Citation

Ryan NP, Catroppa C, Godfrey C, Noble-Haeusslein LJ, Shultz SR, O'Brien TJ, Anderson V, Semple BD. Neurosci. Biobehav. Rev. 2016; 64: 196-214.

Affiliation

Department of Medicine (Royal Melbourne Hospital), The University of Melbourne, Parkville, VIC, Australia. Electronic address: Bridgette.Semple@unimelb.edu.au.

Copyright

(Copyright © 2016, Elsevier Publishing)

DOI

10.1016/j.neubiorev.2016.02.020

PMID

26949224

Abstract

Social dysfunction is common after traumatic brain injury (TBI), contributing to reduced quality of life for survivors. Factors which influence the emergence, development or persistence of social deficits after injury remain poorly understood, particularly in the context of ongoing brain maturation during childhood. Aberrant social interactions have recently been modeled in adult and juvenile rodents after experimental TBI, providing an opportunity to gain new insights into the underlying neurobiology of these behaviors. Here, we review our current understanding of social dysfunction in both humans and rodent models of TBI, with a focus on brain injuries acquired during early development. Modulators of social outcomes are discussed, including injury-related and environmental risk and resilience factors. Disruption of social brain network connectivity and aberrant neuroendocrine function are identified as potential mechanisms of social impairments after pediatric TBI. Throughout, we highlight the overlap and disparities between outcome measures and findings from clinical and experimental approaches, and explore the translational potential of future research to prevent or ameliorate social dysfunction after childhood TBI.

Copyright © 2016. Published by Elsevier Ltd.

Language: en