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Katherine Boudreault, Leonard Levin; Anatomical Locus of Spatial Summation within the Retina and Neuroretinal Disease. Invest. Ophthalmol. Vis. Sci. 2013;54(15):5116.
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When the size of a stimulus on the retina is increased but the sensitivity to light per unit area is not proportionately decreased, incomplete spatial summation is manifested. This can be described by the equation: Ak x L = C, where A is the target area, L is the threshold of luminance, C a constant, and k is the coefficient of summation. The goal of this study was to use the topological variation in the coefficient of summation k in the visual field across disease states from different pathology to give insight into the neural substrate for spatial summation
1Thirteen normal subjects, 14 subjects with optic nerve disease, and 12 subjects with retinal diseases performed Humphrey full-threshold automated visual field tests (Goldmann sizes I and V). The log of the target stimulus area on the retina (log A) was plotted against the log of the differential light sensitivity (DLS) in dB converted to decalamberts (log L), for each locus. Least squares regression was used to calculate the slope of the best-fit line, resulting in the coefficient of summation k. The coefficients of summation calculated from locus with deficit were compared
The mean coefficient of summation k for the 13 normal subjects ranged from 0.4 at the fovea to 0.8 at 27 degrees of eccentricity, similar to that described in previous studies. Spatial summation was more complete (closer to 1) as the visual deficit became greater, and this was true for both retinal and retinal ganglion cell disease. There was nearly identical patterns of coefficients of summation k calculated at equivalent deficits of the visual field for subjects with retinal ganglion cell disease and subjects with retinal disease.
Spatial summation is more complete when a visual field deficit is present, with greater spatial summation with greater deficits. The association of more complete spatial summation with visual field deficits was independent of the locus of damage (retina vs. optic nerve) or the etiology of visual loss. These results suggest that the anatomical substrate for spatial formation is unlikely to be solely at the retinal ganglion cell.
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