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Neurosurgery:
doi: 10.1227/01.neu.0000430739.63491.ba
Science Times

Neuroanatomy Changes With Repetitive Mild Head Injury in Athletes

Jandial, Rahul; Duenas, Matthew J.; Chen, Mike Y.

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The long-term dangers to the cognitive functioning of boxers has been well described and, in retrospect, considered to be a predictable outcome. The essential goal of boxing is to win a combative exchange of blows to score points and, if possible, cause the loss of consciousness of your opponent. This is clearly an example of repetitive head injury. Accordingly, in 1937, the associated decline in cognitive function was termed dementia pugilistica—with clinical features similar to those previously described by the Journal of the Medical Association under a paper titled “punch drunk.”1,2 The histopathology is consistent with what is now termed chronic traumatic encephalopathy (CTE).2 CTE is a progressive neurodegenerative process marked by deposits of hyperphosphorylated tau protein as neurofibrillary tangles in the brain in response to repetitive traumatic brain injury. In the last several years, lay press on the origins and management of concussions has been given significant attention as football players are demonstrating symptoms that in the past were unrecognized or underreported. This increased attention has extended further into the potential deleterious effects not only of severe repetitive head injury, as can occur in boxing, football, or rugby, but also with the aggregate effects of mild repetitive head injury, as can occur in soccer or basketball. In parallel with expanding investigation on the matter, more athletes and military personnel are requesting their brains to be evaluated post-mortem.

In a recent study from Brain, McKee et al examined brains from 85 individuals that described histories of repetitive mild traumatic brain injury. Out of the 85 test subjects, 68 showed evidence of CTE, compared to a control group of 18 age- and sex-matched individuals with no previous history of repetitive mild traumatic brain injury. They performed exhaustive histological evaluation and demonstrated multifocal axonal varicosities and axonal loss in deep cortex and subcortical white matter at all stages of CTE (Figure). They describe an ordered and predictable progression of hyperphosphorylated tau abnormalities through the nervous system in CTE that occurs in conjunction with widespread axonal disruption and loss. Next, they describe common symptoms associated with CTE and assigned them to various stages of progression. Stage I CTE included headache, loss of attention, and lack of concentration. Symptoms in stage II included depression, explosiveness, and short-term memory loss. In stage III, executive dysfunction and cognitive impairment were found, and finally in stage IV, dementia, word-finding difficulty, and aggression were characteristic. They concluded an association between repetitive traumatic brain injury and CTE. Due to admitted limits of autopsy-based studies, however, they propose that in order to get a more telling picture of CTE and its effects on the brain, future investigation will need to include football players and soldiers that have been exposed to repetitive head injury but do not display symptoms.

It is laudable that the authors offer no overreaching conclusions, since subjects with displayed symptoms were more likely to offer their brains for examination after death than those who showed no displayed symptoms. This ascertainment bias is a major limitation in establishing causation, and not just association, between mild repetitive head injury and CTE. Undeniably brain neurodegeneration occurs with repeated head injury. Further important research into this connection includes the type of injury, frequency of injury, genetic susceptibility, and whether or not pediatric patients are at greater risk of injury-induced brain neurodegeneration. This will require large longitudinal studies with a robust inclusion of people not only with a history of repeated head injury, but also those with and without a history yet devoid of symptoms. This will require a large amount of time. In the interim, therefore, prudence should be the guiding principle when any concussive symptoms are suspected, and care should be taken to avoid the risk of repeat injury.

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REFERENCES

1. Millspaugh JA. Dementia pugilistica. US Naval Med Bulletin. 1937;35:297–361.

2. Martland HS. Punch drunk. JAMA. 1928;91(15):1103–1107.

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