The Relation of Focal Lesions to Cortical Thickness in Pediatric Traumatic Brain Injury

Bigler, Erin D.; Zielinski, Brandon A.; Goodrich-Hunsaker, Naomi J.; Black, Garrett; Huff, B. S Trevor; Christiansen, Zachary; Wood, Dawn Marie; Abildskov, Tracy J.; Dennis, Maureen; Taylor, H. Gerry; Rubin, Kenneth H.; Vannatta, Kathryn; Gerhardt, Cynthia A.; Stancin, Terry; Yeates, Keith Owen

doi:10.1177/0883073816654143

Cited by 16 publications

(11 citation statements)

References 55 publications

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“…Although it was difficult to draw conclusions concerning the effect of age on the developing cortex in a cross‐sectional design, we noted a thinner mean prefrontal (MFT) and mean temporal cortex (MTT) in older typically developing children compared to younger ones, which conformed with prior developmental studies . This age effect was to a lesser extent also present in the group with TBI, but contrary to the control cohort the effect was not significant. We interpreted the absence of this typical age effect on prefrontal and temporal cortical thinning in the group with TBI as the result of trauma‐induced cortical grey matter loss .…”

Section: Discussionsupporting

confidence: 86%

Prefrontal and temporal cortical thickness in adolescents with traumatic brain injury

Linden

Verhelst

Verleysen

et al. 2018

Develop Med Child Neuro

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Aim To investigate the impact of traumatic injury on the developing prefrontal‐temporal adolescent cortex, and correlated brain structural measures with neurocognitive functioning. Method Nineteen adolescents (12 males, 7 females, age range: 11–17y, mean 15y 8mo, standard deviation 1y 7mo, median 15y 11mo) with traumatic brain injury (TBI) were included. Cortical thickness of frontal and temporal lobes was assessed using magnetic resonance imaging. We correlated cortical thickness of prefrontal‐temporal regions with age, time since injury, and neurocognitive functioning, and compared these results with a matched control cohort without TBI. Results We found thinner prefrontal (p=0.039) and temporal cortices (p=0.002) in adolescents with TBI compared to typically developing children. Furthermore, significant age effect was observed on the prefrontal (r=−0.75, p=0.003) and temporal (r=−0.66, p=0.013) cortical thickness in typically developing adolescents, but not in adolescents with TBI. Executive function (measured using the Behaviour Rating Inventory of Executive Function questionnaire, with lower scores meaning higher functioning) was correlated with prefrontal cortical thickness in typically developing adolescents (r=0.72, p=0.009). Opposite trends were found for correlations between cortical thickness and executive function in the TBI and control cohort. Interpretation Structural maturation in typically developing adolescents correlates with functional development: the older the adolescent, the thinner the prefrontal cortex, the better executive function. In adolescents with TBI we observed an opposite trend, that appeared significantly different from the control group: the thinner the prefrontal and temporal cortex, the worse executive functioning. What this paper adds Cortical thickness is negatively correlated with age in typically developing adolescents. Prefrontal cortex thickness correlates negatively with executive function in typically developing adolescents. Correlations between cortical thickness and executive functioning rise for adolescents without traumatic brain injury (TBI). Correlations between cortical thickness and executive functioning fall for adolescents with TBI. Adolescents with TBI have a long‐term impairment of adaptive functioning in daily living.

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Section: Discussionsupporting

confidence: 86%

Prefrontal and temporal cortical thickness in adolescents with traumatic brain injury

Linden

Verhelst

Verleysen

et al. 2018

Develop Med Child Neuro

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“…No significant differences were found for the tested subcortical structures.Drijkoningen et al (2017), Belgium3 TFreesurfer (ANOVA, Global-brain, ROI)VolumeICVTotal subcortical GM (not total cortical volume) was smaller in the TBI group compared to controls. No significant differences in cortical ROIs, but subcortically, thalamus, putamen, hippocampus and cerebellar cortex were significantly smaller in TBI.Bigler et al (2016), Canada & USA1.5 TFreesurfer (QDEC, vertex-wise)Cortical ThicknessSex, AgeNo significant effect of group on vertex-wise cortical thickness. Age was significantly related to decreasing cortical thickness, with distribution of age-related changes being similar for TBI and OI.Drijkoningen et al (2015), Belgium3 TSPM8, SUIT toolbox, DARTEL, MRIcron (GLM, Global-brain, Voxel-wise)VolumeICVNo significant differences in total ICV.…”

