Diffusion tensor imaging correlates of saccadic reaction time in children with fetal alcohol spectrum disorder

Eye movement tasks provide a simple method for inferring structural or functional brain deficits in neurodevelopmental disorders. Oculomotor control is impaired in children with fetal alcohol spectrum disorder (FASD), yet the neuroanatomical substrates underlying this are not known. Regions of white matter have been shown by diffusion tensor imaging (DTI) to be different in FASD and thus may play a role in the delayed saccadic eye movements. The objective of this study was to correlate oculomotor performance with regional measures of DTI-derived white matter anisotropy in children with FASD.

Fourteen children (8 to 13 years) with FASD were recruited for oculomotor assessment and DTI. Eye movement control was evaluated using the pro- and antisaccade tasks, in which subjects look at (prosaccade) or away from (antisaccade) a peripheral target. Saccadic reaction time (SRT; time for subjects to move their eyes after the target appears) and direction errors (saccades made in the incorrect direction relative to the instruction) were measured and correlated to fractional anisotropy (FA) on a voxel-by-voxel basis across the whole brain white matter.

A significant positive correlation was observed between antisaccade SRT and FA in a large cluster containing anterior and posterior sections of the corpus callosum just to the right of the midline; prosaccade SRT and FA correlated positively in the genu of the corpus callosum and the right inferior longitudinal fasciculus (ILF), and correlated negatively in the left cerebellum.

The negative correlation for prosaccade SRT and cerebellum demonstrated that individuals with slower reaction times had lower FA values relative to their faster responding counterparts, a finding that implicates cerebellar dysfunction as a significant contributor to deficits in oculomotor control. The higher FA in the corpus callosum and ILF corresponding to longer reaction times for both pro- and antisaccade was opposite to what was expected, but nonetheless implies that altered brain structure in these regions underlies deficits in oculomotor control.