• Nicholas P Ryan, Cathy Catroppa, Celia Godfrey, Linda J Noble-Haeusslein, Sandy R Shultz, Terence J O'Brien, Vicki Anderson, and Bridgette D Semple.
• Australian Centre for Child Neuropsychological Studies, Murdoch Childrens Research Institute, Parkville, VIC, Australia; Melbourne School of Psychological Sciences, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Parkville, VIC, Australia. Electronic address: nicholas.ryan@mcri.edu.au.
• Neurosci Biobehav Rev. 2016 May 1; 64: 196-214.

AbstractSocial dysfunction is common after traumatic brain injury (TBI), contributing to reduced quality of life for survivors. Factors which influence the development or persistence of social deficits after injury remain poorly understood, particularly in the context of ongoing brain maturation during childhood and adolescence. 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. Crown Copyright © 2016. Published by Elsevier Ltd. All rights reserved.

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