The analysis in this study is based on SD-OCT imaging and is compared with previous TD-OCT studies, expanding on those findings. Some of our findings support many of those in previously published articles,2,21,22 including the persisting retinal layers across the fovea, although using SD-OCT allows better determination of which layers actually persist and affect overall image quality. Seo et al4 describe the characteristic TD-OCT findings of albinism as hyporeflectivity of the fovea, lack of foveal depression (which we also noted), and increased reflectivity from the choroidal layer. The hyporeflectivity of the photoreceptor layer of the fovea may have been due to limited image quality from the TD system or from the hyperreflectivity of the nerve fiber layer across the fovea. We did not find a difference in photoreceptor reflectivity in the subjects with OA or suspected OA or the subject with OCA and HPS. Seo and colleagues also describe a “tram track sign” caused by increased transillumination of the choroidal layer and increased reflectivity of the choroidal space. This was not seen in our study. We found increased visualization of the choroidal vessels and sclera in subjects with OA or suspected OA and the subject with OCA and HPS, with hyporeflectivity of the large choroidal vessels contrasting with the prominent hyperreflectivity of the underlying sclera. Reflectivity of a tissue layer on SD-OCT is a function of both the reflectivity of the structure and the shadowing or loss of signal from reflectivity of overlying structures. The absence of pigment in the retinal pigment epithelium and choroid in the subjects with OA or suspected OA and the subject with OCA and HPS results in a pronounced increase in signal (pertinent at the 830-nm central wavelength) extending into the choroid and sclera. Because of increased depth of scanning with this system compared with the TD system, what appeared as a tram track in the previous study is clearly hyperreflectivity from the retinal pigment epithelium on one side and the sclera beneath the hyporeflective choroidal vessels. In their observational case report of a 10-year-old girl with OCA who was imaged using OCT, Meyer et al23,24 also showed a lack of foveal depression. They reported increased foveal thickness greater than 300 μm in their patient with OCA compared with a 150-μm-thick fovea in a control eye. They speculated that the fovea was filled with hyperreflective tissue, possibly including multiple ganglion cell layers. In our study, we believe that the increased foveal thickness in subjects with OA or suspected OA and the subject with OCA and HPS is due to the persisting nerve fiber layer, ganglion cell layer, inner plexiform layer, inner nuclear layer, and outer plexiform layer. In their observational case report of a 79-year-old man with foveal hypoplasia who was imaged using OCT, McGuire et al21 confirm some of our findings as they also found continuation of the outer nuclear layer, inner nuclear layer, and ganglion cell layer across the fovea. However, they describe a prominent photoreceptor layer centrally. In contrast, we found that the photoreceptor layer showed mild loss of thickness in SD-OCT scans across the abnormal site of the fovea in the subjects with OA or suspected OA and in the subject with OCA and HPS when compared with the normal thickening of the photoreceptor layer in the fovea of control eyes.