No neurochemical evidence for brain injury caused by heading in soccer.

BACKGROUND: The possible injurious effect to the brain of heading in soccer is a matter of discussion. OBJECTIVE: To determine whether standardised headings in soccer are associated with increased levels of biochemical markers for neuronal injury in cerebrospinal fluid (CSF) and serum. METHODS: 23 male amateur soccer players took part in a heading training session involving heading a ball kicked from a distance of 30 m at least 10 m forward. Ten players performed 10 and 13 players performed 20 approved headings. The players underwent lumbar puncture and serum sampling 7-10 days after the headings. The study also included 10 healthy male non-athletic control subjects. CSF was analysed for neurofilament light protein, total tau, glial fibrillary acidic protein, S-100B and albumin concentrations. Serum was analysed for S-100B and albumin. RESULTS: None of the biomarker levels were abnormal and there were no significant differences between any of the three groups, except for a slightly increased CSF S-100B concentration in controls compared with headers. Biomarker levels did not correlate with the number of headings performed. CONCLUSION: Repeated low-severity head impacts due to heading in soccer are not associated with any neurochemical signs of injury to the brain.

Neurochemical aftermath of amateur boxing.

BACKGROUND: Little solid information is available on the possible risks for neuronal injury in amateur boxing. OBJECTIVE: To determine whether amateur boxing and severity of hits are associated with elevated levels of biochemical markers for neuronal injury in cerebrospinal fluid. DESIGN: Longitudinal study. SETTING: Referral center specializing in evaluation of neurodegenerative disorders. PARTICIPANTS: Fourteen amateur boxers (11 men and 3 women) and 10 healthy male nonathletic control subjects. INTERVENTIONS: The boxers underwent lumbar puncture 7 to 10 days and 3 months after a bout. The control subjects underwent LP once. MAIN OUTCOME MEASURES: Neurofilament light protein, total tau, glial fibrillary acidic protein, phosphorylated tau, and beta-amyloid protein 1-40 (Abeta([1-40])) and 1-42 (Abeta([1-42])) concentrations in cerebrospinal fluid were measured. RESULTS: Increased levels after a bout compared with after 3 months of rest from boxing were found for 2 markers for neuronal and axonal injury, neurofilament light protein (mean +/- SD, 845 +/- 1140 ng/L vs 208 +/- 108 ng/L; P = .008) and total tau (mean +/- SD, 449 +/- 176 ng/L vs 306 +/- 78 ng/L; P = .006), and for the astroglial injury marker glial fibrillary acidic protein (mean +/- SD, 541 +/- 199 ng/L vs 405 +/- 138 ng/L; P = .003). The increase was significantly higher among boxers who had received many hits (>15) or high-impact hits to the head compared with boxers who reported few hits. In the boxers, concentrations of neurofilament light protein and glial fibrillary acidic protein, but not total tau, were significantly elevated after a bout compared with the nonathletic control subjects. With the exception of neurofilament light protein, there were no significant differences between boxers after 3 months of rest from boxing and the nonathletic control subjects. CONCLUSIONS: Amateur boxing is associated with acute neuronal and astroglial injury. If verified in longitudinal studies with extensive follow-up regarding the clinical outcome, analyses of cerebrospinal fluid may provide a scientific basis for medical counseling of athletes after boxing or head injury.

[There is a strong evidence that professional boxing results in chronic brain damage. The more head punches during a boxer's career, the bigger is the risk]. / Starka belägg för att proffsboxning leder till kroniska hjärnskador. Ju fler slag mot huvudet under en boxares karriär, desto större är risken.

The clinical symptomatology and pathogenic mechanisms of chronic traumatic brain injury associated with boxing (CTBI-B) is reviewed. This syndrome is also known as punch drunk syndrome or dementia pugilistica. Since even milder forms of CTBI-B are rare among amateur boxers, we make a distinction between amateur and professional boxing throughout the review. Focus is also set on the interesting similarities in neurochemical changes and pathogenic mechanisms between CTBI-B, acute traumatic brain injury (e.g. road traffic accidents) and Alzheimer's disease.