Neurobiological and connectivity changes after sports-related concussion

Abstract

Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality worldwide. Sports-related TBI is a subset that encompasses cerebral concussion and chronic traumatic encephalopathy (CTE), the latter of which is a long-term neurodegenerative sequela of repeated mild TBI that affects behaviour, cognition, motor control, and memory. On a cellular level, TBI can result in diffuse axonal injury (DAI). This injury causes axonal transport dysfunction, leading to accumulation of tau and amyloid beta deposits in the brain. Damage occurs in neuronal tracts of both local and distant brain regions. DAI disrupts brain network function, which correlates with decreased cognitive function, by impairing the default mode network’s (DMN) normal ability to deactivate during cognitive tasks. The salience network (SN) can be affected by DAI as well, which ultimately also impairs deactivation of the DMN. These changes coincide with the clinical manifestations of concussions and CTE. Both concussions and CTE are currently clinical diagnoses, as no diagnostic lab tests exist to delineate these conditions. As with many brain disorders of traumatic origin, there is no specific medical treatment for these conditions, though concussion is managed through physical and cognitive rest. The most important consideration for all TBIs, however, is prevention.