Research Reports - Understanding divergent trajectories in pediatric patients with moderate to severe traumatic brain injury

Faisal Rashid, Emily Dennis, Monica Ellis-Blied, Talin Babikian, Jeffry Alger, Julio Villalon-Reina, Yan Jin, Alexander Olsen, Richard Mink, Christopher Babbitt, Jeffrey Johnson, Christopher Giza, Paul Thompson, Robert Asarnow

Neurology Apr 2018, 90 (15 Supplement) S35.007

Objective: To examine changes in the adolescent brain after traumatic brain injury, we used diffusion weighted imaging (dMRI) and magnetic resonance spectroscopy (MRS) to quantify white matter (WM) microstructural changes following moderate to severe TBI (msTBI).

Background: Traumatic brain injury (TBI) is the leading cause of death and disability in children worldwide. TBI can interact with maturational processes in the developing adolescent brain [1], which is especially vulnerable for psychiatric disorders following TBI [2,3].

Design/Methods: We examined 21 children 2–5 (post-acute) and 13–19 months (chronic) after msTBI. To investigate callosal dysfunction, we measured interhemispheric transfer time (IHTT) using event-related potentials (ERPs), and tested its association with DWI measures of WM organization. Using whole brain MRS, we quantified N-acetylaspartate (NAA) levels – a marker of neuronal integrity - and choline (Cho) – a marker of inflammation [4]. Combining dMRI and MRS, we can better relate disruptions in WM organization to underlying biochemical mechanisms.

Results: Approximately half the TBI patients had significantly slower IHTTs at the post-acute phase (TBI-slow, 25.3 ms), while the other had normal IHTTs that did not differ significantly from controls (TBI-normal, 7.8 ms). These effects were also present at the chronic phase (TBI-slow; 26.8 ms, TBI-normal; 8.5 ms). The TBI-slow group shows significant reductions in FA and increases in MD and RD measures in the post-acute and chronic phases. The tracts in the TBI-slow group in the post-acute/chronic phases that had disrupted WM organization also showed lower NAA compared to controls (6 tracts 2–5 months post-injury/7 tracts 13–19 months post-injury), all overlapping. Choline did not show any significant differences.

Conclusions: Our results suggest a diverging neurological trajectory in the outcomes of these groups of patients. Our findings suggest a potential biomarker that identifies as subset of patients with impaired callosal integrity in the first months post-injury who go on to experience continuing degeneration in the first year post-injury.

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