Tan Anna C S, Astroz Polina, Dansingani Kunal K, Slakter Jason S, Yannuzzi Lawrence A, Curcio Christine A, Freund K Bailey
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.
Vitreous Retina Macula Consultants of New York, New York, New York, United States 4Department of Ophthalmology, Intercity Hospital and University Paris Est, Creteil, France.
Invest Ophthalmol Vis Sci. 2017 Apr 1;58(4):2349-2358. doi: 10.1167/iovs.16-21237.
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.
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.
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.
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.
通过光学相干断层扫描(OCT),年龄相关性黄斑变性(AMD)向地图样萎缩(GA)进展途径的组织学细节正逐渐明晰。我们研究了GA眼中一种名为“高原”的OCT特征的起源和演变,并提出了其组织学关联。
对7例患有GA且具有高原特征的患者的8只眼进行了连续的眼跟踪OCT扫描和多模态成像,平均随访7.7年(范围3.7 - 11.6年)。回顾了患有AMD的无关供体眼的组织学情况。
OCT成像上的类玻璃膜疣色素上皮脱离(PED)进展为宽基底丘状特征,顶端扁平,内部低反射但不均匀,外部高反射,类似于先前归因于持续性基底膜沉积物(BLamD)但更大的外层视网膜波纹。这些新特征被描述为“高原”。PED体积及其内容物的低反射性最初增加,随后PED体积减小,归因于上层视网膜色素上皮(RPE)丢失而留下持续性BLamD的上层高反射带变薄。成像和组织学均显示存在带有胶质状Müller细胞突起穿过的缺陷的持续性BLamD。
在OCT成像上,高原特征可追溯到类玻璃膜疣PED。我们推测,在进行性RPE萎缩过程中,Müller细胞通过残余持续性BLamD中的局灶性缺陷延伸,可能导致这些病变内部反射率不均匀。未来研究应探索Müller细胞激活和延伸在AMD发病机制中的作用。