V M Rasmussen1, A E Borgen2, E C Jansen2, P H Rotbøll Nielsen1, M U Werner1. 1. Multidisciplinary Pain Center, Neuroscience Center, Rigshospitalet, Copenhagen University Hospitals, Copenhagen, Denmark. 2. Hyperbaric Unit, Department of Anaesthesia, Head and Orthopedic Center, Rigshospitalet, Copenhagen University Hospitals, Copenhagen, Denmark.
Abstract
BACKGROUND:Hyperbaric oxygen (HBO2 ) treatment has in animal experiments demonstrated antinociceptive effects. It was hypothesized that these effects would attenuate secondary hyperalgesia areas (SHAs), an expression of central sensitization, after a first-degree thermal injury in humans. METHODS:Seventeen healthy volunteers were examined during two sessions using a randomized crossover design. Volunteers were studied during control conditions (ambient pressure, FI O2 = 0.21) and during HBO2 (2.4 standard atmosphere, FI O2 = 1.0, 90 min) conditions in a pressure chamber. Quantitative sensory testing, including assessment of SHAs was performed. RESULTS: A statistically significant overall attenuation of SHAs was seen during the HBO2 sessions compared with the control-sessions (P = 0.011). In the eight volunteers starting with the HBO2 session, no difference in SHAs compared with control was demonstrated. However, in the nine volunteers starting with the control session, a statistical significant attenuation of SHAs was demonstrated in the HBO2 session (P = 0.004). CONCLUSIONS: The results indicate that HBO2 therapy in humans attenuates central sensitization induced by a thermal skin injury, compared with control. These new and original findings in humans corroborate animal experimental data. The thermal injury model may give impetus to future human neurophysiological studies exploring the central effects of hyperbaric oxygen treatment.
RCT Entities:
BACKGROUND: Hyperbaric oxygen (HBO2 ) treatment has in animal experiments demonstrated antinociceptive effects. It was hypothesized that these effects would attenuate secondary hyperalgesia areas (SHAs), an expression of central sensitization, after a first-degree thermal injury in humans. METHODS: Seventeen healthy volunteers were examined during two sessions using a randomized crossover design. Volunteers were studied during control conditions (ambient pressure, FI O2 = 0.21) and during HBO2 (2.4 standard atmosphere, FI O2 = 1.0, 90 min) conditions in a pressure chamber. Quantitative sensory testing, including assessment of SHAs was performed. RESULTS: A statistically significant overall attenuation of SHAs was seen during the HBO2 sessions compared with the control-sessions (P = 0.011). In the eight volunteers starting with the HBO2 session, no difference in SHAs compared with control was demonstrated. However, in the nine volunteers starting with the control session, a statistical significant attenuation of SHAs was demonstrated in the HBO2 session (P = 0.004). CONCLUSIONS: The results indicate that HBO2 therapy in humans attenuates central sensitization induced by a thermal skin injury, compared with control. These new and original findings in humans corroborate animal experimental data. The thermal injury model may give impetus to future human neurophysiological studies exploring the central effects of hyperbaric oxygen treatment.
Authors: Anna M Wahl; Daniel Bidstrup; Isabel G Smidt-Nielsen; Mads U Werner; Ole Hyldegaard; Per Rotbøll-Nielsen Journal: J Pain Res Date: 2019-07-31 Impact factor: 3.133