Didier Ducournau, Yvette Ducournau


To compare the gliosis degree of macular astrocytes and Müller cells in different pathological circumstances with and without cystoid macular edema (CME), in order to understand the neuro-pathological reactional mechanisms and thus explain therapeutical results.


Seven globes -3 with CME and 4 without – enucleated for melanoma or endophthalmitis and presenting vascular pathology and/or retinal detachment (RD) have been investigated in histology and immunohistochemistry with GFAP in order to study astrocytous and Müller cells glia.


There are selective modalities for the expression in GFAP according to the glial cell type and to the nature of pathological process: In 2 cases of isolated ischemia we noticed the presence of a CME predominant in external layers, and of a hypertrophic and hyperplastic astrocytous gliosis at the internal and perivascular layers level, without any Müller cell gliosis. In 2 cases of isolated RD, the Müller cells presented a massive radial gliosis from the internal limiting membrane to the external limiting membrane, without any astrocytous cell gliosis or CME. In 3 cases in which both pathologies were associated, both forms of gliosis were observed without any extensive CME.


Both astrocytous cell gliosis and Müller cell gliosis very likely aim at restoring the bloodretinal barrier and at limiting neuronal apoptosis phenomenon. Müller cell radial gliosis could add a determining and protecting mechanical role on edema. Those results incite to favour therapeutical ways stimulating Müller cell radial gliosis such as the ILM removal or new lasers.

Take Home Message:

Inducing a Müller cell gliosis could prevent from edema development.