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How Concussions Cause Chronic Traumatic Encephalopathy? Research Paper

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Updated: Oct 6th, 2020

Problem Statement

Much of what is known today about long-term consequences of constant head injuries, specifically noted in sports, has only gained important public awareness and interest recently. Specifically, media have concentrated on chronic traumatic encephalopathy (CTE). CTE is defined as a progressive neurodegenerative disease caused by repetitive head trauma (Saulle & Greenwald, 2012; Yi, Padalino, Chin, Montenegro, & Cantu, 2013).

Notably, CTE has gained wider recognition and discourse because of its association with sports, such as football, boxing, soccer, hockey, and professional wrestling. Most affected athletes, mainly retired, tend to suffer from depression, anger, drug abuse, motor/memory disorders, and suicide. Further, postmortem analyses from the affected athletes have demonstrated a relationship between CTE and these cognitive, emotional, and physical disorders (Saulle & Greenwald, 2012).

The evidence available on CTE has created public awareness about the long-term negative effects of concussions and subconcussive brain trauma associated with sports. As previously noted, the conclusive diagnosis of CTE depends on an autopsy analysis, and much effort is now directed toward in vivo confirmatory diagnostic examination that could assist in identifying athletes at greatest risk of experiencing CTE and ascertaining CTE in early stages.

The review, therefore, aims to draw a conclusion on a link between CTE and concussion in retired American footballers, national football league (NFL) players. By identifying athletes with possible CTE, effective intervention strategies could develop earlier to manage the burden of the condition. While research has indicated a link between neurological conditions and constant exposure to mild traumatic brain insults, a clear relationship between long-term effects that are linked to CTE and how and why concussions cause chronic traumatic encephalopathy in retired NFL players remains unclear.

The purpose of this literature review is to examine how and why constant hits to the head or concussions cause chronic traumatic encephalopathy in retired NFL players. Recent literature on CTE specifically referring to NFL retired players has been included in this research to address the research question. The literature review covers progress made in CTE research, clinical symptoms, neuropathology, and clinical implications.

Research Question

This research paper seeks to explore the question of how and why concussions cause chronic traumatic encephalopathy in retired NFL players.

Literature Review

For decades now, it has been claimed that involvement in some contact sporting activities may enhance athletes’ risks of developing a neurodegenerative disease after retirement (Gavett, Stern, & McKee, 2011; Saulle & Greenwald, 2012).

Earlier evidence had established such a relation in boxers, athletes who often sustained multiple hard blows on their heads during sporting activities. Harrison Martland first described the case in 1928 as a clinical spectrum of abnormalities common in boxers who had participated in the game long enough. Later in the 1960s, the term CTE was introduced to replace dementia pugilistica used in the 1920s to refer to conditions of fighters (Korngold, Farrell, & Fozdar, 2013).

The NFL culture promotes toughness and resistance to adversity. In the recent past, however, the majority of the retired NFL players have filed lawsuits based on negligence claims and now require monetary compensations (Abreu, Cromartie, & Spradley, 2016). These claims are based on findings that link repeated concussions to psychological problems and concerns about the neurodegenerative disease, CTE that ultimately impairs cognition, behavior, and movement (Korngold et al., 2013).

Clinical Features

Nearly all studies on CTE have covered clinical manifestations since the 1920s. Martland first used the term ‘punch drunk’ to refer to such signs and symptoms identified in boxers after substantial head trauma. Further, dementia pugilistica was later used to reflect motor deficits and confusion. The CTE was adopted to capture neurologic deterioration that originated after multiple traumatic brain injuries (Yi et al., 2013). Today, it is observed that clinical manifestation of the condition appears similar to other neurodegenerative conditions.

It is shown that concussion and post-concussion symptoms demonstrate momentary conditions of neuronal and axonal instability because CTE is known to take several years or decades after the recovery from acute or post-acute impacts of head trauma (Gavett et al., 2011). Current evidence suggests that the exact association between CTE and concussion is not completely understood (Maroon et al., 2015; Gavett et al., 2011).

Hence, it is vital to define the timeline of how CTE symptoms develop to differentiate it from concussive or post-concussive syndrome (PCS) (Saulle & Greenwald, 2012). Usually, concussion symptoms are headache, amnesia, blurred vision, slurred speech, and fatigue, which disappear in days or weeks if effectively managed. For CTE, it is observed that sustained axonal perturbation could start a series of metabolic, membrane, ionic, and cytoskeletal disorientation, resulting in a pathological reaction that eventually leads to CTE in susceptible athletes.

