July 2013
Volume 13, Issue 9
Free
Vision Sciences Society Annual Meeting Abstract  |   July 2013
Retinotopy of the cortical lesion projection zone in macular degeneration
Author Affiliations
  • Koen V. Haak
    Department of Psychology, University of Minnesota\nLaboratory for Experimental Ophthalmology, University Medical Center Groningen, University of Groningen
  • Antony B. Morland
    York Neuroimaging Centre, Department of Psychology, University of York\nCentre for Neuroscience, Hull-York Medical School, University of York
  • Frans W. Cornelissen
    Laboratory for Experimental Ophthalmology, University Medical Center Groningen, University of Groningen
Journal of Vision July 2013, Vol.13, 606. doi:10.1167/13.9.606
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      Koen V. Haak, Antony B. Morland, Frans W. Cornelissen; Retinotopy of the cortical lesion projection zone in macular degeneration. Journal of Vision 2013;13(9):606. doi: 10.1167/13.9.606.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Macular degeneration (MD) causes lesions to the center of the retina. There is no cure for MD but several promising treatments aimed at restoring retinal lesions are under investigation. These restorative treatments, however, rely on the assumption that the patient's brain can still process the retinal signals once they are restored. Whether this assumption is correct has yet to be determined. In previous work, we already established that the early visual cortex in MD does not reallocate its resources to processing the intact peripheral visual field (Baseler et al. 2011, Nature Neuroscience 14: 649-655), but it is still possible that long-term visual deprivation leads to visual cortical degeneration (Boucard et al. 2009, Brain 132: 1898-1906). Here, we used functional magnetic resonance imaging (fMRI) and a new fMRI data-analysis tool – connective field modeling (Haak et al. 2012, NeuroImage 66: 376-384) – to evaluate the retinotopic organization of the cortical lesion projection zone (LPZ) in 8 MD patients and 12 age-matched controls with simulated retinal lesions. We found that the functional connectivity between the sensory-deprived parts of visual areas V1 and V2 is still retinotopically organized in the patients with MD, although less so than in the controls with simulated retinal lesions. Moreover, the decreased retinotopic functional connectivity in MD correlated strongly with fixation instability, and not with the size of the retinal lesion, suggesting that the difference between MD patients and controls is mainly an artifact of poor fixation. Thus, it appears that the retinotopic configuration of the LPZ remains largely intact, despite the prolonged loss of visual input due to MD. These results are reassuring, because they suggest that the restoration of sight in MD can probably rely on the visual cortex maintaining a largely unchanged mapping of the visual field.

Meeting abstract presented at VSS 2013

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