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Stuart L. Graham, Anina N. Rich, Alexander Klistorner, Mark A. Williams; Functional MRI Reveals Activation Of Visual Cortex By Adjacent Stimuli In Glaucomatous Scotoma Regions - Perceptual Fill-in?. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1647.
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© ARVO (1962-2015); The Authors (2016-present)
Glaucoma patients are rarely aware of their scotomas and "fill-in" the defects. A detailed fMRI protocol was used to examine the response of the deprived cortex to stimuli adjacent to and within the scotoma area.
fMRI testing was performed on 7 glaucoma subjects with small unilateral reproducible focal scotomas close to fixation (Humphrey 24-2 and 10-2 SITA), and 12 normal controls. The scotomas had to include multiple >5 points of absolute loss (dB<0). Subjects were tested monocularly (other eye patched) with 16 sec blocks of retinotopic mapping stimuli (radially oriented alternating black and white checkerboards), placed within the scotoma, at the edges of the scotoma, and across the scotoma. The protocol included 2 runs each eye (6 blocks x 8 repetitions); scotoma run (4 different blocks: within scotoma, foveal region x 2 locations; x 8 repetitions) plus a high-resolution structural scan (MPRAGE). Total protocol ~50mins. We used within-eye controls of diagonally opposing stimuli. Data were collected on a 3T Phillips MRI scanner with axial slices, a TR of 2 secs, 1.4 x 1.4mm in plane resolution, slice thickness of 2mm (+20% gap). Contrasts of the BOLD signal across blocks were all corrected using FWE = .05.
5/7 glaucoma subjects provided high quality data throughout the extended protocol; 2 subjects' data were discarded due to movement artifacts in later sequences. Stimulating the scotoma region resulted in less activation than in the analogous location in the good eye, as previously reported. However, presenting stimuli from the fovea to the edge of the scotoma resulted in significantly greater activation in the cortex representing the damaged eye than in the good eye (p < .05 FWE corrected). Additionally, when the stimulus extended throughout the scotoma region, the cortex from the affected eye also showed greater activation (p < .05).
Visual cortex that loses normal input due to glaucoma is secondarily activated possibly by lateral connections, and appears to ‘extrapolate’ from information presented either side of the scotoma. This may be the neural correlate of the perceptual ‘filling in’. It also allows for the possibility of recruiting this area for vision, despite reports of V1 degeneration in longstanding glaucoma, although the nature and usefulness of the signals generated is yet unknown.
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