• J W Finnie.
• SA Pathology, Hanson Institute Centre for Neurological Diseases and School of Medical and Veterinary Sciences, University of Adelaide, PO Box 14, Rundle Mall, Adelaide, SA 5000, Australia. john.finnie@health.sa.gov.au
• Inflammopharmacology. 2013 Aug 1;21(4):309-20.

AbstractTraumatic brain injury (TBI) is the major cause of death and severe disability in young adults and infants worldwide and many survivors also have mild to moderate neurological deficits which impair their lives. This review highlights the primary and secondary lesions constituting craniocerebral trauma and the main elements of neuroinflammation, one of the most important secondary events evolving after the initial traumatic insult. Neuroinflammation has dual and opposing roles in outcome after TBI, being both beneficial and harmful, its effects often differing between the acute and more delayed phases after injury. Since each patient with TBI has a unique and complex pattern of cerebral damage, developing pharmacological intervention strategies targeted at the multiple cellular and molecular events in the neuroinflammatory cascade is difficult. While there have been very few successful outcomes to date in human clinical trials of drugs developed to treat TBI in general, those that have been devised to modulate neuroinflammation are discussed.

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