Oxidative stress following traumatic brain injury: enhancement of endogenous antioxidant defense systems and the promise of improved outcome.

BACKGROUND: Management of brain injury can pose enormous challenges to the health team. There are many studies aimed at discovering or developing pharmacotherapeutic agents targeted at improving outcome of head-injured patients. This paper reviews the role of oxidative stress in neuronal loss following traumatic brain injury and presents experimental and clinical evidence of the role of exogenous antioxidants as neuroprotectants.
METHOD: We reviewed published literature on reactive oxygen species and their role in experimental and clinical brain injuries in journals and the Internet using Yahoo and Google search engines.
RESULTS: Traumatic brain injury causes massive production of reactive oxygen species with resultant oxidative stress. In experimental brain injury, exogenous antioxidants are useful in limiting oxidative damage. Results with clinical brain injury are however more varied.
CONCLUSION: Oxidative stress due to excessive generation of reactive oxygen species with consequent impairment of endogenous antioxidant defence mechanisms plays a significant role in the secondary events leading to neuronal death. Enhancement of the defence mechanisms through the use of exogenous antioxidants may be neuroprotective, especially if the agents can penetrate cell membranes, are able to cross the blood-brain barrier and if they are administered within the neuroprotective time window.