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Acute sport-related concussion induces transient impairment in dynamic cerebral auto regulation that is related to scat3 performance
  1. Alexander D Wright1,2,3,4,
  2. Jonathan D Smirl4,
  3. Kelsey Bryk4,
  4. Sarah K Fraser2,
  5. Harjas S Grewal5,
  6. Michael Jakovac2,
  7. Jill Dierijck4,
  8. Paul van Donkelaar4
  1. 1University of British Columbia, Vancouver, Canada
  2. 2University of British Columbia Okanagan, Kelowna, Canada
  3. 3Department of Experimental Medicine, Faculty of Medicine, University of British Columbia, Vancouver, Canada
  4. 4School of Health and Exercise Sciences, University of British Columbia Okanagan, Kelowna, Canada
  5. 5Northern Medical Program, University of Northern British Columbia, Prince George, Canada

Abstract

Objective Examine how the frequency-dependent relationship between blood pressure (BP) and cerebral blood velocity (CBV) is affected by acute sport-related concussion.

Design Prospective Cohort.

Setting Laboratory.

Participants: 136 male contact-sport athletes (19.1±1.4 years) recruited, subset of 14 sustained concussions (19±1.4 years).

Intervention Participants completed baseline (T0) and post-injury testing at 72-hours (T1), 2-weeks (T2), and 1-month (T3). BP was monitored via finger photoplethysmography, and transcranial Doppler ultrasound indexed CBV in the middle cerebral artery. Squat-stand manoeuvers were performed at 0.05 and 0.10Hz to enhance BP variation. RM-ANOVA independent variables included time (4) and frequency (2).

Outcome measures Transfer function analysis point estimates quantified coherence (correlation), phase (synchronisation) and gain (amplitude buffer) metrics between BP and CBV waveforms.

Results Significant frequency-time interactions for phase (p=0.007) and gain (p=0.049). Simple effects analysis revealed time effects for phase at 0.10 Hz, indicating reductions at T1 (95% CI: 0.033 – 0.24 rads, p=0.008) and T2 (95% CI: 0.014–0.196 rads, p=0.02) compared to T0. On average, return-to-play occurred at T2 (median 14 days). Phase reductions at T1 were correlated with Standardised Assessment of Concussion performance (r=0.659, p=0.02).

Conclusions These results reveal transient post-concussion impairments in the capacity of the cerebrovasculature to buffer BP oscillations, which exceeded clinical recovery duration. Phase reductions at 0.10Hz suggest the presence of a cerebrovascular autonomic dysregulation, which could leave the brain less protected to BP surges. This key finding may help explain why the brain is more vulnerable to additional trauma during the post-injury recovery period.

Competing interests None.

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