title: Vulnerability of the anterior commissure in moderate to severe pediatric traumatic brain injury.
abstract: In relation to the adult brain, the immature brain might be more vulnerable to damage during and following traumatic brain injury, particularly in white-matter tracts. Given well-established evidence of corpus callosum atrophy, we hypothesized that anterior commissure volume (using quantitative magnetic resonance imaging [MRI]) in this structure would be decreased in children with moderate to severe traumatic brain injury relative to typically developing children. Second, given the purported role of the anterior commissure in interhemispheric axon conveyance between temporal lobes, we hypothesized that temporal lobe white matter, temporal lesion volume, and injury severity (Glasgow Coma Scale score) would be predictive of decreased anterior commissure cross-sectional volume in patients with traumatic brain injury. Finally, we wished to establish the relationship between the anterior commissure and the temporal stem, a major white-matter tract into the temporal lobes, using diffusion tensor imaging fiber-tracking maps for each patient. We also hypothesized that children with traumatic brain injury would exhibit decreased fractional anisotropy in relation to typically developing children in a fiber system including the anterior commissure and the temporal lobes. Decreased anterior commissure cross-sectional volume was observed in patients with traumatic brain injury, and, as predicted, anterior commissure and temporal white-matter volumes were positively related to each other and to higher Glasgow Coma Scale scores. Lesion volume was not independently predictive of anterior commissure volume in the overall model. Diffusion tensor imaging fractional anisotropy values differed between the groups for the temporal stem-anterior commissure system, with the traumatic brain injury group exhibiting decreased fractional anisotropy. The anterior commissure, like the corpus callosum, appears to be highly vulnerable to white-matter degenerative changes resulting from mechanisms such as the direct impact of trauma, progressive axonal injury as tissue in other brain regions atrophies, or myelin degeneration. This is the first systematic examination of anterior commissure atrophy following traumatic brain injury using in vivo quantitative MRI and diffusion tensor imaging fiber tracking in pediatric subjects.
authors.affiliation: Department of Physical Medicine and Rehabilitation, Baylor College of Medicine, 1709 Dryden Road, Houston, TX 77030, USA.
authors.forename: Elisabeth A
authors.initials: EA
authors.lastname: Wilde
authors.forename: Erin D
authors.initials: ED
authors.lastname: Bigler
authors.forename: Janelle M
authors.initials: JM
authors.lastname: Haider
authors.forename: Zili
authors.initials: Z
authors.lastname: Chu
authors.forename: Harvey S
authors.initials: HS
authors.lastname: Levin
authors.forename: Xiaoqi
authors.initials: X
authors.lastname: Li
authors.forename: Jill V
authors.initials: JV
authors.lastname: Hunter
mesh_terms: D000293:Adolescent; D000367:Age Factors; D000704:Analysis of Variance; D016880:Anisotropy; D001284:Atrophy / Q000209:etiology; D001369:Axons / Q000473:pathology*; D001930:Brain Injuries / Q000150:complications / Q000473:pathology*; D016022:Case-Control Studies; D002648:Child; D005260:Female; D015600:Glasgow Coma Scale; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D016555:Matched-Pair Analysis; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology; D009413:Nerve Fibers, Myelinated / Q000473:pathology* / Q000502:physiology; D009434:Neural Pathways / Q000254:growth & development / Q000293:injuries / Q000473:pathology*; D009929:Organ Size; D012016:Reference Values; D013702:Temporal Lobe / Q000254:growth & development / Q000293:injuries / Q000473:pathology*