Martin Szinte¹, Uriel Lascombes¹, Adrien Chopin², Paul V. McGraw³, Denis Schluppeck^3,4; ¹Institut de Neurosciences de la Timone, CNRS, Aix-Marseille Université, Marseille, France, ²The Smith-Kettlewell Eye Research Institute, San Francisco, CA, United States, ³Visual Neuroscience Group, School of Psychology, University of Nottingham, Nottingham, United Kingdom, ⁴Sir Peter Mansfield Imaging Centre, University of Nottingham, Nottingham, United Kingdom

Amblyopia affects 3-5% of adults and is characterized by reduced visual acuity in one eye despite best optical correction and absence of any other overt ocular pathology. While visual deficits are well-documented in amblyopia, the cortical organization underlying these deficits remains debated. Previous measures of population receptive field (pRF) size and cortical magnification in primary visual cortex (V1) have been inconclusive, potentially due to differences in methodology and viewing conditions (monocular vs. binocular). Here, we substantially extend the analysis of a high-resolution 7T fMRI retinotopy dataset previously acquired (monocular stimulation) in participants with strabismic amblyopia (n=12) or no amblyopia (n=9). Our new analysis extends beyond V1 to multiple early and intermediate visual areas (V2, V3, V3AB, hMT+). We examined pRF parameters as a function of eccentricity and cortical area to probe potential reorganization at different levels of visual processing. We next applied surface-based geodesic distance methods to estimate cortical magnification across the visual hierarchy. While the original analysis of this dataset (Schluppeck et al., 2025, Vision Research) found largely preserved V1 organization, it did not explicitly test for alterations in higher visual areas or for changes that may be better captured by a more local cortical magnification measure. This work aims to clarify if and where such reorganization occurs, thereby shedding new light on the quality and extent of potential markers for cortical reorganization in amblyopia, informing ongoing debates about the neural mechanisms underlying amblyopic vision loss.