Abstract
Repetitive subconcussive head impact exposure has been associated with clinical and MRI changes in some non-concussed contact sport athletes over the course of a season. However, analysis of human tolerance for repeated head impacts is complicated by concussion and head impact exposure history, genetics, and other personal factors. Therefore, the objective of the current study was to develop a rodent model for repetitive subconcussive head impact exposure that can be used to understand injury mechanisms and tolerance in the human. This study incorporated the Medical College of Wisconsin Rotational Injury Model to expose rats to multiple low-level head accelerations per day over a 4-week period. The peak magnitude of head accelerations were scaled from our prior human studies of contact sport athletes and the number of exposures per day were based on the median (moderate exposure) and 95th percentile (high exposure) number of exposures per day across the human sample. Following the exposure protocol, rats were assessed for cognitive deficits, emotional changes, blood serum levels of axonal injury biomarkers, and histopathological evidence of injury. High exposure rats demonstrated cognitive deficits and evidence of anxiety-like behaviors relative to shams. Moderate exposure rats did not demonstrate either of those behaviors. Similarly, high exposure rats had histopathological evidence of gliosis [i.e., elevated Iba1 intensity and glial fibrillary acidic protein (GFAP) volume relative to shams] in the basolateral amygdala and other areas. Blood serum levels of neurofilament light (NFL) demonstrated a dose response relationship with increasing numbers of low-level head acceleration exposures with a higher week-to-week rate of NFL increase for the high exposure group compared to the moderate exposure group. These findings demonstrate a cumulative effect of repeated low-level head accelerations and provide a model that can be used in future studies to better understand mechanisms and tolerance for brain injury resulting from repeated low-level head accelerations, with scalable biomechanics between the rat and human.
Highlights
The understanding of biomechanical mechanisms for sportrelated concussion continues to evolve as studies highlight the possible role of repetitive subconcussive head impact exposure for incident concussion and the development of concussion-like symptoms
All rats received a single 5-min exposure to the elevated plus maze (EPM) 5 days following the completion of the head acceleration exposure protocol, the sham protocol, or the single injury exposure
Our prior studies demonstrated that acceleration magnitudes used in this study for the single injury group were consistent with mild traumatic brain injury (Stemper et al, 2015). These findings provided some evidence of a prolonged effect of single injury and high exposure in the analysis of serum neurofilament light protein (NFL) concentrations
Summary
The understanding of biomechanical mechanisms for sportrelated concussion continues to evolve as studies highlight the possible role of repetitive subconcussive head impact exposure for incident concussion and the development of concussion-like symptoms. Despite the fact that concussive impacts are often unremarkable when compared to the severity of head impacts sustained across all athletes, the magnitudes are often remarkable for the individual athlete, with a majority ranking in the top five most severe head impacts sustained by that athlete in their season of injury (Rowson et al, 2018). This individualized concussive impact tolerance may be attributable, at least in part, to recent or within-season HIE. These studies imply a priming effect from HIE that may reduce tolerance and contribute to concussive injury from head impacts/accelerations that would normally be subconcussive
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