title: Frequency analysis unveils cardiac autonomic dysfunction after mild traumatic brain injury.
abstract: Long-term mortality is increased after mild traumatic brain injury (mTBI). Central cardiovascular-autonomic dysregulation resulting from subtle, trauma-induced brain lesions might contribute to cardiovascular events and fatalities. We investigated whether there is cardiovascular-autonomic dysregulation after mTBI. In 20 mTBI patients (37±13 years, 5-43 months post-injury) and 20 healthy persons (26±9 years), we monitored respiration, RR intervals (RRI), blood pressures (BP), while supine and upon standing. We calculated the root mean square successive RRI differences (RMSSD) reflecting cardiovagal modulation, the ratio of maximal and minimal RRIs around the 30th and 15th RRI upon standing (30:15 ratio) reflecting baroreflex sensitivity (BRS), spectral powers of parasympathetic high-frequency (HF: 0.15-0.5 Hz) RRI oscillations, of mainly sympathetic low-frequency (LF: 0.04-0.15 Hz) RRI oscillations, of sympathetic LF-BP oscillations, RRI-LF/HF-ratios reflecting sympathovagal balance, and the gain between BP and RRI oscillations as additional BRS index (BRS(gain)). We compared supine and standing parameters of patients and controls (repeated measures analysis of variance; significance: p<0.05). While supine, patients had lower RRIs (874.2±157.8 vs. 1024.3±165.4 ms), RMSSDs (30.1±23.6 vs. 56.3±31.4 ms), RRI-HF powers (298.1±309.8 vs. 1507.2±1591.4 ms(2)), and BRS(gain) (8.1±4.4 vs. 12.5±8.1 ms·mmHg(-1)), but higher RRI-LF/HF-ratios (3.0±1.9 vs. 1.2±0.7) than controls. Upon standing, RMSSDs and RRI-HF-powers decreased significantly in controls, but not in patients; patients had lower RRI-30:15-ratios (1.3±0.3 vs. 1.6±0.3) and RRI-LF-powers (2450.0±2110.3 vs. 4805.9±3453.5 ms(2)) than controls. While supine, mTBI patients had reduced cardiovagal modulation and BRS. Upon standing, their BRS was still reduced, and patients did not withdraw parasympathetic or augment sympathetic modulation adequately. Impaired autonomic modulation probably contributes to cardiovascular irregularities post-mTBI.
authors.affiliation: Department of Neurology, University of Erlangen-Nuremberg, Erlangen, Germany. max.hilz@nyumc.org
authors.forename: Max J
authors.initials: MJ
authors.lastname: Hilz
authors.forename: Philip A
authors.initials: PA
authors.lastname: DeFina
authors.forename: Stefan
authors.initials: S
authors.lastname: Anders
authors.forename: Julia
authors.initials: J
authors.lastname: Koehn
authors.forename: Christoph J
authors.initials: CJ
authors.lastname: Lang
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Pauli
authors.forename: Steven R
authors.initials: SR
authors.lastname: Flanagan
authors.forename: Stefan
authors.initials: S
authors.lastname: Schwab
authors.forename: Harald
authors.initials: H
authors.lastname: Marthol
mesh_terms: D000293:Adolescent; D000328:Adult; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001342:Autonomic Nervous System Diseases / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology; D001930:Brain Injuries / Q000150:complications* / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D016683:Supine Position