We read with interest the research article by Zucchiatti and associates entitiled “Macular Ganglion Cell Complex and Retinal Nerve Fiber Layer Comparison in Different Stages of Age-Related Macular Degeneration.” This study demonstrated that mean central macular thickness showed a significant increase in the advanced age-related macular degeneration neovascular category (351.4 ± 103 μm) and a significant decrease in the atrophic category (183.9 ± 47 μm), compared with controls. Also, this study showed that thickness of ganglion cell complex was significantly reduced in both atrophic and neovascular age-related macular degeneration compared with healthy subjects.

Although their study provides useful information, some important things should be considered. Based on previous studies, spectral-domain optical coherence tomography measurements may misestimate retinal thickness in eyes affected by retinal diseases that invade the macula, resulting in algorithmic errors due to increased artifacts and deformation of the retinal structure in the presence of choroidal neovascularization, intraretinal cyst, exudates, or subretinal fluid. Also, inter-measurement variability and relatively low resolution of central foveal thickness measurements have been reported in cases of maculopathy. Moreover, the differences in repeatability and reproducibility may result from the inability of patients with retinal diseases to gaze into the beam of light.

In our previous study, we found that the repeatability of ganglion cell–inner plexiform layer thickness measurements was lower in the macular edema and atrophy groups than in the normal eye group. This difference may be explained by a failure of the autosegmentation algorithm to detect boundaries because of changes in macular thickness or distortion of the macular shape caused by retinal diseases. Moreover, we found that the ganglion cell–inner plexiform layer thickness of the edema group was thinner than the average ganglion cell–inner plexiform layer thickness of normal eyes and concluded that this may be attributable to erroneous segmentation of the ganglion cell–inner plexiform layer boundaries owing to changes in macular conditions, rather than actual thinning of the ganglion cell–inner plexiform layer.

Zucchiatti and associates concluded that patients with neovascular and atrophic age-related macular degeneration display reduced ganglion cell complex thickness and that changes of inner retina structure would explain the reason. However, they did not describe the possibility of autosegmentation errors caused by retinal disease–related macular distortion. Also, the information about the signal strength and difference of visual acuity in each group is missing.

We suggest the impact of changes in macular shape caused by various retinal diseases should be taken into consideration when analyzing ganglion cell–inner plexiform layer thickness with retinal diseases.