Eyeball pressure stimulation induces subtle sympathetic activation in patients with a history of moderate or severe traumatic brain injury. Issue 6 (June 2018)

• Record Type: Journal Article
• Authors: Wang, Ruihao; Hösl, Katharina M.; Ammon, Fabian; Markus, Jörg; Koehn, Julia; Roy, Sankanika; Liu, Mao; de Rojas Leal, Carmen; Muresanu, Dafin; Flanagan, Steven R.; Hilz, Max J.
• Is Part Of: Clinical neurophysiology. Volume 129:Issue 6(2018:Jun.)
• Page Start: 1161
• Page End: 1169
• Publication Date: 2018-06
• Subjects: Eyeball pressure stimulation -- Oculocardiac reflex -- Traumatic brain injury -- Central autonomic dysfunction; Neurophysiology -- Periodicals; Electroencephalography -- Periodicals; Electromyography -- Periodicals; Neurology -- Periodicals; 612.8
• DOI: 10.1016/j.clinph.2018.03.011
• Languages: English
• ISSNs: 1388-2457

Abstract

Highlights: Patients with a history of traumatic brain injury (TBI) had impaired blood pressure control at rest. In these patients, eyeball pressure fails to increase cardiovagal outflow but raises blood pressure. These results suggest baroreflex-independent central autonomic dysfunction in patients after TBI. Abstract: Objective: After traumatic brain injury (TBI), there may be persistent central-autonomic-network (CAN) dysfunction causing cardiovascular-autonomic dysregulation. Eyeball-pressure-stimulation (EPS) normally induces cardiovagal activation. In patients with a history of moderate or severe TBI (post-moderate-severe-TBI), we determined whether EPS unveils cardiovascular-autonomic dysregulation. Methods: In 51 post-moderate-severe-TBI patients (32.7 ± 10.5 years old, 43.1 ± 33.4 months post-injury), and 30 controls (29.1 ± 9.8 years), we recorded respiration, RR-intervals (RRI), systolic and diastolic blood-pressure (BPsys, BPdia), before and during EPS (120 sec; 30 mmHg), using an ocular-pressure-device (Okulopressor®). We calculated spectral-powers of mainly sympathetic low (LF: 0.04–0.15 Hz) and parasympathetic high (HF: 0.15–0.5 Hz) frequency RRI-fluctuations, sympathetically mediated LF-powers of BPsys, and calculated normalized (nu) LF- and HF-powers of RRI. We compared parameters between groups before and during EPS by repeated-measurement-analysis-of-variance with post-hoc analysis (significance: p < 0.05). Results: At rest, sympathetically mediated LF-BPsys-powers were significantly lower in the patients than the controls. During EPS, only controls significantly increased RRIs and parasympathetically mediated HFnu-RRI-powers, but decreased LF-RRI-powers, LFnu-RRI-powers, and LF-BPsys-powers; in contrast, the patients slightly though significantly increased BPsys upon EPS, without changing any other parameter. Conclusions: In post-moderate-severe-TBI patients, autonomic BP-modulation was already compromised at rest. During EPS, our patients failed to activate cardiovagal modulation but slightly increased BPsys, indicating persistent CAN dysregulation. Significance: Our findings unveil persistence of subtle cardiovascular-autonomic dysregulation even years after TBI.