According to Gavett et al. (2011), CTE is often noted in mid-life after the retirement of athletes. Behavior is affected mostly in individuals with neuropathological susceptibility who become angry, irritable, show shorter rage, and apathetic while suicidal tendencies are observed as a prominent symptom of the condition (Korngold et al., 2013; Korngold et al., 2013). Further, some individuals also present cases of cognitive difficulties and poor memory as elements of cognitive dysfunction (Saulle & Greenwald, 2012).

Later stages of the disease are characterized by speech, movement (Parkinsonism), and ocular degeneration as cognition deteriorates. A smaller percentage of individuals with neuropathologically-documented CTE normally suffer dementia before deaths. On this note, Gavett et al. (2011) note that dementia is relatively less common because majorities with CTE usually die from suicide, accidents, or drug overdose relatively at an early age. In addition, Saulle and Greenwald (2012) have noted that CTE does not have a clear stage of progression, for instance, from PCS to CTE.

Neuropathology of CTE

Gross pathological results in CTE have been identified as atrophy, enlargement of the lateral and third ventricles, fenestrations of the anterior cavum septum pellucidum, and scarring with neuronal loss of the cerebellar tonsils (Yi et al, 2013; Gavett et al, 2011). These findings are observed as consistent in retired athletes who suffered repeated mild head insults, and they are distinctive results for CTE.

A gross assessment often reveals anterior cavum septum pellucidum and posterior fenestrations, which are thought to be caused by the power of the head impact directed via the ventricular system, thereby distressing functional integrity of nearby or intervening tissues (Yi et al., 2013). The lateral and third ventricles enlargement is also identified as a widely notable feature in CTE. The enlargement makes the third ventricle excessively larger.

Further, atrophy is observed in frontal and temporal cortices and medial temporal lobe, hypothalamic floor diminishing is observed, as well as contraction of the mammillary features, pallor of the substantia nigra, and hippocampal sclerosis (Gavett et al., 2011). Atrophy is usually associated with low brain mass. It is noted that the above-mentioned findings of CTE were first identified in NFL players and described by Omalu in 2002 (Saulle & Greenwald, 2012). They closely resemble some traits identified in most cases of tau deposits with few neurofibrillary tangles (NFTs) and Alzheimer’s disease.

When tau is considered, microscopic neuropathology reveals that CTE is reflected by numerous neurofibrillary inclusions, such as “neurofibrillary tangles (NFTs), neuropil threads (NTs), and glial tangles (GTs)” (Gavett et al., 2011, p. 179). NFT consists of the microtubule-related protein tau. Although CTE may have similar microscopic traits as Alzheimer’s disease and other neurodegenerative diseases, its major differentiating features include tau pathology common in superficial cortical laminae (II and III). It is imperative to note that the exact pathological processes that relate repeated mild head insults to NFT development are not clearly understood.

Some studies have also established that beta-amyloid (Aβ) deposits associated with CTE are observed in 40% to 45% of patients (Gavett et al., 2011; Yi et al., 2013; Saulle & Greenwald, 2012). This is opposed to the extensive presence of Aβ deposits in patients with Alzheimer’s disease. In addition, recent findings have also established prevalent TDP-43 proteinopathy in more than 80% of cases of CTE (Gavett et al., 2011). Additionally, it was also observed that athletes who experienced a progressive motor neuron disease many years before their deaths had prevalent TDP-43 immunoreactive inclusions in the anterior horns of the spinal cord (Gavett et al., 2011).

Clinical Implications

According to an estimate from the Centers for Disease Control and Prevention (CDC), about 3.8 million sports-related concussions occur in the US every year (Kerr et al., 2014). Thus, CTE presents opportunities for clinical implications. CTE has been recognized as having clinical symptoms that can only be identified later in life, normally after athletes have retired from the game. Moreover, just like other neurodegenerative diseases that result in dementia, CTE is also characterized by gradual and harmful onset, as well as progression.

Age plays a critical role in the onset of CTE. According to Gavett et al. (2011), athletes usually experience the condition at an average age of 42.8 years and eight years after retirement, but a small number of athletes experience symptoms immediately after retirement.

Presently, the clinical diagnosis of CTE is challenging. There are no agreements on the current diagnostic criteria or any large studies to support any diagnostic approaches. However, it is noteworthy that the currently used definitive diagnosis of CTE depends on an autopsy examination. Further, research in vivo confirmatory diagnostic is underway to identify persons at greatest risks and development of effective management strategies (Yi et al., 2013; Maroon et al., 2015).

The most important consideration is the differential diagnosis of CTE, which should account for Alzheimer’s disease and frontotemporal dementia (FTD) based on the presenting situation and age of onset (Gavett et al., 2011). For instance, older persons who have conditions of memory deficiencies may seem to have Alzheimer’s disease and CTE neuropathologically. Further, in earlier instances, when the patient is aged between 40 and 50 years old, then FTD should be considered.

