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Fig. 8 | International Journal of Retina and Vitreous

Fig. 8

From: Morphology of partial-thickness macular defects: presumed roles of Müller cells and tissue layer interfaces of low mechanical stability

Fig. 8

Hypothetical mechanisms of the development of partial- and full-thickness macular defects. a Schematic section through a fovea. The Müller cell cone in the foveola is shown in pink. The tissue layer interfaces of low mechanical stability are indicated by red lines: the boundary between the Müller cell cone and the Henle fiber layer (HFL)/outer nuclear layer (ONL) in the foveola, and the interface between the outer plexiform layer (OPL) and HFL in the foveal walls and parafovea. In addition, the vertical stalk of the Müller cell cone in the center of the foveola has a low mechanical stability. b The horizontal layer of the Müller cell cone keeps the inner layers of the foveal walls (nerve fiber layer [NFL] to OPL) together. Normally, the stalk of the Müller cell cone prevents the elevation of the inner layers of the foveal walls. When anteroposterior or tangential tractions exerted by the posterior hyaloid or epiretinal membranes (ERM) disrupt the stalk, foveal pseudocysts associated with an elevation of the inner layers of the foveal walls may develop. The elevation of the inner layers of the foveal walls disrupts the tissue between the OPL and HFL resulting in the formation of schistic cavities which are obliquely traversed by Henle fiber bundles. c, d Anteroposterior or tangential traction may cause a disruption of the connection between the Müller cell cone and the foveal walls, resulting in an elevation of the inner layers of the walls. This may produce a schisis between the OPL and HFL in the foveal walls (c) which may develop to degenerative cavitations of the foveal pit into the lower foveal walls (d). Bundles of Henle fibers composed of photoreceptor axons and the outer processes of Müller cells of the foveal walls keep the schistic cavities together (c). The degenerative cavitations may be enlarged by a degeneration of Henle fibers (d). The formation of a degenerative lamellar hole is often associated with a disruption of the fovea externa (d). Macular pigment-containing cells of the Müller cell cone may contribute to the development of the lamellar hole-associated epiretinal proliferation (LHEP), likely by the formation of a tissue bridge between the foveola and the inner surface of the foveal walls (d). e Anteroposterior traction may cause the formation of an outer lamellar hole characterized by a large pseudocyst in the foveola, schistic splitting of the foveal walls between the OPL and HFL, cystic cavities in the inner nuclear layer (INL), and a gap in the whole central outer retina including the ELM. A disruption of the Müller cell cone produces a full-thickness macular hole (FTMH) from an outer lamellar hole. f Fluid accumulation in the foveal walls may produce edematous cysts between the OPL and HFL, and in the INL. Enlargement of the cysts causes a large elevation of the inner layers of the walls; the Müller cells are obliquely stretched and straightened, and transmit the tension to the outer retina. This produces a detachment and a centrifugal displacement of the central ONL and photoreceptors resulting in an enlargement of the FTMH. g Schematic summary of pathogenic steps which mediate the development of partial-thickness macular defects and FTMH. h Pathogenic events which may be implicated in the development of degenerative cavitations of the foveal pit into the lower foveal walls. EZ: ellipsoid zone; GCL: ganglion cell layer; IPL: inner plexiform layer; IZ: interdigitation zone; NFL: nerve fiber layer; PVD: posterior vitreous detachment; RPE: retinal pigment epithelium; VMA: vitreomacular adhesion; VMT: vitreomacular traction

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