INS NYC 2024 Program

Poster	Poster Session 03 Program Schedule 02/15/2024 09:30 am - 10:40 am Room: Shubert Complex (Posters 1-60) Poster Session 03: Neurotrauma \| Neurovascular Final Abstract #37 Gray Matter Macrostructure Up To Two Years After Pediatric Mild TBI Michael Lee, Georgia State University, Atlanta, United States Brian Brooks, University of Calgary, Calgary, Canada Keith Yeates, University of Calgary, Calgary, Canada Miriam Beauchamp, University of Montreal, Montreal, Canada William Craig, University of Alberta, Edmonton, Canada Quynh Doan, University of British Columbia, University Endowment Lands, Canada Catherine Lebel, University of Calgary, Calgary, United States Andree-Anne Ledoux, University of Ottawa, Ottawa, Canada Roger Zemek, University of Ottawa, Ottawa, Canada Ashley Ware, Georgia State University, Atlanta, United States Category: Concussion/Mild TBI (Child) Keyword 1: concussion/ mild traumatic brain injury Keyword 2: neuroimaging: structural Objective: The long-term neurobiological effects of pediatric mild traumatic brain injury (mTBI) are poorly understood, despite high annual worldwide incidence and prevalence rates. Although advanced structural MRI techniques can detect changes in brain macrostructure post-injury, prospective longitudinal neuroimaging research is needed. This sub-study of Advancing Concussion in Pediatrics (A-CAP) sought to address this gap by examining longitudinal gray matter macrostructural changes in pediatric mTBI relative to mild orthopedic injury (OI) up to 2 years post-injury. Participants and Methods: The A-CAP study recruited 967 children (ages 8-16.99 years) from five pediatric emergency departments within 48 hours of experiencing an mTBI or mild OI. Children returned for two post-injury MRI scans: post-acute and chronic (3 or 6 months via random assignment). Of those, 30 children at one of the sites also completed a third MRI scan at 2 years post-injury. After quality assurance, cortical thickness and subcortical volume of 29 children were estimated in native T1-weighted space for 57 brain regions based on the MICCAI 2012 atlas using the Advanced Normalization Tools automated pipeline. Multiple linear mixed-effects models were used to compare groups on regional brain metrics over time post-injury, with covariates of age at injury, biological sex, and hemisphere, with participant as a random effect. The false discovery rate (FDR) was applied to correct for multiple comparisons (p threshold = .05). Results: The mTBI (n = 19 at all timepoints) and OI (n = 10; 8 post-cute/9 chronic/10 at 2 years post-injury) groups did not differ in terms of age, sex, race, mechanism of injury, parental education, nor socioeconomic status. After FDR correction, time moderated group differences in cortical thickness for several regions. Post-acutely, cortical thickness was lower after mTBI as compared to OI. Calcarine cortical thickness was lower following mTBI relative to OI at chronic timepoints (d range = 1.02 to 1.27). At 6 months post-injury, thickness of the basal forebrain, cuneus, gyrus rectus, lingual gyrus, medial frontal cortex, medial orbital gyrus, medial segment of the superior frontal gyrus, middle temporal gyrus, occipital pole, precentral gyrus, subcallosal area, supplementary motor cortex, superior parietal lobule, and temporal pole (d range = 1.06 to 1.82) were lower following mTBI relative to OI. However, the middle frontal gyrus, postcentral gyrus, and superior frontal gyrus (d range = -1.16 to -0.99) were thicker 2 years after mTBI relative to OI. Groups did not differ in volume of examined subcortical regions. Conclusions: This study provided initial evidence of varying trajectories in cortical but not subcortical gray matter macrostructure up to two years post-injury following mTBI as compared with mild OI in children. Specifically, cortical thickness of several brain regions was lower up to 6 months after mTBI but was higher 2 years after mTBI. Since cortical thinning is typically expected to occur with maturation in this sample’s age range, as observed in the children with OI, these results suggest that pediatric mTBI can disrupt typical age-related changes in cortical development. Future studies should consider the moderating factors of age at injury and sex.

