Atlas of Ophthalmology

Selfrepair of Epiretinal Membrane over 4 Years (SD-OCT)

Retina -> Aquired Macular Diseases
Patient: 55 years of age, female, BCVA 1,0 at OD, 0.8 at OS; IOP 15/16 mmHg General Medical History: -. Ocular Medical History: spontaneous dissolution of epiretinal gliosis at OS, BCVA was in 08/2012 0.7, then always 0.8 and better. Purpose: to show selfrepair of epiretinal gliosis over 4 years. Methods: SD-OCT (Heidelberg Engineering) from 02/2012 to 11/2016. Findings: SD-OCT in 02/2012: loss of the foveal depression, highly reflective epiretinal membrane, intact outer retinal layers, no significant foveal thickening, no intraretinal cysts, no vitreomacular adhesion. SD-OCT in 08/2012: loss of the foveal depression, regression of epiretinal membrane, intact outer retinal layers, significant foveal thickening, no intraretinal cysts, no vitreomacular adhesion. SD-OCT in 11/2012: normalization of the foveal depression, regression of epiretinal membrane, intact outer retinal layers, no foveal thickening, no intraretinal cysts, no vitreomacular adhesion. SD-OCT in 08/2013: normalization of the foveal depression, dissolution of epiretinal membrane, intact outer retinal layers, no foveal thickening, no intraretinal cysts, no vitreomacular adhesion. SD-OCT in 12/2013: regular foveal depression, dissolution of epiretinal membrane, intact outer retinal layers, no foveal thickening, no intraretinal cysts, no vitreomacular adhesion. SD-OCT in 06/2015: regular foveal depression, dissolution of epiretinal membrane, intact outer retinal layers, no foveal thickening, no intraretinal cysts, no vitreomacular adhesion. SD-OCT in 04/2016: regular foveal depression, mainly complete dissolution of epiretinal membrane, intact outer retinal layers, no foveal thickening, no intraretinal cysts, no vitreomacular adhesion. SD-OCT in 11/2016: regular foveal depression, mainly complete dissolution of epiretinal membrane, intact outer retinal layers, no foveal thickening, no intraretinal cysts, no vitreomacular adhesion. SD-OCT in 02/2012, 08/012, and 11/2016: dissolution of epiretinal membrane. Discussion: Almeida DR et al. (1) studied spontaneous release of vitreomacular traction in 61 patients. In 35% of 61 patients developed a spontaneous release of vitreomacular traction. Isolated inner retinal distortion without outer retinal involvement was significantly associated with a spontaneous release of vitreomacular traction. CD45-positive cells were seen in epiretinal cell proliferation of eyes with macular pucker. These cells were suggested to be hyalocytes derived from the hematopoetic monocyte/macrophage lineage. Schumann RG et al. (2) performed an electron microscopic study and suggested a significant role of hyalocytes in epiretinal membrane formation. Müller cells as principle glial cells in the neural retina are responsible for scar formation and epiretinal gliosis. Activation of Müller cells including increased expression of glial fibrillary acid protein (GFAP) is a key response feature of age-related pathologies. GFAP is a protein biomarker activated by Müller cells and contributes to neuroregeneration including protease activation. In a study Jünemann AG et al. (3) found increased levels of glial fibrillary acidic protein (GFAP) in the vitreous body of patients with epiretinal glioses and proposed that glial fibrillary acidic protein (GFAP) in the vitreous body is a protein biomarker for glial response to retinal disorders. Literature: (1 Almeida DR, Chin EK, Rahim K, Folk JC, Russell SR. Factors associated with spontaneous release of vitreomacular traction. ) Retina. 2015 Mar;35(3):492-7. (2) Schumann RG, Gandorfer A, Ziada J, Scheler R, Schaumberger MM, Wolf A, Kampik A, Haritoglou C. Hyalocytes in idiopathic epiretinal membranes: a correlative light and electron microscopic study. ) Graefes Arch Clin Exp Ophthalmol. 2014 Dec;252(12):1887-94. (3) Jünemann AG, Rejdak R, Huchzermeyer C, Maciejewski R, Grieb P, Kruse FE, Zrenner E, Rejdak K, Petzold A. Elevated vitreous body glial fibrillary acidic protein in retinal diseases. Graefes Arch Clin Exp Ophthalmol. 2015 Dec;253(12):2181-6. (4) Hassenstein A, Scholz F, Richard G. OCT in epiretinal gliosis. Ophthalmologe. 2005 Feb;102(2):127-32.

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