Bringmann Andreas, Unterlauft Jan Darius, Wiedemann Renate, Rehak Matus, Wiedemann Peter
Department of Ophthalmology and Eye Hospital, University of Leipzig, Liebigstrasse 10-14, 04103 Leipzig, Germany.
Int J Retina Vitreous. 2020 Jul 6;6:28. doi: 10.1186/s40942-020-00232-1. eCollection 2020.
The pathogenesis of partial-thickness macular defects and the role of Müller glial cells in the development of such defects are not well understood. We document the morphological characteristics of various types of partial-thickness macular defects using spectral-domain optical coherence tomography, with the focus on tractional and degenerative lamellar holes, and discuss possible pathogenic mechanisms.
A retrospective case series of 61 eyes of 61 patients with different types of partial-thickness macular defects is described.
Partial-thickness macular defects are caused by anteroposterior or tangential traction onto the fovea exerted by the partially detached posterior hyaloid and epiretinal membranes, respectively. Tractional elevation of the inner Müller cell layer of the foveola-without (outer lamellar holes, foveal pseudocysts) or with a disruption of this layer (tractional lamellar holes, macular pseudoholes)-produces an elevation of the inner layers of the foveal walls (nerve fiber layer to outer plexiform layer [OPL]) and a schisis between the OPL and Henle fiber layer (HFL). With the exception of outer lamellar holes, the (outer part of the) central outer nuclear layer and the external limiting membrane remain nondisrupted in the various types of partial-thickness defects. Degenerative lamellar holes are characterized by cavitations between the inner plexiform layer and HFL of the foveal walls; many cases have lamellar hole-associated epiretinal proliferation (LHEP). Proliferating cells of the disrupted Müller cell cone may contribute to the development of LHEP and fill the spaces left by degenerated photoreceptors in the foveal center.
It is suggested that morphological characteristics of partial-thickness macular defects can be explained by the disruption of the (stalk of the) Müller cell cone in the foveola and the location of tissue layer interfaces with low mechanical stability: the boundary with no cellular connections between both Müller cell populations in the foveola, and the interface between the OPL and HFL in the foveal walls and parafovea. We propose that the development of the cavitations in degenerative lamellar holes is initiated by traction which produces a schisis between the OPL and HFL, and enlarged by a slow and chronic degeneration of Henle fibers and bipolar cells. retrospectively registered, #143/20-ek, 04/03/2020.
黄斑部分厚度缺损的发病机制以及 Müller 胶质细胞在此类缺损发展过程中的作用尚未完全明确。我们利用频域光学相干断层扫描记录了各种类型黄斑部分厚度缺损的形态学特征，重点关注牵拉性和退行性板层裂孔，并探讨了可能的致病机制。
描述了 61 例不同类型黄斑部分厚度缺损患者的 61 只眼的回顾性病例系列。
黄斑部分厚度缺损分别由部分脱离的后玻璃体和视网膜前膜向黄斑中心凹施加的前后向或切向牵拉所致。黄斑小凹内 Müller 细胞内层的牵拉性抬高——无此层破坏（外层板层裂孔、黄斑假性囊肿）或有此层破坏（牵拉性板层裂孔、黄斑假性裂孔）——导致黄斑壁内层（神经纤维层至外丛状层 [OPL]）抬高以及 OPL 和 Henle 纤维层（HFL）之间的劈裂。除外层板层裂孔外，在各种类型的黄斑部分厚度缺损中，中央外核层（及其外部）和外界膜保持完整。退行性板层裂孔的特征是黄斑壁内丛状层和 HFL 之间有空洞形成；许多病例伴有板层裂孔相关的视网膜前增殖（LHEP）。受损 Müller 细胞锥的增殖细胞可能促成 LHEP 的发展，并填充黄斑中心凹处变性光感受器留下的空间。
提示黄斑部分厚度缺损的形态学特征可通过黄斑小凹内 Müller 细胞锥（的柄）的破坏以及机械稳定性较低的组织层界面位置来解释：黄斑小凹内两个 Müller 细胞群体之间无细胞连接的边界，以及黄斑壁和黄斑旁区域 OPL 和 HFL之间的界面。我们提出，退行性板层裂孔中空洞的形成始于牵拉，牵拉导致 OPL 和 HFL 之间出现劈裂，并因 Henle 纤维和双极细胞的缓慢慢性变性而扩大。回顾性注册，#143/20 - ek，2020 年 3 月 4 日。
