title: Alterations in cerebral oxygen metabolism after traumatic brain injury in children.
abstract: Traumatic brain injury (TBI) is the most common cause of acquired disability in children. Metabolic defects, and in particular mitochondrial dysfunction, are important contributors to brain injury after TBI. Studies of metabolic dysfunction are limited, but magnetic resonance methods suitable for use in children are overcoming this limitation. We performed noninvasive measurements of cerebral blood flow and oxygen metabolic index (OMI) to assess metabolic dysfunction in children with severe TBI. Cerebral blood flow is variable after TBI but hypoperfusion and low OMI are predominant, supporting metabolic dysfunction. This finding is consistent with preclinical and adult clinical studies of brain metabolism and mitochondrial dysfunction after TBI.
authors.affiliation: Department of Pediatrics, Washington University School of Medicine, St Louis, MO, USA.
authors.forename: Dustin K
authors.initials: DK
authors.lastname: Ragan
authors.forename: Robert
authors.initials: R
authors.lastname: McKinstry
authors.forename: Tammie
authors.initials: T
authors.lastname: Benzinger
authors.forename: Jeffrey R
authors.initials: JR
authors.lastname: Leonard
authors.forename: Jose A
authors.initials: JA
authors.lastname: Pineda
mesh_terms: D000293:Adolescent; D001930:Brain Injuries / Q000378:metabolism* / Q000503:physiopathology; D002540:Cerebral Cortex / Q000098:blood supply / Q000378:metabolism* / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D002648:Child; D002675:Child, Preschool; D015600:Glasgow Coma Scale; D006801:Humans; D007223:Infant; D008279:Magnetic Resonance Imaging; D008928:Mitochondria / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism*; D010101:Oxygen Consumption
chemical_list: D010100:Oxygen