Abstract
PurposeThe development of degenerative lamellar macular holes (DLH) is largely unclear. This study was aimed at documenting with spectral-domain optical coherence tomography the tractional development and morphological alterations of DLH.MethodsA retrospective case series of 44 eyes of 44 patients is described.ResultsThe development of DLH is preceded for months or years by tractional deformations of the fovea due to the action of contractile epiretinal membranes (ERM) and/or the partially detached posterior hyaloid, or by cystoid macular edema (CME). DLH may develop after a tractional stretching and thickening of the foveal center, from a foveal pseudocyst, after a detachment of the foveola from the retinal pigment epithelium, a disruption of the foveal structure due to CME, and after surgical treatment of tractional lamellar or full-thickness macular holes (FTMH). The foveal configuration of a DLH can be spontaneously reestablished after short transient episodes of CME and a small FTMH. A DLH can evolve to a FTMH by traction of an ERM. Surgical treatment of a DLH may result in an irregular regeneration of the foveal center without photoreceptors.ConclusionsTractional forces play an important role in the development of DLH and in the further evolution to FTMH. It is suggested that a DLH is the result of a retinal wound repair process after a tractional disruption of the Müller cell cone and a degeneration of Henle fibers, to prevent a further increase in the degenerative cavitations.
Highlights
Various macular diseases are associated with anteroposterior or tangential traction exerted by the partially detached posterior hyaloid and/or contractile epiretinal membranes (ERM)
The common feature of most types of partial-thickness macular defects is a disruption of the Muller cell cone or of the connection between the cone and the foveal walls which results in a deformation of the foveal pit; the central outer nuclear layer (ONL) and the external limiting membrane (ELM) are not disrupted and keep the foveal walls together preventing the formation of a full-thickness macular holes (FTMH) [5]
Tractional forces of an ERM on top of the NFL of this wall caused a deformation of the foveal pit, likely due to a disruption of the connection between the inner Muller cell layer of the foveola to this wall; this resulted in an indentation between the outer plexiform layer (OPL) and Henle fiber layer (HFL)
Summary
Various macular diseases are associated with anteroposterior or tangential traction exerted by the partially detached posterior hyaloid and/or contractile epiretinal membranes (ERM). Full-thickness macular holes (FTMH) develop by a disruption of both the Muller cell cone [1,2,3,4] and the external limiting membrane (ELM) in the foveola. The common feature of most types of partial-thickness macular defects is a disruption of the Muller cell cone or of the connection between the cone and the foveal walls which results in a deformation of the foveal pit; the (outer part of the) central outer nuclear layer (ONL) and the ELM are not disrupted and keep the foveal walls together preventing the formation of a FTMH [5]. A special type of partial-thickness macular defects, the outer layers of the foveola including the ELM are disrupted and the nondisrupted horizontal layer of the Muller cell cone keeps the foveal walls together [6]. The main characteristic of DLH is the development of degenerative cavitations into the lower foveal walls [8,9,10,11,12]; this proceeds by a slow and chronic degeneration of the HFL, OPL, and inner nuclear layer (INL) of the
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