28
2022
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02
[Hospital News] A research achievement of our hospital has been published in an international journal.
Hyperbaric oxygen therapy has achieved widespread consensus in the field as an early rehabilitative intervention for severe traumatic brain injury; however, its therapeutic efficacy remains a subject of ongoing debate. Consequently, researchers in this area are actively investigating the underlying mechanisms of hyperbaric oxygen treatment.
Hyperbaric oxygen therapy has achieved widespread consensus in the field as an early rehabilitation modality for severe traumatic brain injury; however, its therapeutic efficacy remains a subject of ongoing debate. Consequently, researchers in this area are actively investigating the underlying mechanisms of hyperbaric oxygen treatment.
Recently, the research team led by Dr. Duan Lei at Nanjing Zijin Hospital published their findings on “The Effects of Hyperbaric Oxygen Therapy on Flash‑Stimulus Visual Evoked Potentials in Patients with Severe Traumatic Brain Injury” in the latest issue of the international journal NeuroRehabilitation, thereby filling a critical gap in this field and providing further scientific evidence supporting hyperbaric oxygen therapy.
Investigating the mechanisms of hyperbaric oxygen therapy has long been a central focus for scientists in related fields, and neuroelectrophysiological assessments are regarded as the most direct and straightforward clinical research approach. Previous studies have indicated that the basic electroencephalographic rhythms and the somatosensory evoked potential N20 serve as sensitive indicators for evaluating the extent of brain injury. The relevant research findings of Gao Zhiqiang’s team at Nanjing Zijin Hospital were published in 2020 in the Chinese Journal of Naval Medicine and Hyperbaric Medicine.
Visual evoked potentials represent another sensitive indicator of brain function. Because the optic nerve courses between the cerebral hemispheres and the brainstem, its function is profoundly influenced by intracranial pressure and cerebral edema. Consequently, the elicitation rate and latency of visual evoked potentials not only reflect the extent of neural recovery but also serve as markers of improvements in intracranial pressure and cerebral edema. It is widely believed that hyperbaric oxygen therapy can reduce intracranial pressure and cerebral edema following severe traumatic brain injury; however, the scientific evidence supporting this remains limited. Recent research by Dr. Duan Lei’s team at Nanjing Zijin Hospital has demonstrated that, in patients with severe traumatic brain injury, hyperbaric oxygen therapy leads to a shortening of the P2 wave latency and an increase in the elicitation rate of flash‑evoked potentials, with statistically significant differences compared to the control group. These findings suggest that hyperbaric oxygen therapy alleviates cellular edema after brain injury and enhances neurological function.
Nanjing Zijin Hospital was among the first in China to implement hyperbaric oxygen therapy and pioneered a comprehensive treatment protocol centered on hyperbaric oxygen for various types of brain injury. Over its 35 years of operation, more than 7,000 patients with disorders of consciousness have received integrated hyperbaric oxygen–based rehabilitation here, with many emerging from prolonged comas and even reintegrating into society.
References:
1. Lei Duan, Evaluation of the hyperbaric oxygen therapy on the flash visual evoked potential P2 in patients with severe traumatic brain injury. NeuroRehabilitation 50 (2022) 101–104
2. Gao Zhiqiang, Liu Yafeng, Qi Yuliang, et al. The predictive value of the Persistent Vegetative State Scale in Nanjing, China, for assessing the efficacy of hyperbaric oxygen–based comprehensive rehabilitation therapy in patients with long-term disorders of consciousness [J]. Chinese Journal of Maritime Medicine and Hyperbaric Medicine, 2020, 27(04):489-492.
3.Jordan, K. G. (1993). Continuous EEG and evoked potential monitoring in the neuroscience intensive care unit. J Clin Neurophysiol, 10(4), 445-447
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