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J.S. Sunness, B.J. Rosenau, A.S. Greenberg, C.A. Applegate, S. Yantis; Retinotopic Mapping in Patients With Scotomas From Retinal Disease . Invest. Ophthalmol. Vis. Sci. 2005;46(13):4786.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To determine whether there is cortical remapping in the lesion projection zone (LPZ), the region of visual cortex corresponding to the position of the retinal lesion. Methods: We tested five patients with scotomas caused by retinitis pigmentosa (peripheral lesion, spared fovea), chorioretinal atrophy (nasal to the fovea and extending superior and inferior to the fovea in each eye), or age–related macular degeneration (one with eccentric fixation and no sparing of the fovea, one with a central scotoma with a tiny spared foveal area, and one with a thin annular scotoma). Scanning laser ophthalmoscope (SLO) perimetry was used to define the area of dense scotoma and the site and stability of fixation. Subjects met criteria for participation if their scotomas included retina within the central 25.6 degrees of vision and if they could maintain stable fixation. Functional magnetic resonance imaging (fMRI) of visual cortex was performed while patients viewed sequences of five logarithmically scaled annular rings consisting of contrast reversing radial checks that tiled the visual field from 1.5 to 12.8 degrees eccentricity. During scanning, one ring at a time was displayed in 16 second epochs, interspersed with fixation–only epochs. FMRI data from all epochs of each ring were contrasted with data from fixation epochs, separately for each patient. Functional maps from each contrast were projected onto a cortical surface representation. Results: In regions of cortex outside each subject’s LPZ, retinotopic mapping yielded patterns of activation similar to those found in normal subjects: a progressive change of the location of cortical activation evoked by the rings as they stimulated adjacent areas of retina. In the LPZ, four patients failed to exhibit retinotopic activation. In one patient, whose scotoma was in the shape of a thin ring, all stimulus rings that overlaid the scotoma also overlaid areas of intact retina. This prevented a clear demarcation of the LPZ for this thin scotoma. Conclusions: In areas of cortex innervated by intact retina, we observed retinotopically organized cortical activation. Retinotopic activation was absent in the LPZ in four of five patients. If remapping had occurred, activity should have been observed in the LPZ during stimulation of good retina outside the lesion. These results suggest that little significant cortical remapping has occurred in these patients, whose lesions have been present for several years in each case.
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