Cerebrovascular reactivity to carbon dioxide is not altered in otherwise healthy individuals six months post-concussion

Introduction: Concussion, a form of mild traumatic brain injury (TBI), has an estimated annual incidence of 1-4 million cases in the US alone. Studies have documented impairments in cerebral vascular function following concussion which often coincide with other neurocognitive symptoms but, in some cases, persist despite symptom resolution. However, the majority of these studies were performed 3 months or less post-concussion. Therefore, we tested the hypothesis that cerebral vasodilator function is impaired in adults who had a concussion 6 months prior and are asymptomatic relative to healthy age- and sex- matched controls with no known history of concussion. Methods: Six adults (3 Male/3 Female, 26 ± 5 years) with a history of diagnosed concussion ~6 months prior to the study visit (average, 6 ± 1 months) and six controls (3 Male/3 Female, 28 ± 5 years) without a known history of concussion were recruited. Beat-to-beat blood pressure (finger photoplethysomography), middle cerebral artery blood velocity (MCAv; transcranial Doppler ultrasound) and partial pressure of end-tidal carbon dioxide (P ET CO 2 ; capnography) were measured continuously during two-minutes of quiet supine rest and throughout a rebreathing protocol designed to increase P ET CO 2 up to +15mmHg. Cerebral vascular conductance index (CVCi) was calculated as mean MCAv divided by mean arterial pressure (MAP) on a beat-to-beat basis. Cerebrovascular reactivity was assessed as the percent change in MCAv or CVCi at increasing levels of P ET CO 2 (Δ3,6,9,12,15 mmHg P ET CO 2 ) and the gain of the relationship between MCAv or CVCi and P ET CO 2 . Results: Resting MAP (P=0.33), MCAv (control: 76 ± 6 cm/sec; TBI: 74 ± 8 cm/sec, P=0.82), and CVCi (control: 0.91 ± 0.08 cm/sec/mmHg; TBI: 0.86 ± 0.11 cm/sec/mmHg, P=0.72) were not different between groups. The CO2 rebreathing protocol increased MCAv and CVCi in both groups (main effect of time; P<0.001 for both). However, the percent change in MCAv and CVCi did not differ between control and TBI participants throughout the rebreathing protocol (Interaction, P=0.13 and P=0.26, respectively). Likewise, the MCAv (control: 3.5 ± 0.4 cm/sec/mmHg; TBI: 4.0 ± 0.6 cm/sec/mmHg, P=0.51) and CVCi (P=0.72) gains were not different between groups. Conclusion: These preliminary findings suggest that individuals six-months post-concussion who are asymptomatic do not exhibit impaired cerebral vasodilator function. This project was supported by the Henry M Jackson Foundation HU0001-18-2-0016. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.