Poster Communications: Recurrent concussion in retired rugby union players is associated with cerebral hypoperfusion and cognitive impairment

Sports-related concussion (SRC) represents a significant and growing public health concern yet remain one of the least understood injuries facing the sports medicine community today. There is increasing concern that prior recurrent concussion may contribute to long-term neurologic sequelae in later-life as retired contact sport athletes with three or more SRC’s present with a fivefold prevalence of mild cognitive impairment (MCI, 1). To what extent this relates to an accelerated decline in cerebral perfusion, a major risk factor for cognitive decline and dementia, remains to be explored. We recruited 40 aged participants who were divided into two distinct groups; 20 retired rugby union players aged 65 (mean) ± 7 (SD) years with a self-report history of 3 (mean) concussions ± 3 (SD) incurred over the course of their playing careers and 20 non-concussed, non-contact, age, education and fitness-matched controls aged 63 ± 6 years. Middle cerebral artery blood flow velocity (MCAv) was measured via Doppler ultrasomography at rest and in response to hypercapnia/hypocapnia (+/- 5mmHg change in end-tidal PCO2) with cerebral oxygen content (CDO2) calculated retrospectively(2). Ongoing symptoms of concussion were reporting using the Sports Concussion Assessment Tool 5 (SCAT5). Cognitive function was assessed via neuropsychometric testing and screened for MCI using the Montreal Cognitive Assessment (MoCA). Rugby players had played for 23 ± 8 years and reported between 3 – 10 previous concussions with ongoing, persistent symptoms related to concussion (7 ± 6 vs. 3 ± 4, P = 0.01) with greater severity (16 ± 13 vs. 4 ± 8, P = 0.00). Resting cerebral perfusion was lower in rugby players (45 ± 9 cm.s-1 vs. 51 ± 7 cm.s-1, P = 0.01) and in response to hypercapnia (57 ± 10 cm.s-1 vs. 69 ± 15 cm.s-1, P = 0.01). Subsequently, CDO2 was lower in rugby players at rest (1048 ± 170 ml/cm/s vs. 878 ± 184 ml/cm/s, P = 0.00), throughout hypercapnia (1406 ± 289 ml/cm/s vs. 1118 ± 242 ml/cm/s P = 0.00) and hypocapnia (683 ± 136 ml/cm/s vs. 577 ± 139 ml/cm/s P = 0.02). Executive motor function was slower in rugby players using the non-dominant hand on the Grooved Pegboard (92 ± 18 vs. 79 ± 15 seconds, P = 0.02) in addition to lower MoCA scores (24 ± 3 vs. 26 ± 2, P = 0.02). These findings indicate that neurological complications associated with SRC persist after retirement from rugby union. Cerebral hypoperfusion is identified as a haemodynamic risk factor that may precede the observed cognitive impairment that in later-life, may accelerate a (former) player’s trajectory towards neurodegeneration(3, 4). Our prior research has identified that the cerebral hypoperfusion characteristic of SRC, albeit in the younger demographic, is associated with a free radical-mediated reduction in nitric oxide bioavailability(5).