Chronic Traumatic Encephalopathy – The Dangers of Getting Your “Bell Rung”

Throughout his 16 year NFL career, Michael Webster anchored the Pittsburgh Steelers’ offensive line to four Super Bowl championships, nine Pro Bowl and All-Pro selections, and in 1997 was inducted into the Pro Football Hall of Fame. He is considered one of the greatest centers in NFL history. However, despite his long and successful career between the Steelers and Kansas City Chiefs, Webster’s life was cut short by a heart attack in 2002 at the age of 50. Homeless for several years after his retirement, Webster was riddled with various ailments and disabilities, including amnesia, dementia, depression, and chronic pain. Following his death, Webster was diagnosed with chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disease caused by repetitive head trauma. CTE has become a relevant topic recently in many sports, especially American football and hockey, and is associated with depression, substance abuse, anger, memory disturbances, and suicide [1]. Webster’s diagnosis by Dr. Bennet Omalu and colleagues in 2005 was the first documented case of a long-term neurodegenerative disease in an NFL player, and sparked the debate regarding safety in contact sports [2]. In this article, a brief history of CTE will be discussed, followed by the discovery of CTE in Mike Webster’s brain, and how this has impacted neuroscience, sports medicine, and professional sports.

The idea of CTE was first introduced in 1928 by Dr. Harrison Martland, a forensic pathologist, who introduced the term punch-drunk to describe the symptoms related to receiving multiple blows to the head in professional boxing [3]. At the time, symptoms of punch drunk were characterized by unsteadiness in gait and balance, slight mental confusion, and slowing of muscular action. However, more severe cases can include a “peculiar mental attitude”, hesitancy in speech, tremors in the hands, and nodding of the head. In even more severe cases, Martland observed dragging of one or both legs, staggering, vertigo, deafness, and marked mental deterioration that in some cases necessitated commitment to an asylum [3]. Martland hypothesized that punch drunk was caused by a brain injury due to repeated blows on the head or jaw, causing concussive hemorrhages in “deeper portions of the cerebrum.” This 85-year old paper laid the foundation for our understanding of the relationship between concussions and brain disease.

Due to the inability to diagnose CTE until death, there have only been 51 neuropathologically confirmed cases of CTE, 90% of which have occurred in athletes [4]. The most common symptoms in football players are mood disorders (depression), memory loss, paranoia, poor insight or judgment, outbursts of anger or aggression, irritability, apathy, confusion, reduced concentration, and agitation. Telephone interviews with family members of Mike Webster revealed general symptoms of depression, memory and judgment deficits, and parkinsonian symptoms. The autopsy, however, revealed unremarkable meninges, no cerebral atrophy, no cortical contusions, infarcts, or hemorrhages [2]. Following coronal sectioning, there were no gross pathological changes to the cortex, white matter, or deep gray matter structures. Simply put, Mike Webster’s brain was normal. However, what really shocked doctors was what they found in the deep neural tissue of Webster’s brain. Immunohistochemical stains revealed frequent diffuse extracellular amyloid plaques and tau-positive neuropil threads and intraneuronal neurofibrillary tangles in the frontal, temporal, parietal, occipital, and cingulated cortices [2]. Due to the presence of these amyloid plaques and tangles in the cortex, but no tangles in the entorhinal cortex or hippocampus, the diagnosis of Alzheimer’s Disease was ruled out, and the criteria for CTE was met [2].

For many, it was a shocking discovery that multiple concussive blows could lead to Alzheimer’s-like symptoms and pathology. The mechanism by which CTE develops is still being studied and has yet to be completely elucidated. The acceleration and deceleration forces felt by athletes as a result of direct blows to the head can cause serious damage within the brain. Concussive impacts create fluid waves within the ventricles of the brain, which produce shearing forces that can damage neural structures surrounding the ventricles [4]. It is also possible that damage to the blood-brain barrier could release neurotoxins, which then allows for development of tau pathology surrounding the microvasculature of the brain. Acute brain injury is also associated with diffuse axonal injury [5] and the degeneration of cerebral white matter. Axons undergo an uncontrolled influx of calcium, which swells mitochondria, disrupts microtubules, and eventually leads to degeneration of axons. There is also a significant up-regulation of the neuroinflammatory response after traumatic brain injury (TBI) [6]. Following TBI, there is a pronounced increase in MHC class II expression in white matter regions, indicative of some sort of inflammatory immune response in the brain [6].

The connection of CTE to professional sports over the past decade has become an extremely relevant topic in the world science but also for society as a whole. Sports, especially American Football, have a significant cultural impact. For many, it is a way of life. Due to the nature of CTE, the only way to treat it is through preventive measures, which in sports like football and hockey is extremely difficult to attain [1]. Unless extreme technological advancements can be made regarding the safety of helmets, prevention will require the combined efforts of physicians, referees, players, coaches, and administrators. Furthermore, there needs to be more therapeutic support for current and retired athletes.

In the summer of 2011, three National Hockey League (NHL) players were found dead over a four-month period, two of which were apparent suicides, the other from an accidental overdose of alcohol and oxycodone. Derek Boogaard, one of those players, was diagnosed with CTE postmortem. Substance abuse and depression are huge problems amongst “tough guys” and “enforcers” in the NHL, and more needs to be done to provide psychological support for retired players, in both the NHL and NFL. The sheer number of player deaths in both these sports raises the question: what needs to happen in order to change the attitudes of people involved in these sports? More research needs to be conducted on TBI, concussions, CTE, and their relationship with depression and dementia. Finally, there needs to be more funding for the prevention and treatment of concussions so that we can reduce the number of players suffering from this disease both during their careers, and after retirement.


  1.  Saulle, M. and B.D. Greenwald. 2012. Chronic Traumatic Encephalopathy: A Review. Rehabilitation Research and Practice
  2. 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: 128-134.
  3. Martland, H.S. 1928. Punch Drunk. The Journal of the American Medical Association 91(15): 1103-1107.
  4. McKee, A.C., Cantu, R.C., Nowinksi, C.J., Hedley-Whyte, T.E., Gavett, B.E., Budson, A.E., Santini, V.E., Lee, H.S., Kubilus, C.A., Stern, R.A. 2009. Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy After Repetitive Head Injury. J Neuropathol Exp Neurol 68(7): 709-735.
  5. Graham, D.I., McIntosh, T.K., Maxwell, W.L. Recent advances in neurotrauma. J Neuropathol Exp Neurol 59(8):641-651.
  6. Smith, C., Gentleman, S.M., Leclercq, P.D., Murray, L.S., Griffin, W.S.T., Graham, D.I., Nicoll, J.A.R. 2013. The neuroinflammatory response in humans after traumatic brain injury. Neuropathology and Applied Neurobiology 39: 654-666.

Marshal is a fourth year student at the University of Calgary majoring in Neuroscience. He is currently working on an honours thesis, studying the hypoxic effects that follow the induction of a seizure in a rat model of epilepsy. Follow The Triple Helix Online on Twitter and join us on Facebook.