Brain Biomarkers in Children After Mild and Severe Traumatic Brain Injury.

Brain biomarkers (protein S100b and neuron-specific enolase (NSE)), antibodies (aAb) to the NR2 subunit of N-methyl-D-aspartate (NR2(NMDA)) and to the GluR1 subunit of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (GluR1(AMPA)) subtype of glutamate receptors (GluR), NR2 and AMPA peptides, nitrogen oxides (NOx; "nitrites and nitrates"), and 3-nitrotyrosine (NT) were measured in blood from 159 children after mild traumatic brain injury (mTBI), moderate traumatic brain injury (mdTBI), or severe traumatic brain injury (sTBI) within 1-2 days and at intervals during the first 15 days after brain trauma. S100b and NSE levels on the first day were not a strict criterion for injury outcomes. Children with mTBI had the most significant elevations in antibodies to NR2(NMDA) and AMPA peptides, a slight increase in NOx, and, in 25% of cases, appearance of NT in the blood right after TBI. The lowest level of antibodies to NR2(NMDA) GluR detected shortly after the initial TBI was found in children with sTBI, with a negative outcome. The opposite characters of antibodies to NR2(NMDA) on the first day in children with mild and moderate versus severe TBI may be associated with an important mechanism aimed at protecting neurons from Glu excitotoxicity. We hypothesized that a slight increase in NOx after the onset of TBI rapidly activates the innate immune system and contributes to an increase in antibodies to NR2(NMDA). An increase in the AMPA peptide level in mTBI may be early signs of diffuse axonal injury.

Prognosis of Severe Traumatic Brain Injury Outcomes in Children.

OBJECTIVES: We aimed to determine prognostic factors that can influence the outcome of severe traumatic brain injury (TBI) in children. MATERIALS AND METHODS: One hundred and sixty-nine patients with severe TBI were included. Consciousness was evaluated using the Glasgow Coma Scale (GCS). Severity of concomitant injuries was evaluated using the Injury Severity Score (ISS). Computer tomography (CT) scanning was used on admission and later. Intracranial injuries were classified using the Marshall CT scale. Intracranial pressure (ICP) monitoring took place in 80 cases. Serum samples of 65 patients were tested for S-100ß protein and of 43 patients for neuron specific enolase (NSE). Outcomes were evaluated 6 months after trauma using the Glasgow Outcome Scale (GOS). Statistical and mathematical analysis was conducted. The accuracy of our prognostic model was defined in another group of patients (n = 118). RESULTS: GCS, pupil size and photoreaction, ISS, hypotension and hypoxia are significant predictors of outcome of severe TBI in children. CT results complement the forecast significantly. The accuracy of surviving prognosis came to 76% (0.76) in case of S-100ß protein level ≤ 0.25 µg/l and NSE level < 19 µg/l. A mathematical model of outcome prognosis was based on discriminant function analysis. The model of prognosis was tested on the control group. The accuracy of prognosis was 86%. CONCLUSIONS: A personalised prognostic model makes it possible to predict the outcome of severe TBI in children on the first day after trauma.