Spontaneous closure of small full-thickness macular holes: Presumed role of Müller cells.

Abstract

To document with spectral domain optical coherence tomography the formation and spontaneous closure of small full-thickness macular holes and to propose the active role of Müller cells in macular hole closure. A retrospective case series of five patients with spontaneous closure of macular holes is reviewed. In one patient, foveal images were recorded over a period of 18months. In a 66-year-old man, vitreofoveal traction caused a detachment of the inner Müller cell layer of the foveola from the outer nuclear layer (ONL) which was associated with a large pseudocyst and a horizontal gap in the central ONL. The traction caused an elongation and subsequent disruption of the stalk of the Müller cell cone in the foveola. A small full-thickness macular hole developed when a portion of the inner Müller cell layer of the foveola was pulled out. After phacoemulsification and shortly before the subsequent spontaneous closure of the hole, there were rapid increases in the number and size of the cystic cavities in the foveal walls resulting in a narrowing of the hole. The hole closed by bridging the gap in the inner part of the central ONL; a new inner Müller cell layer of the foveola was formed, and the gap of the external limiting membrane (ELM) was closed. The cystic cavities in the foveal walls rapidly disappeared within 2weeks after the closure of the hole. One to 2.5months after hole closure, the thickness of the central ONL increased which decreased the distance between the central ELM and retinal pigment epithelium. In three of the four other patients, the hole also closed by bridging the gap in the inner part of the ONL. It is suggested that the spontaneous closure of small macular holes and the subsequent reconstruction of the normal foveal structure are mediated by active mechanisms of Müller cells which resemble those involved in ontogenetic foveal development.