B25. The Effect of Traumatic Brain Injury on Superficial White Matter in Youth: Towards a Personalized Injury Profile.

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B21. Immunogenic analysis of a CaV2.1 calcium channel C-terminal synaptic vesicle binding site

H. K.-H. MAH, C. SNIDAL, R. H.-C. CHEN, Q. LI, E. F. STANLEY


B21. Immunogenic analysis of a CaV2.1 calcium channel C-terminal synaptic vesicle binding site

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Poster Session 1 - B25

1,2Sonja Stojanovski, 3,4Arash Nazeri, 5Christian Lepage, 6,7,8Aristotle Voineskos, 1,2Anne L Wheeler

1. Neuroscience and Mental Health Program, Hospital for Sick Children, Toronto, Ontario; 2. Department of Physiology, University of Toronto, Toronto, Ontario; 3. Iran/Mallinckrodt Institute of Radiology, Tehran, Iran; 4. Washington University School of Medicine, St. Louis, MO, USA; 5. Toronto Rehabilitation Institute, Toronto, Ontario; 6. Campbell Family Mental Health Institute, Centre for Addiction and Mental Health, Toronto, Ontario. 7. Institute of Medical Science, University of Toronto, Toronto, Ontario; 8. Department of Psychiatry, University of Toronto, Toronto, Ontario

Diffusion Tensor Imaging (DTI) studies of traumatic brain injury (TBI) have focused on alterations in micro-structural features of deep white matter fibers (DWM), though post-mortem studies have demonstrated that injured axons are often observed at the gray-white matter interface where superficial white matter fibers (SWM) mediate local connectivity. The objective of this study was to examine micro-structural alterations in SWM and DWM separately through group-wise comparisons of fractional anisotropy (FA) from DTI, and personalized injury profiles of FA abnormality in youth with: mild TBI (n=63), healthy controls (n=63), and controls with psychopathology symptoms matched to the TBI group (n=63). Group-wise comparisons were used to isolate spatially consistent group differences, while personalized injury profiles provided flexibility to capture spatially heterogeneous individual differences in FA which may result from varied causes of injury. All groups were matched on age, sex, and parental education. Permutation testing, revealed widespread decreases in FA in individuals with TBI compared to healthy controls in DWM and SWM as well as decreases in FA in individuals with TBI compared to their psychopathology matched controls in posterior DWM and SWM. Evaluations of personalized injury profiles revealed more regions with abnormal FA decreases in the DWM of participants with TBI compared to healthy, and psychopathology matched controls as well as more regions with FA decreases in the SWM of participants with TBI compared to healthy controls. Furthermore, in the TBI group, the number of regions in the SWM with increased FA was significantly negatively correlated with the number of internalizing symptoms that individual reported. This relationship was not present in either control groups and suggests a potential compensatory mechanism for SWM FA increases in individuals with history of TBI. These results demonstrate widespread differences in SWM related to mild TBI, a fibre type often overlooked in in vivo imaging in the context of TBI.