Pathophysiology of Traumatic Brain Injury

Pathophysiology of Traumatic Brain Injury
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DOI:
10.1002/msj.20104
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发表时间:
2009-03-01
影响因子:
--
通讯作者:
Zink, Brian J.
Zink, Brian J.
中科院分区:
其他
文献类型:
--
作者:
Greve, Mark W.;Zink, Brian J.

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脑外伤是全球死亡和残疾的主要原因。在改善严重创伤性脑损伤患者的短期结局方面取得了重大成功;然而,我们使严重创伤性脑损伤患者恢复高水平功能的能力仍然存在很大的局限性。原发性脑损伤,由于初始力,导致组织变形和破坏在损伤后早期。临床结果在很大程度上取决于介导初始损伤后发生的双分子和细胞变化。创伤性脑损伤的这些继发性损伤导致细胞功能的改变和损伤的传播,通过诸如去极化、兴奋性毒性、钙稳态破坏、自由基产生、血脑屏障破坏、缺血性损伤、水肿形成和颅内高压的过程。改善创伤性脑损伤患者预后的最大希望是更好地了解这些过程,并开发出可以限制继发性脑损伤的治疗方法。山Sinati J Med 76.97-104,2009(C)2009年西奈山医学院
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 forces, causes tissue distortion and destruction in the early post injury period. Clinical outcomes depend in large part of mediating the bimolecular and cellular changes that occur after the initial injury. These secondary injuries from trumatic 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 of 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. Mt. Sinati J Med 76.97-104, 2009 (C) 2009 Mount Sinai School of Medicine