Medical Complications of Traumatic Brain Injury

Traumatic Brain Injury (TBI) affects five million Americans at an annual cost of over $56 billion and is a significant public health concern.[1] For instance, the Alzheimer’s Association cites an increased Alzheimer’s/dementia late-life disease risk of 2.3 to 4.5 times that of the general population for individuals who did not sustain a TBI early in life. [2]

Signs of compromised brain status include headache, nausea, confusion, dizziness, memory loss, altered thinking, cognitive deficits, and mood and personality changes. The Glasgow Coma Scale classifies and ranks brain injuries.[3] Five points are assigned in each of three categories: (1) eye-opening (E=5 points), (2) verbal responses (V=5 points), and (3) movement = 5 points. Thus, a total score of 15 points is possible on the GCS.[4] A mild TBI event would be scored between 13 and 15. A moderate TBI event would be scored between 9 and 12, and a severe TBI event would be scored between 3 and 8.[5] [6] A Post Concussion Symptom Scale (PCSS) is used to characterize brain injuries sustained during sports activities which ranges from 0 (no symptoms) to 6 (severe symptoms).[7]

A mild TBI (MTBI) event, also known as a concussion, results in neurological and physiological trauma to the brain caused by a series of events resulting in a loss of normal brain activity and function after a significant head impact. [8] Brain damage in concussions results from the violent movement of the brain within the skull cavity and can lead to intracranial bleeding, tissue damage, and diffuse axonal injury. [9]

Researchers have found that the long-term impact of mild TBI (MTBI) ranges from being clinically asymptomatic to experiencing debilitating symptoms in later years. Complications of severe TBI include the development of Alzheimer’s disease, Parkinson’s disease, ALS, and other diseases. [10] [11] A 2014 study found that people who experience a TBI early in life are three times more likely to die early than those who do not. [12] These results could have a dramatic impact on safety considerations for athletes of all ages, the military, and others at increased risk for head injuries.

A frequent complication of TBI is the later development of chronic traumatic encephalopathy (CTE). Defined as “a progressive degenerative disease of the brain found in athletes (and others) with a history of repetitive brain trauma, including symptomatic concussions as well as asymptomatic subconcussive hits to the head,” CTE was first identified in an NFL player by Dr. Bennet Omalu in the early 2000s. [13] [14] [15]

It is uncertain whether TBI patients will eventually develop Alzheimer’s or dementia. Biomarkers (at baseline and after the TBI) can help in predicting the later development of Alzheimer’s and/or dementia and in offering medical counseling to patients and coaches about risk factors for the later development of disease. Additionally, genetic factors can determine increased risk for later disease. [16]

Both MTBI and severe TBI can result in microscopic changes within the brain that are hallmarks for these debilitating diseases. [17] [18] Chronic MTBI leads to the accumulation of tau proteins, neurofibrillary tangles (NFTs), the collection of abnormal protein aggregates, and disruption of the cellular cytoskeleton – which contributes to loss of normal nerve function. The presence of beta-amyloid in severe TBI leads to the development of Alzheimer’s. [19] Genetic factors may play a role in the development of both CTE and Alzheimer’s disease, as well. [20] [21] [22] [23] [24] [25]

Recent reports describe a diagnostic test for tau in CTE (now only definitely diagnosed after death) in living football players after promising preliminary data at UCLA. However, more players need to be tested ensure the viability and accuracy of these early results.[26] [27] [28]

Dorkina Myrick, MD, PhD, MPP, is a physician-scientist and pathologist trained at the National Institutes of Health. Dr. Myrick also previously served as a Senior Health Policy Advisor on the United States Senate Special Committee on Aging in Washington, DC. Dr. Myrick conducted this research during her time in the United States Senate. She is currently a JD candidate at the Boston University School of Law.


[1] “Traumatic Brain Injury: Hope Through Research.” National Institute of Neurological Disorders and Stroke.   Last updated December 30, 2013. Website:   Retrieved January 19, 2014.

[2] Id.

[3] Teasdale, G, Jennett, B. Assessment of coma and impaired consciousness. A practical scale. Lancet 304(7872):81-84, 1974.

[4] Id.

[5] Id.

[6] “Severe TBI.” Centers for Disease Control and Prevention. Online: Retrieved February 23, 2019.

