Medical College, Aga Khan University Hospital, Karachi, Pakistan.
Section of Neurosurgery, Department of Surgery, Aga Khan University Hospital, Karachi, Pakistan.
World Neurosurg. 2019 Nov;131:126-132. doi: 10.1016/j.wneu.2019.07.039. Epub 2019 Jul 10.
Traumatic brain injury (TBI) refers to any insult to the brain resulting in primary (direct) and secondary (indirect) damage to the brain parenchyma. Secondary damage is often linked to the molecular mechanisms that occur post TBI and result in excitotoxicity, neuroinflammation and cytokine damage, oxidative damage, and eventual cell death as prominent mechanisms of cell damage. We present a review highlighting the relation of each of these mechanisms with TBI, their mode of damaging brain tissue, and therapeutic correlation. We also mention the long-term sequelae and their pathophysiology in relation to TBI focusing on Parkinson disease, Alzheimer disease, epilepsy, and chronic traumatic encephalopathy. Understanding of the molecular mechanisms is important in order to realize the secondary and long-term sequelae that follow primary TBI and to devise targeted therapy for quick recovery accordingly.
创伤性脑损伤(TBI)是指任何导致原发性(直接)和继发性(间接)脑实质损伤的脑损伤。继发性损伤通常与 TBI 后发生的分子机制有关,这些机制导致兴奋性毒性、神经炎症和细胞因子损伤、氧化损伤,并最终导致细胞死亡,成为细胞损伤的主要机制。我们提出了一篇综述,强调了这些机制与 TBI 的关系,它们破坏脑组织的方式,以及治疗相关性。我们还提到了与 TBI 相关的长期后果及其病理生理学,重点是帕金森病、阿尔茨海默病、癫痫和慢性创伤性脑病。了解分子机制对于认识原发性 TBI 后出现的继发性和长期后果,并制定相应的靶向治疗方案以实现快速康复非常重要。