The Relationship between Cerebral Vasoreactivity and Post-Concussive Symptom Severity

While pathophysiology underlying post-concussion symptom burden is unknown, data suggest that cerebrovascular dysfunction may be among the culprits. We sought to determine whether the degree of impairment in the ability of cerebrovasculature to buffer against changes in arterial gases (vasoreactivity) is associated with concussion symptoms. In 15 participants (19 ± 5 years, 1 week to 1 year post-injury) diagnosed with concussion, we assessed vasoreactivity from the slope of the linear relationship of beat-by-beat middle cerebral artery blood flow velocity (transcranial Doppler ultrasound) to end-tidal CO₂ during progressive increases in end-tidal CO₂ (air rebreathing). Symptom burden was assessed using the Post-Concussion Symptom Scale. Subsequently, we explored the relationship between vasoreactivity and the severity of post-concussion headache and cognitive difficulties by linear models. During rebreathing, CO₂ increased from 32.6 ± 1.6 to 46.8 ± 1.8 mmHg and cerebrovascular conductance (i.e., flow velocity over pressure) increased from 0.48 ± 0.04 to 0.74 ± 0.06 cms^-1 mmHg^-1. There was a strong linear relationship between the increase in CO₂ and in conductance (R² = 0.81 ± 0.05; p < 0.05). On average, cerebral vasoreactivity was 0.018 ± 0.003 cm^-1 s^-1 mmHg CO₂^-1. Although vasoreactivity tended to be somewhat higher in the asymptotic participants (0.019 ± 0.003 vs. 0.015 ± 0.005 cm^-1 s^-1 mmHg CO₂^-1), this difference was not statistically significant (p = 0.48). Higher vasoreactivity was strongly associated with more severe headaches (R² = 0.57; p < 0.01) and worse cognitive symptoms (R² = 0.71; p < 0.01). Thus, cerebral vasoreactivity relates strongly to post-concussive headache and cognitive symptom burden. This has significant implications for understanding the pathophysiology underlying post-concussive symptom burden and for devising effective treatment options.