LAUSR

BACKGROUND Pediatric traumatic brain injury (TBI) can lead to adverse emotional, social and behavioral consequences. However, post-TBI outcome is difficult to predict due to significant individual variability, likely reflecting a complex interaction between injury- and child-related variables. Among these variables are genetically determined individual differences, which can modulate TBI outcome through their influence on neuroplasticity mechanisms. In this study, we examined the effect of Val66Met, a common polymorphism of the BDNF gene known to be involved in neuroplasticity mechanisms, on behavioral symptoms of mild TBI sustained in early childhood. METHODS This work is part of a prospective, longitudinal cohort study of early TBI. The current sample consisted of 145 children, aged between 18 and 60 months, assigned to one of three participant groups: mild TBI, orthopedic injury and typically developing children. Participants provided a saliva sample to detect the presence of the Val66Met polymorphism, and the Child Behavior Checklist was used to document the presence of behavioral symptoms at 6- and 18-months post-injury. RESULTS Contrary to our initial hypothesis, at 6-months post-injury, non-carriers of the Val66Met polymorphism in the mTBI group presented significantly more internalizing symptoms (e.g., anxiety/depression and somatic complaints) than Val66Met carriers, which were similar to orthopedically injured and typically developing children. However, at 18 months post-injury, all children with mTBI presented more internalizing symptoms, independent of genotype. CONCLUSION The results of the study provide evidence for a protective effect of the Val66Met polymorphism on internalizing behavior symptoms six months after preschool mTBI.