Reynolds JN1, Paolozza A1, Treit S2, Beaulieu C2
1Centre for Neuroscience Studies, Queen’s University, Kingston, Canada
2Centre for Neuroscience, University of Alberta, Edmonton, Canada
The ability to suppress irrelevant impulses to enable goal-directed behavior is critically important for adaptive functioning. Response inhibition deficits are prevalent in children with Fetal Alcohol Spectrum Disorder (FASD), but the underlying neural mechanisms are not clearly understood. The goal of this study was to investigate the relationship between response inhibition during the performance of saccadic eye movement tasks and white matter connectivity in the corpus callosum in children with or without FASD. Participants included 43 children with an FASD diagnosis (12.3 ± 3.1 years old) and 35 typically developing children (12.5 ±3.0 years old) aged 7–18 years, assessed at three sites across Canada. Response inhibition was measured by direction errors in an antisaccade task and timing errors in a delayed memory-guided saccade task. Diffusion tensor imaging (DTI) and manual deterministic tractography were used to delineate six regions of the corpus callosum and calculate fractional anisotropy (FA), mean diffusivity (MD), parallel diffusivity, and perpendicular diffusivity. Group differences in saccade measures were assessed using t-tests, followed by partial correlations between eye movement inhibition scores and corpus callosum FA and MD, controlling for age. Children with FASD made more saccade direction errors and more timing errors, which indicates a deficit in response inhibition. The only group difference in DTI metrics was significantly higher MD of the splenium in the FASD group compared to controls. Direction errors in the antisaccade task were correlated negatively to FA and positively to MD of the splenium in the control group. In contrast, these relationships were not found for the FASD group, which suggests that alterations in connectivity between the two hemispheres of the brain may contribute to inhibition deficits in children with FASD.