Abstract

PurposeTo study the topographical relationship between acute macular neuroretinopathy (AMN) lesions and the choroidal watershed zone (CWZ) or patchy choroidal filling (PCF) using multimodal imaging.MethodsLesions in patients diagnosed with AMN were clinically examined using multimodal imaging, including fundus photography, near-infrared reflectance imaging, spectral-domain optical coherence tomography (OCT), fluorescein angiography, indocyanine green angiography, OCT angiography, and microperimetry. The topographical relationship between AMN and the CWZ or PCF was evaluated.ResultsSeven eyes of six patients were included in the study. The mean age of the patients was 35.8 ± 11.7 years. The AMN lesions were collocated with the CWZ in five eyes and the PCF in one eye. Among these eyes, three had complete patterns, and three had partial patterns. Only one eye showed no topographical relationship between AMN and the CWZ or PCF.ConclusionThe colocation of AMN and CWZ/PCF suggests that the AMN lesions were within an area with a dual-watershed zone: the watershed zone between the retinal deep capillary plexus and choriocapillaris, and the choroidal watershed zone or patchy choroidal filling. This retinal area was highly vulnerable to hypoperfusion. Our results suggest a novel pathophysiological mechanism for AMN.

Highlights

  • In 1975, Bos and Deutman [1] first described four cases of paracentral scotomas and dark-reddish lesions pointing to the fovea; they named this disorder “acute macular neuroretinopathy (AMN).” With the introduction of optical coherence tomography (OCT), reports of AMN have increased within the last decade [2]

  • The colocation of AMN lesions and CWS/patchy choroidal filling (PCF) was detected in six eyes (85.7%); three had complete patterns, and three had partial patterns

  • Some authors have questioned whether the flow void signal within the CC observed on OCT angiography (OCT-A) is due to an artifact caused by a flow signal blockage from the hyper-reflectance of the overlying outer retina [11], and other OCT-A studies have shown that AMN lesions were associated with a reduced signal in the deep capillary plexus (DCP) only [12] or both the DCP and CC [13]

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Summary

Introduction

In 1975, Bos and Deutman [1] first described four cases of paracentral scotomas and dark-reddish lesions pointing to the fovea; they named this disorder “acute macular neuroretinopathy (AMN).” With the introduction of optical coherence tomography (OCT), reports of AMN have increased within the last decade [2]. With the introduction of optical coherence tomography (OCT), reports of AMN have increased within the last decade [2]. AMN is localized at the outer nuclear layer (ONL) and the outer plexiform layer (OPL) on OCT [3], but its underlying pathology is not completely understood. A vascular ischemic etiology has been proposed [3]. The OPL and ONL are within the functional watershed zone between two sources of blood supply to the retina and choroid, and retinal ischemia or choroidal ischemia have been hypothesized as specific etiologies. Each hypothesis on its own cannot fully explain the clinical findings of AMN, and the original location of the vascular impairment of AMN is still debated

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