Traumatic brain injury: can the consequences be stopped?
Traumatic brain injury is a leading cause of morbidity and death in both industrialized and developing countries. To date, there is no targeted pharmacological treatment that effectively limits the progression of secondary injury. The delayed progression of deterioration of grey and white matter gives hope that a meaningful intervention can be applied in a realistic timeframe following initial trauma. In this review we discuss new insights into the subcellular mechanisms of secondary injury that have highlighted numerous potential targets for intervention.
Park
Eugene
E
Cara Phelan Centre for Trauma Research, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ont.
Bell
Joshua D
JD
Baker
Andrew J
AJ
D000818:Animals; D001369:Axons / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D001929:Brain Edema / Q000503:physiopathology; D001930:Brain Injuries / Q000378:metabolism* / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism; D002154:Calpain / Q000378:metabolism; D020833:Diffuse Axonal Injury / Q000503:physiopathology; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D019586:Intracranial Hypertension / Q000503:physiopathology; D018091:Receptors, AMPA / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism
D015415:Biomarkers; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D002154:Calpain; D002118:Calcium