Autonomic nervous system responses to concussion: Arterial pulse contour analysis

Abstract

The arterial pulse wave (APW) has a distinct morphology whose contours reflect dynamics in cardiac function and peripheral vascular tone as a result of sympathetic nervous system (SNS) control. With a transition from rest to increased metabolic demand, the expected augmentation of SNS outflow will not only affect arterial blood pressure and heart rate but it will also induce changes to the contours of the APW. Following a sports concussion, a transient state cardiovascular autonomic dysfunction is present. How this state affects the APW has yet to be described. A prospective, parallel-group study on cardiovascular autonomic control (i.e., digital electrocardiogram and continuous beat-to-beat blood pressure) was performed in the seated upright position in 10 athletes with concussion and 7 non-injured control athletes. Changes in APW were compared at rest and during the first 60 s (F60) of an isometric handgrip test (IHGT) in concussed athletes and non-injured controls within 48 h and 1 week of injury. The concussion group was further separated by the length of time until they were permitted to return to play (RTP > 1week; RTP = 1week). SysSlope, an indirect measurement of stroke volume, was significantly lower in the concussion group at rest and during F60 at 48 h and 1week; a paradoxical decline in SysSlope occurred at each visit during the transition from rest to IHGT F60. The RTP > 1week group had lower SysSlope (405 ± 200; 420 ± 88; 454 ± 236 mmHg/s, respectively) at rest 48 h compared to the RTP = 1week and controls. Similarly at 48 h rest, several measurements of arterial stiffness were abnormal in RTP > 1week compared to RTP = 1week and controls: peak-to-notch latency (0.12 ± 0.04; 0.16 ± 0.02; 0.17 ± 0.05, respectively), notch relative amplitude (0.70 ± 0.03; 0.71 ± 0.04; 0.66 ± 0.14, respectively), and stiffness index (6.4 ± 0.2; 5.7 ± 0.4; 5.8 ± 0.5, respectively). Use of APW revealed that concussed athletes have a transient increase in peripheral artery stiffness, which may be a compensatory adaptation to a paradoxical decline of stroke volume during the transition from rest to a state of increased metabolic demand within 48 h of concussion. This dysfunction of the SNS appeared to be more pronounced among concussed athletes who were removed from participation for >1 week compared to those who resumed play within 7 days.