Emily L Dennis1, Faisal Rashid2, Monica U Ellis2, Talin Babikian2, Roza M Vlasova2, Julio E Villalon-Reina2, Yan Jin2, Alexander Olsen2, Richard Mink2, Christopher Babbitt2, Jeffrey Johnson2, Christopher C Giza2, Paul M Thompson2, Robert F Asarnow2. 1. From the Imaging Genetics Center (E.L.D., F.R., J.E.V.-R., Y.J., P.M.T.), Mary and Mark Stevens Institute for Neuroimaging and Informatics, Keck School of Medicine, University of Southern California, Marina del Rey; Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior (M.U.E., T.B., A.O., R.F.A.), Department of Psychology (R.F.A.), and Brain Research Institute (R.F.A.), UCLA, Los Angeles; Fuller Theological Seminary School of Psychology (M.U.E.), Pasadena; CIBORG Laboratory (R.M.V.), Department of Radiology, Children's Hospital Los Angeles, CA; Department of Psychology (A.O.), Norwegian University of Science and Technology; Department of Physical Medicine and Rehabilitation (A.O.), St. Olavs Hospital, Trondheim University Hospital, Norway; Harbor-UCLA Medical Center and Los Angeles BioMedical Research Institute (R.M.), Department of Pediatrics, Torrance; Miller Children's Hospital (C.B.), Long Beach; Department of Pediatrics (J.J.), LAC+USC Medical Center; Department of Neurosurgery and Division of Pediatric Neurology, UCLA Brain Injury Research Center (C.C.G.), Mattel Children's Hospital; and Departments of Neurology, Pediatrics, Psychiatry, Radiology, Engineering, and Ophthalmology (P.M.T.), USC, Los Angeles, CA. emily.dennis@ini.usc.edu. 2. From the Imaging Genetics Center (E.L.D., F.R., J.E.V.-R., Y.J., P.M.T.), Mary and Mark Stevens Institute for Neuroimaging and Informatics, Keck School of Medicine, University of Southern California, Marina del Rey; Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior (M.U.E., T.B., A.O., R.F.A.), Department of Psychology (R.F.A.), and Brain Research Institute (R.F.A.), UCLA, Los Angeles; Fuller Theological Seminary School of Psychology (M.U.E.), Pasadena; CIBORG Laboratory (R.M.V.), Department of Radiology, Children's Hospital Los Angeles, CA; Department of Psychology (A.O.), Norwegian University of Science and Technology; Department of Physical Medicine and Rehabilitation (A.O.), St. Olavs Hospital, Trondheim University Hospital, Norway; Harbor-UCLA Medical Center and Los Angeles BioMedical Research Institute (R.M.), Department of Pediatrics, Torrance; Miller Children's Hospital (C.B.), Long Beach; Department of Pediatrics (J.J.), LAC+USC Medical Center; Department of Neurosurgery and Division of Pediatric Neurology, UCLA Brain Injury Research Center (C.C.G.), Mattel Children's Hospital; and Departments of Neurology, Pediatrics, Psychiatry, Radiology, Engineering, and Ophthalmology (P.M.T.), USC, Los Angeles, CA.
Abstract
OBJECTIVE: To examine longitudinal trajectories of white matter organization in pediatric moderate/severe traumatic brain injury (msTBI) over a 12-month period. METHODS: We studied 21 children (16 M/5 F) with msTBI, assessed 2-5 months postinjury and again 13-19 months postinjury, as well as 20 well-matched healthy control children. We assessed corpus callosum function through interhemispheric transfer time (IHTT), measured using event-related potentials, and related this to diffusion-weighted MRI measures of white matter (WM) microstructure. At the first time point, half of the patients with TBI had significantly slower IHTT (TBI-slow-IHTT, n = 11) and half were in the normal range (TBI-normal-IHTT, n = 10). RESULTS: The TBI-normal-IHTT group did not differ significantly from healthy controls, either in WM organization in the chronic phase or in the longitudinal trajectory of WM organization between the 2 evaluations. In contrast, the WM organization of the TBI-slow-IHTT group was significantly lower than in healthy controls across a large portion of the WM. Longitudinal analyses showed that the TBI-slow-IHTT group experienced a progressive decline between the 2 evaluations in WM organization throughout the brain. CONCLUSIONS: We present preliminary evidence suggesting a potential biomarker that identifies a subset of patients with impaired callosal organization in the first months postinjury who subsequently experience widespread continuing and progressive degeneration in the first year postinjury.
OBJECTIVE: To examine longitudinal trajectories of white matter organization in pediatric moderate/severe traumatic brain injury (msTBI) over a 12-month period. METHODS: We studied 21 children (16 M/5 F) with msTBI, assessed 2-5 months postinjury and again 13-19 months postinjury, as well as 20 well-matched healthy control children. We assessed corpus callosum function through interhemispheric transfer time (IHTT), measured using event-related potentials, and related this to diffusion-weighted MRI measures of white matter (WM) microstructure. At the first time point, half of the patients with TBI had significantly slower IHTT (TBI-slow-IHTT, n = 11) and half were in the normal range (TBI-normal-IHTT, n = 10). RESULTS: The TBI-normal-IHTT group did not differ significantly from healthy controls, either in WM organization in the chronic phase or in the longitudinal trajectory of WM organization between the 2 evaluations. In contrast, the WM organization of the TBI-slow-IHTT group was significantly lower than in healthy controls across a large portion of the WM. Longitudinal analyses showed that the TBI-slow-IHTT group experienced a progressive decline between the 2 evaluations in WM organization throughout the brain. CONCLUSIONS: We present preliminary evidence suggesting a potential biomarker that identifies a subset of patients with impaired callosal organization in the first months postinjury who subsequently experience widespread continuing and progressive degeneration in the first year postinjury.
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