Boxing has been popular throughout history due to its brutal nature. Injuries are a part of the sport but rarely do brain injuries result in persistent neurological impairment (Lovell et al., 2004). The number of boxing-related fatalities is low, with an estimated 0.13 deaths per 1,000 participants annually (American Medical Association, 1983), which is similar to other high-risk sports. The majority of boxers do not suffer from severe, irreversible neurological impairments, but a correlation has been found between a boxer's overall fight count and the onset of neurologic, mental, or histopathological encephalopathy signs and symptoms (Casson et al., 1984; Drew et al., 1986; Jordan et al., 1997). This paper seeks to inform readers about the potential neuropsychological effects of boxing through second impact syndrome, neurological impairments, post-concussion syndrome, and chronic traumatic encephalopathy.
Second Impact Syndrome (SIS) occurs when an athlete sustains a second brain injury before the initial injury has fully healed (Saunders & Harbaugh, 1984). The second effect may appear modest at first, but it can swiftly progress into respiratory failure and result in death (Cantu, 1995). Case studies on boxers with SIS have connected the syndrome to foramen magnum herniation, vascular engorgement, and cerebral vascular dysregulation. Younger boxers are more vulnerable to SIS, as are younger players in other sports. Animal studies have shown that the developing brain is more susceptible to damage during a "critical time" of maturation because it recovers biochemically and physiologically more slowly than the adult brain. (Prins & Hovda, 2003). The best explanation for the increased mortality in younger animals appears to be brain damage in cognitively underdeveloped animals. As a diagnostic tool, SIS has come under scrutiny. An alternate explanation links mortality in these conditions to diffuse cerebral oedema, an extremely uncommon and serious posttraumatic sequelae of a single, superficially small brain lesion (McCrory, 2001).
The most visible critical neurologic impairment in boxing is a knockout (KO), which causes a rapid loss of consciousness that usually lasts a short time. The cerebellum and brain stem are typically subjected to motion or centrifugal tension when a boxer receives a straight punch to the face, which causes imbalance, and unsteadiness, which eventually renders the combatant unable to stand. However, knockouts cannot solely be used to evaluate neurological impairment because they leave the boxer unable to stand for 10 seconds after being struck, which may or may not signify a true loss of consciousness. The term "groggy state" or, more often, "post-concussion syndrome" is frequently used to describe when some boxers have lasting post-fight cognitive and physical symptoms for days or even weeks, including headaches, vertigo, trouble with balance, and memory issues. Most frequently, the boxer shows symptomatic improvement, reverts to his pre-injury state of physical and mental functioning, and resumes fighting. However, some boxers endure symptoms for longer periods of time (often those with the most extensive combat histories). Boxers are more prone to experience long-term issues, such as the emergence of CTE, when post-concussion symptoms occur frequently and persist for a longer period of time. More research is required to thoroughly evaluate the relevance of persistent post-concussive symptoms in CTE.
Chronic traumatic encephalopathy, known as dementia pugilistica or “Punchdrunk syndrome,” includes a range of neurological conditions that can affect speech, mobility, cognition, behaviour, and personality, and are all caused by long-term cerebral damage (Jordan, 1993). Dysarthria, cerebellar ataxia, parkinsonism, spasticity, and hyperreflexia are a few examples of motor impairments (Jordan, 1987). Personality changes, violent outbursts, impulsivity, and childishness are a few of the characteristic neuropsychiatric manifestations (Johnson, 1969; Mendez, 1995). High boxing exposure alone does not seem to be enough to develop CTE. According to Calne, Eisen, McGeer, and Spencer (1986), a combination of age-related neuronal loss and boxing-related injuries causes late-life dementia that some former professional boxers experience. To put it another way, dementia cannot be caused solely by age-related atrophy; it requires a critical number or percentage of neurons to be harmed or destroyed. Boxers who end their careers with some of their functioning neurons damaged may still not exhibit CTE symptoms as long as a certain percentage of those neurons are still intact (Stern, 2002). This idea of the cognitive reserve could explain why CTE frequently develops after a boxing career ends, although epidemiological research is needed before drawing any firm conclusions (Jordan, 1993). Some boxers may be more susceptible to developing CTE due to genetic reasons, particularly the apolipoprotein E (APOE) genotype, as for Alzheimer's disease and other late-life cognitive diseases, APOE-e4 is a genetic risk factor (Roses et al., 1996).
The APOE-e4 genotype was present in all of the boxers in Jordan and colleagues' study from 1997 who had sustained significant persistent Traumatic brain injury (TBI) and cognitive impairment (Kutner et al., 2000; Teasdale et al., 2005). The APOE-e4 gene may interact with other factors, such as age and the accumulation of mild TBIs, to affect cognitive abilities. While some studies suggest that people with APOE-e4 and a history of head trauma are more likely to develop early-onset dementia than those with APOE-e4 but no history of head trauma, the relationship between APOE-e4 and dementia after head trauma is still not well understood ((Jellinger, 2004). Though difficult to measure and extensively research, factors like a boxer's style and ability may also have an impact on the development of persistent neurological problems. If additional diseases including psychological illnesses, drug addiction, and learning issues are present, the initial diagnosis of CTE may be more difficult. Due to the complexity of the interactions between TBI, additional potential risk factors such as APOE-e4 allele status, concomitant disorders, and cognitive status in later life, further research is necessary before drawing firm conclusions.
Even though a great deal of research has been done on boxing-related brain damage throughout the years, many things remain unclear. The fatality rates for boxing are similar to other high-risk sports, and only a small percentage of boxers experience long-term neurologic damage. Researchers should study factors like the number of fights and sparring sessions, previous concussions, age, genetics, and punch velocity to determine if there is a threshold for impaired cerebral and neurocognitive function. Regular neuropsychological assessments are recommended to track changes in neurocognitive status because they are sensitive to sports-related concussions even when other medical exams are normal. Monitoring the neurocognitive condition of boxers could help improve their neurological health and inform participation decisions. This monitoring would also aid in spotting any early signs of mild neurocognitive deterioration that might develop into more severe CTE symptoms. Further studies are needed to verify some possible claims about the correlation of brain injuries with boxing and sports in general and other subsequent disorders (e.g. Alzheimer's).
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