Abstract
OBJECTIVE: The aim of this study was to investigate the clinical curative effect of hyperbaric oxygen (HBO) treatment and its mechanism in improving dysfunction following traumatic brain injury (TBI). METHODS: Patients were enrolled into control and HBO groups. Glasgow coma scale (GCS) and coma recovery scale-revised (CRS-R) scores were used to measure consciousness; the Rancho Los Amigos scale-revised (RLAS-R) score was used to assess cognitive impairment; the Stockholm computed tomography (CT) score, quantitative electroencephalography (QEEG), and biomarkers, including neuron-specific enolase (NSE), S100 calcium-binding protein beta (S100β), glial fibrillary acidic protein (GFAP), brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and vascular endothelial growth factor (VEGF), were used to assess TBI severity. The patients were followed up 6 months after discharge and assessed with the Glasgow outcome scale-extended (GOSE), functional independence measure (FIM), and the disability rating scale (DRS). RESULTS: The CRS-R scores were higher in the HBO group than the control group at 10 days after treatment. The RLAS-R scores were higher in the HBO group than the control group at 10 and 20 days after treatment. The Stockholm CT scores were significantly lower in the HBO group than the control group at 10 days after treatment. HBO depressed the (δ + θ)/(α + β) ratio (DTABR) of EEG, with lower δ band relative power and higher α band relative power than those in the control group. At 20 days after treatment, the expression of NSE, S100β, and GFAP in the HBO group was lower than that in controls, whereas the expression of BDNF, NGF, and VEGF in the HBO group was higher than that in controls. Six months after discharge, the HBO group had lower DRS scores and higher FIM and GOSE scores than the control group significantly. CONCLUSIONS: HBO may be an effective treatment for patients with TBI to improve consciousness, cognitive function and prognosis through decreasing TBI-induced hematoma volumes, promoting the recovery of EEG rhythm, and modulating the expression of serum NSE, S100β, GFAP, BDNF, NGF, and VEGF.