Although incidence is at epidemic levels, objective indicators of neurologic damage in adolescent concussion remain poorly described. Autonomic markers such as heart rate variability (HRV) have provided equivocal results; however, these predominantly are made under conditions of minimal physiologic stress. The current investigation employs postural stressors to examine underlying neurological outcomes associated with acute concussion and clinical recovery to test the hypothesis that concussion impairs dynamic autonomic adjustments in adolescents. We examined concussed adolescents (CONC; n = 35; 14 males; age 15 ± 1 yrs, range = 12–18 yrs) for up to 6 weekly visits from diagnosis. A group of age and activity level-matched non-concussed adolescents (CTRL; n = 35; 19 males; age 14 ± 2 yrs, range = 12–18 yrs) formed the reference control. HRV (root mean square of successive differences in R-R intervals (RMSSD)) and heart rate were assessed during a sit-to-stand protocol (two trials of seated posture (three minutes), followed by two minutes of standing). Measurements were taken during the last minute of sitting and standing, the ten second period following the postural stress of standing, as well as the ten second period from maximum HR. While seated, RMSSD was lower in CONC (41 ± 24 msec) compared with CTRL (60 ± 40 msec; p < 0.05). 31 patients provided weekly data until clinical discharge. Compared with the first visit (43 ± 25 msec), seated RMSSD in CONC increased (51 ± 36 msec; p = 0.05) at the time of clinical discharge. Upon standing (10 seconds following postural change to standing), RMSSD was lower in CONC versus CTRL (13 ± 7 vs. 18 ± 12 msec; p < 0.05). Compared with the first visit, RMSSD following the induced postural stress did not improve in CONC over the six week recovery period. Following maximal HR, CTRL had increased RMSSD versus CONC (46 ± 30 vs. 34 ± 19 msec; p < 0.05). Compared with CTRL, seated HR was higher in CONC. This tachycardia effect persisted throughout the sit-to-stand protocol (78 ± 12 vs. 72 ± 12 bpm; p < 0.05) and was maintained until the time of clinical discharge (79 ± 13 vs. 72 ± 12 bpm; p < 0.05). In adolescent concussion, autonomic cardiac impairment is demonstrated by reduced RMSSD in the seated position and throughout the adjustment period in response to postural stress. Further, seated HR is increased following acute concussion and remains elevated by the time of clinical discharge. Seated HRV, but not HR, recovered to levels seen in the control population within three to six weeks. Thus, cardiac adjustments to modest postural stress may represent a measurable neurological impairment in adolescent acute concussion which can be objectively monitored throughout clinical recovery.
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