Abstract
The national incidence of traumatic brain injury (TBI) exceeds that of any other disease in the pediatric population. In the United States the Centers for Disease Control and Prevention (CDC) reports 697,347 annual TBIs in children ages 0–19 that result in emergency room visits, hospitalization or deaths. There is a bimodal distribution within the pediatric TBI population, with peaks in both toddlers and adolescents. Preclinical TBI research provides evidence for age differences in acute pathophysiology that likely contribute to long-term outcome differences between age groups. This review will examine the timecourse of acute pathophysiological processes during cerebral maturation, including calcium accumulation, glucose metabolism and cerebral blood flow. Consequences of pediatric TBI are complicated by the ongoing maturational changes allowing for substantial plasticity and windows of vulnerabilities. This review will also examine the timecourse of later outcomes after mild, repeat mild and more severe TBI to establish developmental windows of susceptibility and altered maturational trajectories. Research progress for pediatric TBI is critically important to reveal age-associated mechanisms and to determine knowledge gaps for future studies.
Highlights
Addressing traumatic brain injury (TBI) in the pediatric population is exceptionally complex
The concomitant upregulation of the pentose phosphate pathway (PPP) allows for production of byproducts necessary for DNA repair and activation of glutathione peroxidase (GPx) for detoxification of oxidative stress. 13C-glucose NMR studies in adults after controlled cortical impact (CCI) injury show a 9–13% increase in glucose shunting toward this pathway [14]
The Centers for Disease Control and Prevention (CDC) estimates that 80% of pediatric TBIs are mild, and that patients display acute affective, cognitive and somatic symptoms that resolve within weeks
Summary
The national incidence of traumatic brain injury (TBI) exceeds that of any other disease in the pediatric population. Preclinical TBI research provides evidence for age differences in acute pathophysiology that likely contribute to long-term outcome differences between age groups. This review will examine the timecourse of acute pathophysiological processes during cerebral maturation, including calcium accumulation, glucose metabolism and cerebral blood flow. Consequences of pediatric TBI are complicated by the ongoing maturational changes allowing for substantial plasticity and windows of vulnerabilities. This review will examine the timecourse of later outcomes after mild, repeat mild and more severe TBI to establish developmental windows of susceptibility and altered maturational trajectories. Research progress for pediatric TBI is critically important to reveal age-associated mechanisms and to determine knowledge gaps for future studies
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