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Peer-reviewedCC BYCerebral Cortex

Early postlesional visuomotor capacity after V1 damage in the macaque

  • Alessia Sepe1,2,3
  • Matteo Panormita2,4,3
  • Mark A. G. Eldridge5,6
  • David A. Leopold7,6
  • Luca Bonini1
  • Wim Vanduffel8,2,9,3
  • Marco Tamietto10,4,11
11 affiliations
  1. 1Department of Medicine and Surgery, Neuroscience Unit, University of Parma ,
  2. 2Department of Neurosciences, Laboratory of Neuro- and Psychophysiology, KU Leuven Medical School ,
  3. 3Leuven Brain Institute, KU Leuven ,
  4. 4Department of Psychology and Neuroscience Institute of Turin (NIT), University of Torino ,
  5. 5Biosciences Institute, Newcastle University , Framlington Place, Newcastle upon Tyne, NE2 4HH ,
  6. 6Section on Cognitive Neurophysiology and Imaging, National Institute of Mental Health , 9000 Rockville Pike, Bethesda, MD 20892 ,
  7. 7Neurophysiology Imaging Facility, National Institute of Mental Health, National Institute of Neurological Disorders and Stroke, National Eye Institute , 9000 Rockville Pike, Bethesda, MD 20892,
  8. 8Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital ,
  9. 9Department of Radiology, Harvard Medical School , Boston, 25 Shattuck Street, Boston, MA 02144,
  10. 10Department of Medical and Clinical Psychology, Tilburg University ,
  11. 11Italian Academy for Advanced Studies in America, Columbia University , New York, 1161 Amsterdam Avenue, New York, NY 10027,
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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.

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Cite

BibTeXRIS
BibTeX
@article{sepe2026early,
  title = {{Early postlesional visuomotor capacity after V1 damage in the macaque}},
  author = {Alessia Sepe and Matteo Panormita and Mark A. G. Eldridge and David A. Leopold and Luca Bonini and Wim Vanduffel and Marco Tamietto},
  journal = {Cerebral Cortex},
  year = {2026},
  month = aug,
  doi = {10.1093/cercor/bhag138},
  url = {https://doi.org/10.1093/cercor/bhag138},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Early postlesional visuomotor capacity after V1 damage in the macaque
AU  - Alessia Sepe
AU  - Matteo Panormita
AU  - Mark A. G. Eldridge
AU  - David A. Leopold
AU  - Luca Bonini
AU  - Wim Vanduffel
AU  - Marco Tamietto
PY  - 2026
DA  - 2026/08/21
JO  - Cerebral Cortex
DO  - 10.1093/cercor/bhag138
UR  - https://doi.org/10.1093/cercor/bhag138
AB  - 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.
SN  - 1047-3211
SN  - 1460-2199
ER  -