Control of heart rate by the autonomic nervous system in acute spinal cord injury.
Spinal cord injury may cause loss of cardiovascular reflexes mediated by sympathetic drive due to interruption in the supraspinal control of spinal sympathetic motoneurons. The aim of this study was to analyze sympathovagal balance after acute spinal cord injury demonstrated by linear measures in time and frequency domain of heart rate variability (HRV). The study included 40 tatraplegic patients after acute spinal cord injury and 40 healthy subjects as controls. Cardiac autonomic balance was evaluated by HRV analysis in time and frequency domain. The ratio of low to high frequencies (LF/HF) was statistically significantly (Mann-Whitney U = 0.0; Z = -7.7; P < 0.001) different between the group with cervical spine injuries 0.41 (0158) and control group 1.71 (1875). LH/HF was significantly reduced in the group of patients with acute trauma. This study established HRV analysis by linear methods as an objective measure of normal and abnormal function of the autonomic nervous system. In conclusion, spinal cord injury causes dysfunction of the autonomic cardiovascular regulation and leads to disturbances of the modulatory sympathetic activity on the cardiovascular system. The HRV parameters analyzed indicate decreased but still present sympathetic activity and suggest that descending and ascending fibers of the sympathetic nervous system in isolated segment are undamaged, although without supraspinal control after acute spinal cord injury.
Antonija
A
Krstacić
Goran
G
Krstacić
Dragan
D
Gamberger
D000208:Acute Disease; D001341:Autonomic Nervous System / Q000503:physiopathology*; D017776:Autonomic Pathways / Q000502:physiology; D002574:Cervical Vertebrae / Q000293:injuries*; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology*; D006339:Heart Rate; D006706:Homeostasis; D006801:Humans; D008297:Male; D008875:Middle Aged; D009460:Neurologic Examination; D012016:Reference Values; D013119:Spinal Cord Injuries / Q000150:complications* / Q000503:physiopathology