Poster

02/15/2024
09:30 am - 10:40 am
Room: Shubert Complex (Posters 1-60)

Poster Session 03: Neurotrauma | Neurovascular

Final Abstract #37

Gray Matter Macrostructure Up To Two Years After Pediatric Mild TBI

Michael Lee, Georgia State University, Atlanta, United States
Brian Brooks, University of Calgary, Calgary, Canada
Keith Yeates, University of Calgary, Calgary, Canada
Miriam Beauchamp, University of Montreal, Montreal, Canada
William Craig, University of Alberta, Edmonton, Canada
Quynh Doan, University of British Columbia, University Endowment Lands, Canada
Catherine Lebel, University of Calgary, Calgary, United States
Andree-Anne Ledoux, University of Ottawa, Ottawa, Canada
Roger Zemek, University of Ottawa, Ottawa, Canada
Ashley Ware, Georgia State University, Atlanta, United States

Category: Concussion/Mild TBI (Child)

Keyword 1: concussion/ mild traumatic brain injury
Keyword 2: neuroimaging: structural

Objective:

The long-term neurobiological effects of pediatric mild traumatic brain injury (mTBI) are poorly understood, despite high annual worldwide incidence and prevalence rates. Although advanced structural MRI techniques can detect changes in brain macrostructure post-injury, prospective longitudinal neuroimaging research is needed. This sub-study of Advancing Concussion in Pediatrics (A-CAP) sought to address this gap by examining longitudinal gray matter macrostructural changes in pediatric mTBI relative to mild orthopedic injury (OI) up to 2 years post-injury.

Participants and Methods:

The A-CAP study recruited 967 children (ages 8-16.99 years) from five pediatric emergency departments within 48 hours of experiencing an mTBI or mild OI. Children returned for two post-injury MRI scans: post-acute and chronic (3 or 6 months via random assignment). Of those, 30 children at one of the sites also completed a third MRI scan at 2 years post-injury. After quality assurance, cortical thickness and subcortical volume of 29 children were estimated in native T1-weighted space for 57 brain regions based on the MICCAI 2012 atlas using the Advanced Normalization Tools automated pipeline. Multiple linear mixed-effects models were used to compare groups on regional brain metrics over time post-injury, with covariates of age at injury, biological sex, and hemisphere, with participant as a random effect. The false discovery rate (FDR) was applied to correct for multiple comparisons (p threshold = .05).

Results:

The mTBI (n = 19 at all timepoints) and OI (n = 10; 8 post-cute/9 chronic/10 at 2 years post-injury) groups did not differ in terms of age, sex, race, mechanism of injury, parental education, nor socioeconomic status. After FDR correction, time moderated group differences in cortical thickness for several regions. Post-acutely, cortical thickness was lower after mTBI as compared to OI. Calcarine cortical thickness was lower following mTBI relative to OI at chronic timepoints (d range = 1.02 to 1.27). At 6 months post-injury, thickness of the basal forebrain, cuneus, gyrus rectus, lingual gyrus, medial frontal cortex, medial orbital gyrus, medial segment of the superior frontal gyrus, middle temporal gyrus, occipital pole, precentral gyrus, subcallosal area, supplementary motor cortex, superior parietal lobule, and temporal pole (d range = 1.06 to 1.82) were lower following mTBI relative to OI. However, the middle frontal gyrus, postcentral gyrus, and superior frontal gyrus (d range = -1.16 to -0.99) were thicker 2 years after mTBI relative to OI. Groups did not differ in volume of examined subcortical regions.

Conclusions:

This study provided initial evidence of varying trajectories in cortical but not subcortical gray matter macrostructure up to two years post-injury following mTBI as compared with mild OI in children. Specifically, cortical thickness of several brain regions was lower up to 6 months after mTBI but was higher 2 years after mTBI. Since cortical thinning is typically expected to occur with maturation in this sample’s age range, as observed in the children with OI, these results suggest that pediatric mTBI can disrupt typical age-related changes in cortical development. Future studies should consider the moderating factors of age at injury and sex.