Citation

Zhao S, Wang X, Gao X, Chen J. Sci. Rep. 2018; 8(1): e7339.

Affiliation

Spinal Cord and Brain Injury Research Group, Stark Neuroscience Research Institute, Department of Neurosurgery, Indiana University, 320W 15th street, Indianapolis, IN, 46202, United States. chen204@iupui.edu.

Copyright

(Copyright © 2018, Nature Publishing Group)

DOI

10.1038/s41598-018-25475-9

PMID

29743575

Abstract

Symptoms are commonly more severe in pediatric traumatic brain injury (TBI) patients than in young adult TBI patients. To understand the mechanism, juvenile mice received a controlled cortical impact (CCI) injury at moderate level. Tissue lesion and cell death were measured and compared to our previous reports on brain injury in the young adult mice that received same level of impact using same injury device. Tissue lesion and cell death in the cortex was much less in the juvenile mouse brain in the first few hours after injury. However, once the injury occurred, it developed more rapidly, lasted much longer, and eventually led to exaggerated cell death and a 32.7% larger tissue lesion cavity in the cortex of juvenile mouse brain than of young adult mouse brain. Moreover, we found significant cell death in the thalamus of juvenile brains at 72 h, which was not commonly seen in the young adult mice. In summary, cell death in juvenile mice was delayed, lasted longer, and finally resulted in more severe brain injury than in the young adult mice. The results suggest that pediatric TBI patients may have a longer therapeutic window, but they also need longer intensive clinical care after injury.

Language: en