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Evidence is inconclusive but the absolute risk in modern day boxing is still low
In this week's BMJ, a systematic review of observational studies by Loosemore and colleagues assesses the risk of chronic traumatic brain injury with amateur boxing.1 It finds that the quality of evidence is too poor to come to any definite conclusions. So, do we need to worry about the health of modern boxers, amateur or professional?
Concern over injury to fighters has been a persistent theme throughout the history of boxing. Although boxing was popular in early Rome, the practice was banned by Caesar Augustus, supposedly because of the high rates of injury in Roman legionnaires. The sport resurfaced in England during the 17th century in the form of bare knuckle boxing or prize fighting. The most famous of the rules introduced to protect the injured or incapacitated boxer were the 1867 Queensberry rules, which dictated that fights should be “a fair stand-up boxing match.” Each fighter was given a 10 second count if he was knocked down and the length of bouts was time limited. Gloves of a “fair size” were introduced, which changed the nature of the sport, as bouts became longer and more strategic, with greater importance attached to defensive manoeuvres such as slipping, bobbing, countering, and angling.
As the changing nature of the sport and the use of protective equipment reduced acute injuries, concern began to develop about the chronic neurological risks of boxing. This was fuelled by a study published in 1928, which introduced the lay term “punch drunk” into medical terminology; this term has since become synonymous with impaired boxers.2 Surprisingly, the only clinical case examined in that study concerned idiopathic Parkinson's disease.
Chronic traumatic brain injury has since been described in more detail. In the early stages of the condition, symptoms reflect lesions affecting the pyramidal, cerebellar, and extrapyramidal systems. In the later stages, cognitive and behavioural impairment predominate. About one third of cases are progressive.3 4 5 The pathological features of the condition are similar to Alzheimer's disease, although some specific differences exist.6 7
The crucial risk factor for chronic traumatic brain injury is exposure to head impact. The largest and best of the neuropathological studies included 15 ex-boxers, 12 of whom were professionals.6 7 These boxers had fought in the period 1900-40, and eight of them were national champions or world champions in their weight division. Although the study had methodological flaws—for example, all demographic and boxing exposure data were collected retrospectively—the most striking feature was the fighters' high exposure to boxing. The number of career fights ranged from 400 to 700. Many boxers also worked in fairground boxing booths and had up to 30 or 40 fights each day over several years. The pathological features described have become the essential diagnostic criteria for chronic traumatic brain injury.
These injuries are unlikely to be seen in boxers today because of their relatively short careers. More recent studies of professional boxers find that 95% of registered boxers have fewer than three fights in their careers, and that the theoretical risk of concussive injury from sparring is almost non-existent.8
The other major risk factor for chronic traumatic brain injury is genetic. Recent studies show that boxers with the apolipoprotein E4 (apoE4) allele are susceptible to chronic neurological deficits.9 10 Male boxers who have 12 or more professional fights, as well as the ApoE4 allele are 16 times more likely to have neurological deficits than those without the allele. The ApoE4 allele has also been linked to poor neurological outcome after traumatic brain injury from any cause.11
The precise incidence of chronic traumatic brain injury is difficult to measure, and it may largely be a condition of historical interest. Few prospective epidemiological studies have been performed in boxers, and often they do not distinguish between amateur boxing and professional boxing. A dose-response effect has been suggested, whereby professional boxers have a higher rate of chronic traumatic brain injury than amateurs because of greater exposure to head impacts—bouts are longer (12 rounds versus three rounds) and they do not wear protective headgear. However, this has never been formally tested. Given the quality of the published literature, it is not surprising that Loosemore and colleagues find little conclusive evidence for chronic traumatic brain injury in amateur boxing.1
The difficulty with extrapolating early studies to today's sport is that the nature of the sport has changed substantially. In the 1930s to 1950s, boxers' careers generally lasted 10-20 years, started in childhood, and involved up to 1000 professional fights. Many boxers also became professional sparring partners or boxers in tents and booths, where they fought up to 30-40 unsupervised bouts each day. Fighters were not matched by skill or weight, they had no medical supervision, and they fought with 6 oz gloves. Bouts were often not stopped even when a boxer was overmatched, and bouts lasted longer (up to 20 rounds of two minutes each). There was no mandatory exclusion after a knockout or head injury. Because of the depression in the 1930s, financial reasons kept many boxers competing, despite the onset of neurological symptoms.
No compelling evidence is available to suggest that regular magnetic resonance imaging of the brain, rigorous medical supervision, or currently practised safety measures will influence or prevent the development of chronic traumatic brain injury. However, because today's boxers have shorter careers and reduced exposure to repetitive head trauma, the likelihood of this condition developing is probably low. Whether governing bodies should recommend or mandate genetic testing for the ApoE4 allele in prospective boxers is an ethical question that needs to be debated. One of the reasons for doing so would be to provide an opportunity to counsel boxers about their risk of injury.
This article was posted on bmj.com on 4 October 2007: http://bmj.com/cgi/doi/10.1136/bmj.39352.454792.80
Competing interests: None declared.
Provenance and peer review: Commissioned; not externally peer reviewed.