医学
创伤性脑损伤
兴奋毒性
神经炎症
慢性创伤性脑病
脑损伤
神经科学
疾病
病理生理学
病理
生物信息学
谷氨酸受体
毒物控制
精神科
内科学
伤害预防
受体
脑震荡
环境卫生
生物
作者
Asma Akbar Ladak,Syed Ather Enam,Muhammad Ibrahim
标识
DOI:10.1016/j.wneu.2019.07.039
摘要
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.
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