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Chinese Journal of Neurotraumatic Surgery(Electronic Edition) ›› 2023, Vol. 09 ›› Issue (06): 367-371. doi: 10.3877/cma.j.issn.2095-9141.2023.06.009

• Review • Previous Articles     Next Articles

Characteristic of neurobiology in traumatic brain injury

Chunyu Tang, Qian Li, Shanshan Guo, Qi Ye, Dan Zhang()   

  1. Research Institute of Burn Frostbite and Tissue Functional Reconstruction, Characteristic Medical Center of the PAP, Tianjin 300309, China
    Department of Traditional Chinese Medicine, Characteristic Medical Center of the PLA Rocket Force, Beijing 100088, China
    Department of Treatment for Nuclear Personnel, Characteristic Medical Center of the PLA Rocket Force, Beijing 100088, China
    Department of Nursing, Characteristic Medical Center of the PLA Rocket Force, Beijing 100088, China
    Department of Gastroenterology, Characteristic Medical Center of the PLA Rocket Force, Beijing 100088, China
  • Received:2022-12-15 Online:2023-12-15 Published:2024-02-08
  • Contact: Dan Zhang

Abstract:

Traumatic brain injury (TBI) endangers structural damage to the brain parenchyma, which causes death or lifelong disability in patients. Besides structural damage, the accidental injuries of the brain could cause activation of various deleterious pathways, leading to subsequent neuronal death and permanent dysfunction. The present studies show excitotoxicity, neuroinflammation, edema, oxidative stress, neuronal apoptosis and cerebral metabolic dysfunction could participate in the major pathogenic process in TBI, but few was cleared about the related molecular mechanism study. The available methods could only treated patients symptomatically, and are still not ideal for controlling secondary injuries. This article provides a review of the neurophysiological changes, neurochemical changes, and other pathological manifestations of TBI, with the aim of providing reference for TBI related research and helping clinical development of new treatment strategies to rescue the patient or reduce the occurrence of complications.

Key words: Traumatic brain injury, Excitotoxicity, Neuroinflammation, Oxidative stress, Neuronal apoptosis

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