Amblyopic deficits in monocular processing and binocular interactions revealed by submillimeter 7T fMRI and EEG frequency tagging

Abstract

Disruption of retinal input early in life can lead to amblyopia, a condition characterized by reduced visual acuity despite corrected optics. Although extensive losses of neural activity have been found in the early visual cortex, it remains unclear whether they reflect deficits in feedforward or feedback processing, or abnormal binocular interactions. Combining submillimeter 7T fMRI and EEG frequency tagging, our study revealed the precise neural deficits in monocular processing and binocular interactions in human adults with unilateral amblyopia. Cortical depth-dependent fMRI revealed monocular response deficits in cortical layers of the primary visual cortex (V1) receiving thalamic input, which carried over to the downstream areas (V2-V4) in feedforward processing. Binocular stimulation produced a greater signal loss in the superficial layers of V1, consistent with suppression from the fellow eye by lateral inhibition. EEG data further demonstrate reduced suppression from the amblyopic eye, weakened binocular integration, and delayed monocular and binocular processing. Our results support attenuated and delayed monocular processing in V1 layers receiving thalamic input in human amblyopia, followed by imbalanced binocular suppression and weakened binocular integration in the superficial layers, further reducing signal strength and processing speed. These precise neural deficits can help developing more targeted and effective treatments for the vision disorder.