There is growing scrutiny regarding the link between head trauma and the acquisition of neurological and psychiatric conditions. Head trauma is associated with a significantly increased risk of unipolar and bipolar depression, schizophrenia, and mood disorders (Orlovska et al., 2014; Robinson & Jorge, 2002).
Public attention has now focused on assessing head injuries in athletes participating in contact sports, many of whom have consequently exhibited chronic traumatic encephalopathy (CTE), a neurodegenerative condition resulting from repeated instances of concussions and traumatic brain injuries.
CTE is characterized by neurological atrophy within the central nervous system (CNS), translating pathologically through deposition of the tau protein. Symptomatically, CTE presents in stages, starting with substantial memory disturbances, impulsivity, speech impediments, motor impairments, and depression, before eventually progressing to neurodegeneration in the form of dementia (McKee et al., 2009).
CTE first came to light when many professional boxers exhibited dementia pugilistica, or ‘punch-drunk syndrome,’ which manifested as dementia-like symptoms. Additionally, American football and soccer players who exhibit CTE have often gone on to suffer from dementia (Tartaglia et al., 2014). However, such conclusions have been drawn only from post-mortem analyses. Researchers have the impetus to find means of detecting warning signs for CTE in athletes during their lives.
This process should entail evaluation for biomarkers linked to short and long-term head traumas. Biomarker assessment, when supplemented with neuropsychiatric evaluations and timely medical interventions, will go a long way in preventing many athletes’ lives from being marred by the neuropsychiatric complications of CTE.
One of the most well-documented cases pioneering early interest in the link between head trauma and compromised neuropsychiatric well-being involved Phineas Gage, the American construction foreman. Gage miraculously survived the ordeal of an iron bar thrust through his skull. Though he survived, Gage suffered from permanent frontal lobe damage, which manifested through marked changes in behavior, such as irreverence and inability to take responsibility for his actions (Damasio et al., 1994).
A similar phenomenon is now being considered with respect to participants of contact sports. These sports, while integral parts of everyday recreation and entertainment, carry a high risk of concussion for their participants.
Head Trauma is Rampant Occurrence
Head trauma is a rampant occurrence in contact sports, whether from a blow of a boxing glove, to heading a soccer ball, to collisions with opposition players in strong football tackles. Athletes often experience repeated head impacts, each of which may not be as severe as Phineas Gage’s, but nevertheless, carries its own incremental mark of potential damage.
Recently, neuropathologist Ann McKee, upon examination of brains from 111 deceased American football players from the National Football League (NFL), confirmed that 110 players displayed the pathology of CTE, which was exhibited through the deposition of the tau protein as neurofibrillary tangles in the central nervous system (CNS) (McKee, Mez, & Abdolmohammadi, 2017).
Many of these symptoms have been reported in athletes afflicted by head trauma during their lives. NFL linebacker Fred McNeill was suspected of having CTE after brain scans suggested evidence of tau pathology, an observation validated by a subsequent post-mortem autopsy.
McNeill’s family members indicated that he had suffered from depression and dementia-like memory loss until his death in 2015 (Omalu et al., 2018).
In soccer, a sport characterized by repetitive impacts to the head with the soccer ball, the plight of head trauma and subsequent brain injury has been well-documented. One of the most renowned cases is that of Jeff Astle, a former England and West Bromwich Albion striker.
Astle suffered from marked cognitive decline later in his life before ultimately acquiring dementia. Dementia has also been reported in many other soccer players, including four members of England’s 1966 World Cup winning team. Furthermore, analyses from a cohort of soccer players from 1980 to 2010, all of whom also acquired dementia, indicated a significant prevalence of CTE (Ling et al., 2017).
These findings, while groundbreaking in bringing this phenomenon to public awareness, have all been discovered in post-mortem retrospect. The former players had already suffered from their plight long before their condition could even be detected. Many athletes who suffer from even acute head trauma have been impacted with neuropsychiatric complications.
In 2017, Harvard Medical School psychiatrists diagnosed a living college soccer player, who had a history of concussion, with schizoaffective disorder. He exhibited frontal lobe dysfunction, impulsive behavior, and thought blocking (Adelsky et al., 2017). Given that athletes like him have suffered at such early ages, one can imagine how much of an impact chronic head trauma, culminating in acquiring CTE, can have on the neuropsychiatric well-being of athletes in the long run.
An athlete’s career, even without considering the persistent risks of career-threatening injuries, is truncated relative to other occupations, as athletes often retire in their 30s. However, CTE tends not to present until five to 10 years after repeated brain trauma. Once the athlete acquires CTE, they are consigned to progressively worsening symptomatology throughout the remainder of their lives.
Early Intervention is Limited
Early intervention of CTE has been inherently limited because of a lack of in vivo methods to detect markers of CTE. In addition, CTE results from concussions, which often do not show on magnetic resonance imaging (MRI) or computed tomography (CT) scans, making immediate detection difficult.
One key target in early intervention of CTE is timely detection of its tau neuropathology. This could be done using a radioactive tracer compound to probe for the tau protein on a positron-emission tomography (PET) scan. One such tracer is FDDNP, which can bind to tau proteins.
Moreover, [18F]-T807, a derivative tracer of FDDNP, has recently been found to exhibit highly specificity for the tau protein in in vivo autoradiography results. [18F]-T807 shows great promise as a PET tracer for potential tau analyses going forward. Ideally, provided that the value of [18F]-T807 is substantiated further, this tracer could be used clinically in the future.
For now, FDDNP can more than suffice as an effective probe for the tau protein during PET scans. Alternatively, tau can be assessed by acquiring cerebrospinal fluid (CSF) from lumbar punctures (LPs) and subjecting the CSF to an antibody assay for the tau protein (Gandy et al., 2014).
One potential route worth pursuing is to periodically assess athletes for CTE biomarkers during their involvement in contact sports. As members of professional sports teams, players are subject to regular fitness and medical testing. During such tests, players are assessed for hazardous conditions, such as heart arrhythmias, which, if present, often result in a precautionary termination of the player’s career. Such measures are taken to prolong the player’s life, as there are life-threatening risks like cardiac arrests, which may transpire under the rigorous physical exertion associated with professional sports.
Similar precautions should be taken with CTE assessment. One way to test for tau (and potential CTE) is to have players undergo periodic PET scans and/or CSF-LPs as part of their medical examinations.