Pathophysiology of Traumatic Brain Injury

被引:347
作者
Greve, Mark W. [1 ]
Zink, Brian J. [1 ]
机构
[1] Brown Univ, Dept Emergency Med, Warren Alpert Sch Med, Providence, RI 02912 USA
来源
MOUNT SINAI JOURNAL OF MEDICINE | 2009年 / 76卷 / 02期
关键词
pathophysiology; traumatic brain injury; primary brain injury; secondary brain injury; AXONAL INJURY; CALPAIN; PROTEIN; DAMAGE;
D O I
10.1002/msj.20104
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
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
引用
收藏
页码:97 / 104
页数:8
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