Citation

Huh JW, Raghupathi R. Neuropharmacology 2019; 145(Pt B): 153-159.

Affiliation

Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, PA, USA. Electronic address: RR79@drexel.edu.

Copyright

(Copyright © 2019, Elsevier Publishing)

DOI

10.1016/j.neuropharm.2018.06.025

PMID

29933010

Abstract

Pediatric traumatic brain injury (TBI) remains one of the leading causes of morbidity and mortality in children. Experimental and clinical studies demonstrate that the developmental age, the type of injury (diffuse vs. focal) and sex may play important roles in the response of the developing brain to a traumatic injury. Advancements in acute neurosurgical interventions and neurocritical care have improved and led to a decrease in mortality rates over the past decades. However, survivors are left with life-long behavioral deficits underscoring the need to better define the cellular mechanisms underlying these functional changes. A better understanding of these mechanisms some of which begin in the acute post-traumatic period may likely lead to targeted treatment strategies. Key considerations in designing pre-clinical experiments to test therapeutic strategies in pediatric TBI include the use of age-appropriate and pathologically-relevant models, functional outcomes that are tested as animals age into adolescence and beyond, sex as a biological variable and the recognition that doses and dosing strategies that have been demonstrated to be effective in animal models of adult TBI may not be effective in the developing brain.

Copyright © 2018. Published by Elsevier Ltd.

Language: en

Keywords

Traumatic brain injury; cognition; erythropoietin; neonate; neurodegenerationaxonal injury; plasticity; progesterone