It is also imperative to recognize that the history of head trauma may not necessarily reflect the presence of CTE because it has been previously associated with Alzheimer’s disease, Parkinson’s disease, and other neurodegenerative conditions. This implies that it could be difficult to deliver CTE clinical diagnosis with relatively high confidence levels (Maroon et al., 2015; Gavett et al., 2011).

For risk and protective factors, one must appreciate that CTE research is still emerging, and more research will be required to advance knowledge on diagnosis using various tools. Nevertheless, current evidence provides implications for all stakeholders, including NFL players, athlete trainers, medical professionals, government agencies, and other related associations.

Notably, all studies reviewed have confirmed that repeated head trauma is responsible for CTE as neurodegenerative dementia. It remains unknown whether one hit to the head is enough to start the metabolic cascade that comes before clinical and neuropathological alterations associated with CTE – all known cases have been linked to several head insults. As such, the most possible means to prevent CTE is, at least in theory, to avoid multiple head insults (Maroon et al., 2015; Yi et al., 2013; Gavett et al., 2011).

However, one must observe that this intervention is impossible to realize because collisions and hard hits are expected in contact sports like American football. With the preventive treatment, it would be difficult to attain meaningful outcomes among NFL players. Currently, only symptoms of CTE may be managed because no known treatments are available. With more studies, expectantly, treatments may be found. Meanwhile, the use of protective gear and stringent rules could help in reducing the impacts and frequencies of collisions (Saulle & Greenwald, 2012).

Age is also a critical factor for NFL players because it affects possible CTE risk. Younger players are more susceptible to brain insults (Gavett et al., 2011). Conversely, such players also have enhanced brain plasticity and, thus, it can better compensate for certain injuries. Maroon et al. (2015) found out that the age of death ranged from 17 years to 98 years. In addition, most deaths were related to natural causes, accidents, and suicides. For natural deaths, cardiac disease, respiratory failure, end-stage dementia, and malignancy were common causes, but accidental deaths were linked to severe TBI insults and drug overdose (Maroon et al., 2015).

Genetic differences are also thought to play a critical role in influencing head insults, altered cognition, neuropathological changes, and individual behaviors. The specific gene believed to moderate CTE risk is the apolipoprotein E (APOE) gene, which has been found in patients with Alzheimer’s disease, and it could increase CTE risks (Gavett, 2011). Genetic testing established a significant percentage of persons with confirmed CTE possessed APOE ε4 allele. Conversely, Yi et al. (2013) and Maroon et al. (2015) noted some studies involving genetic testing did not determine how apolipoprotein (ApoE D4) could influence and play a role in increasing CTE risk.


All studies have now confirmed that CTE is a neurodegenerative condition that results from multiple head insults. It mainly affects athletes after retirement with observable symptoms. The definitive diagnosis of CTE is done after death, but significant research is being conducted in vivo to improve diagnostic testing. Current literature still lacks clarity on neuropathological findings. Further studies should focus on clear diagnostic criteria because of CTE shares some symptoms with other known neurodegenerative diseases. New findings would help to improve the diagnosis of the disease. It is imperative to recognize that current treatment is purely preventive, but symptoms can be managed. Still, for NFL players, it would be difficult to reduce cases of blows and hard hits.


Abreu, M. A., Cromartie, F. J., & Spradley, B. D. (2016). . The Sport Journal. Web.

Gavett, B. E., Stern, R. A., & McKee, A. C. (2011). Chronic traumatic encephalopathy: a potential late effect of sport-related concussive and subconcussive head trauma. Clinics in Sports Medicine, 30(1), 179–xi. Web.

Kerr, Z. Y., Evenson, K. R., Rosamond, W. D., Mihalik, J. P., Guskiewicz, K. M., & Marshall, S. W. (2014). Association between concussion and mental health in former collegiate athletes. Injury Epidemiology, 1(1), 28. Web.

Korngold, C., Farrell, H. M., & Fozdar, M. (2013). The National Football League and chronic traumatic encephalopathy: legal implications. Journal of the American Academy of Psychiatry and the Law, 41(3), 430-436.

Maroon, J. C., Winkelman, R., Bost, J., Amos, A., Mathyssek, C., & Miele, V. (2015). Chronic traumatic encephalopathy in contact sports: a systematic review of all reported pathological cases. PLoS ONE, 10(2), e0117338. Web.

Saulle, M., & Greenwald, B. D. (2012). Chronic traumatic encephalopathy: a review. Rehabilitation Research and Practice, 2012, 1-9. Web.

Yi, J., Padalino, D. J., Chin, L. S., Montenegro, P., & Cantu, R. C. (2013). Chronic traumatic encephalopathy. Current Sports Medicine Reports, 12(1), 28-32.

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