Abstract
Monovision is an optical correction for presbyopes that consists of correcting one eye for far distance and the other for near distance, creating a superimposition of an in-focus with a blurred image. Brain adaptation to monovision was studied in unexperienced observers by measuring visual evoked potentials from 64-channels. The first clear effect of monovision on visual evoked potentials was the C1 amplitude reduction, indicating that the unilateral blurring induced by monovision reduces feed-forward activity in primary visual area. Monovision led also to an increased amplitude of the P1 and pP1 components, with the latter originating in prefrontal regions. This effect probably works as an attentional compensatory activity used to compensate for the degraded V1 signal. A common and often successful option to correct presbyopia with contact lenses is monovision. This is an unbalanced correction across the two eyes where one eye is corrected for far vision and the other eye is corrected for near vision. Monovision is therefore a form of acquired anisometropia that causes a superimposition of an in-focus image with a blurred image. In spite of this visual anisometropia, monovision has been successfully used for many decadesl however the brain mechanism supporting monovision is not well understood. The present study aimed to measure the visual evoked potentials with a high-density electrode array (64-channel) in a group of presbyopes and to provide a detailed spatiotemporal analysis of the cortical activity after a short period of adaptation to monovision with contact lenses. When compared with a balanced eye near correction, monovision produced both a clear reduction of the earliest visual evoked potential components, the C1 and the N1, and an amplitude increase of the P1 and pP1. These results indicate that the unilateral blurring induced by wearing monovision contact lenses reduces feed-forward activity in the primary visual area and feedback activity in extrastriate areas (C1 and N1 reduction). Interestingly, other brain activities in both extrastriate visual areas (the P1 component) and in the anterior insula (the pP1 component) appear to compensate for this dysfunction, increasing their activity during monovision. These changes confirm the presence of fluid brain adaptation in visual and non-visual areas during monocular interferences.
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