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创伤性脑损伤的病理生理学

Pathophysiology of traumatic brain injury.

作者信息

Greve Mark W, Zink Brian J

机构信息

Department of Emergency Medicine, Warren Alpert School of Medicine, Brown University, Providence, RI, USA.

出版信息

Mt Sinai J Med. 2009 Apr;76(2):97-104. doi: 10.1002/msj.20104.

Abstract

Traumatic brain injury is a major source of death and disability worldwide. Significant success has been achieved in improving short-term outcomes in severe traumatic brain injury victims; however, there are still great limitations in our ability to return severe traumatic brain injury victims to high levels of functioning. Primary brain injury, due to initial injury forces, causes tissue distortion and destruction in the early postinjury period. Clinical outcomes depend in large part on mediating the bimolecular and cellular changes that occur after the initial injury. These secondary injuries from traumatic brain injury lead to alterations in cell function and propagation of injury through processes such as depolarization, excitotoxicity, disruption of calcium homeostasis, free-radical generation, blood-brain barrier disruption, ischemic injury, edema formation, and intracranial hypertension. The best hope for improving outcome in traumatic brain injury patients is a better understanding of these processes and the development of therapies that can limit secondary brain injury.

摘要

创伤性脑损伤是全球范围内死亡和残疾的主要原因。在改善重度创伤性脑损伤患者的短期预后方面已取得显著成功;然而,我们使重度创伤性脑损伤患者恢复到高功能水平的能力仍存在很大局限性。原发性脑损伤是由初始损伤力导致的,在伤后早期引起组织变形和破坏。临床结果在很大程度上取决于调节初始损伤后发生的双分子和细胞变化。这些创伤性脑损伤引起的继发性损伤会导致细胞功能改变,并通过去极化、兴奋性毒性、钙稳态破坏、自由基生成、血脑屏障破坏、缺血性损伤、水肿形成和颅内高压等过程导致损伤扩散。改善创伤性脑损伤患者预后的最大希望在于更好地理解这些过程,并开发能够限制继发性脑损伤的治疗方法。

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