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Original Contribution
September 2006

Neurochemical Aftermath of Amateur Boxing

Author Affiliations

Author Affiliations: Departments of Experimental Neuroscience (Drs Zetterberg, Popa, Rasulzada, and Blennow), Clinical Chemistry and Transfusion Medicine (Drs Zetterberg and Blennow), Neurology (Drs Hietala and Rosengren), and Psychiatry (Drs Jonsson, Karlsson, Edman, and Wallin, and Ms Styrud), The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden; Neurotec Department, Section of Clinical Geriatrics, Karolinska Institutet, Karolinska University Hospital in Huddinge, Stockholm, Sweden (Drs Andreasen and Wahlund); and Department of Immunology, Institute for Basic Research in Developmental Disabilities, Staten Island, NY (Dr Mehta).

Arch Neurol. 2006;63(9):1277-1280. doi:10.1001/archneur.63.9.1277
Abstract

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 β-amyloid protein 1-40 (Aβ[1-40]) and 1-42 (Aβ[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.

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