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A beta-zone crescent or halo is present in the majority of eyes with glaucoma, but in a minority of other eyes. In glau - comatous eyes, the meridian of a betazone corresponds to the location of cupping and field loss. Teng et al. (579) now confirm that progression is more likely and faster in glaucomatous eyes with a beta zone. The size of the beta zone seems of much less importance than its presence. The anatomy of beta zones and their origins are beyond the data presented, but deserve attention because of unexpressed implications. Parapapillary atrophy (PPA) is a typical designation for zone beta, but 'atrophy' implies acquired loss of retinal pigment epithelium (RPE). There are certainly eyes in which the various layers fail to become aligned during development, so that as a congenital variant, RPE does not define the disc edge. Moreover, in growing eyes that develop high myopia, the retinal edge may be retracted from the disc as the sclera enlarges, but without cellular atrophy. The scleral border tissue, being white, is often included in the area termed PPA or beta-zone, but is a normal anatomic structure.
Could parapapillary zone beta be a causative risk factor, and not be a result of glaucomatous pathogenic processes in the region of the optic disc?
True atrophy has been observed somewhat infrequently as enlargement of zone beta in glaucomatous eyes, and less frequently simply with age. Thus true atrophy does occur, but does not account for all instances of zone beta, and I suspect accounts for only a few. Why make the distinction? 'Atrophy' subconsciously implies that it may result from the same injurious events that cause cupping. Recognition that a zone of absent RPE may be a prior anatomic variant suggests that something about the innate anatomic misalignment produces susceptibility to develop glaucoma and to progression. Zone beta may not be a result of glaucomatous pathogenic processes in the region of the optic disc, but a causative risk factor.