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Structural abnormalities occur in the brains of rugby players.

Thursday, July 22, 2021

injury

Structural abnormalities occur in the brains of rugby players

White matter abnormalities in active elite adult rugby players. 

Karl A Zimmerman, Etienne Laverse, Ravjeet Samra, Maria Yanez Lopez, Amy E Jolly, Niall J Bourke, Neil SN Graham, Maneesh C Patel, John Hardy, Simon Kemp,. Huw R Morris, David J Sharp, White matter abnormalities in active elite adult rugby players, Brain Communications, Volume 3, Issue 3, 2021, fcab133, https: //doi.org/10.1093/braincomms/fcab133

Commentary

This study will examine the state of the brain in rugby players.

In general, recognition, diagnosis and management of mild traumatic brain injury can be difficult and confusing, but there is a lack of mechanistic clarity in the association of persistent injury with brain damage such as diffuse axonal injury, diffuse vascular injury and progressive neurodegeneration.

Advances in neuroimaging technology have allowed us to investigate the neuropathology associated with the acute and long-term effects of injury, and we are investigating the long-term effects of this injury, which is most commonly reported during professional rugby.

Using advanced MRI, a longitudinal observational study was conducted to investigate the relationship between exposure to rugby participation and subacute head trauma in professional adult male and female rugby union and league players.

Diffusion tensor and magnetic susceptibility-weighted images were used to assess white matter structure and evidence of axonal and diffuse vascular injury. Jacobi determinant statistics extracted from serial volume imaging were also used to study changes in brain structure over time.

The study tested 41 male and three female adult elite rugby players, 21 of whom participated after head trauma, 32 non-sport controls, 15 non-collision sport motor controls, and 16 longitudinally assessed controls.

Eighteen rugby players participated in the longitudinal arm of the study.

A second visit was scheduled six months after the initial scan and the results showed that neuroimaging evidence of either axonal or diffuse vascular injury was present in 23% (10/44) of the players.

The non-acutely injured group of rugby players showed partial anisotropy and other abnormalities in diffusion measurements, in contrast non-collision sport motor controls were not classified as showing abnormalities.

Group-level contrast also showed evidence of subacute injury using diffusion tensor imaging in rugby players. Examination of longitudinal images revealed an unexpected decrease in white mass in the elite rugby players studied.

These changes were not related to self-reported history of head trauma or neuropsychological test scores, and may indicate excessive neurodegeneration of white matter tracts affected by the injury.

These findings suggest a link between participation in elite adult rugby and changes in brain structure, and may help us to understand the effects of both repeated and common sports-related head injuries on brain structure and whether the observed abnormalities are associated with increased risk of neurodegenerative and neurocognitive disorders. More well-designed, large-scale studies are needed to clarify whether the observed abnormalities are associated with increased risk of neurodegenerative diseases and neurocognitive disorders.

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