Recently, there has been increased interest regarding when macular visual function is compromised in glaucoma that has resulted in reevaluation of the dogma that glaucoma is a disease of the peripheral visual field until quite late in its course. In this article, Hood et al. test a model of glaucomatous macular (central 8° radius) visual field damage. Their proposition is that the macular representation of the visual field is comprised of a less vulnerable macular region (LVMR), predominantly in the inferior visual field but also including a small part of the cecocentral superior visual field, and a vulnerable macular region (VMR) within the superior visual field. This uneven vulnerability of the central visual field is due to the relative vertical offset of the fovea and optic nerve head (ONH) in the retina and the fact that axons from retinal ganglion cells (RGCs) responsible for the superior macular visual field (in the inferior retina) enter the ONH predominantly in its relatively more susceptible inferior quadrant. Axons from RGCs that are responsible for the LVMR in the inferior macular visual field (in the superior retina) enter the ONH predominantly in its relatively less susceptible temporal quadrant.
In addition, the authors set out to determine if individualizing visual field assessment for each eye, based on its relative positioning of fovea and ONH, improved performance over an analysis that treated all eyes the same. Finally, Hood et al. examined the impact of adding two additional test locations to the commonly used 24-2 visual field pattern on the ability to detect visual field abnormalities in 31 eyes selected because they had scotoma affecting the superior macular region.
Results were fairly decisive. In eyes that were selected because they displayed localized damage to the superior macula visual field, damaged locations were significantly more likely to be in the VMR. Between 35 and 77% of visual field locations in the VMR were damaged, depending on the criterion used, compared to between three and 35% of LVMR locations being damaged when using the same criteria. However, there seemed to be little benefit (i.e., increasing the number of VMR locations showing damage while decreasing the number of LVMR locations showing damage) when visual field analysis was individualized, except perhaps in eyes that displayed the most extreme anatomy. Perhaps the result that had the most immediate clinical applicability was the finding that adding two locations to the 24-2 visual field pattern greatly increased the number of VMR region abnormalities that were detected. The authors suggest that this kind of hybrid test pattern could put us on a path to detecting macular visual field defects without the need to perform both a 24-2 and a 10-2 test. However, the search for best placement of additional test locations was not exhaustive, as only locations that were part of the 10-2 pattern were considered. Therefore, the optimal placement for additional test locations in a hybrid visual field test remains to be determined. Still, the prospect of extracting almost as much information from a hybrid visual field pattern as from the 24-2 and 10-2 tests in combination should be exciting to patients, technicians and physicians alike.