We read with great interest the article titled “Relationship Between Juxtapapillary Choroidal Volume and Beta-Zone Parapapillary Atrophy in Eyes With and Without Primary Open-Angle Glaucoma” by Sullivan-Mee and associates. The authors evaluated peripapillary choroidal thickness and beta zone peripapillary atrophy in glaucoma patients and normal subjects. They found decreased choroidal thickness that associate with peripapillary atrophy in primary open-angle glaucoma. We congratulate the authors for this well-organized study and want to make some contributions.

Intraocular pressure (IOP) is in accordance with ocular tissues. Elevated IOP or hypotony causes some changes in these tissues. One of the ocular structures that is affected by IOP is the sclera. For example, in congenital glaucoma, elevated IOP causes thinning of the sclera and development of high myopia by increase of axial length. Elongation of the posterior side of the eyeball provides a bigger area for the choroid to distribute, which results in choroidal thinning. Peripapillary atrophy in high myopia also develops as a result of this elongation. So, it is evident that the cause of changes in congenital glaucoma is impairment of balance between IOP and the sclera. While congenital glaucoma is a catastrophic situation that causes acute changes and primary open-angle glaucoma (POAG) is a chronic disease that causes long-lasting changes, the underlying mechanism for scleral and choroidal changes in both situations seems to be the relationship between IOP and the sclera.

The existence of the choroid may also have a role in the balance between IOP and the sclera. The choroid contains higher blood flow in the body and seems like a sponge anterior to the sclera that may absorb and distribute the power of IOP. The choroid is absent in the optic disc. The cause of optic disc cupping and peripapillary atrophy may be absence of choroid in this area. Elevated IOP may push the sclera to posterior, which may result in peripapillary atrophy and choroidal thinning.