Aging of the vitreous body is characterized by fibrous degeneration with gel liquefaction.
4,5 Fibrous vitreous liquefaction results from molecular changes causing dissociation of collagen from hyaluronan, forming liquid vitreous (water molecules bound to hyaluronan) and cross-linking of collagen into visible fibers.
6,7 In the presence of myopia, these changes appear earlier in life, and in direct proportion to the degree of axial myopia.
8,9 Consequently, vitreous structure becomes more heterogeneous with the formation of liquefied pockets called lacunae and aggregation of collagen fibrils into larger fibers that present clinically as opacities, which cause the disturbing visual phenomenon of “floaters.”
4,10 Fibrous vitreous liquefaction not only introduces structural heterogeneity, but also promotes posterior vitreous detachment (PVD), a common cause of increased intra-ocular light scattering
11 and floaters, at times with degradation of contrast sensitivity function.
11–13 At this point, the condition attains clinical significance and is called “vision degrading myodesopsia.”
14 Apart from age, other factors contributing to fibrous vitreous liquefaction/degeneration include diabetic vitreopathy,
15 inflammation,
16 and myopic vitreopathy,
9 the latter associated with increased incidence of PVD. Persistent vitreo-retinal adhesion can induce anomalous PVD resulting in vitreo-macular traction syndrome, retinal tears, and detachment,
7 at times splitting of the posterior vitreous cortex (vitreoschisis),
17 contributing to premacular membranes with macular pucker and macular hole formation.
5,14,18 Anterior vitreous opacification can also occur, particularly after surgical interventions of the posterior lens.
19–21 What is not known, however, is whether anterior vitreous changes are associated with central/posterior fibrous liquefaction/degeneration and vision degrading myodesopsia.