Description

The vitreous body fills the posterior chamber of the eye and consists mainly of water. It is kept organized into a gel like structure by numerous collagen fibrils and makes contact with the surrounding retina. This interplay known as the vitreo-retinal interface of the human eye is a complex organization of bridging molecules anchoring the vitreous to the internal limiting membrane. With ageing, the vitreous gel undergoes liquefaction accompanied by progressive weakening of the adhesions at the vitreo-retinal interface resulting in a stepwise process of adhesion release. Since the most firm attachments in the posterior pole are situated at the macular and papillary region, tractional forces exerted during vitreous separation could influence retinal functioning.

Up until now researchers have been looking primarily at the influence of vitreous traction to the macular region of the nerve fiber layer.This research has led to the insight that vitreo-macular traction can result in macular hole formation, and that patients with this condition may benefit from vitreolysis induced by surgery (vitrectomy) or intravitreal injection of ocriplasmin.

More recent reports have focused on the influence of the vitreous on the morphology of the optic disc, showing that VPT altered optic disc architecture, increased average and temporal retinal nerve fiber layer thickness and was associated with more pronounced visual field defects. This could be important as very sensitive scans and diagnostic algorithms were developed for staging and follow up of glaucoma patients' optic nerve head, which could be influenced by the patients' vitreopapillar interface. As the status of this interface changes over time, this could lead to confusion and misinterpretation of the optic disc diagnostic scans.

Besides the diagnostic challenges induced by the vitreopapillar interaction, this interface may also be of pathogenetic relevance in glaucoma. Indeed, the optic disc represents the collection of all ganglion cell axons, and glaucoma is caused by a degeneration of ganglion cells. Some authors have already suggested that vitreopapillary traction (VPT) could play a role in the pathogenesis of optic nerve head hemorrhages, which are regarded as an important risk factor for glaucoma progression. Moreover, one could hypothesize that VPT can cause stress to the ganglion cell axons and therefore contribute more directly to ganglion cell degeneration.

Accordingly, this study aims at investigating the effect of VPT on the ultra-structural level of the optic disc. A possible structure-function relation will be investigated with the help of central visual field tests and focal retinal nerve fiber layer thickness assessment. With increasing knowledge and imaging of VPT, possibly a VPT-staging algorithm can be developed and VPT risk factors defined. Finally, this project may have a therapeutic impact, since it will shed light on the question whether (surgically or chemically) induced vitreolysis might be beneficial in some glaucoma patients with VPT.