
@article{ref1,
title="Cerebrovascular neuroprotection after acute concussion in adolescents",
journal="Annals of neurology",
year="2021",
author="Aaron, Stacey E. and Hamner, J. W. and Ozturk, Erin D. and Hunt, Danielle L. and Iaccarino, Mary Alexis and Meehan, William P. 3rd and Howell, David R. and Tan, Can Ozan",
volume="ePub",
number="ePub",
pages="ePub-ePub",
abstract="OBJECTIVE: To assess acute cerebrovascular function in concussed adolescents (14-21 years of age), whether it related to resting cerebral hemodynamics, and whether it recovered chronically. <br><br>METHODS: Cerebral vasoreactivity and autoregulation, based on middle cerebral artery blood flow velocity, were assessed in 28 concussed participants (≤14 days of injury) and 29 matched controls. The participants in the concussion group returned for an 8-week follow-up assessment. Over the course of those 8-weeks, participants recorded aerobic exercise frequency and duration. <br><br>RESULTS: Between group demographic, clinical, and hemodynamic variables were not significantly different. Vasoreactivity was significantly higher in the concussed group (p=0.02). Within the concussed group, 60% of the variability in resting cerebral blood flow velocity was explained by vasoreactivity and two components of autoregulation - falling slope and effectiveness of autoregulation (adjusted R(2) =0.60, p<0.001). Moreover, lower mean arterial pressure, lower responses to increases in arterial pressure, and lower vasoreactivity were significantly associated with larger symptom burden (adjusted R(2) =0.72, p<0.01). By the 8-week timepoint, symptom burden, but not vasoreactivity, improved in all but four concussed participants (p<0.01). 8-week change in vasoreactivity was positively associated with aerobic exercise volume (adjusted R(2) =0.19, p=0.02). <br><br>INTERPRETATION: Concussion resulted in changes in cerebrovascular regulatory mechanisms, which in turn explained the variability in resting cerebral blood flow velocity and acute symptom burden. Furthermore, these alterations persisted chronically despite symptom resolution, but was positively modified by aerobic exercise volume. These findings provide a mechanistic framework for further investigation into underlying cerebrovascular related symptomatology. This article is protected by copyright. All rights reserved.<p /> <p>Language: en</p>",
language="en",
issn="0364-5134",
doi="10.1002/ana.26082",
url="http://dx.doi.org/10.1002/ana.26082"
}