Epiretinal Macular Edema Associated With Thick Epiretinal Membranes

Doshi, Rishi R.; Lowrance, Matthew D.; Kim, Brian T.; Davis, Janet L.; Rosenfeld, Philip J.

doi:10.3928/23258160-20130909-19

Cited by 7 publications

(3 citation statements)

References 8 publications

(12 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some studies report that the presence of this ERP correlates with greater photoreceptor layer defects, greater LMH external diameters, a thinner floor and worse baseline visual acuity as compared to eyes without ERP [ 9 , 27 , 44 , 49 , 55 , 59 , 60 , 61 , 62 ]. Despite these different morphological characteristics, it appears that once the LMH forms with or without ERP, the LMH remains relatively stable.…”

Section: Epiretinal Proliferation (Erp)mentioning

confidence: 99%

Primary Lamellar Macular Holes: To Vit or Not to Vit

Bradshaw

2022

JCM

View full text Add to dashboard Cite

There is a wide spectrum of macular conditions that are characterized by an irregular foveal contour caused by a break in the inner fovea. These include full-thickness macular hole (FTMH), foveal pseudocyst, lamellar macular hole (LMH) and macular pseudohole (MPH). Clinical examination of vitreomacular interface disorders is notoriously poor in differentiating these conditions. These conditions were initially described with slit-lamp biomicroscopy, and the main goal was to distinguish an FTMH from the others. The introduction of optical coherence tomography (OCT) has revolutionized our understanding of the foveal microstructural anatomy and has facilitated differentiating these conditions from an FTMH. However, the definitions of the other conditions, particularly LMH, has evolved over the past two decades. Initially the term LMH encompassed a wide spectrum of clinical conditions. As OCT became more widely used and observations became more refined, two different phenotypes of LMH became apparent, raising the question of different pathogenic mechanisms for each phenotype. Tractional and degenerative pathological mechanisms were proposed. Epiretinal membranes (ERMs) associated with each phenotype were identified. Typical ERMs were associated with a tractional mechanism, whereas an epiretinal proliferation was associated with a degenerative mechanism. Epiretinal proliferation represents Müller cell proliferation as a reactive process to retinal injury. These two types of ERM were differentiated by their characteristics on SD-OCT. The latest consensus definitions take into account this phenotypic differentiation and classifies these entities into LMH, MPH and ERM foveoschisis. The initial event in both ERM foveoschisis and LMH is a tractional event that disrupts the Müller cell cone in the foveola or the foveal walls. Depending on the extent of Müller cell disruption, either a LMH or an ERM foveoschisis may develop. Although surgical intervention for LMH remains controversial and no clear guidelines exist for pars plana vitrectomy (PPV), eyes with symptomatic, progressive ERM foveoschisis and LMH may benefit from surgical intervention.

show abstract

Section: Epiretinal Proliferation (Erp)mentioning

confidence: 99%

Primary Lamellar Macular Holes: To Vit or Not to Vit

Bradshaw

2022

JCM

View full text Add to dashboard Cite

show abstract

“… 12 Another report by Doshi et al has described intra-LHEP edema but did not notice causative intraretinal vascular abnormalities in the simultaneous presence of the possible confounders age-related macular degeneration (AMD) and post-operative macular edema. 13 …”

Section: Introductionmentioning

confidence: 99%

“…However, reports on the connection of LHEP and retinal vascular dysfunction are scarce, with only one short report by Semoun et al, 2016 describing an intraretinal neovascular network presenting with LHEP, but without any exudation or communication between the two entities 12 . Another report by Doshi et al has described intra-LHEP edema but did not notice causative intraretinal vascular abnormalities in the simultaneous presence of the possible confounders age-related macular degeneration (AMD) and post-operative macular edema 13 …”

Section: Introductionmentioning

confidence: 99%

Lamellar hole-associated epiretinal proliferation presenting with perifoveal exudative vascular anomalous complex

Vounotrypidis

Vogt

Wolf

et al. 2019

American Journal of Ophthalmology Case Reports

View full text Add to dashboard Cite

Purpose Spectral-domain optical coherence tomography (SD-OCT) commonly reveals lamellar-hole-associated epiretinal proliferation (LHEP) as an avascular homogenous layer of premacular material with medium reflectivity, as recently described in various traction maculopathies, mostly in lamellar macular holes (LMH). We have used multimodal imaging to examine a patient suffering from unilateral advanced atrophic LMH presenting LHEP with perifoveal exudative vascular anomalous complex (PEVAC) and intra-LHEP edema fluctuating under anti-vascular endothelial growth factor ( anti -VEGF) therapy. Observation A 77- year-old male presented with decreased vision in the left eye attributable to longstanding LMH. He complained of worsening symptoms for six months. Whereas SD-OCT showed classic tractional epiretinal gliosis in the right eye, the left eye exhibited atrophic LMH and a significant amount of LHEP containing hyperreflective round lesions and hyporeflective cystoid spaces. Fluorescein/indocyanine green angiography demonstrated PEVAC with large anomalous vessels and exudation. OCT angiography revealed abnormal vessels originating from the deep retinal plexus. After anti-vascular endothelial growth factor ( anti -VEGF) therapy, the intraretinal edema seemed to decrease. Conclusions and importance Perifoveal exudative vascular anomalous complex can occur in eyes with advanced LMHs causing edema inside LHEP. Pathologic vessels appear to originate from the deep retinal plexus. Given that LHEP formation is proposed to be a glial-cell-driven process, Müller cells may play a decisive role in the pathogenesis of the presented vascular malformation. Because of spontaneous fluctuation of the associated edema, the role of anti -VEGF remains questionable, while a functional response to therapy might be limited according to the progressive atrophic lamellar defect with intraretinal tissue loss.

show abstract