Altered Cerebrovascular Control in Concussed Patients during Sympathoexcitation

Abstract

Concussed patients (CP) have abnormal regional cerebral blood flow during a hypercapnic challenge and exaggerated increases in brain blood flow during graded intensity whole body exercise. These findings suggest that CP have altered cerebrovascular control. The cold pressor test (CPT) is a general sympathoexcitatory test that increases blood pressure. To buffer against cerebral hyperperfusion during the CPT, cerebrovascular conductance is reduced in healthy controls (HC). However, it is not known if CP exhibit abnormal cerebrovascular conductance response to the CPT.PurposeWe tested the hypothesis that cerebrovascular conductance during the CPT would be higher in CP when compared to HC subjects.MethodsFive symptomatic CP within 10 days of injury (20±1 years; 3 women) and five HC (22±2 years; 2 women) completed a CPT. During the CPT, one hand was submerged up to the wrist in cold water (~0°C) for 120 seconds. Blood pressure (photoplethysmography), middle cerebral artery blood velocity (MCAv, transcranial Doppler), and end‐tidal carbon dioxide tension (PETCO2, capnography) were continuously measured. Cerebrovascular conductance was calculated as MCAv divided by mean arterial pressure. Baseline data were compared using unpaired t‐tests. Data during the CPT were analyzed every 30 seconds, expressed as change from baseline and compared using mixed model repeated measures ANOVA.ResultsBaseline mean arterial pressure (HC: 81±9 mmHg vs. CP: 97±14 mmHg, P=0.06), MCAv (HC: 59±15 mmHg vs. CP: 54±14 mmHg, P=0.59), PETCO2 (HC: 46±3 mmHg vs. CP: 46±2 mmHg, P=0.97), and cerebrovascular conductance (HC: 0.74±0.23 cm/sec/mmHg vs. CP: 0.56±0.15 cm/sec/mmHg, P=0.17) were not different between groups. Mean arterial pressure increased in HC during the CPT at 60 seconds (11±14 mmHg, P=0.04), 90 seconds (22±12 mmHg, P<0.01), and 120 seconds (23±11mmHg, P<0.01). Mean arterial pressure did not change in CP (P>0.20). There were no differences in mean arterial pressure between groups (P>0.08). MCAv did not change from baseline (HC: −1±5, −2±4, −5±5, −4±8 cm/sec; CP 5±5, 1±8, 0±11, −1±11 cm/sec, at 30, 60, 90, and 120 seconds, respectively, time main effect: P=0.18) or between groups (group main effect: P>0.33) (interaction effect: P=0.77). PETCO2 decreased in HC at 90 seconds (3±2 mmHg, P<0.01) and 120 seconds (4±3 mmHg, P<0.01). PETCO2 did not change in CP (P>0.36). There were no differences in PETCO2 between groups (P>0.11). Cerebrovascular conductance decreased in HC at 60 seconds (0.11±0.14 cm/sec/mmHg, P=0.02), 90 seconds (0.21±0.11 cm/sec/mmHg, P<0.01), and 120 seconds (0.20±0.13 cm/sec/mmHg, P<0.01). Cerebrovascular conductance in CP did not change over time (P>0.53). Cerebrovascular conductance was lower in HC vs. CP at 90 seconds (CP: 0.05±0.07 cm/sec/mmHg, P=0.05) and 120 seconds (CP: 0.06±0.06 cm/sec/mmHg, P=0.07).ConclusionCP show an attenuated decrease in cerebrovascular conductance compared to HC during the CPT. These findings suggest that symptomatic CP have altered cerebrovascular control during sympathoexcitation.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.