We thank Taneja and Mathai for their interest in our article. Their letter, however, suggests that they have not fully appreciated important concepts relevant to our article and to the associated literature. They state that “[e]xperimental and histopathological studies have shown irreversible photoreceptor loss (apoptosis), photoreceptor misalignment, neural retinal remodeling, and subretinal pathological abnormalities such as retinal pigment epithelium multilayering to be responsible for poor visual acuity” and cite a reference from Cook et al1 to support this. Although these morphological changes have been demonstrated in experimental systems, no functional correlates exist as yet. Indeed, in a joint article with Lewis et al,2 we previously reviewed the pathological abnormalities seen in experimental retinal detachment and at the same time emphasized that their relationship to visual acuity remains uncertain. We subsequently showed that many of the morphological changes demonstrated in animal models are seen in human proliferative vitreoretinopathy,3 although again the contribution of the observed immunohistological changes to the visual outcome in patients with proliferative vitreoretinopathy (PVR) is not yet established.
Benson SE, Grigoropoulos V, Schlottmann P, Bunce C, Charteris DG. Optical Coherence Tomography in Patients With Decreased Visual Acuity After Successful Surgery for Proliferative Vitreoretinopathy—Reply. Arch Ophthalmol. 2007;125(6):855-856. doi:10.1001/archopht.125.6.855-b