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HERO ID
476081
Reference Type
Journal Article
Title
Pathophysiology of Traumatic Brain Injury
Author(s)
Greve, MW; Zink, BJ
Year
2009
Is Peer Reviewed?
1
Journal
Mount Sinai Journal of Medicine
ISSN:
0027-2507
EISSN:
1931-7581
Volume
76
Issue
2
Page Numbers
97-104
Language
English
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 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
Keywords
pathophysiology; traumatic brain injury; primary brain injury; secondary brain injury; mild head-injury; axonal injury; calpain; neurons; protein; damage
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