Concussion: Hollywood Spotlights Neuroscience


While Hollywood adapts reality to create a good story, it’s worth fact-checking this movie’s science to better clarify chronic traumatic encephalopathy.

Concussion, starring Will Smith as the Nigerian-born forensic pathologist Bennet Omalu, chronicles the heroic struggle of Dr. Omalu to force the corporate goliath that is the National Football League (NFL) to “tell the truth.” The movie puts a human face – and heart – on neuroscience, as the charismatic Will Smith creates a charming and memorable portrait of a man of great integrity.

As a scientist and clinician who sees severe concussion cases in clinic on a daily basis, I enjoyed the movie. I hope it draws attention to and fosters healthy discussion about the risks of brain injury. While Hollywood should always be forgiven for placing importance on telling a good story over giving precise facts and a comprehensive discussion, in this case it is worth fact-checking this movie’s science to increase awareness of chronic traumatic encephalopathy (CTE).

My greatest concern with the movie would actually be the title. This movie is not about concussions, it is about CTE. And it is important not to confuse the two. A concussion or mild traumatic brain injury (mTBI) is a physiological disruption of brain function as the result of a traumatic event that is manifested by at least one of the following: an alteration of consciousness, loss of consciousness, loss of memory, or focal neurological deficit that may or may not be transient.1 It is an acute event, with varying lengths of recovery time. In the brain tissue at a microscopic level, the traumatic event causes the rapid release of the excitatory amino acids glutamine and aspartate while affected neurons experience a calcium influx and microtubule disruption.2

In contrast, CTE is a neurodegenerative disease rather than an event. It is a slowly progressing tauopathy with a clear environmental etiology, characterized neuropathologically by atrophy of the frontal lobe, medial temporal lobe, thalamus, mammillary bodies, and brainstem. Clinically one sees memory disturbance, behavioral and personality changes, Parkinsonism, speech abnormalities, dysphagia, ocular abnormalities, and gait abnormalities.3 Importantly, CTE can only be diagnosed by histopathological examination after death. There is still debate in the field as to whether CTE is caused by concussive blows, subconcussive blows, or a combination.4 But severity of CTE seems to correlate with the length of time engaged in a contact sport and only speculation exists as to the minimum number of closed head injuries necessary to cause CTE.3     

Other issues I took with the movie had to do with scope. While the movie focuses on football, CTE has been found on autopsy in ice hockey players, professional wrestlers, mixed martial artists, rugby players, and major league baseball players, which is not mentioned in the film. The movie also primarily dramatizes the behavioral and personality changes, confusion, and disorientation that can occur in CTE. However, the progressive slowing of muscle movements, dysarthria, vertigo, and deafness can be more prominent than cognitive and behavioral changes in many individuals.  

Finally, and admittedly much too punctiliously on my part, I found a few potentially scientifically misleading moments in the film. Dr. Oamlu did indeed conclude after pathological examination of 50-year-old former Pittsburgh Steeler’s Center Mike Webster – the first case of CTE he discovered – that Webster’s brain was healthy and normal looking,5 just as in the movie. However, atrophy is typically present in CTE with ventricular dilation that would result in a rather unhealthy-looking brain being more typical of CTE. Next, an animated graphic of a blow to the brain early in the movie showed what looked like blood seeping across the brain, which is unrepresentative as hemorrhage is not a common occurrence in concussive or subconcussive blows. Lastly, the images of tissue Dr. Omalu ponders over in the movie showed prominent β-amyloid plaques as well as neurofibulary tangles, characteristic of Alzheimer’s disease. In CTE, less than 50% of cases have shown diffuse β-amyloid plaques.       

In turning from Hollywood to the far less glamorous world of clinical practice, it is important for clinicians who see head injuries to have a functional understanding of this disease. The first description of the syndrome harkens back to the 1920s. Its first mention is typically attributed to Martland in 1928, when he coined the term "punch drunk syndrome" from his study of boxers.6 Lampert and Hardman later termed the same syndrome "dementia pugilistica" in 1984.7 In 2005, Dr. Omalu with DeKosky, Minister, Kamboh, Hamilton, and Wecht named the syndrome CTE in their paper “Chronic Traumatic Encephalopathy in a National Football League Player,” just as portrayed in the movie.

