Retinal structural and vascular features of glaucoma

Glaucoma refers to a group of optic neuropathies characterised by the degeneration of retinal ganglion cells, which if untreated, lead to vision loss. Despite the vast prevalence of glaucoma worldwide, its aetiology is complex and still being established.  

Lowering intraocular pressure is the only known mechanism of treatment intervention to date. However, elevated intraocular pressure is not essential for a glaucoma diagnosis. Glaucoma risk is also affected by older age, family history of glaucoma, ocular factors such as optic disc haemorrhage, thin central cornea and high myopia; and systemic factors such as hypertension.

Vascular insufficiency has been proposed to be a contributing factor to the pathophysiology of glaucoma with reduced retinal blood flow and disrupted retinal microvasculature reported. However, the question remains whether microvasculature perfusion disruption is an early feature in glaucoma or whether it is a consequence of reduced demand due to degeneration of retinal ganglion cells.

In this thesis, vascular features are investigated in the early stages of glaucoma. Vessel density is shown to be reduced, foveal avascular zone area and perimeter are enlarged, foveal circularity is reduced, and wedge-shaped focal vascular defects are identified. Vascular wedge defects are found to be associated with faster global RNFL progression. Vascular wedge defects are compared to localised RNFL defects, and both are shown to be associated with higher genetic risk of glaucoma as determined by a polygenic risk score. These findings provide supporting evidence for vascular involvement in the pathophysiology of glaucoma.