Despite contributing to neurocognitive deficits, intracortical demyelination after traumatic brain injury (TBI) is understudied. This study uses magnetic resonance imaging (MRI) to map intracortical myelin and its change in healthy controls and after mild TBI (mTBI). Acute mTBI involves reductions in relative myelin content primarily in lateral occipital regions. Demyelination mapped ~6 months post-injury is significantly more severe than that observed in typical aging (p < 0.05), with temporal, cingulate, and insular regions losing more myelin (30%, 20%, and 16%, respectively) than most other areas, although occipital regions experience 22% less demyelination. Thus, occipital regions may be more susceptible to primary injury, whereas temporal, cingulate and insular regions may be more susceptible to later manifestations of injury sequelae. The spatial profiles of aging- and mTBI-related chronic demyelination overlap substantially; exceptions include primary motor and somatosensory cortices, where myelin is relatively spared post-mTBI. These features resemble those of white matter demyelination and cortical thinning during Alzheimer's disease, whose risk increases after mTBI.
Mild traumatic brain injury (mTBI) accelerates the rate of age-associated brain atrophy, whose pattern resembles the cortical neurodegeneration pattern observed in Alzheimer’s disease (AD). Because the ratio R of T1-to-T2-weighted magnetic resonance imaging (MRI) intensities is a surrogate measure of cortical myelin concentration, mapping and quantifying changes in this ratio can improve our understanding of demyelination after geriatric mTBI and AD. T1- and T2-weighted MRIs were acquired acutely and ~6 months post-injury from 68 healthy controls (HCs, age (years, y): μ = 76 y, σ = 4 y), 19 mTBIs (age μ = 70 y, σ = 5 y), and 33 ADs (age μ = 77, σ = 6). Volumes were co-registered using 3D Slicer’s BRAINSFit module, and T2-constrained segmentations of T1 volumes were obtained using FreeSurfer. R and its time changes were computed at each cortical location. When comparing mTBI and AD patients to HCs, significant differences in R were found across ~10% and ~23% of the cortex, respectively (p < 0.05). When comparing mTBI to AD, the former exhibited significantly less myelin content in the lateral, medial, and ventral temporal lobes (p < 0.05), on the medial aspects of superior parietal lobules and superior frontal gyri (p < 0.05), and in orbital gyri (p < 0.05), whereas AD subjects had less myelin content on lateral aspect of the parietal lobe (p < 0.05). These results highlight demyelination differences in mTBI and AD. Future studies should examine the long-term trajectories to quantify the risk of neurodegenerative disease after mTBI.
Estimating biological brain age (BA) has the potential of identifying individuals at relatively high risk for accelerated neurodegeneration. This study compares the brain’s chronological age (CA) to its BA and reveals the BA rate of change after mild traumatic brain injury (mTBI) in an aging cohort. Using T1-weighted magnetic resonance imaging (MRI) volumes and cortical thickness, volume, surface area, and Gaussian curvature obtained using FreeSurfer software; we formulated a multivariate linear regression to determine the rate of BA increase associated with mTBI. 95 TBI patients (age in years (y): μ = 41 y, σ = 17 y; range = 18 to 83) were compared to 462 healthy controls (HCs) (age: μ = 69 y, σ = 18 y; range = 25 to 95) over a 6-month time period following mTBI. Across the initial ~6 months following injury, patients’ BAs increased by ~3.0 ± 1.2 years due to their mTBIs alone, i.e., above and beyond typical brain aging. The superior temporal and parahippocampal gyri, two structures involved in memory formation and retrieval, exhibited the fastest rates of TBI-related BA. In both hemispheres, the volume of the hippocampus decreased (left: μ=0.28%, σ=4.40%; right: μ=0.12%, σ=4.84%). These findings illustrate BA estimation techniques’ potential to identify TBI patients with accelerated neurodegeneration, whose rate is strongly associated with the risk for dementia and other aging-related neurological conditions.
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