One of the leading research groups in CTE is the Boston University Center for the Study of Traumatic Encephalopathy (CSTE), which maintains a brain bank of professional athletes’ brains. They have extensively studied a large number of cases. Alarmingly, the youngest CTE case reported was a 17-year-old: Nathan Stiles who died a few hours after playing in the Spring Hill High School homecoming football game in Kansas.8 Perhaps more alarming, I have heard co-founder of CTSE Robert Stern, PhD discuss the high rates of CTE in professional athletes and in September of 2015, the CTSE announced CTE has been found in 87 of 91 former NFL players autopsied. That is 96% of their sample.9

In terms of initial identification, a deficit in executive function may be one of the earliest symptoms of CTE.10 Executive functions are the most complex operations the human brain performs, such as judgment, perspective taking, initiative, inhibition of inappropriate responses and behavior, prioritization, and efficient retrieval of information from memory. Executive functions can be evaluated by a series of non-invasive, neurocognitive tests performed by specialists.  

But identification can be elusive. In clinical practice it can be difficult to differentiate CTE from a post-concussion syndrome. Post-concussion syndrome is the persistence of common concussion symptoms such as confusion, headache, dizziness, fatigue, vision changes, attention/concentration deficit, and physical and cognitive slowing for more than 3 months,11 and the condition generally improves over time. In comparison, CTE generally worsens over time as the disease progresses. Most importantly, post-concussion syndrome is a treatable condition, while there is no cure for CTE.  

Currently, research is looking into what the risk factors are for developing CTE and how CTE might successfully be treated in the future. Concussion should never go ignored and proper rest and treatment are critical to avoid long-term consequences such as CTE.4 Frank and honest discussion with concussion specialists, including sports medicine physicians, neurologists, and neuropsychologists, about any head injuries is the best way to determine proper treatment and what precautions to take to avoid the devastating course of CTE.

At the end of the credits for Concussion, the words “Be Moved” appear (Sony Picture’s slogan). It is my hope that the viewers of this movie will indeed be moved to appreciate the dangers of repetitive head injury and the role of neuroscience in assessment, treatment, and prevention.


1. American Congress of Rehabilitation Medicine. Definition of mild traumatic brain injury. J Head Trauma Rehabil. 1993;8(3):86-87.

2. McAllister TW. Genetic factors. In: Silver JM, et al., eds. Textbook of Traumatic Brain Injury, 2nd ed. Arlington, VA: American Psychiatric Publishing, Inc.; 2011:37-48.

3. McKee AC, et al. Chronic traumatic encephalopathy in athletes: progressive tauopathy following repetitive head injury. J Neuropathol Exp Neurol. 2009;68(7):709-735.

4. Zaslow T. Concussion expert shares important information on sports-related concussions. 26 Dec 2015. Accessed 7 Jan 2016.

5. Omalu BI. Chronic traumatic encephalopathy in a national football league player. Neurosurgery. 2005;57(1):128-134.

6. Martland HS. Punch drunk. JAMA. 1928;91(15):1103-1107.

7. Lampert PW, Hardman JW. Morphological changes in the brains of boxers. JAMA. 1984;251:2676-2679.

8. Kounang N. Brain bank examines athletes’ hard hits. 27 Jan 2012. Accessed 7 Jan 2016.

9. CTE prevalent in deceased players, study shows. ESPN. 15 Oct 2015. Accessed 7 Jan 2016.

10. Seichepine DR, et al. Profile of self-reported problems with executive functioning in college and professional football players. J Neurotrauma. 2013;30:1299-1304.

11. McAllister TW. Mild brain injury. In: Silver JM, et al., eds. Textbook of Traumatic Brain Injury, 2nd ed. Arlington, VA: American Psychiatric Publishing, Inc.; 2011: 239-264.

Related Videos
Ro'ee Gilron, PhD
Monica Verduzco-Gutierrez, MD
Shahid Nimjee, MD, PhD
Peter J. McAllister, MD, FAAN
Video 6 - "Utilization of Neuroimaging in Alzheimer’s Disease"
Video 5 - "Contribution of Multiple Pathways to the Development of Alzheimer’s Disease"
Michael Levy, MD, PhD
© 2024 MJH Life Sciences

All rights reserved.