Section: Resultsmentioning

confidence: 93%

A systematic review of cross-sectional differences and longitudinal changes to the morphometry of the brain following paediatric traumatic brain injury

King

Ellis

Seri

et al. 2019

NeuroImage: Clinical

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Paediatric traumatic brain injury (pTBI) is a leading cause of disability for children and young adults. Children are a uniquely vulnerable group with the disease process that occurs following a pTBI interacting with the trajectory of normal brain development. Quantitative MRI post-injury has suggested a long-term, neurodegenerative effect of TBI on the morphometry of the brain, in both adult and childhood TBI. Changes to the brain beyond that of anticipated, age-dependant differences may allow us to estimate the state of the brain post-injury and produce clinically relevant predictions for long-term outcome. The current review synthesises the existing literature to assess whether, following pTBI, the morphology of the brain exhibits either i) longitudinal change and/or ii) differences compared to healthy controls and outcomes. The current literature suggests that morphometric differences from controls are apparent cross-sectionally at both acute and late-chronic timepoints post-injury, thus suggesting a non-transient effect of injury. Developmental trajectories of morphometry are altered in TBI groups compared to patients, and it is unlikely that typical maturation overcomes damage post-injury, or even ‘catches up’ with that of typically-developing peers. However, there is limited evidence for diverted developmental trajectories being associated with cognitive impairment post-injury. The current review also highlights the apparent challenges to the existing literature and potential methods by which these can be addressed.

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“…Primary injury biomarkers facilitating distinctions between blast and non-blast TBI among living human subjects are not well known, at this time. However, biomarkers have been suggested to distinguish TBI from control subjects, including hemorrhagic lesions (microbleeds), total ventricle volume, parenchymal volume, focal loss of brain tissue (encephalomalacia), and diffuse axonal injury (Bigler et al, 2013; Bigler et al, 2016). Pursuant to findings in previous literature, microbleeds may decrease in size as the time passes following the injury, rendering it increasingly difficult to observe microbleeds in a persistent mTBI population (Lawrence et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Cortical thinning in military blast compared to non-blast persistent mild traumatic brain injuries

Eierud

Nathan

Bonavia

et al. 2019

NeuroImage: Clinical

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In the military, explosive blasts are a significant cause of mild traumatic brain injuries (mTBIs). The symptoms associated with blast mTBIs causes significant economic burdens and a diminished quality of life for many service members. At present, the distinction of the injury mechanism (blast versus non-blast) may not influence TBI diagnosis. However, using noninvasive imaging, this study reveals significant distinctions between the blast and non-blast TBI mechanisms. A cortical whole-brain thickness analysis was performed using structural high-resolution T1-weighted MRI to identify the effects of blasts in persistent mTBI (pmTBI) subjects. A total of 41 blast pmTBI subjects were individually age- and gender-matched to 41 non-blast pmTBI subjects. Using FreeSurfer, cortical thickness was quantified for the blast group, relative to the non-blast group. Cortical thinning was identified within the blast mTBI group, in two clusters bilaterally. In the left hemisphere, the cluster overlapped with the lateral orbitofrontal, rostral middle frontal, medial orbitofrontal, superior frontal, rostral anterior cingulate and frontal pole cortices ( p < 0.02, two-tailed, size = 1680 mm 2 ). In the right hemisphere, the cluster overlapped with the lateral orbitofrontal, rostral middle frontal, medial orbitofrontal, pars orbitalis, pars triangularis and insula cortices ( p < 0.002, two-tailed, cluster size = 2453 mm 2 ). Self-report assessments suggest significant differences in the Post-Traumatic Stress Disorder Checklist-Civilian Version ( p < 0.05, Bonferroni-corrected) and the Neurobehavioral Symptom Inventory ( p < 0.01, uncorrected) between the blast and non-blast mTBI groups. These results suggest that blast may cause a unique injury pattern related to a reduction in cortical thickness within specific brain regions which could affect symptoms. No other study has found cortical thickness difference between blast and non-blast mTBI groups and further replication is needed to confirm these initial observations.

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The Relation of Focal Lesions to Cortical Thickness in Pediatric Traumatic Brain Injury

Cited by 16 publications

References 55 publications

Prefrontal and temporal cortical thickness in adolescents with traumatic brain injury

Prefrontal and temporal cortical thickness in adolescents with traumatic brain injury

A systematic review of cross-sectional differences and longitudinal changes to the morphometry of the brain following paediatric traumatic brain injury

Cortical thinning in military blast compared to non-blast persistent mild traumatic brain injuries

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