UC Davis

Fragile X syndrome (FXS) is a genetic disorder caused by a trinucleotide CGG expansion within the FMR1 gene located on the X chromosome. Children with FXS have been shown to be impaired in dynamic visual attention processing. A key component of dynamic processing is orienting-a perceptual ability that requires disengagement and engagement of attention from one stimulus to fixate on a second. Orienting, specifically the disengagement and engagement of attention, has previously not been studied in young children with FXS. Using an eye tracking gap-overlap task, the present study investigated visual disengagement and engagement in young children with FXS, compared to mental age (MA)- and chronological age (CA)-matched typically developing children. On gap trials, the central stimulus elicited fixation, but then disappeared before the peripheral target appeared, imposing a visual gap between stimuli. On overlap trials, the central stimulus elicited fixation, and remained present when the peripheral target appeared, creating visual competition. A gap effect emerges when latencies to shift to the peripheral target are longer in overlap versus gap conditions, reflecting the recruitment of cortical and subcortical disengagement and engagement mechanisms. The gap effect was measured as the latency to orient attention to the peripheral target during gap versus overlap conditions. Both MA and CA groups showed the expected gap effect, where children were slower to orient to peripheral targets on overlap trials than on gap trials. In contrast, in the FXS group, saccadic latencies between gap and overlap trials were not significantly different, indicating no significant gap effect. These findings suggest disrupted attentional engagement patterns in FXS that may be underlying impairments in attention orienting, and suggest potential targets for attention training in this population.