Congenital idiopathic nystagmus (sometimes known as infantile nystagmus) is a disorder characterised by involuntary eye movements, which leads to decreased acuity and visual function. One such function is visual crowding; a process whereby objects that are easily recognised in isolation become impaired by nearby flankers. Crowding typically occurs in the peripheral visual field, though elevations in foveal vision have been reported in congenital nystagmus, similar to those found with amblyopia (another developmental visual disorder). Here we examine whether the elevated foveal crowding with nystagmus is driven by similar mechanisms to those documented in amblyopia (long-term neural changes associated with a sensory deficit) or by the momentary displacement of the stimulus through nystagmus eye movements. We used a Landolt-C orientation identification task to measure threshold gap sizes with and without flanker Landolt-Cs that were either horizontally or vertically placed. Because nystagmus is predominantly horizontal, crowding should be stronger with horizontal flankers if eye movements cause the interference, whereas a sensory deficit should be equivalent for the two dimensions. Consistent with an origin in eye movements, we observe elevations in nystagmic crowding that are above that of typical vision, and stronger with horizontal than vertical flankers. This horizontal elongation was not found in either amblyopic or typical vision. We further demonstrate that the same pattern of performance can be obtained in typical vision with stimulus movement that simulates nystagmus. We consequently propose that the origin of nystagmic crowding lies in the eye movements, either through relocation of the stimulus into peripheral retina or image smear of the target and flanker elements.
bioRxiv Subject Collection: Neuroscience