Eye movements elevate crowding in idiopathic infantile nystagmus syndrome

Abstract

Idiopathic infantile nystagmus syndrome is a disorder characterised by involuntary eye movements, whichleads to decreased acuity and visual function. One suchfunction is visual crowding – a process whereby objectsthat are easily recognised in isolation become impairedby nearby flankers. Crowding typically occurs in theperipheral visual field, although elevations in fovealvision have been reported in congenital nystagmus,similar to those found with amblyopia. Here, weexamine whether elevated foveal crowding withnystagmus is driven by similar mechanisms to those ofamblyopia – long-term neural changes associated with asensory deficit – or by the momentary displacement ofthe stimulus through nystagmus eye movements. ALandolt-C orientation identification task was used tomeasure threshold gap sizes with and without either horizontally or vertically placed Landolt-C flankers.Weassume that a sensory deficit should give equivalentcrowding in these two dimensions, whereas an origin ineye movements should give stronger crowding withhorizontal flankers given the predominantly horizontaleye movements of nystagmus.We observe elevations innystagmic crowding that are above crowding in typicalvision but below that of amblyopia. Consistent with anorigin in eye movements, elevations were stronger withhorizontal than vertical flankers in nystagmus, but not intypical or amblyopic vision.We further demonstrate thesame horizontal elongation in typical vision withstimulus movement that simulates nystagmus.Consequently, we propose that the origin of nystagmiccrowding lies in the eye movements, either throughimage smear of the target and flanker elements or through relocation of the stimulus into the peripheralretina