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Epiretinal gliosis (makular pucker)

The frequency of idiopathic epiretinal membranes is strongly dependent on age and increases from 2% in the age of 50 to about 20% in the 70- to 80-year-olds.1,2

Various mechanisms can play a role in the development of epiretinal gliosis. If there are pre-existing conditions in which a hole has been found in the retina, this hole can lead to cells from the retinal pigment epithelium, which is located under the retina, into the eye's interior. These cells then settle on the retina and finally form an epiretinal gliosis. Typical for epiretinal gliosis is that it affects the central site of the retina.

Furthermore, inflammatory disorders of the eye, vascular occlusions or diabetes can trigger an epiretinal gliosis. Frequently, however, no pre-existing diseases are found, so that it is postulated that so-called glial cells emerge from the reticulum of the retina and form the epiretinal gliosis.

Through the supports on the central retina there is a visual impairment. The epiretinal gliosis can lead to a distortion of the underlying retina. This not only results in a loss of vision loss but also image distortions, which can be considerably disturbing. The disease does not lead to blindness. The central vision is affected, while peripheral vision remains intact.

The epiretinal gliosis is determined by an ophthalmological examination and can be well represented by means of device tests such as optical coherence tomography (OCT).

   

 


1. Pearlstone, A. D. The incidence of idiopathic preretinal macular gliosis. Ann Ophthalmol 17, 378-380 (1985).

2. Roth, A. M. & Foos, R. Y. Surface wrinkling retinopathy in eyes enucleated at autopsy. Trans Am Acad Ophthalmol Otolaryngol 75, 1047-1058 (1971).

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