[7] Lovell, M. R., & Collins, M. W. (1998). Neuropsychological assessment of the college football player.Journal of Head Trauma Rehabilitation, 13(2), 9–26.

[8] “Heads Up: Facts for Physicians About Mild Traumatic Brain Injury (MTBI).” U.S. Department of Health and Hman Services. Centers for Disease Control and Prevention. p.2. Website: Retrieved January 19, 2014.

[9] “Pathophysiology: Primary Injury – Coup and Contrecoup Contusions” in Dawodu, Segun. “Traumatic Brain Injury (TBI) – Definition, Epidemiology, Pathophysiology.” Medscape. Updated March 6, 2013.

[10] “Traumatic Brain Injury: Hope Through Research.” National Institute of Neurological Disorders and Stroke. Last updated December 30, 2013. Website: Retrieved January 16, 2014.

[11] Lehman et al. “Neurodegenerative Causes of Death among Retired National Football League Players.” Neurology 2012; 79: 1970-1974.

[12] Fazel et al. “Suicide, Fatal Injuries, and Other Causes of Premature Mortality in Patients with Traumatic Brain Injury: : A 41-Year Swedish Population Study.” JAMA Psychiatry. Published online January 15, 2014. Retrieved January 16, 2014.

[13] “What is CTE? Center for the Study of Traumatic Encephalopathy” Website:

[14] Miller. “Mental after-effects of head injury.” Proc R Soc Med. 1966 Mar; 59(3):257-61.

[15] Omalu BI, DeKosky ST, Minster RL, Kamboh MI, Hamilton RL, Wecht CH. “Chronic traumatic encephalopathy in a National Football League player.” Neurosurgery. 2005 Jul;57(1):128-34; discussion 128-34. Website: Retrieved January 20, 2014.

[16] Zetterberg et al. “Biomarkers of mild traumatic brain injury in cerebrospinal fluid and blood.” Nature Reviews Neurology. Nature Reviews Neurology 9, 201-210 (April 2013). Website: Retrieved January 19, 2014.

[17] Figure 1: “Spectrum of pathological features and outcomes of mild and severe TBI.” in DeKosky, Steven et al. “Acute and chronic traumatic encephalopathies: pathogenesis and biomarkers.” Nature Reviews Neurology 9, 192-200 (April 2013). Retrieved January 19, 2014.

[18] “Traumatic Brain Injury.” Online:

[19] Id. at Figure 1: “Spectrum of pathological features and outcomes of mild and severe TBI.”

[20] Id. at”Acute and chronic traumatic encephalopathies: pathogenesis and biomarkers.”

[21] Small et al. “PET Scanning of Brain Tau in Retired National Football League Players: Preliminary Findings.” American Journal of Geriatric Psychiatry. 21:2. February 2013. Retrieved May 20, 2014.

[22] Mielke et al. “Head Trauma and in vivo Measures of Amyloid and Neurodegeneration in a Population-Based Study.” Neurology 82 January 7, 2014.

[23] Glenn Smith, Ph.D. “Alzheimer’s: Can A Head Injury Increase My Risk? Can A Head Injury Cause or Hasten Alzheimer’s Disease or Other Types of Dementia?” Mayo Clinic Website. Updated July 13, 2013. Website: Retrieved December 24 2013.

[24] Belson, Ken. “New Tests for Brain Trauma Create Hope, and Skepticism.” New York Times. December 25, 2013. Website: Retrieved January 21, 2014.

[25] “Chronic Traumatic Encephalopathy in a National Football League player.”

[26] Barrio et al. In vivo Characterization of Chronic Traumatic Encephalopathy Using [F-18] FDDNP PET Brain Imaging.” Proceedings of the National Academy of Sciences, April 21, 2015.

[27] Correction for Barrio et al., In vivo characterization of chronic traumatic encephalopathy using [F-18] FDDNP PET brain imaging. Proceedings of the National Academy of Sciences. June 2, 2015 112 (22) E2981; published ahead of print May 11, 2015.

[28] Conflict of interest statement: “J.R.B., G.W.S., and S.-C.H. are co-inventors of the [F-18]FDDNP PET technology that is covered under University of California, Los Angeles patents and licensed to TauMark, LLC. J.R.B., G.W.S., R.P.F., and B.O. have a financial interest in TauMark, LLC.”


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