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Journal of neurotrauma · Nov 2017
A prospective transcranial Doppler ultrasound-based evaluation of the acute and cumulative effects of sport-related concussion on neurovascular coupling response dynamics.
- Alexander D Wright, Jonathan D Smirl, Kelsey Bryk, and Paul van Donkelaar.
- 1 School of Health and Exercise Sciences, University of British Columbia , Kelowna, British Columbia, Canada .
- J. Neurotrauma. 2017 Nov 15; 34 (22): 3097-3106.
AbstractSport-related concussion has been shown to alter cerebral blood flow (CBF) both acutely and chronically, and may exert cumulative effects across multiple injuries. Such dysfunction may be mediated by trauma-induced deficits to CBF control mechanisms, though our understanding of these effects is limited, including dynamics of neurovascular coupling (NVC) responses (i.e., CBF responses to neurologic demand). A total of 179 junior-level contact sport athletes completed preseason testing; 42 reported never having experienced a concussion (Hx-) while 31 had endured three or more (Hx3+). A total of 18 athletes suffered concussions during the study period and were re-tested 3 days, 2 weeks, and 1 month post-injury. NVC dynamics were indexed via CBF velocity in the posterior (PCAv) and middle (MCAv) cerebral arteries during cycles of 20 sec eyes closed and 40 sec eyes open to a visual stimulus (reading). Acutely following concussion, peak rate of PCAv increase during the activation phase was delayed by over 50% and PCAv response magnitude was elevated by over 30%, compared with preseason. Response magnitude remained elevated at 2 weeks despite symptom resolution. Independent medical clearance for full return-to-play was inversely related to the magnitude of increase in the NVC response at 3 days post-injury. No post-injury changes were observed in MCAv, blood pressure, or end-tidal carbon dioxide levels during visual stimulation. No NVC metric differences were observed between the Hx- and Hx3+ groups at preseason. Via multiple potential mechanisms, acute sport-related concussion may induce compensatory alterations in NVC response dynamics that may be related to clinical recovery. Such effects do not appear to be persistent across multiple injuries.
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