Blunted Autonomic and Cardiovascular Activation during Face Cooling in Symptomatic Concussed Athletes
Authors: Johnson Blair D. , McBryde Muhamed , O'Leary Morgan C. , Sackett James R. , Schlader Zachary J. , Leddy John J. 
Published: June 2021

Concussed patients have abnormal parasympathetic responses to sympathoexcitatory maneuvers. However, it is not known if concussed patients have abnormal parasympathetic responses during physiological tests that activate the parasympathetic nervous system. Cooling the forehead, eyes, and cheeks (i.e., face cooling) transiently (~1–2 min) stimulates the trigeminal nerve and activates the parasympathetic nervous system followed by more sustained sympathetically‐mediated increases in heart rate and blood pressure.

Purpose

We tested the hypothesis that symptomatic concussed patients have blunted cardiac parasympathetic and sympathetically‐mediated cardiovascular responses during face cooling.

Methods

Ten symptomatic concussed athletes (CA; 20 ± 2 years; 5 women) who were within 10 days of injury and ten active healthy controls (HC; 23 ± 2 years; 5 women) participated. Face cooling was induced by placing a pliable plastic bag filled with ice water (~0°C) on the forehead, eyes, and cheeks for 3 min. Heart rate (ECG) and blood pressure (photoplethysmography) were continuously measured. Root mean square of successive differences (RMSSD) from the time domain and high frequency (HF) power from spectral analyses were calculated from the R‐R interval as markers of cardiac parasympathetic activity. Data were analyzed in one minute increments and compared as a change from baseline.

Results

There were no differences in baseline heart rate (CA: 60 ± 12; HC: 61 ± 11 bpm; P = 0.78), mean arterial pressure (CA: 97 ± 12; HC: 94 ± 10 mmHg; P = 0.55), R‐R interval (CA: 995 ± 170; HC: 1022 ± 197 ms; P = 0.75), RMSSD (CA: 102 ± 102; HC: 101 ± 83 ms; P = 0.99), or HF (CA: 2348 ± 2134; HC: 2294 ± 2314 ms2; P = 0.96). Heart rate did not change over time (P = 0.07), was not different between groups (P = 0.68), and there was no interaction effect (P = 0.34). Mean arterial pressure in CA was increased at 1 min (6 ± 6 mmHg; P < 0.01), 2 min (11 ± 7 mmHg; P < 0.01) and 3 min (12 ± 7 mmHg; P < 0.01). Mean arterial pressure in HC was increased at 1 min (12 ± 6 mmHg; P < 0.01), 2 min (21 ± 7 mmHg; P < 0.01), and 3 min (20 ± 6 mmHg; P < 0.01). The increase in mean arterial pressure was lower in CA at each minute vs. HC (P < 0.02 for all). R‐R interval in CA did not change from baseline (P = 0.51 for all) (peak increase at 1 min; 60 ± 76 ms). R‐R interval in HC was increased at 2 min (134 ± 225 ms; P = 0.02). There were no differences between groups for R‐R interval (P > 0.67 for all). RMSSD in CA did not change from baseline (P > 0.65 for all) (peak increase at 1 min; 31 ± 149 ms; P = 0.66). RMSSD in HC was increased at 1 min (106 ± 105 ms; P < 0.01). There were no differences between groups for RMSSD (P > 0.25 for all). HF in CA did not change from baseline (P > 0.80 for all) (peak increase at 1 min; 1800 ± 4475 ms2; P = 0.81). HF in HC was increased at 1 min (12354 ± 11489 ms2; P < 0.01) and 2 min (5832 ± 8002 ms2; P = 0.02). The increase in HF was greater in HC at 1 min vs. CA (P < 0.01).

Conclusion

These data indicate that CA have impaired cardiac parasympathetic and sympathetic responses to a physiological test that activates both branches of the autonomic nervous system.

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.