Journal
CRITICAL CARE CLINICS
Volume 19, Issue 3, Pages 529-+Publisher
W B SAUNDERS CO
DOI: 10.1016/S0749-0704(03)00014-9
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Funding
- NINDS NIH HHS [R01 NS38087, R01 NS38620] Funding Source: Medline
- PHS HHS [P01 30318] Funding Source: Medline
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After traumatic brain injury (TBI), irreparable brain damage, termed primary injury, results from direct disruption of brain parenchyma. Potentially reversible secondary injury, caused by altered hemodynamic and respiratory functions and cellular derangement, also takes place. Traumatic brain injury triggers a common pathway of neuronal death involving posttraumatic ischemia, energy failure, excitotoxicity, mitochondrial failure, oxidative stress, and secondary cerebral swelling. In this article, the experimental and clinical data on secondary mechanisms of TBI pathophysiology and current therapeutic strategies are discussed.
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