Anna C S Tan1, Polina Astroz2, Kunal K Dansingani3, Jason S Slakter4, Lawrence A Yannuzzi5, Christine A Curcio6, K Bailey Freund7. 1. Vitreous Retina Macula Consultants of New York, New York, New York, United States 2The LuEsther T. Mertz Retinal Research Center, New York, New York, United States 3Singapore National Eye Center/Singapore Eye Research Institute/Duke-NUS Medical School, Singapore, Singapore. 2. Vitreous Retina Macula Consultants of New York, New York, New York, United States 4Department of Ophthalmology, Intercity Hospital and University Paris Est, Creteil, France. 3. Vitreous Retina Macula Consultants of New York, New York, New York, United States 2The LuEsther T. Mertz Retinal Research Center, New York, New York, United States 5Truhlsen Eye Institute, University of Nebraska Medical Center, Omaha, Nebraska, United States. 4. Vitreous Retina Macula Consultants of New York, New York, New York, United States. 5. Vitreous Retina Macula Consultants of New York, New York, New York, United States 2The LuEsther T. Mertz Retinal Research Center, New York, New York, United States. 6. Department of Ophthalmology, University of Alabama School of Medicine, Birmingham, Alabama, United States. 7. Vitreous Retina Macula Consultants of New York, New York, New York, United States 2The LuEsther T. Mertz Retinal Research Center, New York, New York, United States 7Department of Ophthalmology, New York University School of Medicine, New York, New York, United States.
Abstract
Purpose: Histologic details of progression routes to geographic atrophy (GA) in AMD are becoming available through optical coherence tomography (OCT). We studied the origins and evolution of an OCT signature called plateau in eyes with GA and suggested a histologic correlate. Methods: Serial eye-tracked OCT scans and multimodal imaging were acquired from eight eyes of seven patients with GA and plateau signatures over a mean follow-up of 7.7 years (range, 3.7-11.6). The histology of unrelated donor eyes with AMD was reviewed. Results: Drusenoid pigment epithelial detachment (PED) on OCT imaging progressed into wide-based mound-like signatures with flattened apices characterized by a hyporeflective yet heterogeneous interior and an overlying hyperreflective exterior, similar to outer retinal corrugations previously ascribed to persistent basal laminar deposit (BLamD) but larger. These new signatures are described as "plateaus." An initial increase of the PED volume and hyporeflectivity of its contents was followed by a decrease in PED volume and thinning of an overlying hyperreflective band attributable to the loss of the overlying RPE leaving persistent BLamD. Both imaging and histology revealed persistent BLamD with defects through which gliotic Müller cell processes pass. Conclusions: Plateaus can be traced back to drusenoid PEDs on OCT imaging. We hypothesize that during progressive RPE atrophy, Müller cell extension through focal defects in the residual persistent BLamD may contribute to the heterogeneous internal reflectivity of these entities. The role of Müller cell activation and extension in the pathogenesis of AMD should be explored in future studies.
Purpose: Histologic details of progression routes to geographic atrophy (GA) in AMD are becoming available through optical coherence tomography (OCT). We studied the origins and evolution of an OCT signature called plateau in eyes with GA and suggested a histologic correlate. Methods: Serial eye-tracked OCT scans and multimodal imaging were acquired from eight eyes of seven patients with GA and plateau signatures over a mean follow-up of 7.7 years (range, 3.7-11.6). The histology of unrelated donor eyes with AMD was reviewed. Results:Drusenoid pigment epithelial detachment (PED) on OCT imaging progressed into wide-based mound-like signatures with flattened apices characterized by a hyporeflective yet heterogeneous interior and an overlying hyperreflective exterior, similar to outer retinal corrugations previously ascribed to persistent basal laminar deposit (BLamD) but larger. These new signatures are described as "plateaus." An initial increase of the PED volume and hyporeflectivity of its contents was followed by a decrease in PED volume and thinning of an overlying hyperreflective band attributable to the loss of the overlying RPE leaving persistent BLamD. Both imaging and histology revealed persistent BLamD with defects through which gliotic Müller cell processes pass. Conclusions: Plateaus can be traced back to drusenoid PEDs on OCT imaging. We hypothesize that during progressive RPE atrophy, Müller cell extension through focal defects in the residual persistent BLamD may contribute to the heterogeneous internal reflectivity of these entities. The role of Müller cell activation and extension in the pathogenesis of AMD should be explored in future studies.
Authors: Chandrakumar Balaratnasingam; Jeffrey D Messinger; Kenneth R Sloan; Lawrence A Yannuzzi; K Bailey Freund; Christine A Curcio Journal: Ophthalmology Date: 2017-01-30 Impact factor: 12.079
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Authors: Miaoling Li; Rosa Dolz-Marco; Carrie Huisingh; Jeffrey D Messinger; Richard M Feist; Daniela Ferrara; K Bailey Freund; Christine A Curcio Journal: Retina Date: 2019-04 Impact factor: 4.256