Reduced visual acuity disrupts fixational stability but fails to fully capture amblyopic eye movements.

Abstract

Purpose: Amblyopia is a neurodevelopmental disorder characterized by diminished visual acuity (VA) and aberrant fixational eye movements (FEMs), affecting both the amblyopic and fellow eyes. While previous studies have established a strong correlation between impaired VA and increased fixational instability (FI), whether this reflects a causal relationship-or a shared downstream consequence of cortical dysfunction-remains unclear. We sought to determine whether reduced VA alone is sufficient to alter FEMs in the absence of developmental abnormalities.

Methods: To investigate whether reduced VA alone is sufficient to alter FEMs, we induced retinal defocus using convex lenses in neurotypical individuals (n = 5) and compared their FEM characteristics-microsaccade amplitude, latency, drift magnitude, and FI-with those of individuals with amblyopia (n = 7), under both monocular (nondominant eye only) and binocular viewing conditions. In addition to a control (0.0 logMAR), defocus was introduced using convex lenses to simulate interocular VA differences of 0.2, 0.4, 0.6, and 0.8 logMAR in both viewing conditions resulting in a total of 10 conditions.

Results: Retinal defocus in neurotypical observers increased drift magnitude and FI during monocular viewing, partially reproducing amblyopic oculomotor behavior. However, microsaccade amplitude and latency remained unchanged across all defocus levels. No significant effects of defocus were observed during binocular viewing.

Conclusions: Reduced VA is sufficient to increase FI but does not reproduce the broader oculomotor abnormalities characteristic of amblyopia. These data suggest that FI in amblyopia arises from additional neurodevelopmental mechanisms beyond visual cortex, likely involving higher-order visuomotor circuits.