Traumatic brain injury, symptoms of depression and sleep dysfunction in former elite rugby players

While self-reported repetitive head impact (RHI) exposure in former athletes has been associated with symptoms of depression and sleep dysfunction, it is uncertain whether these symptoms are mediated by changes in brain structure. We used cross-sectional data from 57 middle-aged, cognitively healthy, former elite rugby players and 114 propensity-matched controls. Questionnaires were used to collect self-reported traumatic brain injury (srTBI: number of blows to the head (nBL); number of times of feeling dazed and confused (nDC); number of times of loss of consciousness (nLC)), RHI exposure (career length, play at the highest level, and playing position), medical history, symptoms of depression (Center for Epidemiological Studies Depression scale) and sleep dysfunction (Pittsburgh Sleep Quality Index). Grey matter volumes and diffusion tensor imaging measures (fractional anisotropy (FA), mean (MD), axial (AxD) and radial diffusivity (RD)) were obtained using FreeSurfer (v7.1.0, v7.4.2) and FSL (v6.0.5). We assessed how srTBI, RHI exposure, symptoms of depression, sleep dysfunction, and the imaging markers were related using spearman correlations, multivariate regression models and partial least squares structural equation modelling. Although former rugby players reported higher nBL (9.8 vs 5.4, p<0.001), nDC (4.5 vs 1.7, p<0.001), and nLC (1.9 vs 0.7, p<0.001), they were less likely to report a past diagnosis of anxiety (7% vs. 22%, p=0.03) or sleep disorders (2% vs. 15%, p=0.02) than controls. In rugby players, srTBI correlated poorly with RHI exposure. Furthermore, srTBI, but not RHI exposure was associated with previous depression, anxiety and sleep disorders. Higher srTBI was directly associated with more symptoms of depression (B:0.52[95%CI:0.21-0.74]), and indirectly associated with more sleep dysfunction (B:0.18[95%CI:0.03-0.39]), fully mediated through symptoms of depression. Higher srTBI was also associated with a larger putamen (r=0.28,p=0.03) and inferior-tubular hypothalamus (r=0.35,p=0.007), thicker medial orbitofrontal (r=0.32,p=0.02) and insular cortices (r=0.40,p=0.002), lower AxD of the inferior cerebellar peduncle (r=-0.28,p=0.03) and uncinate fasciculus (r=-0.26,p=0.048), lower FA (r=-0.44,p<0.001) and higher RD (r=0.29,p=0.03) of the tapetum. Symptoms of depression were associated with thicker superior (r=0.30,p=0.02) and inferior (r=0.33,p=0.01) parietal cortices, higher FA of the hippocampal cingulum (r=0.27,p=0.04) and lower MD of the fornix (r=-0.28,p=0.03). None of these imaging markers mediated the association between srTBI and symptoms of depression. SrTBI, but not RHI exposure, was associated with symptoms of depression in former rugby players. However, this relationship was not mediated through differences in brain structure suggesting that psychosocial or methodological factors such as recall bias and common method bias may be more important.