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Prospective Study of Gray Matter Atrophy Following Pediatric Mild Traumatic Brain Injury
Andrew R Mayer1, Timothy B Meier2, Andrew B Dodd2
1From the The Mind Research Network/Lovelace Biomedical Research Institute (A.R.M., A.B.D., D.D.S., C.R.R.-B., J.M.L., S.P.R., V.Z., K.V., J.P.P., A.A.V.); Department of Psychology (A.R.M.), Department of Neurology (A.R.M., J.P.P.), and Department of Psychiatry & Behavioral Sciences (A.R.M., R.A.C.), University of New Mexico, Albuquerque; Department of Neurosurgery (T.B.M.), Department of Cell Biology, Neurobiology and Anatomy (T.B.M.), and Department of Biomedical Engineering (T.B.M.), Medical College of Wisconsin, Milwaukee; and Department of Emergency Medicine (R.E.S.), and Department of Mathematics and Statistics (E.B.E.), University of New Mexico, Albuquerque. amayer@mrn.org.
Insights
Pediatric mild traumatic brain injuries (pmTBI) can cause persistent structural brain changes up to 4 months post-injury. These abnormalities, while not linked to age at injury, may indicate prolonged recovery in children.
Area of Science:
- Neuroscience
- Pediatric Neurology
- Radiology
Background:
- The recovery timeline following pediatric mild traumatic brain injury (pmTBI) is not well understood.
- Structural brain changes and the influence of age at injury require further investigation.
Purpose of the Study:
- To prospectively examine structural brain changes (cortical thickness, subcortical volumes) in children after pmTBI.
- To investigate the association between age at injury and these structural changes.
- To assess the relationship between structural abnormalities and clinical outcomes.
Main Methods:
- Prospective cohort study with 208 pmTBI patients and 176 healthy controls.
- Structural brain imaging (3 T MRI) and clinical evaluations at subacute (SA) and early chronic (EC) stages post-injury.
- Quantification of cortical thickness and subcortical volumes using FreeSurfer software.
Main Results:
- Reduced cortical thickness and hippocampal volumes were observed in pmTBI patients up to 4 months post-injury.
- These structural changes were not associated with age at injury.
- Hippocampal volume recovery was influenced by loss of consciousness and posttraumatic amnesia.
- Structural abnormalities improved classification accuracy for pmTBI detection.
Conclusions:
- Structural brain abnormalities may persist for at least 4 months after pmTBI in children.
- Injury severity markers, not age at injury, appear to mediate these changes.
- Findings support the hypothesis of prolonged physiologic recovery post-pmTBI.
Background And Objectives:
The clinical and physiologic time course for recovery following pediatric mild traumatic brain injury (pmTBI) remains actively debated. The primary objective of the current study was to prospectively examine structural brain changes (cortical thickness and subcortical volumes) and age-at-injury effects. A priori study hypotheses predicted reduced cortical thickness and hippocampal volumes up to 4 months postinjury, which would be inversely associated with age at injury.
Methods:
Prospective cohort study design with consecutive recruitment. Study inclusion adapted from American Congress of Rehabilitation Medicine (upper threshold) and Zurich Concussion in Sport Group (minimal threshold) and diagnosed by Emergency Department and Urgent Care clinicians. Major neurologic, psychiatric, or developmental disorders were exclusionary. Clinical (Common Data Element) and structural (3 T MRI) evaluations within 11 days (subacute visit [SA]) and at 4 months (early chronic visit [EC]) postinjury. Age- and sex-matched healthy controls (HC) to control for repeat testing/neurodevelopment. Clinical outcomes based on self-report and cognitive testing. Structural images quantified with FreeSurfer (version 7.1.1).
Results:
A total of 208 patients with pmTBI (age = 14.4 ± 2.9; 40.4% female) and 176 HC (age = 14.2 ± 2.9; 42.0% female) were included in the final analyses (>80% retention). Reduced cortical thickness (right rostral middle frontal gyrus; d = -0.49) and hippocampal volumes (d = -0.24) observed for pmTBI, but not associated with age at injury. Hippocampal volume recovery was mediated by loss of consciousness/posttraumatic amnesia. Significantly greater postconcussive symptoms and cognitive deficits were observed at SA and EC visits, but were not associated with the structural abnormalities. Structural abnormalities slightly improved balanced classification accuracy above and beyond clinical gold standards (∆+3.9%), with a greater increase in specificity (∆+7.5%) relative to sensitivity (∆+0.3%).
Discussion:
Current findings indicate that structural brain abnormalities may persist up to 4 months post-pmTBI and are partially mediated by initial markers of injury severity. These results contribute to a growing body of evidence suggesting prolonged physiologic recovery post-pmTBI. In contrast, there was no evidence for age-at-injury effects or physiologic correlates of persistent symptoms in our sample.
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