Authors
Alessia Sepe, Matteo Panormita, Mark A G Eldridge, David A Leopold, Luca Bonini, Wim Vanduffel, Marco Tamietto
Published in
Cerebral cortex (New York, N.Y. : 1991). Volume 36. Issue 9. Sep 01, 2026.
Abstract
Damage to the primary visual cortex (V1) causes field defects in conscious vision, yet stimuli in the affected field may still guide saccades and other visuomotor responses ("blindsight"). Chronic blindsight is well documented, but early postlesional saccade profiles to scotoma stimuli remain poorly characterized. We mapped visuomotor functions in two macaques 3 to 4 weeks after a unilateral V1 lesion using a perimetry-like saccade assay up to 35° eccentricity, with analyses of saccade direction and catch-trial baselines. Targets had either unpredictable onset, as in clinical perimetry, or temporally cued onset. With unpredictable onsets, monkeys typically failed to initiate movements toward the affected hemifield, and correct saccades to scotoma targets were rare. Temporal cueing increased saccade initiation toward contralesional targets, including positions meeting conventional criteria for blindness, primarily as delayed saccades with initial misdirection or multistep trajectories. A scotoma-related spatial bias, largely independent of the target, was evident in catch-trial and misdirected saccades, whereas a minority of delayed ("out-of-time") saccades reached toward the target location without meeting the temporal criterion. Fine-grained saccade phenotyping may offer a sensitive marker of residual visuomotor processing after V1 damage in monkeys and, potentially, humans.
PMID:
42831685
Bibliographic data and abstract were imported from PubMed on 05 Oct 2026.
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