Bringmann Andreas, Duncker Tobias, Jochmann Claudia, Barth Thomas, Duncker Gernot I W, Wiedemann Peter
Department of Ophthalmology and Eye Hospital, University of Leipzig, Leipzig, Germany.
Institute of Ophthalmology, Halle, Germany.
Acta Ophthalmol. 2020 Jun;98(4):e447-e456. doi: 10.1111/aos.14289. Epub 2019 Oct 26.
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 18 months.
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 2 weeks after the closure of the hole. One to 2.5 months 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.
利用频域光学相干断层扫描记录小的全层黄斑裂孔的形成及自发闭合情况，并提出米勒细胞在黄斑裂孔闭合中的积极作用。
回顾性分析5例黄斑裂孔自发闭合患者的病例系列。其中1例患者在18个月内记录了中央凹图像。
在1例66岁男性患者中，玻璃体黄斑牵拉导致中央凹内米勒细胞层与外核层分离，伴有一个大的假性囊肿和中央外核层的水平间隙。牵拉导致中央凹内米勒细胞锥体的柄伸长并随后中断。当中央凹内米勒细胞层的一部分被拉出时，形成了一个小的全层黄斑裂孔。白内障超声乳化术后，在裂孔随后自发闭合前不久，中央凹壁上的囊腔数量和大小迅速增加，导致裂孔变窄。裂孔通过桥接中央外核层内部的间隙而闭合；形成了新的中央凹内米勒细胞层，外部限制膜的间隙也闭合了。裂孔闭合后2周内，中央凹壁上的囊腔迅速消失。裂孔闭合后1至2.5个月，中央外核层厚度增加，减少了中央外部限制膜与视网膜色素上皮之间的距离。在其他4例患者中的3例，裂孔也通过桥接外核层内部的间隙而闭合。
提示小黄斑裂孔的自发闭合及随后正常中央凹结构的重建是由米勒细胞的主动机制介导的，这些机制类似于胚胎期中央凹发育过程中涉及的机制。
