Autor: |
Merkley TL; Department of Psychology and Brigham Young University, Provo, Utah, USA.; Neuroscience Center, Brigham Young University, Provo, Utah, USA., Halter C; Department of Psychology and Brigham Young University, Provo, Utah, USA., Graul B; Neuroscience Center, Brigham Young University, Provo, Utah, USA., Gale SD; Department of Psychology and Brigham Young University, Provo, Utah, USA.; Neuroscience Center, Brigham Young University, Provo, Utah, USA., Junge C; Neuroscience Center, Brigham Young University, Provo, Utah, USA., Reading M; Department of Psychology and Brigham Young University, Provo, Utah, USA., Jarvis S; Department of Psychology and Brigham Young University, Provo, Utah, USA., Greer K; Department of Psychology and Brigham Young University, Provo, Utah, USA., Squires C; Department of Psychology and Brigham Young University, Provo, Utah, USA., Bigler ED; Department of Psychology and Brigham Young University, Provo, Utah, USA.; Neuroscience Center, Brigham Young University, Provo, Utah, USA., Taylor HG; Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, Ohio, USA., Vannatta K; Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, Ohio, USA.; Departments of Pediatrics and Psychology, The Ohio State University, Columbus, Ohio, USA., Gerhardt CA; Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, Ohio, USA.; Departments of Pediatrics and Psychology, The Ohio State University, Columbus, Ohio, USA., Rubin KH; Department of Human Development and Quantitative Methodology, University of Maryland, College Park, Maryland, USA., Stancin T; MetroHealth System, Case Western Reserve University, Cleveland, Ohio, USA., Yeates KO; Department of Psychology, University of Calgary, Calgary, Alberta, Canada., Cobia D; Department of Psychology and Brigham Young University, Provo, Utah, USA.; Neuroscience Center, Brigham Young University, Provo, Utah, USA. |
Abstrakt: |
A decline in intellectual functioning (intelligence quotient [IQ]) is often observed following more severe forms of traumatic brain injury (TBI) and is a useful index for long-term outcome. Identifying brain correlates of IQ can serve to inform developmental trajectories of behavior in this population. Using magnetic resonance imaging (MRI), we examined the relationship between intellectual abilities and patterns of cortical thickness in children with a history of TBI or with orthopedic injury (OI) in the chronic phase of injury recovery. Participants were 47 children with OI and 58 children with TBI, with TBI severity ranging from complicated-mild to severe. Ages ranged from 8 to 14 years old, with an average age of 10.47 years, and an injury-to-test range of ∼1-5 years. The groups did not differ in age or sex. The intellectual ability estimate (full-scale [FS]IQ-2) was derived from a two-form (Vocabulary and Matrix Reasoning subtests) Wechsler Abbreviated Scale of Intelligence (WASI). MRI data were processed using the FreeSurfer toolkit and harmonized across data collection sites using neuroComBat procedures, while holding demographic features (i.e., sex, socioeconomic status [SES]), TBI status, and FSIQ-2 constant. Separate general linear models per group (TBI and OI) and a single interaction model with all participants were conducted with all significant results withstanding correction for multiple comparisons via permutation testing. Intellectual ability was higher ( p < 0.001) in the OI group (FSIQ-2 = 110.81) than in the TBI group (FSIQ-2 = 99.81). In children with OI, bi-hemispheric regions, including the right pre-central gyrus and precuneus and bilateral inferior temporal and left occipital areas were related to IQ, such that higher IQ was associated with thicker cortex in these regions. In contrast, only cortical thickness in the right pre-central gyrus and bilateral cuneus positively related to IQ in children with TBI. Significant interaction effects were found in the bilateral temporal, parietal, and occipital lobes and left frontal regions, indicating that the relationship between IQ and cortical thickness differed between groups in these regions. Changes in cortical associations with IQ after TBI may reflect direct injury effects and/or adaptation in cortical structure and intellectual functioning, particularly in the bilateral posterior parietal and inferior temporal regions. This suggests that the substrates of intellectual ability are particularly susceptible to acquired injury in the integrative association cortex. Longitudinal work is needed to account for normal developmental changes and to investigate how cortical thickness and intellectual functioning and their association change over time following TBI. Improved understanding of how TBI-related cortical thickness alterations relate to cognitive outcome could lead to improved predictions of outcome following brain injury. |