创伤性颅脑损伤（TBI）是累及到大脑实质的结构性损害，可导致患者死亡或终生残疾。除结构性损害外，脑部意外创伤还会引起多种有害途径的激活导致继发性神经元死亡及永久性功能障碍。现有研究表明兴奋性毒性、神经炎症、水肿、氧化应激、神经元凋亡、代谢功能障碍等参与TBI主要致病过程，但相关分子机制研究仍不清楚。现有的治疗手段仅能对症处理，对控制继发性损伤仍不理想。本文通过对TBI神经生理学变化、神经化学变化以及其他病理表现作一综述，旨在为TBI相关研究提供参考，同时帮助临床制定新的治疗策略以尽可能挽救患者生命或减少并发症发生。

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.