This may occur because of the fact that PCCC and AV eliminate the vitreous and hyaloid face as a scaffold for the LECs' migration to the visual axis.

This hyaloid version of identity as decentered and destabilized is reflected in the postmodern writing by revealing the foundations and construction process of the identity.

(1,2,3) Mechanisms implicated in the pathogenesis of MH include abnormal interactions/adhesions between the posterior hyaloid membrane (i.e., the posterior cortical vitreous) and the macular surface (especially in the central fovea), as well as the forces exerted by anterior-posterior and tangential vitreous traction on the fovea.

Here the anterior hyaloid membrane can provide a foundation for ongrowth of lens epithelial cells.

Ocular defects were reported as retinal hemorrhage, abnormalities of the optic nerve, severe attenuation of normal retinal vasculature, anomalies of the optic nerve, and abnormal hyaloid artery development.

The premacular haemorrhage is anatomically located either under the internal limiting membrane (ILM) or under the posterior hyaloid or both [2].

If microphthalmia originates at the stage of the neural plate/optic sulcus, it is frequently associated with multiple ocular malformations (e.g., anterior segment dysgenesis, cataract, retinal dysplasia, and persistent hyaloid artery) [2].

Although SDOCT and OCT angiography (OCTA) can localize NV location relative to the posterior hyaloid and retinal surface, blood flow assessment in OCTA is currently limited to certain blood flow velocities [14, 39, 40].

After removing the detached vitreous gel and the posterior hyaloid membrane, removal of the ERM was performed using intraocular forceps.

[3-5] Nd:YAG laser posterior capsulotomy possibly combined with complications such as cystoid macular edema, transient rise in intraocular pressure (IOP), endophthalmitis, anterior hyaloid disruption, and lens pitting.