population. In Australia, one report estimated the direct hospital costs for all TBI in the 2004–05 financial year at $184 million.14.
According to the US Centers for Disease Control and Prevention (CDC), the economic cost of TBI in the United States in 2010, including direct and indirect medical costs, was estimated at $76.5 billion.15.
1. Perel P, Wasserberg J, Ravi RR, Shakur H, Edwards P, Roberts I (2007) Prognosis following head injury: a survey of doctors from developing and developed countries. J Eval Clin Pract 13:464-465. doi:10.1111/j.1365-2753.2006.00713.x
2. Rosenfeld JV, Maas AI, Bragge P, Morganti-Kossmann MC, Manley GT, Gruen RL (2012) Early management of severe traumatic brain injury. Lancet 380:1088-1098. doi:10.1016/S0140-6736(12)60864-2
3.V.G. Coronado, L.C. McGuire, K. Sarmiento, J. Bell, M.R. Lionbarger, C.D. Jones, A.I. Geller, N. Khoury, and L. Xu (2012). Trends in traumatic brain injury in the U.S. and the public health response: 1995–2009. J Safety Res.
4. Faul M, Xu L, Wald MM, Coronado VG. Centers for Disease Control and Prevention. Traumatic brain injury in the United States. GA, USA.
5. C.A. Molgaard, E.P. Stanford, D.J. Morton, L.A. Ryden, K.R. Schubert, and A.L. Golbeck (1990). Epidemiology of head trauma and neurocognitive impairment in a multi-ethnic population. Neuroepidemiology 9, 233–242.
6. J.A. Mortimer, L.R. French, J.T. Hutton, and L.M. Schuman (1985). Head injury as a risk factor for Alzheimer's disease. Neurology 35, 264–267.
7. J.A. Mortimer, C.M. van Duijn, V. Chandra, L. Fratiglioni, A.B. Graves, A. Heyman, A.F. Jorm, E. Kokmen, K. Kondo, W.A. Rocca, and et al. (1991). Head trauma as a risk factor for Alzheimer's disease: a collaborative re-analysis of case-control studies. EURODEM Risk Factors Research Group. Int. J. Epidemiol. 20, Suppl 2, S28–S35.
8. E.S. O'Meara, W.A. Kukull, L. Sheppard, J.D. Bowen, W.C. McCormick, L. Teri, M. Pfanschmidt, J.D. Thompson, G.D. Schellenberg, and E.B. Larson (1997). Head injury and risk of Alzheimer's disease by apolipoprotein E genotype. Am. J. Epidemiol. 146, 373–384.
9. Z. Guo, L.A. Cupples, A. Kurz, S.H. Auerbach, L. Volicer, H. Chui, R.C. Green, A.D. Sadovnick, R. Duara, C. DeCarli, K. Johnson, R.C. Go, J.H. Growdon, J.L. Haines, W.A. Kukull, and L.A. Farrer (2000). Head injury and the risk of AD in the MIRAGE study. Neurology 54, 1316–1323.
10. B.L. Plassman, R.J. Havlik, D.C. Steffens, M.J. Helms, T.N. Newman, D. Drosdick, C. Phillips, B.A. Gau, K.A. Welsh-Bohmer, J.R. Burke, J.M. Guralnik, and J.C. Breitner (2000). Documented head injury in early adulthood and risk of Alzheimer's disease and other dementias. Neurology 55, 1158–1166.
11. V.E. Johnson, W. Stewart, and D.H. Smith (2012). Widespread tau and amyloid‐beta pathology many years after a single traumatic brain injury in humans. Brain Pathol. 22, 142–149. 12. P. Corso, E. Finkelstein, T. Miller, I. Fiebelkorn, and E. Zaloshnja (2006). Incidence and lifetime costs of injuries in the United States. Inj. Prev. 12, 212–218.
13. Marc Dalecki, et al. Concussion May 12, 2016.
14. Caroline F Finch, Angela J Clapperton and Paul McCrory. Increasing incidence of hospitalisation for sport-related concussion in Victoria, Australia. Med J Aust 2013; 198 (8): 427-430.
15. CDC. Severe traumatic brain injury. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/TraumaticBrainInjury/severe.html. Accessed: Jul 14, 2015.
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