In football, players run like bulldozers, ramming everyone in their way. If the heads of two football players collide, the impact can reach up to more than 100 g [1], similar to forces in a car crash; a high school football player experiences about thousand blows to the head each season [2]!
Rising Awareness Since 2005
Football has been played since 1869, but awareness that repetitive concussions and sub-concussive hits to the head may have long term neurodegenerative effects has been rising only since 2005. It all started when Bennet Omalu autopsied the brain of Mike Webster, a four-time winner of the Super Bowl who died at the age 50. After retiring from a long football career, he developed depression, took drugs, had memory and concentration problems, as well as shaking hands.
Mike Webster’s brain showed amyloid plaques and neurofibrillary tangles in the neocortex, reminiscent of Alzheimer's disease (AD). Omalu diagnosed chronic traumatic encephalopathy (CTE) and hypothesised that head-to-head collisions were the cause [3]. With accumulating case studies, he also started making connections between repetitive mild brain injuries and depression. Later, a second group led by Ann McKee reported CTE in a larger cohort of post-mortem samples and confirmed many of Omalu's hypotheses [4].
Upon Impact, the Brain Hits the Skull
Helmets worn by the players only prevent skull fractures, but not internal damage; the brain hits the skull from the inside, referred to as “Brain Slosh”. The shearing of brain tissue leads to excessive toxic release of neurotransmitters, changes in glucose-metabolism, immune activation, and damage of blood vessels. This leads to secondary injury: breakdown of the blood brain barrier, disturbances in cerebral blood flow, formation of hematomas, neuroinflammation and so on.
The results are neurological symptoms during acute injury (dizziness, headache, nausea) which collectively persist in long-term deficits [5]. Neuronal damage and traumatic axonal injury further lead to accumulation of a-beta amyloid, tau and ApoE components [5]. Though sharing many similarities with AD, CTE-associated tauopathy differs with regard to the distribution: in CTE, tau is most prominent in superficial cortical layers and sulci, and tends to surround blood vessels [5].
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| by Jack Kurzenknabe, via flickr |
Diagnostic Difficulties
The clinical phenotype of CTE is still incomplete, because most of the knowledge comes from post-mortem analyses and retrospective data. In the 158 autopsy cases analysed so far, 80% showed signs of CTE [6]. However it is difficult to asses how natural age-related changes, unrelated psychiatric illness, alcohol/drug use or coexisting cognitive impiarment contribute to the current picture of CTE; due to the long latency of CTE, co-morbidities are often present.
As of yet, there have been no established diagnostic criteria or in vivo biomarkers, meaning that CTE can only be diagnosed post mortem. But there is hope: Recent research developed means for premorbid identification of neurodegeneration in contact-sports athletes. NFL players with histories of mood and cognitive symptoms were subjected to positron emission tomography (PET) scans, which revealed that they had higher tau deposits than controls in all subcortical regions and the amygdala, areas known to produce tau deposits following trauma [7].
However the incidence and prevalence of CTE are still unknown and, to date, there is no consensus regarding which intensity of head blows is tolerable. Large-scale prospective, longitudinal studies of concussed and non-concussed individuals are needed to provide a better picture.INCIDENCE AND PREVALENCE STILL UNKNOWN
To further advance the research on biomarkers and treatment approaches, a mouse model has been developed. It uses controlled closed-head impacts on unanaesthetized mice to recapitulate the spectrum of behavioural symptoms noted in patients diagnosed with CTE [8].
What are the Consequences?
Until recently, the National Football league (NFL) did not recognize these injuries as consequence of the sport itself. Rather, a common argument suggests that former players can’t cope with not being the focus of attention anymore, which is why they develop depression and take drugs, which then goes on to eventually cause neurodegeneration. Several former NFL players sued the league for allegedly misleading them about the risks of brain injury and one player even resigned from the NFL because he feared the consequences of the daily brain trauma.
Is This the End for Football?
Football has been played for 150 years. In 1905, 19 players died in a single season, most due to head and spine injuries. President Roosevelt, an avid football fan, ordered football coaches to reform the rules eliminating the more brutal features of the game. Since then, the sport has changed time and again. As a reaction to the current discoveries, President Barack Obama also expressed concern about college football players and the “problems with concussions and so forth” [9]. Football is just too big of a cult for this to be the end. New rules will hopefully be enforced to make the games safer for the athletes and still satisfying for fans.
[1] Funk et al, Ann Biomed Eng, 2012
[2] Beckwith et al, Med Sci Sports Exerc. 2013
[3] Omalu et al, Neurosurgery, 2005
[4] Stein et al, Alzheimers Res Ther, 2014
[5] Chauhan, Restor Neurol Neurosci, 2014
[6] Gardner et al, Br J Sports Med, 2014
[7] Small et al, Am J Geriatr Psychiatry, 2013
[7] Petraglia et al, J Neurotrauma, 2014
[9] Foer and Hughes, New Republic, 2013
by Claudia Willmes, PhD Alumna AG Eickholt / AG Schmitz
this article originally appeared June 2016 in Volume 09 Issue 2 "The Sporty Brain"
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