Time-domain OCT studies have shown nonspecific hyperreflectivity in the outer retinal layers.1- 3 Clouding of the RPE cell cytoplasm and/or an increase in cellularity due to inflammation have been proposed as the underlying cause. Anterior displacement of the neuroretina and outer reflective band have been observed and are proposed to be due to choroiditis.4 However, details of the actual layers within the outer retina are limited by the resolution of time-domain OCT (10 μm). One study using a research tool, ultra–high-resolution OCT (3-μm resolution), described outer nuclear layer backscattering during the acute phase followed by photoreceptor atrophy.5 We report here changes in the acute and resolved phases of APMPPE studied with commercially available SD-OCT (5-μm resolution), clearly showing photoreceptor layer disruption during the acute phase. While APMPPE often has a relatively benign prognosis, a recent series found incomplete visual recovery in a large proportion of patients.6 In our patient, despite visual acuity returning to 20/20, SD-OCT clearly showed photoreceptor atrophy and lack of reconstitution of the 2 hyperreflective bands representing the inner and outer segment junction and the Verhoeff membrane. While the border between affected and unaffected areas appeared well demarcated during the acute phase, pigmentary and atrophic changes seen in the resolved phases were much more diffuse on both funduscopy and SD-OCT. In particular, disruption of the hyperreflective bands representing the inner and outer segment junction and the Verhoeff membrane was seen in areas that initially appeared normal tomographically during the acute phase (Figure 2B and C). We hypothesize that in addition to the inflammatory component, secondary progressive degenerative changes of the photoreceptor and RPE may play a role in tissue destruction, resulting in the commonly recognized pigmentary changes in resolved APMPPE.